Mr. S, 64, has a history of posttraumatic stress disorder (PTSD), which has been well controlled for the past 15 years with cognitive-processing therapy and fluoxetine, 40 mg/d. However, over the past 6 weeks, Mr. S has experienced increased hypervigilance, nightmares, and flashbacks. He states that his primary care provider recommended an adjustment in pharmacotherapy to address this exacerbation of symptoms. Previous medication trials include sertraline, 200 mg/d, discontinued due to lack of perceived efficacy, and venlafaxine, 150 mg/d, discontinued due to increased blood pressure.

Mr. S’s medical history includes hypertension, dyslipidemia, and myocardial infarction (MI) 5 years ago. His family history includes sudden cardiac death (mother and father) and major depressive disorder (sister). His blood pressure is currently uncontrolled on lisinopril, 5 mg/d, and metoprolol succinate, 50 mg/d. Today, serial blood pressure readings measured approximately 180/90 mm Hg, with a pulse 50-60 beats per minute.

What is the next step in treating Mr. S’s hypertension and PTSD symptoms? Is there any evidence to support concomitant therapy?

PTSD is characterized by emotional and behavioral symptoms following exposure to a traumatic event. Its 12-month prevalence in the United States is estimated at 3.5%. Diagnostic criteria necessitate the presence of intrusive symptoms, persistent effortful avoidance of distressing trauma-related stimuli, negative cognitions or mood, and alterations in arousal and reactivity. PTSD negatively impacts social and occupational functioning.¹

ACEIs, ARBs, beta blockers, and calcium channel blockers

Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) inhibit the renin-angiotensin system: ACEIs prevent formation of angiotensin II, a potent vasoconstrictor, and ARBs prevent interaction between angiotensin II and its receptor. In one study, patients were recruited from a large public hospital serving primarily a highly traumatized, low-income population. Patients taking an ACEI or ARB who had experienced at least 1 traumatic event exhibited significantly decreased hyperarousal symptoms and decreased intrusive thoughts on the PTSD Symptom Scale and Clinician Administered PTSD Scale.⁵ Other studies have reported that blockade of angiotensin II AT1 receptors may result in decreased stress, anxiety, and inflammation.¹⁵

Evidence supports the use of the centrally acting, beta-adrenergic antagonist propranolol for decreasing the physiologic reactivity to acute trauma. Emotional arousal enhances the consolidation of emotional experiences into long-term memories via the adrenal stress hormones epinephrine and corticosterone. The amygdala mediates these stress hormones and releases norepinephrine, which subsequently activates noradrenergic receptors essential for memory enhancement. Several studies have reported that patients who received propranolol within several hours of a traumatic event experienced fewer physiologic signs of PTSD at follow-up 1 month later.¹⁶ Moreover, researchers have hypothesized that chronic treatment with propranolol may be effective in decreasing hyperarousal symptoms in patients with chronic PTSD by reducing tonically elevated norepinephrine signaling.⁶

Chronic elevation of noradrenergic activity may induce lipoprotein lipase and suppress low-density lipoprotein (LDL) receptor activity, which in turn elevates serum cholesterol levels. The results of one study suggested that verapamil, a non-dihydropyridine calcium channel blocker, significantly improves serum cholesterol levels in patients with PTSD by increasing LDL receptor activity and decreasing norepinephrine release.⁷

Alpha-1 and alpha-2 antagonists

Alpha-1 antagonists relax vascular smooth muscle by blocking norepinephrine stimulation at postsynaptic α-1-adrenergic receptors. They frequently are prescribed for hypertension and benign prostatic hypertrophy. One α-1 antagonist in particular, prazosin, appears especially useful in treating sleep disturbances, which occur in up to 90% of patients with PTSD.¹⁷ Because of its relatively greater lipophilicity, prazosin crosses the blood–brain barrier and acts centrally to reduce the fight-or-flight and hyperarousal reactions related to nightmares caused by PTSD.¹⁸ Common adverse effects include dizziness and orthostatic hypotension. These usually can be mitigated with titration to effective dose. In a study of active-duty soldiers who returned from Iraq and Afghanistan, Raskind et al⁸ found that prazosin doses up to 25 mg/d in men and 12 mg/d in women were tolerated with weekly adjustments and blood pressure monitoring.

Other α-1 antagonists have shown efficacy in a limited number of trials and may be considered second-line treatment of PTSD hyperarousal symptoms. Doxazosin has a longer half-life compared with prazosin (22 hours vs 3 hours) and may be useful in treating daytime hyperarousal with once-daily dosing. However, its hydrophilicity prevents it from crossing the blood–brain barrier to the same degree as prazosin.¹⁹ Terazosin also has a longer half-life (12 hours) and reaches peak plasma concentration in 1 hour. It undergoes minimal first-pass metabolism, leaving almost the entire circulating dose in the parent form, but clinical data are limited to only a small case report.¹⁰

Alpha-2 agonists inhibit sympathetic outflow in the CNS, which ultimately relaxes vascular smooth muscle like α-1 antagonists. Clonidine exhibits sedative properties, which derive from its non­specific binding to α-2a-, -2b-, and -2c-adrenergic receptors. Several case studies have described a reduction in agitation in PTSD patients with the use of clonidine, likely through the induction of sleep and relaxation. Guanfacine, on the other hand, selectively binds to the α-2a-adrenergic receptor and therefore lacks the sedative properties of clonidine. Several placebo-controlled trials showed no alleviation of PTSD symptoms in adults with the use of guanfacine.¹¹ However, case reports and open-label trials have suggested that guanfacine may reduce trauma-induced nightmares in pediatric patients. Further investigation is needed to clarify the potential use of guanfacine in pediatric PTSD.¹⁹

Antihistamines and antidepressants

Several second-line pharmacologic agents may be useful in patients with PTSD who are already taking cardiovascular medication. A limited number of studies have demonstrated reduced frequency of PTSD nightmares with the histamine-1 antagonists cyproheptadine and hydroxyzine, both of which exhibit minor anti-serotonergic properties.^12,13 Likewise, the serotonin antagonists nefazodone and trazodone have been shown to reduce the frequency of PTSD nightmares, as well as improve overall sleep quality.¹⁴ Nefazodone should be considered an option only after treatment failure of multiple other medications, because it is associated with a small, but significant, risk of life-threatening hepatotoxicity.²⁰

Tricyclic antidepressants (TCAs) may reduce anxiety and depression associated with PTSD to the same degree as SSRIs.²¹ However, their effect on PTSD-associated sleep disturbances is much less pronounced than other available medications.¹⁴ TCAs should be avoided in patients with CVD because they may exacerbate cardiac conduction abnormalities. This is especially true for those recovering from acute MI.²²

CASE CONTINUED

Mr. S is started on prazosin, 1 mg at bedtime, titrated weekly to 6 mg at bedtime with regular blood pressure monitoring because of the risk of orthostatic hypotension. Although the frequency of his nightmares decreases to 1 or 2 per month, he still experiences flashbacks at the same frequency and intensity as before. Prazosin, 1 mg every morning, is added, titrated weekly to 4 mg every morning. This combination of morning and bedtime dosing leads to resolution of both nightmares and flashbacks along with a significant reduction in hyperarousal. Lisinopril is increased from 5 to 10 mg/d to address Mr. S’s uncontrolled hypertension; this change also could have contributed to the reduction in hyperarousal. CPT and fluoxetine are continued.

Mr. S, 64, has a history of posttraumatic stress disorder (PTSD), which has been well controlled for the past 15 years with cognitive-processing therapy and fluoxetine, 40 mg/d. However, over the past 6 weeks, Mr. S has experienced increased hypervigilance, nightmares, and flashbacks. He states that his primary care provider recommended an adjustment in pharmacotherapy to address this exacerbation of symptoms. Previous medication trials include sertraline, 200 mg/d, discontinued due to lack of perceived efficacy, and venlafaxine, 150 mg/d, discontinued due to increased blood pressure.

Mr. S’s medical history includes hypertension, dyslipidemia, and myocardial infarction (MI) 5 years ago. His family history includes sudden cardiac death (mother and father) and major depressive disorder (sister). His blood pressure is currently uncontrolled on lisinopril, 5 mg/d, and metoprolol succinate, 50 mg/d. Today, serial blood pressure readings measured approximately 180/90 mm Hg, with a pulse 50-60 beats per minute.

What is the next step in treating Mr. S’s hypertension and PTSD symptoms? Is there any evidence to support concomitant therapy?

PTSD is characterized by emotional and behavioral symptoms following exposure to a traumatic event. Its 12-month prevalence in the United States is estimated at 3.5%. Diagnostic criteria necessitate the presence of intrusive symptoms, persistent effortful avoidance of distressing trauma-related stimuli, negative cognitions or mood, and alterations in arousal and reactivity. PTSD negatively impacts social and occupational functioning.¹

ACEIs, ARBs, beta blockers, and calcium channel blockers

Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) inhibit the renin-angiotensin system: ACEIs prevent formation of angiotensin II, a potent vasoconstrictor, and ARBs prevent interaction between angiotensin II and its receptor. In one study, patients were recruited from a large public hospital serving primarily a highly traumatized, low-income population. Patients taking an ACEI or ARB who had experienced at least 1 traumatic event exhibited significantly decreased hyperarousal symptoms and decreased intrusive thoughts on the PTSD Symptom Scale and Clinician Administered PTSD Scale.⁵ Other studies have reported that blockade of angiotensin II AT1 receptors may result in decreased stress, anxiety, and inflammation.¹⁵

Evidence supports the use of the centrally acting, beta-adrenergic antagonist propranolol for decreasing the physiologic reactivity to acute trauma. Emotional arousal enhances the consolidation of emotional experiences into long-term memories via the adrenal stress hormones epinephrine and corticosterone. The amygdala mediates these stress hormones and releases norepinephrine, which subsequently activates noradrenergic receptors essential for memory enhancement. Several studies have reported that patients who received propranolol within several hours of a traumatic event experienced fewer physiologic signs of PTSD at follow-up 1 month later.¹⁶ Moreover, researchers have hypothesized that chronic treatment with propranolol may be effective in decreasing hyperarousal symptoms in patients with chronic PTSD by reducing tonically elevated norepinephrine signaling.⁶

Chronic elevation of noradrenergic activity may induce lipoprotein lipase and suppress low-density lipoprotein (LDL) receptor activity, which in turn elevates serum cholesterol levels. The results of one study suggested that verapamil, a non-dihydropyridine calcium channel blocker, significantly improves serum cholesterol levels in patients with PTSD by increasing LDL receptor activity and decreasing norepinephrine release.⁷

Alpha-1 and alpha-2 antagonists

Alpha-1 antagonists relax vascular smooth muscle by blocking norepinephrine stimulation at postsynaptic α-1-adrenergic receptors. They frequently are prescribed for hypertension and benign prostatic hypertrophy. One α-1 antagonist in particular, prazosin, appears especially useful in treating sleep disturbances, which occur in up to 90% of patients with PTSD.¹⁷ Because of its relatively greater lipophilicity, prazosin crosses the blood–brain barrier and acts centrally to reduce the fight-or-flight and hyperarousal reactions related to nightmares caused by PTSD.¹⁸ Common adverse effects include dizziness and orthostatic hypotension. These usually can be mitigated with titration to effective dose. In a study of active-duty soldiers who returned from Iraq and Afghanistan, Raskind et al⁸ found that prazosin doses up to 25 mg/d in men and 12 mg/d in women were tolerated with weekly adjustments and blood pressure monitoring.

Other α-1 antagonists have shown efficacy in a limited number of trials and may be considered second-line treatment of PTSD hyperarousal symptoms. Doxazosin has a longer half-life compared with prazosin (22 hours vs 3 hours) and may be useful in treating daytime hyperarousal with once-daily dosing. However, its hydrophilicity prevents it from crossing the blood–brain barrier to the same degree as prazosin.¹⁹ Terazosin also has a longer half-life (12 hours) and reaches peak plasma concentration in 1 hour. It undergoes minimal first-pass metabolism, leaving almost the entire circulating dose in the parent form, but clinical data are limited to only a small case report.¹⁰

Alpha-2 agonists inhibit sympathetic outflow in the CNS, which ultimately relaxes vascular smooth muscle like α-1 antagonists. Clonidine exhibits sedative properties, which derive from its non­specific binding to α-2a-, -2b-, and -2c-adrenergic receptors. Several case studies have described a reduction in agitation in PTSD patients with the use of clonidine, likely through the induction of sleep and relaxation. Guanfacine, on the other hand, selectively binds to the α-2a-adrenergic receptor and therefore lacks the sedative properties of clonidine. Several placebo-controlled trials showed no alleviation of PTSD symptoms in adults with the use of guanfacine.¹¹ However, case reports and open-label trials have suggested that guanfacine may reduce trauma-induced nightmares in pediatric patients. Further investigation is needed to clarify the potential use of guanfacine in pediatric PTSD.¹⁹

Antihistamines and antidepressants

Several second-line pharmacologic agents may be useful in patients with PTSD who are already taking cardiovascular medication. A limited number of studies have demonstrated reduced frequency of PTSD nightmares with the histamine-1 antagonists cyproheptadine and hydroxyzine, both of which exhibit minor anti-serotonergic properties.^12,13 Likewise, the serotonin antagonists nefazodone and trazodone have been shown to reduce the frequency of PTSD nightmares, as well as improve overall sleep quality.¹⁴ Nefazodone should be considered an option only after treatment failure of multiple other medications, because it is associated with a small, but significant, risk of life-threatening hepatotoxicity.²⁰

Tricyclic antidepressants (TCAs) may reduce anxiety and depression associated with PTSD to the same degree as SSRIs.²¹ However, their effect on PTSD-associated sleep disturbances is much less pronounced than other available medications.¹⁴ TCAs should be avoided in patients with CVD because they may exacerbate cardiac conduction abnormalities. This is especially true for those recovering from acute MI.²²

CASE CONTINUED

Mr. S is started on prazosin, 1 mg at bedtime, titrated weekly to 6 mg at bedtime with regular blood pressure monitoring because of the risk of orthostatic hypotension. Although the frequency of his nightmares decreases to 1 or 2 per month, he still experiences flashbacks at the same frequency and intensity as before. Prazosin, 1 mg every morning, is added, titrated weekly to 4 mg every morning. This combination of morning and bedtime dosing leads to resolution of both nightmares and flashbacks along with a significant reduction in hyperarousal. Lisinopril is increased from 5 to 10 mg/d to address Mr. S’s uncontrolled hypertension; this change also could have contributed to the reduction in hyperarousal. CPT and fluoxetine are continued.

Mr. S, 64, has a history of posttraumatic stress disorder (PTSD), which has been well controlled for the past 15 years with cognitive-processing therapy and fluoxetine, 40 mg/d. However, over the past 6 weeks, Mr. S has experienced increased hypervigilance, nightmares, and flashbacks. He states that his primary care provider recommended an adjustment in pharmacotherapy to address this exacerbation of symptoms. Previous medication trials include sertraline, 200 mg/d, discontinued due to lack of perceived efficacy, and venlafaxine, 150 mg/d, discontinued due to increased blood pressure.

Mr. S’s medical history includes hypertension, dyslipidemia, and myocardial infarction (MI) 5 years ago. His family history includes sudden cardiac death (mother and father) and major depressive disorder (sister). His blood pressure is currently uncontrolled on lisinopril, 5 mg/d, and metoprolol succinate, 50 mg/d. Today, serial blood pressure readings measured approximately 180/90 mm Hg, with a pulse 50-60 beats per minute.

What is the next step in treating Mr. S’s hypertension and PTSD symptoms? Is there any evidence to support concomitant therapy?

PTSD is characterized by emotional and behavioral symptoms following exposure to a traumatic event. Its 12-month prevalence in the United States is estimated at 3.5%. Diagnostic criteria necessitate the presence of intrusive symptoms, persistent effortful avoidance of distressing trauma-related stimuli, negative cognitions or mood, and alterations in arousal and reactivity. PTSD negatively impacts social and occupational functioning.¹

ACEIs, ARBs, beta blockers, and calcium channel blockers

Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) inhibit the renin-angiotensin system: ACEIs prevent formation of angiotensin II, a potent vasoconstrictor, and ARBs prevent interaction between angiotensin II and its receptor. In one study, patients were recruited from a large public hospital serving primarily a highly traumatized, low-income population. Patients taking an ACEI or ARB who had experienced at least 1 traumatic event exhibited significantly decreased hyperarousal symptoms and decreased intrusive thoughts on the PTSD Symptom Scale and Clinician Administered PTSD Scale.⁵ Other studies have reported that blockade of angiotensin II AT1 receptors may result in decreased stress, anxiety, and inflammation.¹⁵

Evidence supports the use of the centrally acting, beta-adrenergic antagonist propranolol for decreasing the physiologic reactivity to acute trauma. Emotional arousal enhances the consolidation of emotional experiences into long-term memories via the adrenal stress hormones epinephrine and corticosterone. The amygdala mediates these stress hormones and releases norepinephrine, which subsequently activates noradrenergic receptors essential for memory enhancement. Several studies have reported that patients who received propranolol within several hours of a traumatic event experienced fewer physiologic signs of PTSD at follow-up 1 month later.¹⁶ Moreover, researchers have hypothesized that chronic treatment with propranolol may be effective in decreasing hyperarousal symptoms in patients with chronic PTSD by reducing tonically elevated norepinephrine signaling.⁶

Chronic elevation of noradrenergic activity may induce lipoprotein lipase and suppress low-density lipoprotein (LDL) receptor activity, which in turn elevates serum cholesterol levels. The results of one study suggested that verapamil, a non-dihydropyridine calcium channel blocker, significantly improves serum cholesterol levels in patients with PTSD by increasing LDL receptor activity and decreasing norepinephrine release.⁷

Alpha-1 and alpha-2 antagonists

Alpha-1 antagonists relax vascular smooth muscle by blocking norepinephrine stimulation at postsynaptic α-1-adrenergic receptors. They frequently are prescribed for hypertension and benign prostatic hypertrophy. One α-1 antagonist in particular, prazosin, appears especially useful in treating sleep disturbances, which occur in up to 90% of patients with PTSD.¹⁷ Because of its relatively greater lipophilicity, prazosin crosses the blood–brain barrier and acts centrally to reduce the fight-or-flight and hyperarousal reactions related to nightmares caused by PTSD.¹⁸ Common adverse effects include dizziness and orthostatic hypotension. These usually can be mitigated with titration to effective dose. In a study of active-duty soldiers who returned from Iraq and Afghanistan, Raskind et al⁸ found that prazosin doses up to 25 mg/d in men and 12 mg/d in women were tolerated with weekly adjustments and blood pressure monitoring.

