Stuart B. Black

Within the past year, major developments have occurred that will have a significant impact on the future of medicine. The Patient Protection and Affordable Care Act (ACA) was signed into law by Congress in March 2010. On March 31, 2011, the Centers for Medicare and Medicaid Services released the proposed rules and guidance regarding the development and implementation of accountable care organizations (ACOs). Almost a month later, on April 23, the CMS announced the Bundled Payments for Care Improvement Initiative (BPCII) as a reimbursement model in which the fees of multiple providers are bundled into a single, comprehensive payment that covers all of the services involved in the patient's care.

The BPCII payment system appears to be somewhere between fee-for-service and capitation. The fee-for-service approach puts the full insurance risk on the payer. There is much criticism that fee-for-service ties reimbursement directly to the volume of services provided instead of quality, and is the root cause for poor coordination of care and overuse of expensive, and sometimes unnecessary, services. Capitation provides a lump sum for the medical care of each individual which transfers the full insurance risk to the provider. Bundled payments focus on a single payment for a defined group of services rather than paying separately for each item or service. A bundled payment system will also require providers to bear more of the financial responsibility for outcomes.

This kind of bundled payment model will need to have some type of integrated delivery system consisting of an administrative structure to determine the continuing medical needs of patients and how much each participating provider should be reimbursed for care. ACOs are being considered as one appropriate entity to manage bundled payments on behalf of providers and to develop collaborative and contractual relationships with facilities such as hospitals in providing patient care coordination.

The ACO/Medicare Shared Savings Proposed Rule, which outlined the statutory framework of ACOs, is rather limiting and allows a narrow scope of providers who can apply, but the BPCII is more flexible and allows applications from not only physicians and hospitals but also from other health care providers, including rehabilitation facilities, home health agencies, and skilled nursing facilities.

In the three retrospective models for episodes of careo applicants would set a target payment amount for a defined episode of care. That price would be negotiated at a discount of 2%-3% off the original Medicare fee-for-service rate. Total payment would then be reconciled against the predetermined target price. For models involving inpatient stay and posthospital care, any profit or shared savings beyond the target price would be paid to the participants. This would be synergistic with the ACO concept of better outcomes for less cost. Costs above targets would be paid back to the CMS.

Presumably, by introducing different options of involvement, it should be easier for providers of different sizes and readiness to participate in the BPCII initiative.

There are numerous concerns as well as multiple potential operational and design issues which must be addressed before bundled payments are universally implemented. Examples of questions neurologists may have include:

▸ Are neurologists willing to have a hospital be in charge of administering their reimbursements and developing an equitable agreed-upon fee for both the hospital and physician group?

▸ How will bundled payments be divided among various physicians including procedural and nonprocedural specialists? Who will make that decision?

▸ Will neurologists be willing to make an expensive investment in a new contracting and claims infrastructure to handle the new payment model, and which disease entities and services should be included in a bundled payment?

▸ Will bundling with hospitals require an integrated health care system with hospital-based neurohospitalists?

▸ In the absence of integration and existing contractual relationships, would a general neurology practice be expected to provide neurohospitalist services?

Neurologists would be well advised to exercise due diligence before entering into an agreement such as an ACO or bundled payment contract without appropriate professional and legal counsel.

Within the past year, major developments have occurred that will have a significant impact on the future of medicine. The Patient Protection and Affordable Care Act (ACA) was signed into law by Congress in March 2010. On March 31, 2011, the Centers for Medicare and Medicaid Services released the proposed rules and guidance regarding the development and implementation of accountable care organizations (ACOs). Almost a month later, on April 23, the CMS announced the Bundled Payments for Care Improvement Initiative (BPCII) as a reimbursement model in which the fees of multiple providers are bundled into a single, comprehensive payment that covers all of the services involved in the patient's care.

