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Genetics of Migraine
Migraine Workup
Severe pulsing headache
On the basis of the patient's presentation and described history, the likely diagnosis is migraine. By adolescence, migraine is much more common among female patients and can be connected to the menstrual cycle. The early symptoms before onset of head pain reported by this patient characterize the prodromal phase, which can occur 1-2 days before the headache, followed by the aura phase. Approximately one third of patients with migraine experience episodes with aura, like the visual disturbance described in this case.
Migraine can be diagnosed on a clinical basis, but certain neurologic symptoms with headache should be considered red flags and prompt further workup (ie, stiff neck or fever, or history of head injury or major trauma). Spontaneous internal carotid artery dissection, for example, should be investigated in the differential of younger patients who have severe headache before onset of neurologic symptoms. Patients who present with migraine are very frequently misdiagnosed as having sinus headaches or sinusitis. Relevant clinical findings of acute sinusitis are sinus tenderness or pressure; pain over the cheek which radiates to the frontal region or teeth; redness of nose, cheeks, or eyelids; pain to the vertex, temple, or occiput; postnasal discharge; a blocked nose; coughing or pharyngeal irritation; facial pain; and hyposmia. Tension-type headaches usually are associated with mild or moderate bilateral pain, causing a steady ache as opposed to the throbbing of migraines. Basilar migraine, common among female patients, is marked by vertebrobasilar insufficiency.
The American Headache Society defines migraine by the occurrence of at least five episodes. These attacks must last 4-72 hours and have at least two of these four characteristics: unilateral location, pulsating quality, moderate or severe pain intensity, and aggravation by or causing avoidance of routine physical activity. During these episodes, the patient must experience either photophobia and phonophobia or nausea and/or vomiting. If these signs and symptoms cannot be explained by another diagnosis, the patient is very likely presenting with migraine.
Identifying an effective treatment for migraines is often associated with a trial-and-error period, with an average 4-year gap between diagnosis and initiation of preventive medications. Because the patient's migraines do not seem to respond to non-steroidal anti inflammatory drugs, she may be a candidate for other treatments of mild-to-moderate migraines: nonopioid analgesics, acetaminophen, or caffeinated analgesic combinations. If attacks are moderate or severe, or even mild to moderate but do not respond well to therapy, migraine-specific agents are recommended: triptans, dihydroergotamine (DHE), small-molecule calcitonin gene-related peptide (CGRP) receptor antagonists (gepants), and selective serotonin (5-HT1F) receptor agonists (ditans).
Jasmin Harpe, MD, MPH, Headache Fellow, Department of Neurology, Harvard University, John R. Graham Headache Center, Mass General Brigham, Boston, MA
Jasmin Harpe, MD, MPH, has disclosed no relevant financial relationships.
Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.
On the basis of the patient's presentation and described history, the likely diagnosis is migraine. By adolescence, migraine is much more common among female patients and can be connected to the menstrual cycle. The early symptoms before onset of head pain reported by this patient characterize the prodromal phase, which can occur 1-2 days before the headache, followed by the aura phase. Approximately one third of patients with migraine experience episodes with aura, like the visual disturbance described in this case.
Migraine can be diagnosed on a clinical basis, but certain neurologic symptoms with headache should be considered red flags and prompt further workup (ie, stiff neck or fever, or history of head injury or major trauma). Spontaneous internal carotid artery dissection, for example, should be investigated in the differential of younger patients who have severe headache before onset of neurologic symptoms. Patients who present with migraine are very frequently misdiagnosed as having sinus headaches or sinusitis. Relevant clinical findings of acute sinusitis are sinus tenderness or pressure; pain over the cheek which radiates to the frontal region or teeth; redness of nose, cheeks, or eyelids; pain to the vertex, temple, or occiput; postnasal discharge; a blocked nose; coughing or pharyngeal irritation; facial pain; and hyposmia. Tension-type headaches usually are associated with mild or moderate bilateral pain, causing a steady ache as opposed to the throbbing of migraines. Basilar migraine, common among female patients, is marked by vertebrobasilar insufficiency.
The American Headache Society defines migraine by the occurrence of at least five episodes. These attacks must last 4-72 hours and have at least two of these four characteristics: unilateral location, pulsating quality, moderate or severe pain intensity, and aggravation by or causing avoidance of routine physical activity. During these episodes, the patient must experience either photophobia and phonophobia or nausea and/or vomiting. If these signs and symptoms cannot be explained by another diagnosis, the patient is very likely presenting with migraine.