Other α-1 antagonists have shown efficacy in a limited number of trials and may be considered second-line treatment of PTSD hyperarousal symptoms. Doxazosin has a longer half-life compared with prazosin (22 hours vs 3 hours) and may be useful in treating daytime hyperarousal with once-daily dosing. However, its hydrophilicity prevents it from crossing the blood–brain barrier to the same degree as prazosin.¹⁹ Terazosin also has a longer half-life (12 hours) and reaches peak plasma concentration in 1 hour. It undergoes minimal first-pass metabolism, leaving almost the entire circulating dose in the parent form, but clinical data are limited to only a small case report.¹⁰

Alpha-2 agonists inhibit sympathetic outflow in the CNS, which ultimately relaxes vascular smooth muscle like α-1 antagonists. Clonidine exhibits sedative properties, which derive from its non­specific binding to α-2a-, -2b-, and -2c-adrenergic receptors. Several case studies have described a reduction in agitation in PTSD patients with the use of clonidine, likely through the induction of sleep and relaxation. Guanfacine, on the other hand, selectively binds to the α-2a-adrenergic receptor and therefore lacks the sedative properties of clonidine. Several placebo-controlled trials showed no alleviation of PTSD symptoms in adults with the use of guanfacine.¹¹ However, case reports and open-label trials have suggested that guanfacine may reduce trauma-induced nightmares in pediatric patients. Further investigation is needed to clarify the potential use of guanfacine in pediatric PTSD.¹⁹

Antihistamines and antidepressants

Several second-line pharmacologic agents may be useful in patients with PTSD who are already taking cardiovascular medication. A limited number of studies have demonstrated reduced frequency of PTSD nightmares with the histamine-1 antagonists cyproheptadine and hydroxyzine, both of which exhibit minor anti-serotonergic properties.^12,13 Likewise, the serotonin antagonists nefazodone and trazodone have been shown to reduce the frequency of PTSD nightmares, as well as improve overall sleep quality.¹⁴ Nefazodone should be considered an option only after treatment failure of multiple other medications, because it is associated with a small, but significant, risk of life-threatening hepatotoxicity.²⁰

Tricyclic antidepressants (TCAs) may reduce anxiety and depression associated with PTSD to the same degree as SSRIs.²¹ However, their effect on PTSD-associated sleep disturbances is much less pronounced than other available medications.¹⁴ TCAs should be avoided in patients with CVD because they may exacerbate cardiac conduction abnormalities. This is especially true for those recovering from acute MI.²²

CASE CONTINUED

Mr. S is started on prazosin, 1 mg at bedtime, titrated weekly to 6 mg at bedtime with regular blood pressure monitoring because of the risk of orthostatic hypotension. Although the frequency of his nightmares decreases to 1 or 2 per month, he still experiences flashbacks at the same frequency and intensity as before. Prazosin, 1 mg every morning, is added, titrated weekly to 4 mg every morning. This combination of morning and bedtime dosing leads to resolution of both nightmares and flashbacks along with a significant reduction in hyperarousal. Lisinopril is increased from 5 to 10 mg/d to address Mr. S’s uncontrolled hypertension; this change also could have contributed to the reduction in hyperarousal. CPT and fluoxetine are continued.

CASE Unusual behavior, thoughts

Mr. L, age 28, an immigrant from Burma, is brought to his primary care physician’s clinic by his wife for follow-up on a rash. During the evaluation, his wife reports that Mr. L recently has had suicidal ideation, depression, and increased anger. She says Mr. L had made statements about wanting to kill himself with a gun. Mr. L had driven his car to a soccer field with a knife in hand and was contemplating suicide. She is concerned about her own safety and their children’s safety because of Mr. L’s anger. The physician refers Mr. L to the emergency department, and he is admitted to the medical floor for a rheumatological flare-up and suicidal ideation.

Mr. L starts displaying inappropriate behaviors, including masturbating in front of the patient safety attendant, telling the attendant “You are going to die today,” and assaulting a female attendant by trying to grab her breasts. He is given IM haloperidol, 2 mg, which effectively alleviates these behaviors. Between episodes of unusual behavior and outbursts, Mr. L is docile, quiet, and cooperative, and denies any memory of these episodes.

One month earlier, Mr. L had been hospitalized for progressive weakness and inability to ambulate. He was diagnosed with necrotizing myositis and a rash consistent with subacute cutaneous lupus. He was started on IV methylprednisolone, 1 g, and transitioned to oral prednisolone, 40 mg/d, which he continued taking after discharge. He also started taking azathioprine, which was increased from 50 to 100 mg/d. His condition improved shortly after beginning this regimen.

[polldaddy:9796586]

The authors’ observations

DSM-5 defines brief psychotic disorder as positive symptoms or disorganized or catatonic behavior appearing suddenly and lasting between 1 day to 1 month.¹ Mr. L had a sudden onset of his symptoms and marked stressors as a result of his worsening health. However, the possibility of his general medical conditions or medications causing his symptoms needed to be investigated and ruled out before this diagnosis could be assigned.

Another consideration is the culture-bound syndrome amok. Although DSM-5 does not use the term “culture-bound syndrome,” which was used in DSM-IV, it does recognize cultural conceptualizations of distress. Amok is described as a dissociative episode in which an individual has a period of brooding followed by outbursts that include violent, aggressive, and suicidal and/or homicidal ideation. The individual may exhibit persecutory and paranoid thinking, amnesia of the outbursts, and a return to typical behavior when the episode concludes.² However, it remained unclear whether Mr. L’s violent behavior was a manifestation of psychiatric or organic disease.

Identifying the possibility of amok is important not only for alleviating the patient’s distress but also for preventing violent outbursts that can result in injury or death.³ Amok should be considered only in the context of possible psychiatric or organic brain disease, such as corticosteroid-induced psychosis (CIP) or systemic lupus erythematosus-induced psychosis (SLEIP).⁴

EVALUATION Informants, labs

Mr. L immigrated to the United States when he was 5 years old. He does not speak English, and interviews are conducted with interpreting services at the hospital. Mr. L answers most questions with or 1 to 2 words. His medical and psychiatric histories are notable for hypothyroidism, hepatitis, non-ischemic cardiomyopathy, necrotizing myositis, subacute cutaneous lupus, and depression. Mr. L denies a personal or family history of mental illness; however, records show he has a history of unspecified depressive disorder.

Mr. L reports his current mood is “okay,” but he has felt different in the past few weeks. He denies auditory or visual hallucinations, or suicidal or homicidal ideation, but exhibits paranoid thoughts. Mr. L believes everyone “lied” to him, and he repeats this frequently. Collateral information from friends reveals that he had threatened to burn down their houses. A family friend states that Mr. L has been depressed and angry over the past 5 days.

During his prior and current hospitalizations, many labs were completed. Thyroid, urine drug screen, C-reactive protein, urine analysis, ethanol, complete blood count, and comprehensive metabolic panel were negative. Erythrocyte sedimentation rate was 30. Lumbar puncture cell count was notable for mildly elevated lymphocytes at 84%. Antinuclear antibody (ANA) was positive. Lupus anticoagulant panel revealed a mildly prolonged partial thromboplastin time at 38.9 seconds. DNA double-stranded antibody (anti-dsDNA) was positive. Anti-Smith antibody was negative. Anti-Ro/SSA and anti-La/SSB antibodies were elevated. Albumin was low. A MRI of the brain showed dystrophic-appearing right parieto-occipital calcification and mild cerebral volume loss.

Based on Mr. L’s presentation and imaging, the rheumatology team suspects CNS lupus and that his prescribed steroids could be playing a role in his behavior.

The authors’ observations

Differentiating CIP from SLEIP can be difficult. The clinical features and criteria for CIP and SLEIP are listed in Table 1.^5-7 Several studies have highlighted the difficulties in separating the 2 diagnoses:
 

• Kampylafka et al⁸ found that CNS involvement, including stroke, myelopathy, seizures, optic neuritis, and meningitis, was present in 4.3% of their sample of patients with systematic lupus erythematosus (SLE), of whom 6.3% presented with SLEIP. Of patients with CNS involvement, 94% had positive ANA and 69% had positive anti-dsDNA antibodies. It remains difficult to definitively diagnose SLEIP rather than CIP, however, because 100% of patients in this study were taking corticosteroids, with 25% taking azathioprine, as was Mr. L.⁸
• Appenzeller et al⁹ found that acute psychosis was associated with SLE in 11.3% of their sample. Psychosis in patients with SLE was accompanied by other manifestations of CNS involvement. On follow-up these patients had mild increases in white blood cell count in their CSF, and MRI demonstrated hyperdense lesions and cerebral atrophy. Hypoalbuminemia, although often seen in SLEIP, also is observed in patients with CIP and cannot be used to differentiate these 2 conditions.⁹
• Monov and Monova⁵ recommended criteria for SLEIP that include 3 stages. The first stage is determining that there is evidence of an exacerbation of SLE, and ruling out other causes for neurologic and psychiatric symptoms. The second stage involves using clinical, laboratory, or imaging tests to define the lesion as central and/or peripheral and diffuse and/or focal. The third stage requires diagnosing SLEIP using criteria from 2 groups of signs and symptoms: the first group includes seizure, psychosis, cerebrovascular event, lesion of cranial nerves, and quantitative alterations of consciousness; the second group includes cognitive dysfunction, lupus headache, peripheral neuropathy, MRI changes, EEG changes, electroneuromyography changes, and a positive replication protein A or antiphospholipid-positive antibody. Diagnosing SLEIP requires ≥1 criterion from group 1 and ≥2 criteria from group 2.⁵
• Patten and Neutel⁶ found that patients taking prednisolone, Symbol Std<40 mg/d, had significantly higher rates of psychosis than those taking <40 mg/d.⁶
• Bhangle et Myriad Proal⁷ found that one of the major distinguishing factors between CIP and SLEIP is the timing of the onset of symptoms, with CIP occurring within 8 weeks of initiation of a corticosteroid, and SLEIP being more likely to occur when additional CNS symptoms are present.⁷

TREATMENT Decreased dosage

Mr. L starts quetiapine, 25 mg at bedtime, increased to 75 mg at bedtime. Prednisolone is decreased to 10 mg/d. Over the next few days Mr. L’s mood, psychosis, and aggression improve. He becomes calm and cooperative, and denies suicidal or homicidal ideation. Mr. L’s wife, who was initially scared to visit him, comes to see him and confirms that he has improved. After 3 consecutive days with no abnormal behaviors or psychiatric symptoms, Mr. L is discharged and continues taking quetiapine, 75 mg at bedtime, and prednisolone, 10 mg/d, with outpatient follow-up.

The authors’ observations

Table 2^10,11 describes approaches to treating CIP and SLEIP. Managing CIP typically consists of reducing the corticosteroid dosage. CIP treatment also includes adjunct therapy with psychotropics if the corticosteroid dose cannot be lowered enough to reduce psychiatric symptoms while suppressing symptoms of the disease for which the corticosteroid was prescribed.⁶

When treating SLEIP, the corticosteroid dosage often is increased. Corticosteroids often are used to treat SLEIP while suppressing symptoms of SLE.¹⁰ The main treatment of SLEIP is focused on the disease and using psychotropic medications to control symptoms that don’t respond after exacerbation of the disease has been controlled.¹⁰

The presence of Mr. L’s multiple SLE symptoms, as well as MRI findings, could indicate SLEIP. However, corticosteroids also were a possible cause of his psychotic symptoms. Mr. L’s psychosis began within 8 weeks of starting a corticosteroid (prednisolone, 40 mg/d), and his symptoms improved when the corticosteroid dosage was reduced. The difference between CIP and SLEIP may best be distinguished by reducing the corticosteroid dosage and seeing if psychotic symptoms improve. Because it is important to control SLE symptoms in those with CIP, prescribing psychotropics may be warranted, as well as alternative treatments for immunosuppression.

Because steroids are frequently prescribed for lupus, it is important for clinicians to be aware of their psychiatric effects as well as how to manage those effects. When distinguishing CIP from SLEIP, consider decreasing the corticosteroid dosage and see if psychotic symptoms improve. Use adjunct therapy as needed.

CASE Unusual behavior, thoughts

Mr. L, age 28, an immigrant from Burma, is brought to his primary care physician’s clinic by his wife for follow-up on a rash. During the evaluation, his wife reports that Mr. L recently has had suicidal ideation, depression, and increased anger. She says Mr. L had made statements about wanting to kill himself with a gun. Mr. L had driven his car to a soccer field with a knife in hand and was contemplating suicide. She is concerned about her own safety and their children’s safety because of Mr. L’s anger. The physician refers Mr. L to the emergency department, and he is admitted to the medical floor for a rheumatological flare-up and suicidal ideation.

Mr. L starts displaying inappropriate behaviors, including masturbating in front of the patient safety attendant, telling the attendant “You are going to die today,” and assaulting a female attendant by trying to grab her breasts. He is given IM haloperidol, 2 mg, which effectively alleviates these behaviors. Between episodes of unusual behavior and outbursts, Mr. L is docile, quiet, and cooperative, and denies any memory of these episodes.

One month earlier, Mr. L had been hospitalized for progressive weakness and inability to ambulate. He was diagnosed with necrotizing myositis and a rash consistent with subacute cutaneous lupus. He was started on IV methylprednisolone, 1 g, and transitioned to oral prednisolone, 40 mg/d, which he continued taking after discharge. He also started taking azathioprine, which was increased from 50 to 100 mg/d. His condition improved shortly after beginning this regimen.

[polldaddy:9796586]

The authors’ observations

DSM-5 defines brief psychotic disorder as positive symptoms or disorganized or catatonic behavior appearing suddenly and lasting between 1 day to 1 month.¹ Mr. L had a sudden onset of his symptoms and marked stressors as a result of his worsening health. However, the possibility of his general medical conditions or medications causing his symptoms needed to be investigated and ruled out before this diagnosis could be assigned.

Another consideration is the culture-bound syndrome amok. Although DSM-5 does not use the term “culture-bound syndrome,” which was used in DSM-IV, it does recognize cultural conceptualizations of distress. Amok is described as a dissociative episode in which an individual has a period of brooding followed by outbursts that include violent, aggressive, and suicidal and/or homicidal ideation. The individual may exhibit persecutory and paranoid thinking, amnesia of the outbursts, and a return to typical behavior when the episode concludes.² However, it remained unclear whether Mr. L’s violent behavior was a manifestation of psychiatric or organic disease.

Identifying the possibility of amok is important not only for alleviating the patient’s distress but also for preventing violent outbursts that can result in injury or death.³ Amok should be considered only in the context of possible psychiatric or organic brain disease, such as corticosteroid-induced psychosis (CIP) or systemic lupus erythematosus-induced psychosis (SLEIP).⁴

EVALUATION Informants, labs

Mr. L immigrated to the United States when he was 5 years old. He does not speak English, and interviews are conducted with interpreting services at the hospital. Mr. L answers most questions with or 1 to 2 words. His medical and psychiatric histories are notable for hypothyroidism, hepatitis, non-ischemic cardiomyopathy, necrotizing myositis, subacute cutaneous lupus, and depression. Mr. L denies a personal or family history of mental illness; however, records show he has a history of unspecified depressive disorder.

Mr. L reports his current mood is “okay,” but he has felt different in the past few weeks. He denies auditory or visual hallucinations, or suicidal or homicidal ideation, but exhibits paranoid thoughts. Mr. L believes everyone “lied” to him, and he repeats this frequently. Collateral information from friends reveals that he had threatened to burn down their houses. A family friend states that Mr. L has been depressed and angry over the past 5 days.

During his prior and current hospitalizations, many labs were completed. Thyroid, urine drug screen, C-reactive protein, urine analysis, ethanol, complete blood count, and comprehensive metabolic panel were negative. Erythrocyte sedimentation rate was 30. Lumbar puncture cell count was notable for mildly elevated lymphocytes at 84%. Antinuclear antibody (ANA) was positive. Lupus anticoagulant panel revealed a mildly prolonged partial thromboplastin time at 38.9 seconds. DNA double-stranded antibody (anti-dsDNA) was positive. Anti-Smith antibody was negative. Anti-Ro/SSA and anti-La/SSB antibodies were elevated. Albumin was low. A MRI of the brain showed dystrophic-appearing right parieto-occipital calcification and mild cerebral volume loss.

Based on Mr. L’s presentation and imaging, the rheumatology team suspects CNS lupus and that his prescribed steroids could be playing a role in his behavior.

The authors’ observations

Differentiating CIP from SLEIP can be difficult. The clinical features and criteria for CIP and SLEIP are listed in Table 1.^5-7 Several studies have highlighted the difficulties in separating the 2 diagnoses:
 

• Kampylafka et al⁸ found that CNS involvement, including stroke, myelopathy, seizures, optic neuritis, and meningitis, was present in 4.3% of their sample of patients with systematic lupus erythematosus (SLE), of whom 6.3% presented with SLEIP. Of patients with CNS involvement, 94% had positive ANA and 69% had positive anti-dsDNA antibodies. It remains difficult to definitively diagnose SLEIP rather than CIP, however, because 100% of patients in this study were taking corticosteroids, with 25% taking azathioprine, as was Mr. L.⁸
• Appenzeller et al⁹ found that acute psychosis was associated with SLE in 11.3% of their sample. Psychosis in patients with SLE was accompanied by other manifestations of CNS involvement. On follow-up these patients had mild increases in white blood cell count in their CSF, and MRI demonstrated hyperdense lesions and cerebral atrophy. Hypoalbuminemia, although often seen in SLEIP, also is observed in patients with CIP and cannot be used to differentiate these 2 conditions.⁹
• Monov and Monova⁵ recommended criteria for SLEIP that include 3 stages. The first stage is determining that there is evidence of an exacerbation of SLE, and ruling out other causes for neurologic and psychiatric symptoms. The second stage involves using clinical, laboratory, or imaging tests to define the lesion as central and/or peripheral and diffuse and/or focal. The third stage requires diagnosing SLEIP using criteria from 2 groups of signs and symptoms: the first group includes seizure, psychosis, cerebrovascular event, lesion of cranial nerves, and quantitative alterations of consciousness; the second group includes cognitive dysfunction, lupus headache, peripheral neuropathy, MRI changes, EEG changes, electroneuromyography changes, and a positive replication protein A or antiphospholipid-positive antibody. Diagnosing SLEIP requires ≥1 criterion from group 1 and ≥2 criteria from group 2.⁵
• Patten and Neutel⁶ found that patients taking prednisolone, Symbol Std<40 mg/d, had significantly higher rates of psychosis than those taking <40 mg/d.⁶
• Bhangle et Myriad Proal⁷ found that one of the major distinguishing factors between CIP and SLEIP is the timing of the onset of symptoms, with CIP occurring within 8 weeks of initiation of a corticosteroid, and SLEIP being more likely to occur when additional CNS symptoms are present.⁷

TREATMENT Decreased dosage

Mr. L starts quetiapine, 25 mg at bedtime, increased to 75 mg at bedtime. Prednisolone is decreased to 10 mg/d. Over the next few days Mr. L’s mood, psychosis, and aggression improve. He becomes calm and cooperative, and denies suicidal or homicidal ideation. Mr. L’s wife, who was initially scared to visit him, comes to see him and confirms that he has improved. After 3 consecutive days with no abnormal behaviors or psychiatric symptoms, Mr. L is discharged and continues taking quetiapine, 75 mg at bedtime, and prednisolone, 10 mg/d, with outpatient follow-up.