The BPCII payment system appears to be somewhere between fee-for-service and capitation. The fee-for-service approach puts the full insurance risk on the payer. There is much criticism that fee-for-service ties reimbursement directly to the volume of services provided instead of quality, and is the root cause for poor coordination of care and overuse of expensive, and sometimes unnecessary, services. Capitation provides a lump sum for the medical care of each individual which transfers the full insurance risk to the provider. Bundled payments focus on a single payment for a defined group of services rather than paying separately for each item or service. A bundled payment system will also require providers to bear more of the financial responsibility for outcomes.

This kind of bundled payment model will need to have some type of integrated delivery system consisting of an administrative structure to determine the continuing medical needs of patients and how much each participating provider should be reimbursed for care. ACOs are being considered as one appropriate entity to manage bundled payments on behalf of providers and to develop collaborative and contractual relationships with facilities such as hospitals in providing patient care coordination.

The ACO/Medicare Shared Savings Proposed Rule, which outlined the statutory framework of ACOs, is rather limiting and allows a narrow scope of providers who can apply, but the BPCII is more flexible and allows applications from not only physicians and hospitals but also from other health care providers, including rehabilitation facilities, home health agencies, and skilled nursing facilities.

In the three retrospective models for episodes of careo applicants would set a target payment amount for a defined episode of care. That price would be negotiated at a discount of 2%-3% off the original Medicare fee-for-service rate. Total payment would then be reconciled against the predetermined target price. For models involving inpatient stay and posthospital care, any profit or shared savings beyond the target price would be paid to the participants. This would be synergistic with the ACO concept of better outcomes for less cost. Costs above targets would be paid back to the CMS.

Presumably, by introducing different options of involvement, it should be easier for providers of different sizes and readiness to participate in the BPCII initiative.

There are numerous concerns as well as multiple potential operational and design issues which must be addressed before bundled payments are universally implemented. Examples of questions neurologists may have include:

▸ Are neurologists willing to have a hospital be in charge of administering their reimbursements and developing an equitable agreed-upon fee for both the hospital and physician group?

▸ How will bundled payments be divided among various physicians including procedural and nonprocedural specialists? Who will make that decision?

▸ Will neurologists be willing to make an expensive investment in a new contracting and claims infrastructure to handle the new payment model, and which disease entities and services should be included in a bundled payment?

▸ Will bundling with hospitals require an integrated health care system with hospital-based neurohospitalists?

▸ In the absence of integration and existing contractual relationships, would a general neurology practice be expected to provide neurohospitalist services?

Neurologists would be well advised to exercise due diligence before entering into an agreement such as an ACO or bundled payment contract without appropriate professional and legal counsel.

Within the past year, major developments have occurred that will have a significant impact on the future of medicine. The Patient Protection and Affordable Care Act (ACA) was signed into law by Congress in March 2010. On March 31, 2011, the Centers for Medicare and Medicaid Services released the proposed rules and guidance regarding the development and implementation of accountable care organizations (ACOs). Almost a month later, on April 23, the CMS announced the Bundled Payments for Care Improvement Initiative (BPCII) as a reimbursement model in which the fees of multiple providers are bundled into a single, comprehensive payment that covers all of the services involved in the patient's care.

The BPCII payment system appears to be somewhere between fee-for-service and capitation. The fee-for-service approach puts the full insurance risk on the payer. There is much criticism that fee-for-service ties reimbursement directly to the volume of services provided instead of quality, and is the root cause for poor coordination of care and overuse of expensive, and sometimes unnecessary, services. Capitation provides a lump sum for the medical care of each individual which transfers the full insurance risk to the provider. Bundled payments focus on a single payment for a defined group of services rather than paying separately for each item or service. A bundled payment system will also require providers to bear more of the financial responsibility for outcomes.

This kind of bundled payment model will need to have some type of integrated delivery system consisting of an administrative structure to determine the continuing medical needs of patients and how much each participating provider should be reimbursed for care. ACOs are being considered as one appropriate entity to manage bundled payments on behalf of providers and to develop collaborative and contractual relationships with facilities such as hospitals in providing patient care coordination.