Identifying an effective treatment for migraines is often associated with a trial-and-error period, with an average 4-year gap between diagnosis and initiation of preventive medications. Because the patient's migraines do not seem to respond to non-steroidal anti inflammatory drugs, she may be a candidate for other treatments of mild-to-moderate migraines: nonopioid analgesics, acetaminophen, or caffeinated analgesic combinations. If attacks are moderate or severe, or even mild to moderate but do not respond well to therapy, migraine-specific agents are recommended: triptans, dihydroergotamine (DHE), small-molecule calcitonin gene-related peptide (CGRP) receptor antagonists (gepants), and selective serotonin (5-HT1F) receptor agonists (ditans).
Jasmin Harpe, MD, MPH, Headache Fellow, Department of Neurology, Harvard University, John R. Graham Headache Center, Mass General Brigham, Boston, MA
Jasmin Harpe, MD, MPH, has disclosed no relevant financial relationships.
Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.
On the basis of the patient's presentation and described history, the likely diagnosis is migraine. By adolescence, migraine is much more common among female patients and can be connected to the menstrual cycle. The early symptoms before onset of head pain reported by this patient characterize the prodromal phase, which can occur 1-2 days before the headache, followed by the aura phase. Approximately one third of patients with migraine experience episodes with aura, like the visual disturbance described in this case.
Migraine can be diagnosed on a clinical basis, but certain neurologic symptoms with headache should be considered red flags and prompt further workup (ie, stiff neck or fever, or history of head injury or major trauma). Spontaneous internal carotid artery dissection, for example, should be investigated in the differential of younger patients who have severe headache before onset of neurologic symptoms. Patients who present with migraine are very frequently misdiagnosed as having sinus headaches or sinusitis. Relevant clinical findings of acute sinusitis are sinus tenderness or pressure; pain over the cheek which radiates to the frontal region or teeth; redness of nose, cheeks, or eyelids; pain to the vertex, temple, or occiput; postnasal discharge; a blocked nose; coughing or pharyngeal irritation; facial pain; and hyposmia. Tension-type headaches usually are associated with mild or moderate bilateral pain, causing a steady ache as opposed to the throbbing of migraines. Basilar migraine, common among female patients, is marked by vertebrobasilar insufficiency.
The American Headache Society defines migraine by the occurrence of at least five episodes. These attacks must last 4-72 hours and have at least two of these four characteristics: unilateral location, pulsating quality, moderate or severe pain intensity, and aggravation by or causing avoidance of routine physical activity. During these episodes, the patient must experience either photophobia and phonophobia or nausea and/or vomiting. If these signs and symptoms cannot be explained by another diagnosis, the patient is very likely presenting with migraine.
Identifying an effective treatment for migraines is often associated with a trial-and-error period, with an average 4-year gap between diagnosis and initiation of preventive medications. Because the patient's migraines do not seem to respond to non-steroidal anti inflammatory drugs, she may be a candidate for other treatments of mild-to-moderate migraines: nonopioid analgesics, acetaminophen, or caffeinated analgesic combinations. If attacks are moderate or severe, or even mild to moderate but do not respond well to therapy, migraine-specific agents are recommended: triptans, dihydroergotamine (DHE), small-molecule calcitonin gene-related peptide (CGRP) receptor antagonists (gepants), and selective serotonin (5-HT1F) receptor agonists (ditans).
Jasmin Harpe, MD, MPH, Headache Fellow, Department of Neurology, Harvard University, John R. Graham Headache Center, Mass General Brigham, Boston, MA
Jasmin Harpe, MD, MPH, has disclosed no relevant financial relationships.
Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.
An 18-year-old female patient presents with severe pulsing headache that began about 6 hours earlier. She describes feeling tired and irritable for the past 2 days and that she has had difficulty concentrating. Earlier in the day, before headache onset, she became extremely fatigued. Describing a "blinding light" in her vision, she is currently highly photophobic. The patient took four ibuprofen 2 hours ago. There is no significant medical history. She is on a regimen of estrogen-progestin and spironolactone for acne. Following advice from her primary care practitioner, she takes magnesium and vitamin B for headache prevention. The patient reports that she does not believe that she has migraines because she has never vomited during an episode. The patient explains that she has always had frequent headaches but that this is the sixth or seventh episode of this type and severity that she has had in the past year. The headaches do not seem to align with her menstrual cycle.