The authors’ observations

Table 2^10,11 describes approaches to treating CIP and SLEIP. Managing CIP typically consists of reducing the corticosteroid dosage. CIP treatment also includes adjunct therapy with psychotropics if the corticosteroid dose cannot be lowered enough to reduce psychiatric symptoms while suppressing symptoms of the disease for which the corticosteroid was prescribed.⁶

When treating SLEIP, the corticosteroid dosage often is increased. Corticosteroids often are used to treat SLEIP while suppressing symptoms of SLE.¹⁰ The main treatment of SLEIP is focused on the disease and using psychotropic medications to control symptoms that don’t respond after exacerbation of the disease has been controlled.¹⁰

The presence of Mr. L’s multiple SLE symptoms, as well as MRI findings, could indicate SLEIP. However, corticosteroids also were a possible cause of his psychotic symptoms. Mr. L’s psychosis began within 8 weeks of starting a corticosteroid (prednisolone, 40 mg/d), and his symptoms improved when the corticosteroid dosage was reduced. The difference between CIP and SLEIP may best be distinguished by reducing the corticosteroid dosage and seeing if psychotic symptoms improve. Because it is important to control SLE symptoms in those with CIP, prescribing psychotropics may be warranted, as well as alternative treatments for immunosuppression.

Because steroids are frequently prescribed for lupus, it is important for clinicians to be aware of their psychiatric effects as well as how to manage those effects. When distinguishing CIP from SLEIP, consider decreasing the corticosteroid dosage and see if psychotic symptoms improve. Use adjunct therapy as needed.

CASE Unusual behavior, thoughts

Mr. L, age 28, an immigrant from Burma, is brought to his primary care physician’s clinic by his wife for follow-up on a rash. During the evaluation, his wife reports that Mr. L recently has had suicidal ideation, depression, and increased anger. She says Mr. L had made statements about wanting to kill himself with a gun. Mr. L had driven his car to a soccer field with a knife in hand and was contemplating suicide. She is concerned about her own safety and their children’s safety because of Mr. L’s anger. The physician refers Mr. L to the emergency department, and he is admitted to the medical floor for a rheumatological flare-up and suicidal ideation.

Mr. L starts displaying inappropriate behaviors, including masturbating in front of the patient safety attendant, telling the attendant “You are going to die today,” and assaulting a female attendant by trying to grab her breasts. He is given IM haloperidol, 2 mg, which effectively alleviates these behaviors. Between episodes of unusual behavior and outbursts, Mr. L is docile, quiet, and cooperative, and denies any memory of these episodes.

One month earlier, Mr. L had been hospitalized for progressive weakness and inability to ambulate. He was diagnosed with necrotizing myositis and a rash consistent with subacute cutaneous lupus. He was started on IV methylprednisolone, 1 g, and transitioned to oral prednisolone, 40 mg/d, which he continued taking after discharge. He also started taking azathioprine, which was increased from 50 to 100 mg/d. His condition improved shortly after beginning this regimen.

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The authors’ observations

DSM-5 defines brief psychotic disorder as positive symptoms or disorganized or catatonic behavior appearing suddenly and lasting between 1 day to 1 month.¹ Mr. L had a sudden onset of his symptoms and marked stressors as a result of his worsening health. However, the possibility of his general medical conditions or medications causing his symptoms needed to be investigated and ruled out before this diagnosis could be assigned.

Another consideration is the culture-bound syndrome amok. Although DSM-5 does not use the term “culture-bound syndrome,” which was used in DSM-IV, it does recognize cultural conceptualizations of distress. Amok is described as a dissociative episode in which an individual has a period of brooding followed by outbursts that include violent, aggressive, and suicidal and/or homicidal ideation. The individual may exhibit persecutory and paranoid thinking, amnesia of the outbursts, and a return to typical behavior when the episode concludes.² However, it remained unclear whether Mr. L’s violent behavior was a manifestation of psychiatric or organic disease.

Identifying the possibility of amok is important not only for alleviating the patient’s distress but also for preventing violent outbursts that can result in injury or death.³ Amok should be considered only in the context of possible psychiatric or organic brain disease, such as corticosteroid-induced psychosis (CIP) or systemic lupus erythematosus-induced psychosis (SLEIP).⁴

EVALUATION Informants, labs

Mr. L immigrated to the United States when he was 5 years old. He does not speak English, and interviews are conducted with interpreting services at the hospital. Mr. L answers most questions with or 1 to 2 words. His medical and psychiatric histories are notable for hypothyroidism, hepatitis, non-ischemic cardiomyopathy, necrotizing myositis, subacute cutaneous lupus, and depression. Mr. L denies a personal or family history of mental illness; however, records show he has a history of unspecified depressive disorder.

Mr. L reports his current mood is “okay,” but he has felt different in the past few weeks. He denies auditory or visual hallucinations, or suicidal or homicidal ideation, but exhibits paranoid thoughts. Mr. L believes everyone “lied” to him, and he repeats this frequently. Collateral information from friends reveals that he had threatened to burn down their houses. A family friend states that Mr. L has been depressed and angry over the past 5 days.

During his prior and current hospitalizations, many labs were completed. Thyroid, urine drug screen, C-reactive protein, urine analysis, ethanol, complete blood count, and comprehensive metabolic panel were negative. Erythrocyte sedimentation rate was 30. Lumbar puncture cell count was notable for mildly elevated lymphocytes at 84%. Antinuclear antibody (ANA) was positive. Lupus anticoagulant panel revealed a mildly prolonged partial thromboplastin time at 38.9 seconds. DNA double-stranded antibody (anti-dsDNA) was positive. Anti-Smith antibody was negative. Anti-Ro/SSA and anti-La/SSB antibodies were elevated. Albumin was low. A MRI of the brain showed dystrophic-appearing right parieto-occipital calcification and mild cerebral volume loss.

Based on Mr. L’s presentation and imaging, the rheumatology team suspects CNS lupus and that his prescribed steroids could be playing a role in his behavior.

The authors’ observations

Differentiating CIP from SLEIP can be difficult. The clinical features and criteria for CIP and SLEIP are listed in Table 1.^5-7 Several studies have highlighted the difficulties in separating the 2 diagnoses:
 

• Kampylafka et al⁸ found that CNS involvement, including stroke, myelopathy, seizures, optic neuritis, and meningitis, was present in 4.3% of their sample of patients with systematic lupus erythematosus (SLE), of whom 6.3% presented with SLEIP. Of patients with CNS involvement, 94% had positive ANA and 69% had positive anti-dsDNA antibodies. It remains difficult to definitively diagnose SLEIP rather than CIP, however, because 100% of patients in this study were taking corticosteroids, with 25% taking azathioprine, as was Mr. L.⁸
• Appenzeller et al⁹ found that acute psychosis was associated with SLE in 11.3% of their sample. Psychosis in patients with SLE was accompanied by other manifestations of CNS involvement. On follow-up these patients had mild increases in white blood cell count in their CSF, and MRI demonstrated hyperdense lesions and cerebral atrophy. Hypoalbuminemia, although often seen in SLEIP, also is observed in patients with CIP and cannot be used to differentiate these 2 conditions.⁹
• Monov and Monova⁵ recommended criteria for SLEIP that include 3 stages. The first stage is determining that there is evidence of an exacerbation of SLE, and ruling out other causes for neurologic and psychiatric symptoms. The second stage involves using clinical, laboratory, or imaging tests to define the lesion as central and/or peripheral and diffuse and/or focal. The third stage requires diagnosing SLEIP using criteria from 2 groups of signs and symptoms: the first group includes seizure, psychosis, cerebrovascular event, lesion of cranial nerves, and quantitative alterations of consciousness; the second group includes cognitive dysfunction, lupus headache, peripheral neuropathy, MRI changes, EEG changes, electroneuromyography changes, and a positive replication protein A or antiphospholipid-positive antibody. Diagnosing SLEIP requires ≥1 criterion from group 1 and ≥2 criteria from group 2.⁵
• Patten and Neutel⁶ found that patients taking prednisolone, Symbol Std<40 mg/d, had significantly higher rates of psychosis than those taking <40 mg/d.⁶
• Bhangle et Myriad Proal⁷ found that one of the major distinguishing factors between CIP and SLEIP is the timing of the onset of symptoms, with CIP occurring within 8 weeks of initiation of a corticosteroid, and SLEIP being more likely to occur when additional CNS symptoms are present.⁷

TREATMENT Decreased dosage

Mr. L starts quetiapine, 25 mg at bedtime, increased to 75 mg at bedtime. Prednisolone is decreased to 10 mg/d. Over the next few days Mr. L’s mood, psychosis, and aggression improve. He becomes calm and cooperative, and denies suicidal or homicidal ideation. Mr. L’s wife, who was initially scared to visit him, comes to see him and confirms that he has improved. After 3 consecutive days with no abnormal behaviors or psychiatric symptoms, Mr. L is discharged and continues taking quetiapine, 75 mg at bedtime, and prednisolone, 10 mg/d, with outpatient follow-up.

The authors’ observations

Table 2^10,11 describes approaches to treating CIP and SLEIP. Managing CIP typically consists of reducing the corticosteroid dosage. CIP treatment also includes adjunct therapy with psychotropics if the corticosteroid dose cannot be lowered enough to reduce psychiatric symptoms while suppressing symptoms of the disease for which the corticosteroid was prescribed.⁶

When treating SLEIP, the corticosteroid dosage often is increased. Corticosteroids often are used to treat SLEIP while suppressing symptoms of SLE.¹⁰ The main treatment of SLEIP is focused on the disease and using psychotropic medications to control symptoms that don’t respond after exacerbation of the disease has been controlled.¹⁰

The presence of Mr. L’s multiple SLE symptoms, as well as MRI findings, could indicate SLEIP. However, corticosteroids also were a possible cause of his psychotic symptoms. Mr. L’s psychosis began within 8 weeks of starting a corticosteroid (prednisolone, 40 mg/d), and his symptoms improved when the corticosteroid dosage was reduced. The difference between CIP and SLEIP may best be distinguished by reducing the corticosteroid dosage and seeing if psychotic symptoms improve. Because it is important to control SLE symptoms in those with CIP, prescribing psychotropics may be warranted, as well as alternative treatments for immunosuppression.

Because steroids are frequently prescribed for lupus, it is important for clinicians to be aware of their psychiatric effects as well as how to manage those effects. When distinguishing CIP from SLEIP, consider decreasing the corticosteroid dosage and see if psychotic symptoms improve. Use adjunct therapy as needed.

Twenty-eight states and Washington, DC, have legalized marijuana for treating certain medical conditions, but the United States Drug Enforcement Administration (DEA) still classifies marijuana as a Schedule I drug “with no currently accepted medical use and a high potential for abuse.”¹ In certain states, clinicians can recommend, but not prescribe, medical marijuana. There is limited guidance in caring for patients who use medical marijuana and request or use DEA-controlled prescription medications, such as benzodiazepines, stimulants, and/or opiates. Physicians can take the following steps to ensure safe care for patients who use medical marijuana and request or take a DEA-controlled prescription medication:

1. Understand your patients’ point of view. Talk with patients who use medical marijuana about the history, frequency, and method of use, and reasons for using medical marijuana. Assess for psychiatric illnesses and any past or active treatment with DEA-controlled prescription medications.

2. Perform screens. Screen for risk factors, past psychiatric history, and prior or current substance use disorders. Treat any existing substance use disorders as appropriate.

3. Provide education. Discuss the risks of marijuana use and its potential adverse effects on the patient’s illness. Explain that marijuana is not currently an FDA-approved treatment and that there often are safer, efficacious alternatives.

4. Set clear boundaries. Be upfront about what is safe clinical practice or the usual standard of medical care and practice within the scope of state and federal laws. Document treatment agreements, utilize prescription drug monitoring programs, and use blood and/or urine toxicology screens as needed. Be aware that a routine drug screen can detect marijuana exposure but may vary in detecting the quantity or length of marijuana use.²

5. Try harm reduction. Any marijuana use, including use that falls short of a Cannabis use disorder, may adversely impact cognition, mood, and/or anxiety.³ Reducing use or abstaining from marijuana use for at least 4 weeks^4,5 or reducing or discontinuing the DEA-controlled medication if a patient continues marijuana use are reasonable interventions to see if psychiatric symptoms improve or remit. Polypharmacy with marijuana may place a patient at risk for substance use disorders or additive adverse effects or can hinder the recovery process.

6. Consider alternatives. If a patient feels strongly about continuing medical marijuana use, and you feel that their marijuana use is not clinically harmful and that psychiatric symptoms require treatment, consider medications without a known potential for abuse (eg, antidepressants, buspirone, or hydroxyzine for anxiety; alpha-agonists or atomoxetine for attention-deficit/hyperactivity disorder, etc.). Start such medications at low dosages, titrate slowly, and monitor for benefits and adverse effects.

7. Continue the conversation. Maintain an open and nonjudgmental stance when discussing medical marijuana. Roll with resistance, and frame discussions toward a shared goal of improving the patient’s mental health as safely as possible while using the best medical evidence available.

8. Offer additional support. Refer patients any additional services as appropriate, which may include psychotherapy, a pain specialist, or a substance abuse specialist.

Twenty-eight states and Washington, DC, have legalized marijuana for treating certain medical conditions, but the United States Drug Enforcement Administration (DEA) still classifies marijuana as a Schedule I drug “with no currently accepted medical use and a high potential for abuse.”¹ In certain states, clinicians can recommend, but not prescribe, medical marijuana. There is limited guidance in caring for patients who use medical marijuana and request or use DEA-controlled prescription medications, such as benzodiazepines, stimulants, and/or opiates. Physicians can take the following steps to ensure safe care for patients who use medical marijuana and request or take a DEA-controlled prescription medication:

1. Understand your patients’ point of view. Talk with patients who use medical marijuana about the history, frequency, and method of use, and reasons for using medical marijuana. Assess for psychiatric illnesses and any past or active treatment with DEA-controlled prescription medications.

2. Perform screens. Screen for risk factors, past psychiatric history, and prior or current substance use disorders. Treat any existing substance use disorders as appropriate.

3. Provide education. Discuss the risks of marijuana use and its potential adverse effects on the patient’s illness. Explain that marijuana is not currently an FDA-approved treatment and that there often are safer, efficacious alternatives.

4. Set clear boundaries. Be upfront about what is safe clinical practice or the usual standard of medical care and practice within the scope of state and federal laws. Document treatment agreements, utilize prescription drug monitoring programs, and use blood and/or urine toxicology screens as needed. Be aware that a routine drug screen can detect marijuana exposure but may vary in detecting the quantity or length of marijuana use.²

5. Try harm reduction. Any marijuana use, including use that falls short of a Cannabis use disorder, may adversely impact cognition, mood, and/or anxiety.³ Reducing use or abstaining from marijuana use for at least 4 weeks^4,5 or reducing or discontinuing the DEA-controlled medication if a patient continues marijuana use are reasonable interventions to see if psychiatric symptoms improve or remit. Polypharmacy with marijuana may place a patient at risk for substance use disorders or additive adverse effects or can hinder the recovery process.

6. Consider alternatives. If a patient feels strongly about continuing medical marijuana use, and you feel that their marijuana use is not clinically harmful and that psychiatric symptoms require treatment, consider medications without a known potential for abuse (eg, antidepressants, buspirone, or hydroxyzine for anxiety; alpha-agonists or atomoxetine for attention-deficit/hyperactivity disorder, etc.). Start such medications at low dosages, titrate slowly, and monitor for benefits and adverse effects.

7. Continue the conversation. Maintain an open and nonjudgmental stance when discussing medical marijuana. Roll with resistance, and frame discussions toward a shared goal of improving the patient’s mental health as safely as possible while using the best medical evidence available.

8. Offer additional support. Refer patients any additional services as appropriate, which may include psychotherapy, a pain specialist, or a substance abuse specialist.

Twenty-eight states and Washington, DC, have legalized marijuana for treating certain medical conditions, but the United States Drug Enforcement Administration (DEA) still classifies marijuana as a Schedule I drug “with no currently accepted medical use and a high potential for abuse.”¹ In certain states, clinicians can recommend, but not prescribe, medical marijuana. There is limited guidance in caring for patients who use medical marijuana and request or use DEA-controlled prescription medications, such as benzodiazepines, stimulants, and/or opiates. Physicians can take the following steps to ensure safe care for patients who use medical marijuana and request or take a DEA-controlled prescription medication:

1. Understand your patients’ point of view. Talk with patients who use medical marijuana about the history, frequency, and method of use, and reasons for using medical marijuana. Assess for psychiatric illnesses and any past or active treatment with DEA-controlled prescription medications.

2. Perform screens. Screen for risk factors, past psychiatric history, and prior or current substance use disorders. Treat any existing substance use disorders as appropriate.

3. Provide education. Discuss the risks of marijuana use and its potential adverse effects on the patient’s illness. Explain that marijuana is not currently an FDA-approved treatment and that there often are safer, efficacious alternatives.

4. Set clear boundaries. Be upfront about what is safe clinical practice or the usual standard of medical care and practice within the scope of state and federal laws. Document treatment agreements, utilize prescription drug monitoring programs, and use blood and/or urine toxicology screens as needed. Be aware that a routine drug screen can detect marijuana exposure but may vary in detecting the quantity or length of marijuana use.²

5. Try harm reduction. Any marijuana use, including use that falls short of a Cannabis use disorder, may adversely impact cognition, mood, and/or anxiety.³ Reducing use or abstaining from marijuana use for at least 4 weeks^4,5 or reducing or discontinuing the DEA-controlled medication if a patient continues marijuana use are reasonable interventions to see if psychiatric symptoms improve or remit. Polypharmacy with marijuana may place a patient at risk for substance use disorders or additive adverse effects or can hinder the recovery process.