The ACO/Medicare Shared Savings Proposed Rule, which outlined the statutory framework of ACOs, is rather limiting and allows a narrow scope of providers who can apply, but the BPCII is more flexible and allows applications from not only physicians and hospitals but also from other health care providers, including rehabilitation facilities, home health agencies, and skilled nursing facilities.

In the three retrospective models for episodes of careo applicants would set a target payment amount for a defined episode of care. That price would be negotiated at a discount of 2%-3% off the original Medicare fee-for-service rate. Total payment would then be reconciled against the predetermined target price. For models involving inpatient stay and posthospital care, any profit or shared savings beyond the target price would be paid to the participants. This would be synergistic with the ACO concept of better outcomes for less cost. Costs above targets would be paid back to the CMS.

Presumably, by introducing different options of involvement, it should be easier for providers of different sizes and readiness to participate in the BPCII initiative.

There are numerous concerns as well as multiple potential operational and design issues which must be addressed before bundled payments are universally implemented. Examples of questions neurologists may have include:

▸ Are neurologists willing to have a hospital be in charge of administering their reimbursements and developing an equitable agreed-upon fee for both the hospital and physician group?

▸ How will bundled payments be divided among various physicians including procedural and nonprocedural specialists? Who will make that decision?

▸ Will neurologists be willing to make an expensive investment in a new contracting and claims infrastructure to handle the new payment model, and which disease entities and services should be included in a bundled payment?

▸ Will bundling with hospitals require an integrated health care system with hospital-based neurohospitalists?

▸ In the absence of integration and existing contractual relationships, would a general neurology practice be expected to provide neurohospitalist services?

Neurologists would be well advised to exercise due diligence before entering into an agreement such as an ACO or bundled payment contract without appropriate professional and legal counsel.

The relationship between cortical spreading depression (CSD) and migraine aura has a pathophysiological overlap that has led to the widely accepted theory that CSD is the electrophysiological substrate underlying the migraine aura. The question as to whether CSD is the brain mechanism causing the migraine headache is more controversial. Although circumstantial evidence and indirect data, including neuroimaging studies, provide strong evidence that CSD does occur in migraine, there is still no definitive demonstration in a migraine patient that CSD causes the proposed activation of nociceptors in the cranial pain-sensitive structures, specifically the meninges, large blood vessels, and large venous sinuses.

The fact that the majority of migraine attacks are not preceded by aura is explained by the theory that CSD events may have variations in expression and may occur in subcortical tissue such as the hippocampus, cerebellum, and striatum. In this situation, an intense and steady depolarization propagates centrifugally in grey matter and occurs within regions of the brain that remain clinically silent. The depolarization does not follow functional divisions or arterial territories, and quickly depresses brain function by transiently abolishing all spontaneous and evoked synaptic activity. Although CSD can be evoked experimentally in subcortical tissue, if this were to happen in a migraineur, one could postulate that the patient may not experience an aura but would still develop headache as a consequence of trigeminal activation. Thus, while CSD has been implicated in both aura and headache, it is less clear as to whether this pandepolarization actually initiates the migraine pain in humans.

In 1941, Karl Spencer Lashley, Ph.D., an eminent psychologist at Harvard University, published a classic paper, “Patterns of cerebral integration indicated by scatomas of migraine,” in which he described his own visual aura (Arch. Neurol. Psychiatry 1941;46:331-9). He meticulously mapped his aura and postulated that if his aura migrated, so did the underlying CNS process. Using those sketches, he was able to calculate that his migraine aura resulted from a wave of intense excitation of the visual cortex followed by complete inhibition of activity. He concluded that the cortical process progressed at a speed of 3 mm/min across the visual cortex. The migraine scotomata he drew have become known as “Lashley's aura.”