Migraine Headache Medications
Episodes of visual disturbance
On the basis of the history, examination, and investigations, retinal migraine was diagnosed according to the International Classification of Headache Disorders, third edition (1.2 migraine with aura; 1.2.4 retinal migraine). This classification system describes retinal migraine as a subtype of migraine with aura.
Retinal migraine (also called ophthalmic or ocular migraine) is relatively rare but is sometimes a cause of transient monocular blindness in young adults. It manifests as recurrent attacks of unilateral visual disturbance (positive symptoms) or blindness (negative symptoms) lasting from minutes to 1 hour, associated with minimal or no headache.
Some patients describe a positive visual symptom/disturbance in a mosaic pattern of scotomata that gradually enlarge, producing total or near-total unilateral visual loss. Precipitating factors may include emotional stress, hypertension, and hormonal contraceptive pills, as well as exercise, high altitude, dehydration, smoking, hypoglycemia, and hyperthermia.
Retinal migraine is believed to result from transient vasospasm of the choroidal or retinal arteries. A history of recurrent attacks of transient monocular visual disturbance or blindness, with or without a headache and without other neurologic symptoms, can suggest retinal migraine. A personal or family history of migraine can confirm the diagnosis.
Ruling out eye disease or vascular causes, especially when risk factors for arteriosclerosis exist, is important; that is, the condition must be differentiated from ocular or vascular causes of transient monocular blindness, mainly carotid artery disease.
Carotid duplex ultrasonography, transcranial Doppler ultrasonography, magnetic resonance angiography, or CT angiography of the brain may be helpful. Fluorescein or cerebral angiography is rarely necessary. A hypercoagulability workup and evaluation of the erythrocyte sedimentation rate may be useful in excluding other coagulation disorders associated with retinal vasculopathy.
Regarding management, calcium-channel blockers have shown some efficacy. Even in patients with low blood pressure, nifedipine 10-20 mg/d is generally tolerated. From the available literature on treatment of this condition, it is recommended that triptans, ergots, and beta-blockers be used with caution or avoided in patients with retinal migraine owing to the potential for exacerbating vasoconstriction of the retinal artery. Transient vision loss in retinal migraine has been associated with future onset of permanent vision loss from occlusive conditions such as central retinal artery occlusion and branch retinal artery occlusion.
Jasmin Harpe, MD, MPH, Headache Fellow, Department of Neurology, Harvard University, John R. Graham Headache Center, Mass General Brigham, Boston, MA
Jasmin Harpe, MD, MPH, has disclosed no relevant financial relationships.
Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.
On the basis of the history, examination, and investigations, retinal migraine was diagnosed according to the International Classification of Headache Disorders, third edition (1.2 migraine with aura; 1.2.4 retinal migraine). This classification system describes retinal migraine as a subtype of migraine with aura.
Retinal migraine (also called ophthalmic or ocular migraine) is relatively rare but is sometimes a cause of transient monocular blindness in young adults. It manifests as recurrent attacks of unilateral visual disturbance (positive symptoms) or blindness (negative symptoms) lasting from minutes to 1 hour, associated with minimal or no headache.
Some patients describe a positive visual symptom/disturbance in a mosaic pattern of scotomata that gradually enlarge, producing total or near-total unilateral visual loss. Precipitating factors may include emotional stress, hypertension, and hormonal contraceptive pills, as well as exercise, high altitude, dehydration, smoking, hypoglycemia, and hyperthermia.
Retinal migraine is believed to result from transient vasospasm of the choroidal or retinal arteries. A history of recurrent attacks of transient monocular visual disturbance or blindness, with or without a headache and without other neurologic symptoms, can suggest retinal migraine. A personal or family history of migraine can confirm the diagnosis.
Ruling out eye disease or vascular causes, especially when risk factors for arteriosclerosis exist, is important; that is, the condition must be differentiated from ocular or vascular causes of transient monocular blindness, mainly carotid artery disease.
Carotid duplex ultrasonography, transcranial Doppler ultrasonography, magnetic resonance angiography, or CT angiography of the brain may be helpful. Fluorescein or cerebral angiography is rarely necessary. A hypercoagulability workup and evaluation of the erythrocyte sedimentation rate may be useful in excluding other coagulation disorders associated with retinal vasculopathy.