6. Consider alternatives. If a patient feels strongly about continuing medical marijuana use, and you feel that their marijuana use is not clinically harmful and that psychiatric symptoms require treatment, consider medications without a known potential for abuse (eg, antidepressants, buspirone, or hydroxyzine for anxiety; alpha-agonists or atomoxetine for attention-deficit/hyperactivity disorder, etc.). Start such medications at low dosages, titrate slowly, and monitor for benefits and adverse effects.

7. Continue the conversation. Maintain an open and nonjudgmental stance when discussing medical marijuana. Roll with resistance, and frame discussions toward a shared goal of improving the patient’s mental health as safely as possible while using the best medical evidence available.

8. Offer additional support. Refer patients any additional services as appropriate, which may include psychotherapy, a pain specialist, or a substance abuse specialist.

Certain clinical features of posttraumatic stress disorder (PTSD) appear in other psychiatric diagnoses and therefore can confound accurate diagnosis and treatment. PTSD is frequently comorbid with other classes of psychiatric disorders, including mood, personality, substance use, and psychotic disorders, which can further complicate diagnostic clarity. Comorbidity in PTSD is important to recognize because it has been associated with worse treatment outcomes.¹

In DSM-5, the updated criteria for PTSD included Criterion D: “Negative alterations in cognitions and mood associated with the traumatic event(s) ….”² In addition to inability to remember an important aspect of the traumatic event, this criterion may be met by developing persistent and exaggerated negative beliefs or expectations about oneself, blaming oneself or others for the event, and developing a persistent negative emotional state and decreased interest.² These characteristics overlap with DSM-5 criteria for major depressive disorder (MDD), including low self-worth, guilt, depression, and anhedonia. It is easy to imagine how one could diagnose MDD based on these features if a full history has not been obtained. Similarly, many of the elements in Criterion D overlap with the criteria for anxiety disorders, including irritable behavior, problems with concentration, and sleep disturbance. Re-experiencing symptoms can exist on a continuum with primary psychotic symptoms, and comorbid substance use disorders can add additional diagnostic complexity.

We created the mnemonic FIGHT to help remember the updated DSM-5 criteria for PTSD when considering the differential diagnosis.

Flight. Avoidant symptoms, including efforts to avoid distressing memories, thoughts, or feelings about the traumatic event, as well as avoidance of external reminders.

Intrusive symptoms, such as distressing dreams, intrusive memories, and physiological distress when exposed to cues.

Gloomy cognitions. Negative cognitions and mood associated with the traumatic event.

Hypervigilance. Alterations in arousal, such as irritability, angry outbursts, reckless behavior, and exaggerated startle response.

Trauma. Exposure to actual or threatened death, serious injury, or sexual violence.

A diagnosis of PTSD requires ≥1 month of symptoms that cause significant distress or impairment and are not attributable to the physiological effects of a substance or medical condition. Specifiers in DSM-5 include with depersonalization or derealization, as well as delayed expression.²

Vigilance in the assessment and treatment of PTSD will aid the clinician and patient in producing better care outcomes.

Certain clinical features of posttraumatic stress disorder (PTSD) appear in other psychiatric diagnoses and therefore can confound accurate diagnosis and treatment. PTSD is frequently comorbid with other classes of psychiatric disorders, including mood, personality, substance use, and psychotic disorders, which can further complicate diagnostic clarity. Comorbidity in PTSD is important to recognize because it has been associated with worse treatment outcomes.¹

In DSM-5, the updated criteria for PTSD included Criterion D: “Negative alterations in cognitions and mood associated with the traumatic event(s) ….”² In addition to inability to remember an important aspect of the traumatic event, this criterion may be met by developing persistent and exaggerated negative beliefs or expectations about oneself, blaming oneself or others for the event, and developing a persistent negative emotional state and decreased interest.² These characteristics overlap with DSM-5 criteria for major depressive disorder (MDD), including low self-worth, guilt, depression, and anhedonia. It is easy to imagine how one could diagnose MDD based on these features if a full history has not been obtained. Similarly, many of the elements in Criterion D overlap with the criteria for anxiety disorders, including irritable behavior, problems with concentration, and sleep disturbance. Re-experiencing symptoms can exist on a continuum with primary psychotic symptoms, and comorbid substance use disorders can add additional diagnostic complexity.

We created the mnemonic FIGHT to help remember the updated DSM-5 criteria for PTSD when considering the differential diagnosis.

Flight. Avoidant symptoms, including efforts to avoid distressing memories, thoughts, or feelings about the traumatic event, as well as avoidance of external reminders.

Intrusive symptoms, such as distressing dreams, intrusive memories, and physiological distress when exposed to cues.

Gloomy cognitions. Negative cognitions and mood associated with the traumatic event.

Hypervigilance. Alterations in arousal, such as irritability, angry outbursts, reckless behavior, and exaggerated startle response.

Trauma. Exposure to actual or threatened death, serious injury, or sexual violence.

A diagnosis of PTSD requires ≥1 month of symptoms that cause significant distress or impairment and are not attributable to the physiological effects of a substance or medical condition. Specifiers in DSM-5 include with depersonalization or derealization, as well as delayed expression.²

Vigilance in the assessment and treatment of PTSD will aid the clinician and patient in producing better care outcomes.

Certain clinical features of posttraumatic stress disorder (PTSD) appear in other psychiatric diagnoses and therefore can confound accurate diagnosis and treatment. PTSD is frequently comorbid with other classes of psychiatric disorders, including mood, personality, substance use, and psychotic disorders, which can further complicate diagnostic clarity. Comorbidity in PTSD is important to recognize because it has been associated with worse treatment outcomes.¹

In DSM-5, the updated criteria for PTSD included Criterion D: “Negative alterations in cognitions and mood associated with the traumatic event(s) ….”² In addition to inability to remember an important aspect of the traumatic event, this criterion may be met by developing persistent and exaggerated negative beliefs or expectations about oneself, blaming oneself or others for the event, and developing a persistent negative emotional state and decreased interest.² These characteristics overlap with DSM-5 criteria for major depressive disorder (MDD), including low self-worth, guilt, depression, and anhedonia. It is easy to imagine how one could diagnose MDD based on these features if a full history has not been obtained. Similarly, many of the elements in Criterion D overlap with the criteria for anxiety disorders, including irritable behavior, problems with concentration, and sleep disturbance. Re-experiencing symptoms can exist on a continuum with primary psychotic symptoms, and comorbid substance use disorders can add additional diagnostic complexity.

We created the mnemonic FIGHT to help remember the updated DSM-5 criteria for PTSD when considering the differential diagnosis.

Flight. Avoidant symptoms, including efforts to avoid distressing memories, thoughts, or feelings about the traumatic event, as well as avoidance of external reminders.

Intrusive symptoms, such as distressing dreams, intrusive memories, and physiological distress when exposed to cues.

Gloomy cognitions. Negative cognitions and mood associated with the traumatic event.

Hypervigilance. Alterations in arousal, such as irritability, angry outbursts, reckless behavior, and exaggerated startle response.

Trauma. Exposure to actual or threatened death, serious injury, or sexual violence.

A diagnosis of PTSD requires ≥1 month of symptoms that cause significant distress or impairment and are not attributable to the physiological effects of a substance or medical condition. Specifiers in DSM-5 include with depersonalization or derealization, as well as delayed expression.²

Vigilance in the assessment and treatment of PTSD will aid the clinician and patient in producing better care outcomes.

As psychiatrists, we all come across patients who press our buttons and engender negative feelings, such as anger, frustration, and inadequacy.¹ These patients have been referred to as “hateful” or “difficult” because they disrupt the treatment alliance.^1,2 We are quick to point our fingers at such patients for making our jobs harder, being noncompliant, resisting the therapeutic alliance, and in general, being “problem patients.”³ However, the physician–patient relationship is a 2-way street. Although our patients knowingly or unknowingly play a role in this dynamic, we could be overlooking our role in adversely affecting this relationship. The following factors influence the physician–patient bond.^1,2

Countertransference. We may have negative feelings toward a patient based on our personalities and/or if the patient reminds us of someone we may not like, which could lead us to overprescribe or under­prescribe medications, conduct unnecessary medical workups, distance ourselves from the patient, etc. Accepting our disdain for certain patients and understanding why we have these emotions will allow us to better understand them, ensure that we are not impeding the delivery of appropriate clinical care, and improve rapport.

Listening. It may seem obvious that not listening to our patients negatively impacts rapport. However, in today’s technological world, we may not be really listening to our patients even when we think we are. Answering a text message or reading the patient’s electronic medical record while they are talking to us may increase productivity, but doing so also can interfere with our ability to form a therapeutic alliance. Although we may hear what our patients are saying, such distractions can create a hurdle in listening to what they are telling us.

Empathy often is confused for sympathy. Sympathy entails expressing concern and compassion for one’s distress, whereas empathy includes recognizing and sharing the patient’s emotions. Identifying with and understanding our patients’ situations, drives, and feelings allows us to understand what they are experiencing, see why they are reacting in a negative manner, and protect them from unnecessary emotional distress. Empathy can lead us to know what needs to be said and what should be said. It also can demystify a patient’s suffering. Not providing empathy or substituting sympathy can disrupt the therapeutic alliance.

Projective identification. Patients can project intolerable and negative feelings onto us and coerce us into identifying with what has been projected, allowing them to indirectly take control of our emotions. Our subsequent reactions can unsettle the physician–patient relationship. We need to be attuned to this process and recognize what the patient is provoking within us. Once we understand the process, we can realize that this is how they deal with others under similarly stressful conditions, and then react in a more supportive and healthy manner, rather than reviling our patients and negatively impacting the therapeutic relationship.

As psychiatrists, we all come across patients who press our buttons and engender negative feelings, such as anger, frustration, and inadequacy.¹ These patients have been referred to as “hateful” or “difficult” because they disrupt the treatment alliance.^1,2 We are quick to point our fingers at such patients for making our jobs harder, being noncompliant, resisting the therapeutic alliance, and in general, being “problem patients.”³ However, the physician–patient relationship is a 2-way street. Although our patients knowingly or unknowingly play a role in this dynamic, we could be overlooking our role in adversely affecting this relationship. The following factors influence the physician–patient bond.^1,2

Countertransference. We may have negative feelings toward a patient based on our personalities and/or if the patient reminds us of someone we may not like, which could lead us to overprescribe or under­prescribe medications, conduct unnecessary medical workups, distance ourselves from the patient, etc. Accepting our disdain for certain patients and understanding why we have these emotions will allow us to better understand them, ensure that we are not impeding the delivery of appropriate clinical care, and improve rapport.

Listening. It may seem obvious that not listening to our patients negatively impacts rapport. However, in today’s technological world, we may not be really listening to our patients even when we think we are. Answering a text message or reading the patient’s electronic medical record while they are talking to us may increase productivity, but doing so also can interfere with our ability to form a therapeutic alliance. Although we may hear what our patients are saying, such distractions can create a hurdle in listening to what they are telling us.

Empathy often is confused for sympathy. Sympathy entails expressing concern and compassion for one’s distress, whereas empathy includes recognizing and sharing the patient’s emotions. Identifying with and understanding our patients’ situations, drives, and feelings allows us to understand what they are experiencing, see why they are reacting in a negative manner, and protect them from unnecessary emotional distress. Empathy can lead us to know what needs to be said and what should be said. It also can demystify a patient’s suffering. Not providing empathy or substituting sympathy can disrupt the therapeutic alliance.

Projective identification. Patients can project intolerable and negative feelings onto us and coerce us into identifying with what has been projected, allowing them to indirectly take control of our emotions. Our subsequent reactions can unsettle the physician–patient relationship. We need to be attuned to this process and recognize what the patient is provoking within us. Once we understand the process, we can realize that this is how they deal with others under similarly stressful conditions, and then react in a more supportive and healthy manner, rather than reviling our patients and negatively impacting the therapeutic relationship.

As psychiatrists, we all come across patients who press our buttons and engender negative feelings, such as anger, frustration, and inadequacy.¹ These patients have been referred to as “hateful” or “difficult” because they disrupt the treatment alliance.^1,2 We are quick to point our fingers at such patients for making our jobs harder, being noncompliant, resisting the therapeutic alliance, and in general, being “problem patients.”³ However, the physician–patient relationship is a 2-way street. Although our patients knowingly or unknowingly play a role in this dynamic, we could be overlooking our role in adversely affecting this relationship. The following factors influence the physician–patient bond.^1,2

Countertransference. We may have negative feelings toward a patient based on our personalities and/or if the patient reminds us of someone we may not like, which could lead us to overprescribe or under­prescribe medications, conduct unnecessary medical workups, distance ourselves from the patient, etc. Accepting our disdain for certain patients and understanding why we have these emotions will allow us to better understand them, ensure that we are not impeding the delivery of appropriate clinical care, and improve rapport.

Listening. It may seem obvious that not listening to our patients negatively impacts rapport. However, in today’s technological world, we may not be really listening to our patients even when we think we are. Answering a text message or reading the patient’s electronic medical record while they are talking to us may increase productivity, but doing so also can interfere with our ability to form a therapeutic alliance. Although we may hear what our patients are saying, such distractions can create a hurdle in listening to what they are telling us.

Empathy often is confused for sympathy. Sympathy entails expressing concern and compassion for one’s distress, whereas empathy includes recognizing and sharing the patient’s emotions. Identifying with and understanding our patients’ situations, drives, and feelings allows us to understand what they are experiencing, see why they are reacting in a negative manner, and protect them from unnecessary emotional distress. Empathy can lead us to know what needs to be said and what should be said. It also can demystify a patient’s suffering. Not providing empathy or substituting sympathy can disrupt the therapeutic alliance.

Projective identification. Patients can project intolerable and negative feelings onto us and coerce us into identifying with what has been projected, allowing them to indirectly take control of our emotions. Our subsequent reactions can unsettle the physician–patient relationship. We need to be attuned to this process and recognize what the patient is provoking within us. Once we understand the process, we can realize that this is how they deal with others under similarly stressful conditions, and then react in a more supportive and healthy manner, rather than reviling our patients and negatively impacting the therapeutic relationship.

Photo by Aurimas Rimsa

Researchers say they have published the most extensive data ever collected on childhood cancer in sub-Saharan Africa.

On the African continent, only South Africa operates a childhood cancer registry on the national level.

Researchers brought together data from 16 of the smaller, local registries, collecting this information for the first time and presenting it in an accessible format.

The data were published in ecancermedicalscience.

Examining the data in context allowed the researchers to notice trends in cancer incidence. For example, they found that, in Blantyre, Malawi’s second-largest city, the cumulative risk of a child developing Burkitt lymphoma is 2 in every thousand.

The researchers called this incidence “remarkable” and noted that the global research community is largely unaware of this.

“Everything starts with awareness,” said study author Cristina Stefan, global clinical leader of oncology for Roche Diagnostics International Ltd of Switzerland and director of the African Medical Research and Innovation Institute.

“It is highly necessary to publicize these data, which, at the moment, represent the best image of the malignant disease in children in the respective regions.”

The researchers also noted that factors such as the prevalence of malaria and the Epstein-Barr virus contribute to the unique epidemiology of childhood cancer in Africa.

“Our colleagues can learn that the patterns and distribution of cancers in Africa are totally different from Europe, and there is a need for further research into the roles of factors such as genetic predispositions and the influence of infections and other comorbidities in the evolution of cancer,” Dr Stefan said.

“We have learned many universal lessons about data collection as we prepared this work. Our hope is that the publication of this monograph will open the forums for future discussions and that the work will be referenced for the better understanding of cancer in children in Africa and used to improve outcomes for children affected there.”

Photo by Aurimas Rimsa

Researchers say they have published the most extensive data ever collected on childhood cancer in sub-Saharan Africa.

On the African continent, only South Africa operates a childhood cancer registry on the national level.

Researchers brought together data from 16 of the smaller, local registries, collecting this information for the first time and presenting it in an accessible format.

The data were published in ecancermedicalscience.

Examining the data in context allowed the researchers to notice trends in cancer incidence. For example, they found that, in Blantyre, Malawi’s second-largest city, the cumulative risk of a child developing Burkitt lymphoma is 2 in every thousand.

The researchers called this incidence “remarkable” and noted that the global research community is largely unaware of this.

“Everything starts with awareness,” said study author Cristina Stefan, global clinical leader of oncology for Roche Diagnostics International Ltd of Switzerland and director of the African Medical Research and Innovation Institute.

“It is highly necessary to publicize these data, which, at the moment, represent the best image of the malignant disease in children in the respective regions.”

The researchers also noted that factors such as the prevalence of malaria and the Epstein-Barr virus contribute to the unique epidemiology of childhood cancer in Africa.

“Our colleagues can learn that the patterns and distribution of cancers in Africa are totally different from Europe, and there is a need for further research into the roles of factors such as genetic predispositions and the influence of infections and other comorbidities in the evolution of cancer,” Dr Stefan said.

“We have learned many universal lessons about data collection as we prepared this work. Our hope is that the publication of this monograph will open the forums for future discussions and that the work will be referenced for the better understanding of cancer in children in Africa and used to improve outcomes for children affected there.”

Photo by Aurimas Rimsa

Researchers say they have published the most extensive data ever collected on childhood cancer in sub-Saharan Africa.

On the African continent, only South Africa operates a childhood cancer registry on the national level.

Researchers brought together data from 16 of the smaller, local registries, collecting this information for the first time and presenting it in an accessible format.

The data were published in ecancermedicalscience.

Examining the data in context allowed the researchers to notice trends in cancer incidence. For example, they found that, in Blantyre, Malawi’s second-largest city, the cumulative risk of a child developing Burkitt lymphoma is 2 in every thousand.

The researchers called this incidence “remarkable” and noted that the global research community is largely unaware of this.

“Everything starts with awareness,” said study author Cristina Stefan, global clinical leader of oncology for Roche Diagnostics International Ltd of Switzerland and director of the African Medical Research and Innovation Institute.

“It is highly necessary to publicize these data, which, at the moment, represent the best image of the malignant disease in children in the respective regions.”

The researchers also noted that factors such as the prevalence of malaria and the Epstein-Barr virus contribute to the unique epidemiology of childhood cancer in Africa.

“Our colleagues can learn that the patterns and distribution of cancers in Africa are totally different from Europe, and there is a need for further research into the roles of factors such as genetic predispositions and the influence of infections and other comorbidities in the evolution of cancer,” Dr Stefan said.

“We have learned many universal lessons about data collection as we prepared this work. Our hope is that the publication of this monograph will open the forums for future discussions and that the work will be referenced for the better understanding of cancer in children in Africa and used to improve outcomes for children affected there.”