Coincidentally, Aristides Leão, a researcher from Brazil, was also at Harvard working toward his Ph.D. in physiology. Early in his studies, he noted an interesting cortical response elicited by stimulation of the cortex in rabbits. The distinctive feature of the response was a spread of electrical activity, with a recovery of the initial pattern of spontaneous activity occurring after 5-10 minutes. The speed of the spread was in the range of 3 mm/min, exactly the rate reported by Lashley. Despite being totally unaware of Lashley's publication 3 years earlier, Leão noticed the similarity of this spreading depression to the migraine aura. In 1944, he published his research paper, “Spreading depression of activity in the cerebral cortex” (J. Neurophysiol. 1944;7:359-90). This original paper on CSD is still considered one of the classics in the field of neurophysiology. Dr. Lashley's and Dr. Leão's observations changed the way migraine pathophysiology is scientifically conceived.

A review of the early contributors who set the foundation of our current understanding of headache would not be complete without reference to Dr. Harold G. Wolff. His enormous contribution to neurology included landmark studies that led to the modernization of the science of migraine and the anatomy of headache. One such contribution was the discovery that the brain itself is largely insensate. In a 1940 paper coauthored with neurosurgeon Dr. Bronson Ray, Dr. Wolff reported that mechanical stimulation of the brain parenchyma did not cause pain in patients during craniotomy, but that the crucial structures that produced pain were the dura mater, large intracranial blood vessels, and the venous sinuses (Arch. Surg. 1940;41:813-56). The innervation of the pain-sensitive intracranial structures is largely supplied by branches of the first division of the trigeminal nerve. Because the dura mater and large intracranial vessels are pain producing, they have been used in research to model trigeminovascular nociception.

It should also be noted that Dr. Wolff wrote the first textbook on headaches, entitled “Wolff's Headache and Other Head Pain.” He wrote the first (1948) and second editions (1963) entirely by himself.

The recent study by Dr. Zhang and colleagues at Beth Israel Deaconess Medical Center, Boston, is an extension of earlier work by Dr. Lashley, Dr. Leão, Dr. Wolff, and others. The purpose of this elegant study was to determine whether CSD can give rise to activation of nociceptors that innervate the meninges. The discovery that the induction of CSD by focal stimulation of the rat visual cortex can lead to long-lasting activation of meningeal receptors is extremely important, especially if it is assumed that the headache phase of migraine is driven by ongoing neuronal activity along the trigeminovascular pathway. It is important to recognize that we have no definitive demonstration to document that what occurs in the animal model directly translates into what takes place in the brain of a migraineur. However, it is this type of sophisticated research that allows us to work toward a better understanding of the mechanisms of migraine with and without aura. The recognition that CSD can trigger activation of nociceptive meningeal receptors in an animal model that has blood vessels and anatomy similar to humans provides important scientific data that could lead to beneficial clinical application.

The relationship between cortical spreading depression (CSD) and migraine aura has a pathophysiological overlap that has led to the widely accepted theory that CSD is the electrophysiological substrate underlying the migraine aura. The question as to whether CSD is the brain mechanism causing the migraine headache is more controversial. Although circumstantial evidence and indirect data, including neuroimaging studies, provide strong evidence that CSD does occur in migraine, there is still no definitive demonstration in a migraine patient that CSD causes the proposed activation of nociceptors in the cranial pain-sensitive structures, specifically the meninges, large blood vessels, and large venous sinuses.

The fact that the majority of migraine attacks are not preceded by aura is explained by the theory that CSD events may have variations in expression and may occur in subcortical tissue such as the hippocampus, cerebellum, and striatum. In this situation, an intense and steady depolarization propagates centrifugally in grey matter and occurs within regions of the brain that remain clinically silent. The depolarization does not follow functional divisions or arterial territories, and quickly depresses brain function by transiently abolishing all spontaneous and evoked synaptic activity. Although CSD can be evoked experimentally in subcortical tissue, if this were to happen in a migraineur, one could postulate that the patient may not experience an aura but would still develop headache as a consequence of trigeminal activation. Thus, while CSD has been implicated in both aura and headache, it is less clear as to whether this pandepolarization actually initiates the migraine pain in humans.