Regarding management, calcium-channel blockers have shown some efficacy. Even in patients with low blood pressure, nifedipine 10-20 mg/d is generally tolerated. From the available literature on treatment of this condition, it is recommended that triptans, ergots, and beta-blockers be used with caution or avoided in patients with retinal migraine owing to the potential for exacerbating vasoconstriction of the retinal artery. Transient vision loss in retinal migraine has been associated with future onset of permanent vision loss from occlusive conditions such as central retinal artery occlusion and branch retinal artery occlusion.
Jasmin Harpe, MD, MPH, Headache Fellow, Department of Neurology, Harvard University, John R. Graham Headache Center, Mass General Brigham, Boston, MA
Jasmin Harpe, MD, MPH, has disclosed no relevant financial relationships.
Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.
On the basis of the history, examination, and investigations, retinal migraine was diagnosed according to the International Classification of Headache Disorders, third edition (1.2 migraine with aura; 1.2.4 retinal migraine). This classification system describes retinal migraine as a subtype of migraine with aura.
Retinal migraine (also called ophthalmic or ocular migraine) is relatively rare but is sometimes a cause of transient monocular blindness in young adults. It manifests as recurrent attacks of unilateral visual disturbance (positive symptoms) or blindness (negative symptoms) lasting from minutes to 1 hour, associated with minimal or no headache.
Some patients describe a positive visual symptom/disturbance in a mosaic pattern of scotomata that gradually enlarge, producing total or near-total unilateral visual loss. Precipitating factors may include emotional stress, hypertension, and hormonal contraceptive pills, as well as exercise, high altitude, dehydration, smoking, hypoglycemia, and hyperthermia.
Retinal migraine is believed to result from transient vasospasm of the choroidal or retinal arteries. A history of recurrent attacks of transient monocular visual disturbance or blindness, with or without a headache and without other neurologic symptoms, can suggest retinal migraine. A personal or family history of migraine can confirm the diagnosis.
Ruling out eye disease or vascular causes, especially when risk factors for arteriosclerosis exist, is important; that is, the condition must be differentiated from ocular or vascular causes of transient monocular blindness, mainly carotid artery disease.
Carotid duplex ultrasonography, transcranial Doppler ultrasonography, magnetic resonance angiography, or CT angiography of the brain may be helpful. Fluorescein or cerebral angiography is rarely necessary. A hypercoagulability workup and evaluation of the erythrocyte sedimentation rate may be useful in excluding other coagulation disorders associated with retinal vasculopathy.
Regarding management, calcium-channel blockers have shown some efficacy. Even in patients with low blood pressure, nifedipine 10-20 mg/d is generally tolerated. From the available literature on treatment of this condition, it is recommended that triptans, ergots, and beta-blockers be used with caution or avoided in patients with retinal migraine owing to the potential for exacerbating vasoconstriction of the retinal artery. Transient vision loss in retinal migraine has been associated with future onset of permanent vision loss from occlusive conditions such as central retinal artery occlusion and branch retinal artery occlusion.
Jasmin Harpe, MD, MPH, Headache Fellow, Department of Neurology, Harvard University, John R. Graham Headache Center, Mass General Brigham, Boston, MA
Jasmin Harpe, MD, MPH, has disclosed no relevant financial relationships.
Image Quizzes are fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.
A 23-year-old woman presents with sudden recurrent episodes of visual disturbance (extreme blurriness and partial blindness) in her right eye. She had seven or eight episodes over 30 hours; each episode lasted for 5-7 minutes, with spontaneous and full recovery. These were not associated with flashes of light, tingling, numbness, fever, or headache. She was asymptomatic between episodes.
She had normal vision in her left eye during these episodes, which she checked by covering both eyes alternately with her hands. The only significant history was four episodes of migraine with aura 3 years ago, which resolved spontaneously and did not recur. Family history was noncontributory. She had no history of illicit drug use or alcohol use.
On examination, her vital signs were normal. Blood pressure was 110/80 mm Hg, pulse 85 beats/min, and respiratory rate 16 breaths/min. There was no lymphadenopathy, and jugular venous pressure was not elevated. Visual acuity was 6/6, with normal visual fields and perimetry. Fundoscopy was normal. Complete blood count, liver function tests, renal function tests, erythrocyte sedimentation rate, antineutrophil antibodies, electrocardiography, transthoracic echocardiography, carotid Doppler, and MRI of the brain with contrast were all normal. She is taking no medications.