Primary care physicians are frequently the first to evaluate hand, wrist, and forearm pain in patients, making knowledge of the symptoms, causes, and treatment of common diagnoses in the upper extremities imperative. Primary symptoms usually include pain and/or swelling. While most tendon disorders originating in the hand and wrist are idiopathic in nature, some patients occasionally report having recently performed unusual manual activity or having experienced trauma to the area days or weeks prior. A significant portion of patients are injured as a result of chronic repetitive activities at work.¹

Most diagnoses can be made by pairing your knowledge of hand and forearm anatomy with an understanding of which tender points are indicative of which common conditions. (Care, of course, must be taken to ensure that there is no underlying infection.) Common conditions can often be treated nonsurgically with conservative treatments such as physical therapy, bracing/splinting, nonsteroidal anti-inflammatory drugs (NSAIDs), and injections of corticosteroids (eg, betamethasone, hydrocortisone, methylprednisolone, and triamcinolone) (TABLE 1^2-4) with or without the use of ultrasound. The benefits of corticosteroid injections for these conditions are well studied and documented in the literature, although physicians should always warn patients of the possible adverse effects prior to injection^3,5 (TABLE 2⁴).

To help you refine your skills, we review some of the more common hand and forearm conditions you are likely to encounter in the office and provide photos that reveal underlying anatomy so that you can administer injections without, in many cases, the need for ultrasound.

Trigger finger/thumb: New pathophysiologic findings?

Trigger finger most commonly occurs in the dominant hand. It is also more common in women, patients in their 50s, and in individuals with diabetes.⁶ Trigger finger/thumb is caused by inflammation and constriction of the flexor tendon sheath, which carries the flexor tendons through the palm and into the fingers and thumb. This, in turn, causes irritation of the tendons, sometimes via the formation of tendinous nodules, which may impinge upon the sheath’s “pulley system.”

When the “pulley” is compromised. The retinacular sheath is composed of 5 annular ligaments, or pulleys, that hold the tendons of the fingers close to the bone and allow the fingers to flex properly. The A1 pulley, at the level of the metacarpal head, is the first part of the sheath and is subject to the highest force; high forces may subsequently lead to the finger becoming locked in a flexed, or trigger, position.⁶ Patients may experience pain in the distal palm at the level of the A1 pulley and clicking of the finger.⁶

Additionally . . . recent studies show discrete histologic changes in trigger finger tendons, similar to findings with Achilles tendinosis and tendinopathy.⁷ In trigger finger tendons, collagen type 1A1 and 3A1, aggrecan, and biglycan are up-regulated, while metalloproteinase inhibitor 3 (TIMP-3) and matrix metallopeptidase³ (MMP-3) are down-regulated, a situation also described in Achilles tendinosis.⁷ This similarity in conditions provides new insight into the pathophysiology of the condition and may help provide future treatments.

Making the Dx: Look for swelling, check for carpal tunnel

During the examination, first look at both hands for swelling, arthropathy, or injury, and note the presence of any joint contractures. Next, examine all of the digits in flexion and extension while noting which ones are triggering, as the problem can occur in multiple digits on one hand. Then palpate the palms over the patient’s metacarpal heads, feeling for tender nodules.

Most diagnoses can be made by pairing your knowledge of hand and forearm anatomy with an understanding of which tender points are indicative of which common conditions.

Finally, examine the patient for carpal tunnel syndrome (CTS). A positive Tinel’s sign (shooting pain into the hand when the median nerve in the wrist is percussed), a positive Phalen maneuver (numbness or pain, usually within one minute of full wrist flexion), or thenar muscle wasting are highly indicative of CTS (compression of the median nerve at the transverse carpal ligament in the carpal tunnel). It is important to check for CTS when examining a patient for trigger finger because the 2 conditions frequently co-occur.⁶ (For more on CTS, see here.)

Treatment: Consider corticosteroids first

First-line treatment for patients with trigger finger or thumb is a corticosteroid injection into the subcutaneous tissue around the tendon sheath (FIGURES 1 and 2). (For this indication and for the others discussed throughout the article, there isn’t tremendous evidence for one particular type of corticosteroid over another; see TABLE 1^2-4 for choices.) Up to 57% of cases resolve with one injection, and 86% resolve with 2,⁸ but keep in mind that it may take up to 2 weeks to achieve the full clinical benefit.

Patients with multiple trigger fingers can be treated with oral corticosteroids (eg, a methylprednisolone dose pack). Peters-Veluthamaningal et al performed a systematic review in 2009 and found 2 randomized controlled trials involving 63 patients (34 received injections of a corticosteroid [either methylprednisolone or betamethasone] and lidocaine and 29 received lidocaine only).² The corticosteroid/lidocaine combination was more effective at 4 weeks (relative risk [RR]=3.15; 95% confidence interval [CI], 1.34 to 7.40).²

If 2 corticosteroid injections 6 weeks apart fail to provide benefit, or the finger is irreversibly locked in flexion, surgical release of the pulley is required and is performed through a palmar incision at the level of the A1 pulley. Complications from this surgery, including nerve damage, are exceedingly rare, but injury can occur, given the proximity of the digital nerves to the A1 pulley.

Patient is a child? Refer children with trigger finger or thumb to a hand surgeon for evaluation and management because the indications for nonoperative treatment in the pediatric population are unclear.⁹

Carpometacarpal arthritis: Common, with many causes

Osteoarthritis of the first carpometacarpal (CMC) joint is the most common site of arthritis in the hand/wrist region, affecting up to 11% of men and 33% of women in their 50s and 60s.¹⁰ Because the CMC joint lacks a bony restraint, it relies on a number of ligaments for stability—the strongest and most important of which is the palmar oblique “beak” ligament.¹¹ A major cause of degenerative arthritis of this joint is attenuation and laxity of these ligaments, leading to abnormal and increased stress loads, which, in turn, can lead to loss of cartilage and bony impingement. While the exact mechanism of this process is not fully understood,^10,12 acute or chronic trauma, advanced age, hormonal factors, and genetic factors seem to play a role.¹¹

Many believe there is a relationship between a patient's occupation and the development of CMC arthritis, but studies are inconclusive.¹³ At risk are secretarial workers, tailors, domestic helpers/cleaners, and individuals whose jobs involve repetitive thumb use and/or insufficient rest of the joint throughout the day.

Making the Dx: Perform the Grind test

A detailed patient history (which is usually void of trauma to the hand) and physical examination are the keys to making the diagnosis of CMC arthritis. A history of pain at the base of the thumb during pinching and gripping tasks is often elucidated. Classically, patients describe pain upon turning keys, opening jars, and gripping doorknobs.¹¹

It's important to focus on the dorsoradial aspect of the thumb during the physical exam and to rule out other causes of pain, such as de Quervain’s tenosynovitis, flexor carpi radialis tendinitis, CTS, and trigger thumb.¹¹ Typical findings include pain with palpation directly over the dorsoradial aspect of the CMC joint and pain with axial loading and upon circumduction during a Grind test of the CMC joint. (The Grind test is performed by moving the metacarpal bone of the thumb in a circle and loading it with gentle axial forces. People with thumb joint arthritis generally experience sudden sharp pain at the CMC joint.)

Radiographic findings can be useful as a diagnostic adjunct, with staging of the disease, and in determining who can benefit from conservative management.¹¹

Treatment: Start with NSAIDs and splinting

Depending on the degree of arthritis, management may include both conservative and surgical options.¹⁰ Patient education describing activity modification is useful during all stages of CMC arthritis. Research has shown that avoiding inciting activities, such as key turning, pinching, and grasping, helps to alleviate symptoms.¹⁴ Patients may also obtain relief from NSAIDs, especially when they are used in conjunction with activity modification and splinting. NSAIDs, however, do not halt or reverse the disease process; they only reduce inflammation, synovitis, and pain.¹¹

Splinting. Studies have shown splinting of the thumb CMC joint to provide pain relief and to potentially slow disease progression.¹⁵ Because splints decrease motion and increase joint stability, they are especially useful for patients with joint hypermobility. The long opponens thumb spica splint is commonly used; it immobilizes the wrist and CMC, while leaving the thumb interphalangeal joint free. Short thumb spica and neoprene splints are also commercially available, and studies have shown that they provide good results.¹⁵ Splinting is most beneficial in patients with early-stage disease and may be used for either short-term flares or long-term treatment.¹¹

Cortisone injections. For those patients who do not respond to activity modification, NSAIDs, and/or splinting, consider cortisone injections (FIGURE 3). Intra-articular cortisone injections can decrease inflammation and provide good pain relief, especially in patients with early-stage disease. The effectiveness of cortisone injections in patients with more advanced disease is not clear; no benefit has been shown in studies to date.¹⁶ Equally unclear is the long-term benefit of injections.¹¹ Patients who do not respond to conservative treatments will often require surgical care.

Carpal tunnel syndrome: Moving slower to surgery

CTS is one of the most common conditions of the upper extremities. Researchers estimate that 491 women per 100,000 person-years and 258 men per 100,000 person-years will develop CTS, with 109 per 100,000 person-years receiving carpal tunnel release surgery.¹⁷ Risk factors for the development of CTS include diabetes, hypothyroidism, rheumatoid arthritis, pregnancy, obesity, family history, trauma, and occupations that involve repetitive tasks or long hours working at a computer.¹⁸

CTS is caused by compression of the median nerve as it passes through the carpal tunnel.¹⁹ The elevated pressure in the carpal tunnel restricts epineural blood flow and supply, causing the pain felt with CTS.²⁰ Even after surgical decompression, recurrent or persistent CTS can be a problem.²¹

Making the Dx: Perform the Phalen maneuver, Durkan’s test

Patients typically present with complaints of weakness, pain, and/or numbness in at least 2 of 4 radial digits (thumb, index, middle, ring).^19,22 The most common time of day for patients to have symptoms is at night.²¹

The diagnostic tools. Tinel’s sign is a useful diagnostic tool when you suspect carpal tunnel syndrome. Tinel’s sign is positive if percussion over the median nerve at the carpal tunnel elicits pain or paresthesia.¹⁸

When employing the Phalen maneuver, be certain to have the patient flex his/her wrist to 90 degrees and to document the number of seconds it takes for numbness to present in the fingers. Pain or paresthesia should occur in <60 seconds for the test to be positive.¹⁸

Median nerve compression over the carpal tunnel, also known as Durkan’s test, may also elicit symptoms. With Durkan’s test, you apply direct pressure over the transverse carpal ligament. If pain or paresthesia occurs in <30 seconds, the test is positive.¹⁸ Often clinicians will combine the Phalen maneuver and Durkan’s test to increase sensitivity and specificity.¹⁸ Nerve conduction studies are often performed to confirm the clinical diagnosis.

Is more than one condition at play? It is important to determine whether cervical spine disease and/or peripheral neuropathy is contributing to the patient’s symptoms, along with CTS; patients may have more than one condition contributing to their pain. We routinely check cervical spine motion, tenderness, and nerve compression as part of the exam on a patient with suspected CTS. In the office, a monofilament test or 2-point discrimination test can help make the clinical diagnosis by uncovering decreased sensation in the thumb, index, and/or middle fingers.²³

The 5.07 monofilament test is performed with the clinician applying the monofilament to different dermatomal or sensory distributions while the patient has his/her eyes closed. The 2-point discrimination test is performed with a caliper device that measures the distance at which the patient can feel 2 separate stimuli. Often electromyography or nerve conduction studies are necessary.¹⁸

Treatment: Pursue nonoperative approaches

A survey of the membership of the American Society for Surgery of the Hand revealed that surgeons are utilizing nonoperative treatments for a longer duration of time and are employing narrowed surgical indications.²⁴ Thus, clinicians are more likely to try splints and steroid injections before proceeding to operative release.²⁴

Nonsurgical management. In our practice, we commonly recommend corticosteroid injections (TABLE 1^2-4) into the carpal tunnel (FIGURES 4 and 5) to patients who are poor candidates for surgery (ie, those who have too many medical comorbidities or wound healing concerns). This is one indication for which you may want to consider ultrasound-guided injections because the improved accuracy may provide symptom relief faster than “blind” or palpation-guided injections.²⁵

A recent randomized controlled trial from Sweden showed that injections of methylprednisolone relieved symptoms in patients with mild to moderate CTS at 10 weeks and reduced the rate of surgery one year after treatment; however, 3 out of 4 patients still went on to have surgery within a year.²² Patients in the study had failed a 2-month trial of splinting and were given either 80 mg or 40 mg of methylprednisolone or saline. There was no statistical difference between the doses of methylprednisolone in preventing surgery at one year. Compared to placebo, the 80-mg methylprednisolone group was less likely to have surgery with an odds ratio of 0.24 (P=.042).²²

Recent studies show discrete histologic changes in trigger finger tendons, similar to findings with Achilles tendinosis and tendinopathy.

There is evidence that oral steroids, injected steroids, ultrasound, electromagnetic field therapy, nocturnal splinting, and use of ergonomic keyboards are effective nonoperative modalities in the short term, but evidence is sparse for mid- or long-term use.¹⁹ In addition, at least one randomized trial found traditional cupping therapy applied around the shoulder alleviated carpal tunnel symptoms in the short-term.²⁶ Other nonoperative therapies include rest, NSAIDs, extracorporeal shock wave therapy, and activity modification.^19,27

Surgical outcomes by either endoscopic, mini-open, or open surgical techniques are typically good.^20,21 Surgical release involves cutting the transverse carpal ligament over the carpal tunnel to decompress the median nerve.²⁴ You should inform patients of the risks and inconveniences associated with surgery, including the cost, absence from work, infection, and chronic pain. Patients who have recurrent or persistent symptoms after surgery may have had an incompletely released transverse carpal ligament or there may be no identifiable cause.²¹ Overall, surgical treatment, combined with physical therapy, seems to be more effective than splinting or NSAIDs for mid- and long-term treatment of CTS.²⁸

De Quervain’s tenosynovitis: Common during pregnancy

De Quervain’s tenosynovitis (radial styloid tenosynovitis) involves painful inflammation of the 2 tendons in the first dorsal compartment of the wrist—the abductor pollicis longus (APL) and the extensor pollicis brevis (EPB). The tendons comprise the radial border of the anatomic snuffbox.

The APL abducts and extends the thumb at the CMC joint, while the EPB extends the thumb proximal phalanx at the metacarpophalangeal joint. These tendons are contained in a synovial sheath that is subject to inflammation and constriction and subsequent wear and damage.²⁹ In addition, the extensor retinaculum in patients with de Quervain’s disease demonstrates increased vascularity and deposition of dense fibrous tissue resulting in thickening of the tendon up to 5 times its normal width.³⁰

As a result, degeneration and thickening of the tendon sheath, as well as radial-sided wrist pain elicited at the first dorsal compartment, are common pathophysiologic and clinical findings.³¹ Pain is often accompanied by the build-up of protuberances and nodulations of the tendon sheath.

De Quervain’s disease commonly occurs during and after pregnancy.³² Other risk factors include racquet sports, golfing, wrist trauma, and other activities involving repetitive hand and wrist motions.³³ Often, however, de Quervain’s is idiopathic.

Making the Dx: Perform a Finkelstein's test

The major finding in patients with de Quervain’s tenosynovitis is a positive Finkelstein's test. To perform Finkelstein's test (FIGURE 6), ask the patient to oppose the thumb into the palm and flex the fingers of the same hand over the thumb. Holding the patient’s fingers around the thumb, ulnarly deviate the wrist. Finkelstein's test puts strain on the APL and EPB, causing pain along the radial border of the wrist and forearm in patients with de Quervain’s tenosynovitis. Since the maneuver can be uncomfortable, complete the exam on the unaffected side for comparison.

Stenosis of the tendon sheath may lead to crepitus over the first dorsal wrist compartment. This should be distinguished from intersection syndrome (tenosynovitis at the intersection of the first and second extensor compartments), which can also present with forearm and wrist crepitus. Patients usually have swelling of the wrist with marked discomfort upon palpation of the radial tendons. An x-ray can be useful to evaluate for CMC or radiocarpal arthritis, which may be an underlying cause.

Treatment: Select an approach based on symptom severity

In a retrospective analysis, Lane et al concluded that classification of patients with de Quervain’s disease based on pretreatment symptoms may assist physicians in selecting the most efficacious treatment and in providing prognostic information to their patients (TABLE 3³⁴). Patients with mild to moderate (Types 1 and 2) de Quervain’s may benefit from immobilization in a thumb spica splint, rest, NSAIDs, and physical or occupational therapy. If work conditions played a role in causing the symptoms, they need to be addressed to improve outcomes. Types 2 and 3 can be initially treated with a corticosteroid injection, but may eventually require surgery.³³

Treatment with NSAIDs or corticosteroid injections (see TABLE 1^2-4 for choices) in the first compartment of the extensor retinaculum (FIGURE 7) is usually adequate to provide relief. Peters-Veluthamaningal et al performed a systematic review in 2009 and found only one controlled trial of 18 participants (all pregnant or lactating women) who were either injected with corticosteroids or given a thumb spica splint.³⁵ All 9 patients in the injection group had complete pain relief, whereas no one in the splint group had complete resolution of symptoms.³⁵ Typical anatomic placement of corticosteroid injections is shown in FIGURE 7.

More complicated injection methods have been described, but injecting the first dorsal compartment is usually satisfactory. Patients will feel the tendon sheath filling with the injection material. The 2-point technique, implemented by Sawaizumi et al, which involves injecting corticosteroid into 2 points over the EPB and APL tendon in the area of maximum pain and soft tissue thickening, is more effective than the 1-point injection technique.³⁶

Severe, recalcitrant cases. Professional and college athletes may be prone to recalcitrant de Quervain’s tenosynovitis. A 2010 study by Pagonis et al showed that recurrent symptomatic episodes commonly occur in athletes who engage in high-resistance, intense athletic training. In these severe cases, a 4-point injection technique offers better distribution of corticosteroid solution to the first extensor compartment than other methods.³⁷ Consider referring severe cases to a hand surgeon.

Check for carpal tunnel syndrome when examining a patient with trigger finger; the 2 conditions often co-occur.

Surgical release of the first dorsal compartmental sheath around the tendons serves as a final option for patients who fail conservative treatment. Care should be taken to release both tendons completely, as there may be at least 2 tendon slips of the APL or there may be a distinct EPB sheath dorsally.³⁸

“Tennis elbow”— you don’t have to play tennis to have it

Lateral epicondylitis (tennis elbow) is a painful condition involving microtears within the extensor carpi radialis brevis muscle and the subsequent development of angiofibroblastic dysplasia.³⁹ According to Regan et al who studied the histopathologic features of 11 patients with lateral epicondylitis, the underlying cause of recalcitrant lateral epicondylitis is, in fact, degenerative, rather than inflammatory.⁴⁰

Determine whether cervical spin disease and/or peripheral neuropathy are contributing to the patient's symptoms, as patients with carpal tunnel syndrome may have more than one condition at play.