In 1941, Karl Spencer Lashley, Ph.D., an eminent psychologist at Harvard University, published a classic paper, “Patterns of cerebral integration indicated by scatomas of migraine,” in which he described his own visual aura (Arch. Neurol. Psychiatry 1941;46:331-9). He meticulously mapped his aura and postulated that if his aura migrated, so did the underlying CNS process. Using those sketches, he was able to calculate that his migraine aura resulted from a wave of intense excitation of the visual cortex followed by complete inhibition of activity. He concluded that the cortical process progressed at a speed of 3 mm/min across the visual cortex. The migraine scotomata he drew have become known as “Lashley's aura.”

Coincidentally, Aristides Leão, a researcher from Brazil, was also at Harvard working toward his Ph.D. in physiology. Early in his studies, he noted an interesting cortical response elicited by stimulation of the cortex in rabbits. The distinctive feature of the response was a spread of electrical activity, with a recovery of the initial pattern of spontaneous activity occurring after 5-10 minutes. The speed of the spread was in the range of 3 mm/min, exactly the rate reported by Lashley. Despite being totally unaware of Lashley's publication 3 years earlier, Leão noticed the similarity of this spreading depression to the migraine aura. In 1944, he published his research paper, “Spreading depression of activity in the cerebral cortex” (J. Neurophysiol. 1944;7:359-90). This original paper on CSD is still considered one of the classics in the field of neurophysiology. Dr. Lashley's and Dr. Leão's observations changed the way migraine pathophysiology is scientifically conceived.

A review of the early contributors who set the foundation of our current understanding of headache would not be complete without reference to Dr. Harold G. Wolff. His enormous contribution to neurology included landmark studies that led to the modernization of the science of migraine and the anatomy of headache. One such contribution was the discovery that the brain itself is largely insensate. In a 1940 paper coauthored with neurosurgeon Dr. Bronson Ray, Dr. Wolff reported that mechanical stimulation of the brain parenchyma did not cause pain in patients during craniotomy, but that the crucial structures that produced pain were the dura mater, large intracranial blood vessels, and the venous sinuses (Arch. Surg. 1940;41:813-56). The innervation of the pain-sensitive intracranial structures is largely supplied by branches of the first division of the trigeminal nerve. Because the dura mater and large intracranial vessels are pain producing, they have been used in research to model trigeminovascular nociception.

It should also be noted that Dr. Wolff wrote the first textbook on headaches, entitled “Wolff's Headache and Other Head Pain.” He wrote the first (1948) and second editions (1963) entirely by himself.

The recent study by Dr. Zhang and colleagues at Beth Israel Deaconess Medical Center, Boston, is an extension of earlier work by Dr. Lashley, Dr. Leão, Dr. Wolff, and others. The purpose of this elegant study was to determine whether CSD can give rise to activation of nociceptors that innervate the meninges. The discovery that the induction of CSD by focal stimulation of the rat visual cortex can lead to long-lasting activation of meningeal receptors is extremely important, especially if it is assumed that the headache phase of migraine is driven by ongoing neuronal activity along the trigeminovascular pathway. It is important to recognize that we have no definitive demonstration to document that what occurs in the animal model directly translates into what takes place in the brain of a migraineur. However, it is this type of sophisticated research that allows us to work toward a better understanding of the mechanisms of migraine with and without aura. The recognition that CSD can trigger activation of nociceptive meningeal receptors in an animal model that has blood vessels and anatomy similar to humans provides important scientific data that could lead to beneficial clinical application.

The relationship between cortical spreading depression (CSD) and migraine aura has a pathophysiological overlap that has led to the widely accepted theory that CSD is the electrophysiological substrate underlying the migraine aura. The question as to whether CSD is the brain mechanism causing the migraine headache is more controversial. Although circumstantial evidence and indirect data, including neuroimaging studies, provide strong evidence that CSD does occur in migraine, there is still no definitive demonstration in a migraine patient that CSD causes the proposed activation of nociceptors in the cranial pain-sensitive structures, specifically the meninges, large blood vessels, and large venous sinuses.