Although the condition has been nicknamed “tennis elbow,” only about 5% of tennis players have the condition.⁴¹ In tennis players, males are more often affected than females, whereas in the general population, incidence is approximately equal in men and women.⁴¹ Lateral epicondylitis occurs between 4 and 7 times more frequently than medial-sided elbow pain.⁴²

Making the Dx: Look for localized pain, normal ROM

The diagnosis of lateral epicondylitis is based upon a history of pain over the lateral epicondyle and findings on physical examination, including local tenderness directly over the lateral epicondyle,⁴³ pain aggravated by resisted wrist extension and radial deviation, pain with resisted middle finger extension, and decreased grip strength or pain aggravated by strong gripping. These findings typically occur in the presence of normal elbow range of motion.

Treatment: Choose from a range of options

Since lateral epicondylitis was first described, researchers have proposed a wide variety of treatments as initial interventions including rest, activity, equipment modification, NSAIDs, wrist bracing/elbow straps, and physical therapy. If initial treatment does not produce the desired effect, second-line treatments include corticosteroid injections (FIGURE 8), prolotherapy (injection of an irritant, often dextrose; see “Prolotherapy: Can it help your patient?” J Fam Pract. 2015;64:763-768), autologous blood injections, platelet-rich plasma injections (see “Is platelet-rich plasma right for your patient?” J Fam Pract. 2016;65:319-328), and needling of the extensor tendon origin. Refer patients who do not improve after one corticosteroid injection to an orthopedic surgeon for consideration of open or arthroscopic treatment.

CORRESPONDENCE
Gregory R. Waryasz, MD, Rhode Island Hospital, Department of Orthopaedic Surgery, 593 Eddy St., Providence, RI 02903; gregory.waryasz.md@gmail.com.

Primary care physicians are frequently the first to evaluate hand, wrist, and forearm pain in patients, making knowledge of the symptoms, causes, and treatment of common diagnoses in the upper extremities imperative. Primary symptoms usually include pain and/or swelling. While most tendon disorders originating in the hand and wrist are idiopathic in nature, some patients occasionally report having recently performed unusual manual activity or having experienced trauma to the area days or weeks prior. A significant portion of patients are injured as a result of chronic repetitive activities at work.¹

Most diagnoses can be made by pairing your knowledge of hand and forearm anatomy with an understanding of which tender points are indicative of which common conditions. (Care, of course, must be taken to ensure that there is no underlying infection.) Common conditions can often be treated nonsurgically with conservative treatments such as physical therapy, bracing/splinting, nonsteroidal anti-inflammatory drugs (NSAIDs), and injections of corticosteroids (eg, betamethasone, hydrocortisone, methylprednisolone, and triamcinolone) (TABLE 1^2-4) with or without the use of ultrasound. The benefits of corticosteroid injections for these conditions are well studied and documented in the literature, although physicians should always warn patients of the possible adverse effects prior to injection^3,5 (TABLE 2⁴).

To help you refine your skills, we review some of the more common hand and forearm conditions you are likely to encounter in the office and provide photos that reveal underlying anatomy so that you can administer injections without, in many cases, the need for ultrasound.

Trigger finger/thumb: New pathophysiologic findings?

Trigger finger most commonly occurs in the dominant hand. It is also more common in women, patients in their 50s, and in individuals with diabetes.⁶ Trigger finger/thumb is caused by inflammation and constriction of the flexor tendon sheath, which carries the flexor tendons through the palm and into the fingers and thumb. This, in turn, causes irritation of the tendons, sometimes via the formation of tendinous nodules, which may impinge upon the sheath’s “pulley system.”

When the “pulley” is compromised. The retinacular sheath is composed of 5 annular ligaments, or pulleys, that hold the tendons of the fingers close to the bone and allow the fingers to flex properly. The A1 pulley, at the level of the metacarpal head, is the first part of the sheath and is subject to the highest force; high forces may subsequently lead to the finger becoming locked in a flexed, or trigger, position.⁶ Patients may experience pain in the distal palm at the level of the A1 pulley and clicking of the finger.⁶

Additionally . . . recent studies show discrete histologic changes in trigger finger tendons, similar to findings with Achilles tendinosis and tendinopathy.⁷ In trigger finger tendons, collagen type 1A1 and 3A1, aggrecan, and biglycan are up-regulated, while metalloproteinase inhibitor 3 (TIMP-3) and matrix metallopeptidase³ (MMP-3) are down-regulated, a situation also described in Achilles tendinosis.⁷ This similarity in conditions provides new insight into the pathophysiology of the condition and may help provide future treatments.

Making the Dx: Look for swelling, check for carpal tunnel

During the examination, first look at both hands for swelling, arthropathy, or injury, and note the presence of any joint contractures. Next, examine all of the digits in flexion and extension while noting which ones are triggering, as the problem can occur in multiple digits on one hand. Then palpate the palms over the patient’s metacarpal heads, feeling for tender nodules.

Most diagnoses can be made by pairing your knowledge of hand and forearm anatomy with an understanding of which tender points are indicative of which common conditions.

Finally, examine the patient for carpal tunnel syndrome (CTS). A positive Tinel’s sign (shooting pain into the hand when the median nerve in the wrist is percussed), a positive Phalen maneuver (numbness or pain, usually within one minute of full wrist flexion), or thenar muscle wasting are highly indicative of CTS (compression of the median nerve at the transverse carpal ligament in the carpal tunnel). It is important to check for CTS when examining a patient for trigger finger because the 2 conditions frequently co-occur.⁶ (For more on CTS, see here.)

Treatment: Consider corticosteroids first

First-line treatment for patients with trigger finger or thumb is a corticosteroid injection into the subcutaneous tissue around the tendon sheath (FIGURES 1 and 2). (For this indication and for the others discussed throughout the article, there isn’t tremendous evidence for one particular type of corticosteroid over another; see TABLE 1^2-4 for choices.) Up to 57% of cases resolve with one injection, and 86% resolve with 2,⁸ but keep in mind that it may take up to 2 weeks to achieve the full clinical benefit.

Patients with multiple trigger fingers can be treated with oral corticosteroids (eg, a methylprednisolone dose pack). Peters-Veluthamaningal et al performed a systematic review in 2009 and found 2 randomized controlled trials involving 63 patients (34 received injections of a corticosteroid [either methylprednisolone or betamethasone] and lidocaine and 29 received lidocaine only).² The corticosteroid/lidocaine combination was more effective at 4 weeks (relative risk [RR]=3.15; 95% confidence interval [CI], 1.34 to 7.40).²

If 2 corticosteroid injections 6 weeks apart fail to provide benefit, or the finger is irreversibly locked in flexion, surgical release of the pulley is required and is performed through a palmar incision at the level of the A1 pulley. Complications from this surgery, including nerve damage, are exceedingly rare, but injury can occur, given the proximity of the digital nerves to the A1 pulley.

Patient is a child? Refer children with trigger finger or thumb to a hand surgeon for evaluation and management because the indications for nonoperative treatment in the pediatric population are unclear.⁹

Carpometacarpal arthritis: Common, with many causes

Osteoarthritis of the first carpometacarpal (CMC) joint is the most common site of arthritis in the hand/wrist region, affecting up to 11% of men and 33% of women in their 50s and 60s.¹⁰ Because the CMC joint lacks a bony restraint, it relies on a number of ligaments for stability—the strongest and most important of which is the palmar oblique “beak” ligament.¹¹ A major cause of degenerative arthritis of this joint is attenuation and laxity of these ligaments, leading to abnormal and increased stress loads, which, in turn, can lead to loss of cartilage and bony impingement. While the exact mechanism of this process is not fully understood,^10,12 acute or chronic trauma, advanced age, hormonal factors, and genetic factors seem to play a role.¹¹

Many believe there is a relationship between a patient's occupation and the development of CMC arthritis, but studies are inconclusive.¹³ At risk are secretarial workers, tailors, domestic helpers/cleaners, and individuals whose jobs involve repetitive thumb use and/or insufficient rest of the joint throughout the day.

Making the Dx: Perform the Grind test

A detailed patient history (which is usually void of trauma to the hand) and physical examination are the keys to making the diagnosis of CMC arthritis. A history of pain at the base of the thumb during pinching and gripping tasks is often elucidated. Classically, patients describe pain upon turning keys, opening jars, and gripping doorknobs.¹¹

It's important to focus on the dorsoradial aspect of the thumb during the physical exam and to rule out other causes of pain, such as de Quervain’s tenosynovitis, flexor carpi radialis tendinitis, CTS, and trigger thumb.¹¹ Typical findings include pain with palpation directly over the dorsoradial aspect of the CMC joint and pain with axial loading and upon circumduction during a Grind test of the CMC joint. (The Grind test is performed by moving the metacarpal bone of the thumb in a circle and loading it with gentle axial forces. People with thumb joint arthritis generally experience sudden sharp pain at the CMC joint.)

Radiographic findings can be useful as a diagnostic adjunct, with staging of the disease, and in determining who can benefit from conservative management.¹¹

Treatment: Start with NSAIDs and splinting

Depending on the degree of arthritis, management may include both conservative and surgical options.¹⁰ Patient education describing activity modification is useful during all stages of CMC arthritis. Research has shown that avoiding inciting activities, such as key turning, pinching, and grasping, helps to alleviate symptoms.¹⁴ Patients may also obtain relief from NSAIDs, especially when they are used in conjunction with activity modification and splinting. NSAIDs, however, do not halt or reverse the disease process; they only reduce inflammation, synovitis, and pain.¹¹

Splinting. Studies have shown splinting of the thumb CMC joint to provide pain relief and to potentially slow disease progression.¹⁵ Because splints decrease motion and increase joint stability, they are especially useful for patients with joint hypermobility. The long opponens thumb spica splint is commonly used; it immobilizes the wrist and CMC, while leaving the thumb interphalangeal joint free. Short thumb spica and neoprene splints are also commercially available, and studies have shown that they provide good results.¹⁵ Splinting is most beneficial in patients with early-stage disease and may be used for either short-term flares or long-term treatment.¹¹

Cortisone injections. For those patients who do not respond to activity modification, NSAIDs, and/or splinting, consider cortisone injections (FIGURE 3). Intra-articular cortisone injections can decrease inflammation and provide good pain relief, especially in patients with early-stage disease. The effectiveness of cortisone injections in patients with more advanced disease is not clear; no benefit has been shown in studies to date.¹⁶ Equally unclear is the long-term benefit of injections.¹¹ Patients who do not respond to conservative treatments will often require surgical care.

Carpal tunnel syndrome: Moving slower to surgery

CTS is one of the most common conditions of the upper extremities. Researchers estimate that 491 women per 100,000 person-years and 258 men per 100,000 person-years will develop CTS, with 109 per 100,000 person-years receiving carpal tunnel release surgery.¹⁷ Risk factors for the development of CTS include diabetes, hypothyroidism, rheumatoid arthritis, pregnancy, obesity, family history, trauma, and occupations that involve repetitive tasks or long hours working at a computer.¹⁸

CTS is caused by compression of the median nerve as it passes through the carpal tunnel.¹⁹ The elevated pressure in the carpal tunnel restricts epineural blood flow and supply, causing the pain felt with CTS.²⁰ Even after surgical decompression, recurrent or persistent CTS can be a problem.²¹

Making the Dx: Perform the Phalen maneuver, Durkan’s test

Patients typically present with complaints of weakness, pain, and/or numbness in at least 2 of 4 radial digits (thumb, index, middle, ring).^19,22 The most common time of day for patients to have symptoms is at night.²¹

The diagnostic tools. Tinel’s sign is a useful diagnostic tool when you suspect carpal tunnel syndrome. Tinel’s sign is positive if percussion over the median nerve at the carpal tunnel elicits pain or paresthesia.¹⁸

When employing the Phalen maneuver, be certain to have the patient flex his/her wrist to 90 degrees and to document the number of seconds it takes for numbness to present in the fingers. Pain or paresthesia should occur in <60 seconds for the test to be positive.¹⁸

Median nerve compression over the carpal tunnel, also known as Durkan’s test, may also elicit symptoms. With Durkan’s test, you apply direct pressure over the transverse carpal ligament. If pain or paresthesia occurs in <30 seconds, the test is positive.¹⁸ Often clinicians will combine the Phalen maneuver and Durkan’s test to increase sensitivity and specificity.¹⁸ Nerve conduction studies are often performed to confirm the clinical diagnosis.

Is more than one condition at play? It is important to determine whether cervical spine disease and/or peripheral neuropathy is contributing to the patient’s symptoms, along with CTS; patients may have more than one condition contributing to their pain. We routinely check cervical spine motion, tenderness, and nerve compression as part of the exam on a patient with suspected CTS. In the office, a monofilament test or 2-point discrimination test can help make the clinical diagnosis by uncovering decreased sensation in the thumb, index, and/or middle fingers.²³

The 5.07 monofilament test is performed with the clinician applying the monofilament to different dermatomal or sensory distributions while the patient has his/her eyes closed. The 2-point discrimination test is performed with a caliper device that measures the distance at which the patient can feel 2 separate stimuli. Often electromyography or nerve conduction studies are necessary.¹⁸

Treatment: Pursue nonoperative approaches

A survey of the membership of the American Society for Surgery of the Hand revealed that surgeons are utilizing nonoperative treatments for a longer duration of time and are employing narrowed surgical indications.²⁴ Thus, clinicians are more likely to try splints and steroid injections before proceeding to operative release.²⁴

Nonsurgical management. In our practice, we commonly recommend corticosteroid injections (TABLE 1^2-4) into the carpal tunnel (FIGURES 4 and 5) to patients who are poor candidates for surgery (ie, those who have too many medical comorbidities or wound healing concerns). This is one indication for which you may want to consider ultrasound-guided injections because the improved accuracy may provide symptom relief faster than “blind” or palpation-guided injections.²⁵

A recent randomized controlled trial from Sweden showed that injections of methylprednisolone relieved symptoms in patients with mild to moderate CTS at 10 weeks and reduced the rate of surgery one year after treatment; however, 3 out of 4 patients still went on to have surgery within a year.²² Patients in the study had failed a 2-month trial of splinting and were given either 80 mg or 40 mg of methylprednisolone or saline. There was no statistical difference between the doses of methylprednisolone in preventing surgery at one year. Compared to placebo, the 80-mg methylprednisolone group was less likely to have surgery with an odds ratio of 0.24 (P=.042).²²

Recent studies show discrete histologic changes in trigger finger tendons, similar to findings with Achilles tendinosis and tendinopathy.

There is evidence that oral steroids, injected steroids, ultrasound, electromagnetic field therapy, nocturnal splinting, and use of ergonomic keyboards are effective nonoperative modalities in the short term, but evidence is sparse for mid- or long-term use.¹⁹ In addition, at least one randomized trial found traditional cupping therapy applied around the shoulder alleviated carpal tunnel symptoms in the short-term.²⁶ Other nonoperative therapies include rest, NSAIDs, extracorporeal shock wave therapy, and activity modification.^19,27

Surgical outcomes by either endoscopic, mini-open, or open surgical techniques are typically good.^20,21 Surgical release involves cutting the transverse carpal ligament over the carpal tunnel to decompress the median nerve.²⁴ You should inform patients of the risks and inconveniences associated with surgery, including the cost, absence from work, infection, and chronic pain. Patients who have recurrent or persistent symptoms after surgery may have had an incompletely released transverse carpal ligament or there may be no identifiable cause.²¹ Overall, surgical treatment, combined with physical therapy, seems to be more effective than splinting or NSAIDs for mid- and long-term treatment of CTS.²⁸

De Quervain’s tenosynovitis: Common during pregnancy

De Quervain’s tenosynovitis (radial styloid tenosynovitis) involves painful inflammation of the 2 tendons in the first dorsal compartment of the wrist—the abductor pollicis longus (APL) and the extensor pollicis brevis (EPB). The tendons comprise the radial border of the anatomic snuffbox.

The APL abducts and extends the thumb at the CMC joint, while the EPB extends the thumb proximal phalanx at the metacarpophalangeal joint. These tendons are contained in a synovial sheath that is subject to inflammation and constriction and subsequent wear and damage.²⁹ In addition, the extensor retinaculum in patients with de Quervain’s disease demonstrates increased vascularity and deposition of dense fibrous tissue resulting in thickening of the tendon up to 5 times its normal width.³⁰

As a result, degeneration and thickening of the tendon sheath, as well as radial-sided wrist pain elicited at the first dorsal compartment, are common pathophysiologic and clinical findings.³¹ Pain is often accompanied by the build-up of protuberances and nodulations of the tendon sheath.

De Quervain’s disease commonly occurs during and after pregnancy.³² Other risk factors include racquet sports, golfing, wrist trauma, and other activities involving repetitive hand and wrist motions.³³ Often, however, de Quervain’s is idiopathic.

Making the Dx: Perform a Finkelstein's test

The major finding in patients with de Quervain’s tenosynovitis is a positive Finkelstein's test. To perform Finkelstein's test (FIGURE 6), ask the patient to oppose the thumb into the palm and flex the fingers of the same hand over the thumb. Holding the patient’s fingers around the thumb, ulnarly deviate the wrist. Finkelstein's test puts strain on the APL and EPB, causing pain along the radial border of the wrist and forearm in patients with de Quervain’s tenosynovitis. Since the maneuver can be uncomfortable, complete the exam on the unaffected side for comparison.

Stenosis of the tendon sheath may lead to crepitus over the first dorsal wrist compartment. This should be distinguished from intersection syndrome (tenosynovitis at the intersection of the first and second extensor compartments), which can also present with forearm and wrist crepitus. Patients usually have swelling of the wrist with marked discomfort upon palpation of the radial tendons. An x-ray can be useful to evaluate for CMC or radiocarpal arthritis, which may be an underlying cause.