The fact that the majority of migraine attacks are not preceded by aura is explained by the theory that CSD events may have variations in expression and may occur in subcortical tissue such as the hippocampus, cerebellum, and striatum. In this situation, an intense and steady depolarization propagates centrifugally in grey matter and occurs within regions of the brain that remain clinically silent. The depolarization does not follow functional divisions or arterial territories, and quickly depresses brain function by transiently abolishing all spontaneous and evoked synaptic activity. Although CSD can be evoked experimentally in subcortical tissue, if this were to happen in a migraineur, one could postulate that the patient may not experience an aura but would still develop headache as a consequence of trigeminal activation. Thus, while CSD has been implicated in both aura and headache, it is less clear as to whether this pandepolarization actually initiates the migraine pain in humans.

In 1941, Karl Spencer Lashley, Ph.D., an eminent psychologist at Harvard University, published a classic paper, “Patterns of cerebral integration indicated by scatomas of migraine,” in which he described his own visual aura (Arch. Neurol. Psychiatry 1941;46:331-9). He meticulously mapped his aura and postulated that if his aura migrated, so did the underlying CNS process. Using those sketches, he was able to calculate that his migraine aura resulted from a wave of intense excitation of the visual cortex followed by complete inhibition of activity. He concluded that the cortical process progressed at a speed of 3 mm/min across the visual cortex. The migraine scotomata he drew have become known as “Lashley's aura.”

Coincidentally, Aristides Leão, a researcher from Brazil, was also at Harvard working toward his Ph.D. in physiology. Early in his studies, he noted an interesting cortical response elicited by stimulation of the cortex in rabbits. The distinctive feature of the response was a spread of electrical activity, with a recovery of the initial pattern of spontaneous activity occurring after 5-10 minutes. The speed of the spread was in the range of 3 mm/min, exactly the rate reported by Lashley. Despite being totally unaware of Lashley's publication 3 years earlier, Leão noticed the similarity of this spreading depression to the migraine aura. In 1944, he published his research paper, “Spreading depression of activity in the cerebral cortex” (J. Neurophysiol. 1944;7:359-90). This original paper on CSD is still considered one of the classics in the field of neurophysiology. Dr. Lashley's and Dr. Leão's observations changed the way migraine pathophysiology is scientifically conceived.

A review of the early contributors who set the foundation of our current understanding of headache would not be complete without reference to Dr. Harold G. Wolff. His enormous contribution to neurology included landmark studies that led to the modernization of the science of migraine and the anatomy of headache. One such contribution was the discovery that the brain itself is largely insensate. In a 1940 paper coauthored with neurosurgeon Dr. Bronson Ray, Dr. Wolff reported that mechanical stimulation of the brain parenchyma did not cause pain in patients during craniotomy, but that the crucial structures that produced pain were the dura mater, large intracranial blood vessels, and the venous sinuses (Arch. Surg. 1940;41:813-56). The innervation of the pain-sensitive intracranial structures is largely supplied by branches of the first division of the trigeminal nerve. Because the dura mater and large intracranial vessels are pain producing, they have been used in research to model trigeminovascular nociception.

It should also be noted that Dr. Wolff wrote the first textbook on headaches, entitled “Wolff's Headache and Other Head Pain.” He wrote the first (1948) and second editions (1963) entirely by himself.

The recent study by Dr. Zhang and colleagues at Beth Israel Deaconess Medical Center, Boston, is an extension of earlier work by Dr. Lashley, Dr. Leão, Dr. Wolff, and others. The purpose of this elegant study was to determine whether CSD can give rise to activation of nociceptors that innervate the meninges. The discovery that the induction of CSD by focal stimulation of the rat visual cortex can lead to long-lasting activation of meningeal receptors is extremely important, especially if it is assumed that the headache phase of migraine is driven by ongoing neuronal activity along the trigeminovascular pathway. It is important to recognize that we have no definitive demonstration to document that what occurs in the animal model directly translates into what takes place in the brain of a migraineur. However, it is this type of sophisticated research that allows us to work toward a better understanding of the mechanisms of migraine with and without aura. The recognition that CSD can trigger activation of nociceptive meningeal receptors in an animal model that has blood vessels and anatomy similar to humans provides important scientific data that could lead to beneficial clinical application.