Treatment: Select an approach based on symptom severity

In a retrospective analysis, Lane et al concluded that classification of patients with de Quervain’s disease based on pretreatment symptoms may assist physicians in selecting the most efficacious treatment and in providing prognostic information to their patients (TABLE 3³⁴). Patients with mild to moderate (Types 1 and 2) de Quervain’s may benefit from immobilization in a thumb spica splint, rest, NSAIDs, and physical or occupational therapy. If work conditions played a role in causing the symptoms, they need to be addressed to improve outcomes. Types 2 and 3 can be initially treated with a corticosteroid injection, but may eventually require surgery.³³

Treatment with NSAIDs or corticosteroid injections (see TABLE 1^2-4 for choices) in the first compartment of the extensor retinaculum (FIGURE 7) is usually adequate to provide relief. Peters-Veluthamaningal et al performed a systematic review in 2009 and found only one controlled trial of 18 participants (all pregnant or lactating women) who were either injected with corticosteroids or given a thumb spica splint.³⁵ All 9 patients in the injection group had complete pain relief, whereas no one in the splint group had complete resolution of symptoms.³⁵ Typical anatomic placement of corticosteroid injections is shown in FIGURE 7.

More complicated injection methods have been described, but injecting the first dorsal compartment is usually satisfactory. Patients will feel the tendon sheath filling with the injection material. The 2-point technique, implemented by Sawaizumi et al, which involves injecting corticosteroid into 2 points over the EPB and APL tendon in the area of maximum pain and soft tissue thickening, is more effective than the 1-point injection technique.³⁶

Severe, recalcitrant cases. Professional and college athletes may be prone to recalcitrant de Quervain’s tenosynovitis. A 2010 study by Pagonis et al showed that recurrent symptomatic episodes commonly occur in athletes who engage in high-resistance, intense athletic training. In these severe cases, a 4-point injection technique offers better distribution of corticosteroid solution to the first extensor compartment than other methods.³⁷ Consider referring severe cases to a hand surgeon.

Check for carpal tunnel syndrome when examining a patient with trigger finger; the 2 conditions often co-occur.

Surgical release of the first dorsal compartmental sheath around the tendons serves as a final option for patients who fail conservative treatment. Care should be taken to release both tendons completely, as there may be at least 2 tendon slips of the APL or there may be a distinct EPB sheath dorsally.³⁸

“Tennis elbow”— you don’t have to play tennis to have it

Lateral epicondylitis (tennis elbow) is a painful condition involving microtears within the extensor carpi radialis brevis muscle and the subsequent development of angiofibroblastic dysplasia.³⁹ According to Regan et al who studied the histopathologic features of 11 patients with lateral epicondylitis, the underlying cause of recalcitrant lateral epicondylitis is, in fact, degenerative, rather than inflammatory.⁴⁰

Determine whether cervical spin disease and/or peripheral neuropathy are contributing to the patient's symptoms, as patients with carpal tunnel syndrome may have more than one condition at play.

Although the condition has been nicknamed “tennis elbow,” only about 5% of tennis players have the condition.⁴¹ In tennis players, males are more often affected than females, whereas in the general population, incidence is approximately equal in men and women.⁴¹ Lateral epicondylitis occurs between 4 and 7 times more frequently than medial-sided elbow pain.⁴²

Making the Dx: Look for localized pain, normal ROM

The diagnosis of lateral epicondylitis is based upon a history of pain over the lateral epicondyle and findings on physical examination, including local tenderness directly over the lateral epicondyle,⁴³ pain aggravated by resisted wrist extension and radial deviation, pain with resisted middle finger extension, and decreased grip strength or pain aggravated by strong gripping. These findings typically occur in the presence of normal elbow range of motion.

Treatment: Choose from a range of options

Since lateral epicondylitis was first described, researchers have proposed a wide variety of treatments as initial interventions including rest, activity, equipment modification, NSAIDs, wrist bracing/elbow straps, and physical therapy. If initial treatment does not produce the desired effect, second-line treatments include corticosteroid injections (FIGURE 8), prolotherapy (injection of an irritant, often dextrose; see “Prolotherapy: Can it help your patient?” J Fam Pract. 2015;64:763-768), autologous blood injections, platelet-rich plasma injections (see “Is platelet-rich plasma right for your patient?” J Fam Pract. 2016;65:319-328), and needling of the extensor tendon origin. Refer patients who do not improve after one corticosteroid injection to an orthopedic surgeon for consideration of open or arthroscopic treatment.

CORRESPONDENCE
Gregory R. Waryasz, MD, Rhode Island Hospital, Department of Orthopaedic Surgery, 593 Eddy St., Providence, RI 02903; gregory.waryasz.md@gmail.com.

Primary care physicians are frequently the first to evaluate hand, wrist, and forearm pain in patients, making knowledge of the symptoms, causes, and treatment of common diagnoses in the upper extremities imperative. Primary symptoms usually include pain and/or swelling. While most tendon disorders originating in the hand and wrist are idiopathic in nature, some patients occasionally report having recently performed unusual manual activity or having experienced trauma to the area days or weeks prior. A significant portion of patients are injured as a result of chronic repetitive activities at work.¹

Most diagnoses can be made by pairing your knowledge of hand and forearm anatomy with an understanding of which tender points are indicative of which common conditions. (Care, of course, must be taken to ensure that there is no underlying infection.) Common conditions can often be treated nonsurgically with conservative treatments such as physical therapy, bracing/splinting, nonsteroidal anti-inflammatory drugs (NSAIDs), and injections of corticosteroids (eg, betamethasone, hydrocortisone, methylprednisolone, and triamcinolone) (TABLE 1^2-4) with or without the use of ultrasound. The benefits of corticosteroid injections for these conditions are well studied and documented in the literature, although physicians should always warn patients of the possible adverse effects prior to injection^3,5 (TABLE 2⁴).

To help you refine your skills, we review some of the more common hand and forearm conditions you are likely to encounter in the office and provide photos that reveal underlying anatomy so that you can administer injections without, in many cases, the need for ultrasound.

Trigger finger/thumb: New pathophysiologic findings?

Trigger finger most commonly occurs in the dominant hand. It is also more common in women, patients in their 50s, and in individuals with diabetes.⁶ Trigger finger/thumb is caused by inflammation and constriction of the flexor tendon sheath, which carries the flexor tendons through the palm and into the fingers and thumb. This, in turn, causes irritation of the tendons, sometimes via the formation of tendinous nodules, which may impinge upon the sheath’s “pulley system.”

When the “pulley” is compromised. The retinacular sheath is composed of 5 annular ligaments, or pulleys, that hold the tendons of the fingers close to the bone and allow the fingers to flex properly. The A1 pulley, at the level of the metacarpal head, is the first part of the sheath and is subject to the highest force; high forces may subsequently lead to the finger becoming locked in a flexed, or trigger, position.⁶ Patients may experience pain in the distal palm at the level of the A1 pulley and clicking of the finger.⁶

Additionally . . . recent studies show discrete histologic changes in trigger finger tendons, similar to findings with Achilles tendinosis and tendinopathy.⁷ In trigger finger tendons, collagen type 1A1 and 3A1, aggrecan, and biglycan are up-regulated, while metalloproteinase inhibitor 3 (TIMP-3) and matrix metallopeptidase³ (MMP-3) are down-regulated, a situation also described in Achilles tendinosis.⁷ This similarity in conditions provides new insight into the pathophysiology of the condition and may help provide future treatments.

Making the Dx: Look for swelling, check for carpal tunnel

During the examination, first look at both hands for swelling, arthropathy, or injury, and note the presence of any joint contractures. Next, examine all of the digits in flexion and extension while noting which ones are triggering, as the problem can occur in multiple digits on one hand. Then palpate the palms over the patient’s metacarpal heads, feeling for tender nodules.

Most diagnoses can be made by pairing your knowledge of hand and forearm anatomy with an understanding of which tender points are indicative of which common conditions.

Finally, examine the patient for carpal tunnel syndrome (CTS). A positive Tinel’s sign (shooting pain into the hand when the median nerve in the wrist is percussed), a positive Phalen maneuver (numbness or pain, usually within one minute of full wrist flexion), or thenar muscle wasting are highly indicative of CTS (compression of the median nerve at the transverse carpal ligament in the carpal tunnel). It is important to check for CTS when examining a patient for trigger finger because the 2 conditions frequently co-occur.⁶ (For more on CTS, see here.)

Treatment: Consider corticosteroids first

First-line treatment for patients with trigger finger or thumb is a corticosteroid injection into the subcutaneous tissue around the tendon sheath (FIGURES 1 and 2). (For this indication and for the others discussed throughout the article, there isn’t tremendous evidence for one particular type of corticosteroid over another; see TABLE 1^2-4 for choices.) Up to 57% of cases resolve with one injection, and 86% resolve with 2,⁸ but keep in mind that it may take up to 2 weeks to achieve the full clinical benefit.

Patients with multiple trigger fingers can be treated with oral corticosteroids (eg, a methylprednisolone dose pack). Peters-Veluthamaningal et al performed a systematic review in 2009 and found 2 randomized controlled trials involving 63 patients (34 received injections of a corticosteroid [either methylprednisolone or betamethasone] and lidocaine and 29 received lidocaine only).² The corticosteroid/lidocaine combination was more effective at 4 weeks (relative risk [RR]=3.15; 95% confidence interval [CI], 1.34 to 7.40).²

If 2 corticosteroid injections 6 weeks apart fail to provide benefit, or the finger is irreversibly locked in flexion, surgical release of the pulley is required and is performed through a palmar incision at the level of the A1 pulley. Complications from this surgery, including nerve damage, are exceedingly rare, but injury can occur, given the proximity of the digital nerves to the A1 pulley.

Patient is a child? Refer children with trigger finger or thumb to a hand surgeon for evaluation and management because the indications for nonoperative treatment in the pediatric population are unclear.⁹

Carpometacarpal arthritis: Common, with many causes

Osteoarthritis of the first carpometacarpal (CMC) joint is the most common site of arthritis in the hand/wrist region, affecting up to 11% of men and 33% of women in their 50s and 60s.¹⁰ Because the CMC joint lacks a bony restraint, it relies on a number of ligaments for stability—the strongest and most important of which is the palmar oblique “beak” ligament.¹¹ A major cause of degenerative arthritis of this joint is attenuation and laxity of these ligaments, leading to abnormal and increased stress loads, which, in turn, can lead to loss of cartilage and bony impingement. While the exact mechanism of this process is not fully understood,^10,12 acute or chronic trauma, advanced age, hormonal factors, and genetic factors seem to play a role.¹¹

Many believe there is a relationship between a patient's occupation and the development of CMC arthritis, but studies are inconclusive.¹³ At risk are secretarial workers, tailors, domestic helpers/cleaners, and individuals whose jobs involve repetitive thumb use and/or insufficient rest of the joint throughout the day.

Making the Dx: Perform the Grind test

A detailed patient history (which is usually void of trauma to the hand) and physical examination are the keys to making the diagnosis of CMC arthritis. A history of pain at the base of the thumb during pinching and gripping tasks is often elucidated. Classically, patients describe pain upon turning keys, opening jars, and gripping doorknobs.¹¹

It's important to focus on the dorsoradial aspect of the thumb during the physical exam and to rule out other causes of pain, such as de Quervain’s tenosynovitis, flexor carpi radialis tendinitis, CTS, and trigger thumb.¹¹ Typical findings include pain with palpation directly over the dorsoradial aspect of the CMC joint and pain with axial loading and upon circumduction during a Grind test of the CMC joint. (The Grind test is performed by moving the metacarpal bone of the thumb in a circle and loading it with gentle axial forces. People with thumb joint arthritis generally experience sudden sharp pain at the CMC joint.)

Radiographic findings can be useful as a diagnostic adjunct, with staging of the disease, and in determining who can benefit from conservative management.¹¹

Treatment: Start with NSAIDs and splinting

Depending on the degree of arthritis, management may include both conservative and surgical options.¹⁰ Patient education describing activity modification is useful during all stages of CMC arthritis. Research has shown that avoiding inciting activities, such as key turning, pinching, and grasping, helps to alleviate symptoms.¹⁴ Patients may also obtain relief from NSAIDs, especially when they are used in conjunction with activity modification and splinting. NSAIDs, however, do not halt or reverse the disease process; they only reduce inflammation, synovitis, and pain.¹¹

Splinting. Studies have shown splinting of the thumb CMC joint to provide pain relief and to potentially slow disease progression.¹⁵ Because splints decrease motion and increase joint stability, they are especially useful for patients with joint hypermobility. The long opponens thumb spica splint is commonly used; it immobilizes the wrist and CMC, while leaving the thumb interphalangeal joint free. Short thumb spica and neoprene splints are also commercially available, and studies have shown that they provide good results.¹⁵ Splinting is most beneficial in patients with early-stage disease and may be used for either short-term flares or long-term treatment.¹¹

Cortisone injections. For those patients who do not respond to activity modification, NSAIDs, and/or splinting, consider cortisone injections (FIGURE 3). Intra-articular cortisone injections can decrease inflammation and provide good pain relief, especially in patients with early-stage disease. The effectiveness of cortisone injections in patients with more advanced disease is not clear; no benefit has been shown in studies to date.¹⁶ Equally unclear is the long-term benefit of injections.¹¹ Patients who do not respond to conservative treatments will often require surgical care.

Carpal tunnel syndrome: Moving slower to surgery

CTS is one of the most common conditions of the upper extremities. Researchers estimate that 491 women per 100,000 person-years and 258 men per 100,000 person-years will develop CTS, with 109 per 100,000 person-years receiving carpal tunnel release surgery.¹⁷ Risk factors for the development of CTS include diabetes, hypothyroidism, rheumatoid arthritis, pregnancy, obesity, family history, trauma, and occupations that involve repetitive tasks or long hours working at a computer.¹⁸

CTS is caused by compression of the median nerve as it passes through the carpal tunnel.¹⁹ The elevated pressure in the carpal tunnel restricts epineural blood flow and supply, causing the pain felt with CTS.²⁰ Even after surgical decompression, recurrent or persistent CTS can be a problem.²¹

Making the Dx: Perform the Phalen maneuver, Durkan’s test

Patients typically present with complaints of weakness, pain, and/or numbness in at least 2 of 4 radial digits (thumb, index, middle, ring).^19,22 The most common time of day for patients to have symptoms is at night.²¹

The diagnostic tools. Tinel’s sign is a useful diagnostic tool when you suspect carpal tunnel syndrome. Tinel’s sign is positive if percussion over the median nerve at the carpal tunnel elicits pain or paresthesia.¹⁸

When employing the Phalen maneuver, be certain to have the patient flex his/her wrist to 90 degrees and to document the number of seconds it takes for numbness to present in the fingers. Pain or paresthesia should occur in <60 seconds for the test to be positive.¹⁸

Median nerve compression over the carpal tunnel, also known as Durkan’s test, may also elicit symptoms. With Durkan’s test, you apply direct pressure over the transverse carpal ligament. If pain or paresthesia occurs in <30 seconds, the test is positive.¹⁸ Often clinicians will combine the Phalen maneuver and Durkan’s test to increase sensitivity and specificity.¹⁸ Nerve conduction studies are often performed to confirm the clinical diagnosis.

Is more than one condition at play? It is important to determine whether cervical spine disease and/or peripheral neuropathy is contributing to the patient’s symptoms, along with CTS; patients may have more than one condition contributing to their pain. We routinely check cervical spine motion, tenderness, and nerve compression as part of the exam on a patient with suspected CTS. In the office, a monofilament test or 2-point discrimination test can help make the clinical diagnosis by uncovering decreased sensation in the thumb, index, and/or middle fingers.²³

The 5.07 monofilament test is performed with the clinician applying the monofilament to different dermatomal or sensory distributions while the patient has his/her eyes closed. The 2-point discrimination test is performed with a caliper device that measures the distance at which the patient can feel 2 separate stimuli. Often electromyography or nerve conduction studies are necessary.¹⁸

Treatment: Pursue nonoperative approaches

A survey of the membership of the American Society for Surgery of the Hand revealed that surgeons are utilizing nonoperative treatments for a longer duration of time and are employing narrowed surgical indications.²⁴ Thus, clinicians are more likely to try splints and steroid injections before proceeding to operative release.²⁴

Nonsurgical management. In our practice, we commonly recommend corticosteroid injections (TABLE 1^2-4) into the carpal tunnel (FIGURES 4 and 5) to patients who are poor candidates for surgery (ie, those who have too many medical comorbidities or wound healing concerns). This is one indication for which you may want to consider ultrasound-guided injections because the improved accuracy may provide symptom relief faster than “blind” or palpation-guided injections.²⁵

A recent randomized controlled trial from Sweden showed that injections of methylprednisolone relieved symptoms in patients with mild to moderate CTS at 10 weeks and reduced the rate of surgery one year after treatment; however, 3 out of 4 patients still went on to have surgery within a year.²² Patients in the study had failed a 2-month trial of splinting and were given either 80 mg or 40 mg of methylprednisolone or saline. There was no statistical difference between the doses of methylprednisolone in preventing surgery at one year. Compared to placebo, the 80-mg methylprednisolone group was less likely to have surgery with an odds ratio of 0.24 (P=.042).²²

Recent studies show discrete histologic changes in trigger finger tendons, similar to findings with Achilles tendinosis and tendinopathy.

There is evidence that oral steroids, injected steroids, ultrasound, electromagnetic field therapy, nocturnal splinting, and use of ergonomic keyboards are effective nonoperative modalities in the short term, but evidence is sparse for mid- or long-term use.¹⁹ In addition, at least one randomized trial found traditional cupping therapy applied around the shoulder alleviated carpal tunnel symptoms in the short-term.²⁶ Other nonoperative therapies include rest, NSAIDs, extracorporeal shock wave therapy, and activity modification.^19,27

Surgical outcomes by either endoscopic, mini-open, or open surgical techniques are typically good.^20,21 Surgical release involves cutting the transverse carpal ligament over the carpal tunnel to decompress the median nerve.²⁴ You should inform patients of the risks and inconveniences associated with surgery, including the cost, absence from work, infection, and chronic pain. Patients who have recurrent or persistent symptoms after surgery may have had an incompletely released transverse carpal ligament or there may be no identifiable cause.²¹ Overall, surgical treatment, combined with physical therapy, seems to be more effective than splinting or NSAIDs for mid- and long-term treatment of CTS.²⁸

De Quervain’s tenosynovitis: Common during pregnancy

De Quervain’s tenosynovitis (radial styloid tenosynovitis) involves painful inflammation of the 2 tendons in the first dorsal compartment of the wrist—the abductor pollicis longus (APL) and the extensor pollicis brevis (EPB). The tendons comprise the radial border of the anatomic snuffbox.

The APL abducts and extends the thumb at the CMC joint, while the EPB extends the thumb proximal phalanx at the metacarpophalangeal joint. These tendons are contained in a synovial sheath that is subject to inflammation and constriction and subsequent wear and damage.²⁹ In addition, the extensor retinaculum in patients with de Quervain’s disease demonstrates increased vascularity and deposition of dense fibrous tissue resulting in thickening of the tendon up to 5 times its normal width.³⁰

As a result, degeneration and thickening of the tendon sheath, as well as radial-sided wrist pain elicited at the first dorsal compartment, are common pathophysiologic and clinical findings.³¹ Pain is often accompanied by the build-up of protuberances and nodulations of the tendon sheath.

De Quervain’s disease commonly occurs during and after pregnancy.³² Other risk factors include racquet sports, golfing, wrist trauma, and other activities involving repetitive hand and wrist motions.³³ Often, however, de Quervain’s is idiopathic.

Making the Dx: Perform a Finkelstein's test

The major finding in patients with de Quervain’s tenosynovitis is a positive Finkelstein's test. To perform Finkelstein's test (FIGURE 6), ask the patient to oppose the thumb into the palm and flex the fingers of the same hand over the thumb. Holding the patient’s fingers around the thumb, ulnarly deviate the wrist. Finkelstein's test puts strain on the APL and EPB, causing pain along the radial border of the wrist and forearm in patients with de Quervain’s tenosynovitis. Since the maneuver can be uncomfortable, complete the exam on the unaffected side for comparison.

Stenosis of the tendon sheath may lead to crepitus over the first dorsal wrist compartment. This should be distinguished from intersection syndrome (tenosynovitis at the intersection of the first and second extensor compartments), which can also present with forearm and wrist crepitus. Patients usually have swelling of the wrist with marked discomfort upon palpation of the radial tendons. An x-ray can be useful to evaluate for CMC or radiocarpal arthritis, which may be an underlying cause.

Treatment: Select an approach based on symptom severity

In a retrospective analysis, Lane et al concluded that classification of patients with de Quervain’s disease based on pretreatment symptoms may assist physicians in selecting the most efficacious treatment and in providing prognostic information to their patients (TABLE 3³⁴). Patients with mild to moderate (Types 1 and 2) de Quervain’s may benefit from immobilization in a thumb spica splint, rest, NSAIDs, and physical or occupational therapy. If work conditions played a role in causing the symptoms, they need to be addressed to improve outcomes. Types 2 and 3 can be initially treated with a corticosteroid injection, but may eventually require surgery.³³

Treatment with NSAIDs or corticosteroid injections (see TABLE 1^2-4 for choices) in the first compartment of the extensor retinaculum (FIGURE 7) is usually adequate to provide relief. Peters-Veluthamaningal et al performed a systematic review in 2009 and found only one controlled trial of 18 participants (all pregnant or lactating women) who were either injected with corticosteroids or given a thumb spica splint.³⁵ All 9 patients in the injection group had complete pain relief, whereas no one in the splint group had complete resolution of symptoms.³⁵ Typical anatomic placement of corticosteroid injections is shown in FIGURE 7.

More complicated injection methods have been described, but injecting the first dorsal compartment is usually satisfactory. Patients will feel the tendon sheath filling with the injection material. The 2-point technique, implemented by Sawaizumi et al, which involves injecting corticosteroid into 2 points over the EPB and APL tendon in the area of maximum pain and soft tissue thickening, is more effective than the 1-point injection technique.³⁶

Severe, recalcitrant cases. Professional and college athletes may be prone to recalcitrant de Quervain’s tenosynovitis. A 2010 study by Pagonis et al showed that recurrent symptomatic episodes commonly occur in athletes who engage in high-resistance, intense athletic training. In these severe cases, a 4-point injection technique offers better distribution of corticosteroid solution to the first extensor compartment than other methods.³⁷ Consider referring severe cases to a hand surgeon.

Check for carpal tunnel syndrome when examining a patient with trigger finger; the 2 conditions often co-occur.

Surgical release of the first dorsal compartmental sheath around the tendons serves as a final option for patients who fail conservative treatment. Care should be taken to release both tendons completely, as there may be at least 2 tendon slips of the APL or there may be a distinct EPB sheath dorsally.³⁸

“Tennis elbow”— you don’t have to play tennis to have it

Lateral epicondylitis (tennis elbow) is a painful condition involving microtears within the extensor carpi radialis brevis muscle and the subsequent development of angiofibroblastic dysplasia.³⁹ According to Regan et al who studied the histopathologic features of 11 patients with lateral epicondylitis, the underlying cause of recalcitrant lateral epicondylitis is, in fact, degenerative, rather than inflammatory.⁴⁰

Determine whether cervical spin disease and/or peripheral neuropathy are contributing to the patient's symptoms, as patients with carpal tunnel syndrome may have more than one condition at play.

Although the condition has been nicknamed “tennis elbow,” only about 5% of tennis players have the condition.⁴¹ In tennis players, males are more often affected than females, whereas in the general population, incidence is approximately equal in men and women.⁴¹ Lateral epicondylitis occurs between 4 and 7 times more frequently than medial-sided elbow pain.⁴²

Making the Dx: Look for localized pain, normal ROM

The diagnosis of lateral epicondylitis is based upon a history of pain over the lateral epicondyle and findings on physical examination, including local tenderness directly over the lateral epicondyle,⁴³ pain aggravated by resisted wrist extension and radial deviation, pain with resisted middle finger extension, and decreased grip strength or pain aggravated by strong gripping. These findings typically occur in the presence of normal elbow range of motion.

Treatment: Choose from a range of options

Since lateral epicondylitis was first described, researchers have proposed a wide variety of treatments as initial interventions including rest, activity, equipment modification, NSAIDs, wrist bracing/elbow straps, and physical therapy. If initial treatment does not produce the desired effect, second-line treatments include corticosteroid injections (FIGURE 8), prolotherapy (injection of an irritant, often dextrose; see “Prolotherapy: Can it help your patient?” J Fam Pract. 2015;64:763-768), autologous blood injections, platelet-rich plasma injections (see “Is platelet-rich plasma right for your patient?” J Fam Pract. 2016;65:319-328), and needling of the extensor tendon origin. Refer patients who do not improve after one corticosteroid injection to an orthopedic surgeon for consideration of open or arthroscopic treatment.

CORRESPONDENCE
Gregory R. Waryasz, MD, Rhode Island Hospital, Department of Orthopaedic Surgery, 593 Eddy St., Providence, RI 02903; gregory.waryasz.md@gmail.com.

Image by Peter H. Seeberger

The earliest documented case of β-thalassemia in Sardinia suggests malaria was widespread on the island long before the Middle Ages, according to researchers.

The team noted that Sardinia has one of the highest incidence rates of β-thalassemia in Europe due to its long history of endemic malaria.

However, it has been assumed that malaria was only endemic on the island since the Middle Ages (500-1500 CE).

New research, published in the American Journal of Physical Anthropology, suggests malaria was probably already endemic on Sardinia during the Roman period.

Since ancient DNA of malaria is difficult to extract, the researchers studied thalassemia and other genetic adaptations in its place.

The team studied a thalassemia allele called cod39 β-thalassemia, which is dominant on Sardinia. They were able to confirm the presence of the cod39 allele in the 2000-year-old (approximately 300 BCE to 100 CE) remains of a Roman man.

“This is the very first documented case of the genetic adaptation to malaria on Sardinia,” said study author Claudia Vigano, of the Institute for Evolutionary Medicine of the University of Zurich in Switzerland.

“We also discovered that the person was genetically a Sardinian in all probability and not an immigrant from another area.”

“Our study shows the importance of a multidisciplinary approach to history,” said Abigail Bouwman, also of the Institute for Evolutionary Medicine of the University of Zurich.

“We are researching the evolution of today’s diseases, such as malaria, to explain why the human body becomes sick at all and how adaptations occur.”

Image by Peter H. Seeberger

The earliest documented case of β-thalassemia in Sardinia suggests malaria was widespread on the island long before the Middle Ages, according to researchers.

The team noted that Sardinia has one of the highest incidence rates of β-thalassemia in Europe due to its long history of endemic malaria.

However, it has been assumed that malaria was only endemic on the island since the Middle Ages (500-1500 CE).

New research, published in the American Journal of Physical Anthropology, suggests malaria was probably already endemic on Sardinia during the Roman period.

Since ancient DNA of malaria is difficult to extract, the researchers studied thalassemia and other genetic adaptations in its place.

The team studied a thalassemia allele called cod39 β-thalassemia, which is dominant on Sardinia. They were able to confirm the presence of the cod39 allele in the 2000-year-old (approximately 300 BCE to 100 CE) remains of a Roman man.

“This is the very first documented case of the genetic adaptation to malaria on Sardinia,” said study author Claudia Vigano, of the Institute for Evolutionary Medicine of the University of Zurich in Switzerland.

“We also discovered that the person was genetically a Sardinian in all probability and not an immigrant from another area.”

“Our study shows the importance of a multidisciplinary approach to history,” said Abigail Bouwman, also of the Institute for Evolutionary Medicine of the University of Zurich.

“We are researching the evolution of today’s diseases, such as malaria, to explain why the human body becomes sick at all and how adaptations occur.”

Image by Peter H. Seeberger

The earliest documented case of β-thalassemia in Sardinia suggests malaria was widespread on the island long before the Middle Ages, according to researchers.

The team noted that Sardinia has one of the highest incidence rates of β-thalassemia in Europe due to its long history of endemic malaria.

However, it has been assumed that malaria was only endemic on the island since the Middle Ages (500-1500 CE).

New research, published in the American Journal of Physical Anthropology, suggests malaria was probably already endemic on Sardinia during the Roman period.

Since ancient DNA of malaria is difficult to extract, the researchers studied thalassemia and other genetic adaptations in its place.

The team studied a thalassemia allele called cod39 β-thalassemia, which is dominant on Sardinia. They were able to confirm the presence of the cod39 allele in the 2000-year-old (approximately 300 BCE to 100 CE) remains of a Roman man.

“This is the very first documented case of the genetic adaptation to malaria on Sardinia,” said study author Claudia Vigano, of the Institute for Evolutionary Medicine of the University of Zurich in Switzerland.

“We also discovered that the person was genetically a Sardinian in all probability and not an immigrant from another area.”

“Our study shows the importance of a multidisciplinary approach to history,” said Abigail Bouwman, also of the Institute for Evolutionary Medicine of the University of Zurich.

“We are researching the evolution of today’s diseases, such as malaria, to explain why the human body becomes sick at all and how adaptations occur.”

Photo by Rhoda Baer

The American Society of Clinical Oncology (ASCO) has updated its clinical practice guidelines on the use of antiemetics in cancer patients.

The update, published in the Journal of Clinical Oncology, provides new evidence-based information on the appropriate use of olanzapine, NK1 receptor antagonists, and dexamethasone.

“The adverse impact of inadequately controlled nausea and vomiting on patients’ quality of life is well documented,” said Paul J. Hesketh, MD, co-chair of the ASCO expert panel that updated the guidelines.

“By following the ASCO antiemetics guideline, clinicians have the opportunity to improve patients’ quality of life by minimizing treatment-induced emesis.”

To update ASCO’s guidelines on antiemetics, the expert panel conducted a systematic review of the medical literature published between November 2009 and June 2016. The panel included members with expertise in medical oncology, radiation oncology, nursing, pharmacy, and health services research, as well as a patient representative.

“Tremendous progress has been realized over the last 25 years in the prevention of chemotherapy-induced nausea and vomiting with the introduction of new classes of antiemetic agents,” said Mark G. Kris, MD, co-chair of the expert panel that updated the guidelines.

“The full benefit of these treatment advances will only be realized, however, if evidence-based guidelines are fully implemented.”

Key recommendations in the updated guidelines include:

For adults receiving chemotherapy with a high risk for nausea and vomiting (eg, cisplatin or the combination of cyclophosphamide and an anthracycline), olanzapine should be added to standard antiemetic regimens (the combination of a 5-HT3 receptor antagonist, an NK1 receptor antagonist, and dexamethasone). Olanzapine also helps individuals who experience symptoms despite receiving medicines to prevent vomiting before chemotherapy is given.

For adults receiving carboplatin-based chemotherapy or high-dose chemotherapy and children receiving chemotherapy with a high risk for nausea and vomiting, an NK1 receptor antagonist should be added to the standard antiemetic regimen (the combination of 5-HT3 receptor antagonist and dexamethasone).

Dexamethasone treatment can be limited to the day of chemotherapy administration in patients receiving an anthracycline and cyclophosphamide.

Dronabinol and nabilone, cannabinoids approved by the US Food and Drug Administration, can be used to treat nausea and vomiting that is resistant to standard antiemetic therapies. Evidence remains insufficient to recommend medical marijuana for either prevention or treatment of nausea and vomiting in patients with cancer receiving chemotherapy or radiation therapy.

Photo by Rhoda Baer

The American Society of Clinical Oncology (ASCO) has updated its clinical practice guidelines on the use of antiemetics in cancer patients.

The update, published in the Journal of Clinical Oncology, provides new evidence-based information on the appropriate use of olanzapine, NK1 receptor antagonists, and dexamethasone.

“The adverse impact of inadequately controlled nausea and vomiting on patients’ quality of life is well documented,” said Paul J. Hesketh, MD, co-chair of the ASCO expert panel that updated the guidelines.

“By following the ASCO antiemetics guideline, clinicians have the opportunity to improve patients’ quality of life by minimizing treatment-induced emesis.”

To update ASCO’s guidelines on antiemetics, the expert panel conducted a systematic review of the medical literature published between November 2009 and June 2016. The panel included members with expertise in medical oncology, radiation oncology, nursing, pharmacy, and health services research, as well as a patient representative.

“Tremendous progress has been realized over the last 25 years in the prevention of chemotherapy-induced nausea and vomiting with the introduction of new classes of antiemetic agents,” said Mark G. Kris, MD, co-chair of the expert panel that updated the guidelines.

“The full benefit of these treatment advances will only be realized, however, if evidence-based guidelines are fully implemented.”

Key recommendations in the updated guidelines include:

For adults receiving chemotherapy with a high risk for nausea and vomiting (eg, cisplatin or the combination of cyclophosphamide and an anthracycline), olanzapine should be added to standard antiemetic regimens (the combination of a 5-HT3 receptor antagonist, an NK1 receptor antagonist, and dexamethasone). Olanzapine also helps individuals who experience symptoms despite receiving medicines to prevent vomiting before chemotherapy is given.

For adults receiving carboplatin-based chemotherapy or high-dose chemotherapy and children receiving chemotherapy with a high risk for nausea and vomiting, an NK1 receptor antagonist should be added to the standard antiemetic regimen (the combination of 5-HT3 receptor antagonist and dexamethasone).

Dexamethasone treatment can be limited to the day of chemotherapy administration in patients receiving an anthracycline and cyclophosphamide.

Dronabinol and nabilone, cannabinoids approved by the US Food and Drug Administration, can be used to treat nausea and vomiting that is resistant to standard antiemetic therapies. Evidence remains insufficient to recommend medical marijuana for either prevention or treatment of nausea and vomiting in patients with cancer receiving chemotherapy or radiation therapy.

Photo by Rhoda Baer

The American Society of Clinical Oncology (ASCO) has updated its clinical practice guidelines on the use of antiemetics in cancer patients.

The update, published in the Journal of Clinical Oncology, provides new evidence-based information on the appropriate use of olanzapine, NK1 receptor antagonists, and dexamethasone.

“The adverse impact of inadequately controlled nausea and vomiting on patients’ quality of life is well documented,” said Paul J. Hesketh, MD, co-chair of the ASCO expert panel that updated the guidelines.

“By following the ASCO antiemetics guideline, clinicians have the opportunity to improve patients’ quality of life by minimizing treatment-induced emesis.”

To update ASCO’s guidelines on antiemetics, the expert panel conducted a systematic review of the medical literature published between November 2009 and June 2016. The panel included members with expertise in medical oncology, radiation oncology, nursing, pharmacy, and health services research, as well as a patient representative.

“Tremendous progress has been realized over the last 25 years in the prevention of chemotherapy-induced nausea and vomiting with the introduction of new classes of antiemetic agents,” said Mark G. Kris, MD, co-chair of the expert panel that updated the guidelines.

“The full benefit of these treatment advances will only be realized, however, if evidence-based guidelines are fully implemented.”

Key recommendations in the updated guidelines include:

For adults receiving chemotherapy with a high risk for nausea and vomiting (eg, cisplatin or the combination of cyclophosphamide and an anthracycline), olanzapine should be added to standard antiemetic regimens (the combination of a 5-HT3 receptor antagonist, an NK1 receptor antagonist, and dexamethasone). Olanzapine also helps individuals who experience symptoms despite receiving medicines to prevent vomiting before chemotherapy is given.

For adults receiving carboplatin-based chemotherapy or high-dose chemotherapy and children receiving chemotherapy with a high risk for nausea and vomiting, an NK1 receptor antagonist should be added to the standard antiemetic regimen (the combination of 5-HT3 receptor antagonist and dexamethasone).

Dexamethasone treatment can be limited to the day of chemotherapy administration in patients receiving an anthracycline and cyclophosphamide.

Dronabinol and nabilone, cannabinoids approved by the US Food and Drug Administration, can be used to treat nausea and vomiting that is resistant to standard antiemetic therapies. Evidence remains insufficient to recommend medical marijuana for either prevention or treatment of nausea and vomiting in patients with cancer receiving chemotherapy or radiation therapy.

Thirty-six percent of children enrolled in Medicaid have noncomplex chronic diseases (NC-CDs), such as asthma, diabetes, or depression, accounting for a third of Medicaid pediatric expenditures, according to a retrospective, cross-sectional analysis.

Generalizing to the 35 million children on Medicaid nationally, the NC-CD population accounts for $35 billion in annual Medicaid spending (Pediatrics. 2017. doi: 10.1542/peds.2017-0492).

sndr/istockphoto

mkalaycio@frontinemedcom.com

Thirty-six percent of children enrolled in Medicaid have noncomplex chronic diseases (NC-CDs), such as asthma, diabetes, or depression, accounting for a third of Medicaid pediatric expenditures, according to a retrospective, cross-sectional analysis.

Generalizing to the 35 million children on Medicaid nationally, the NC-CD population accounts for $35 billion in annual Medicaid spending (Pediatrics. 2017. doi: 10.1542/peds.2017-0492).

sndr/istockphoto

mkalaycio@frontinemedcom.com

Thirty-six percent of children enrolled in Medicaid have noncomplex chronic diseases (NC-CDs), such as asthma, diabetes, or depression, accounting for a third of Medicaid pediatric expenditures, according to a retrospective, cross-sectional analysis.

Generalizing to the 35 million children on Medicaid nationally, the NC-CD population accounts for $35 billion in annual Medicaid spending (Pediatrics. 2017. doi: 10.1542/peds.2017-0492).

sndr/istockphoto

mkalaycio@frontinemedcom.com