eMedicine Specialties > Neurology > Inflammatory and Demyelinating Diseases

Marchiafava-Bignami Disease

Jennifer Ault, DO, DPT, Resident Physician, Department of Neurology, Dartmouth-Hitchcock Medical Center
Stephen A Berman, MD, PhD, Professor, Department of Internal Medicine, Section of Neurology, Dartmouth Medical School; Chief, Neurology Service, White River Junction Veterans Medical Center; Mardjohan Hardjasudarma, MD, Chief of Neuroradiology, Program Director, Professor, Departments of Clinical Radiology and Ophthalmology, Louisiana State University Health Sciences Center; Eric Dinnerstein, MD, Consulting Staff Neurologist, Maine Neurology

Updated: Nov 16, 2009

Introduction

Background

In 1903, 2 Italian pathologists named Marchiafava and Bignami described 3 alcoholic men who died after having seizures and coma. In each patient, the middle two-thirds of the corpus callosum was found to be severely necrotic. Through the years, the medical literature has accumulated hundreds of cases of what is now termed Marchiafava-Bignami disease (MBD).¹ Most of these cases are alcoholic men, but the disease does occur in nonalcoholics, although rarely.

In 2007, 2 case reports were published describing MBD in nonalcoholics. Celik et al reported a case of a nonalcoholic patient with acute Marchiafava-Bignami disease that was associated with a gynecologic malignancy. The authors raise the question of a possible paraneoplastic Marchiafava-Bignami disease.² Rusche-Skolarus et al have described a case of Marchiafava-Bignami disease in a postoperative nonalcoholic female who presented with an encephalopathy.³

For years, Italian heritage was thought to be important because Italian pathologists originally described the disease. However, MBD has since been found in persons from all over the world. In 2004, Heinrich et al described 2 clinical subtypes based on a review of 50 radiologic cases diagnosed in vivo:⁴

• Type A had predominant features of coma and stupor. This subtype is associated with a high prevalence of pyramidal-tract symptoms. Radiologic features include involvement of the entire corpus callosum.
• Type B is characterized by normal or mildly impaired mental status. Radiologic features are partial or focal callosal lesions.

Pathophysiology

Single-photon emission CT (SPECT) scanning has yielded interesting pathophysiologic data related to MBD. In a published case reported by Ferracci et al in 1999, SPECT scanning showed a bilateral reduction in cerebral blood flow. The patient had left hemispatial neglect in addition to the expected left-handed apraxia and agraphia.⁵

In 2006, Nardone et al reported an interesting study on a partially recovered patient with MBD who demonstrated impairment of transcallosal inhibition. When performed properly, transcranial magnetic stimulation of the motor cortex elicits excitatory responses in contralateral hand muscles and suppresses tonic voluntary activity in ipsilateral muscles. The corpus callosum conveys the inhibitory signal. This inhibition was reduced this patient.⁶

Frequency

United States

MBD is a very rare condition. In 2001, Helenius et al wrote that they had found approximately 250 cases in published reports, although they also suggested that many cases had gone undiagnosed.⁷

Since 1966, 176 papers have been published. The authors estimate approximately 300 cases in published reports as of November 2008. Another 40 or 50 cases have been mentioned in textbooks that are too old to have been included in the author's PubMed search.

Now, with the availability of MRI, fewer cases are going undiagnosed. No accurate epidemiological data are available as of November 2008.

International

International cases are similar to US cases, but one additional detail deserves mention. Some of the old literature on MBD suggests that this condition is more common in Italians. This is solely an artifact of the initial cases' being found in Italy and Italian physicians' appearing to be the only ones interested in finding such cases at first. It is now firmly believed that no national, geographic, ethnic, or racial predilection is known. However, with such few reports, the numbers of cases reported from each country could not be expected to be exactly in proportion to the population size of each country. In 2006, Staszewski et al described the first case in Poland, which was detected by MRI.⁸

Race

No racial predilection is known to exist.

Sex

Although this disease occurs in both men and women, most cases are found in men.

Age

Most cases of MBD occur in persons older than 45 years.

Clinical

History

• Most patients diagnosed with Marchiafava-Bignami disease (MBD) have a history of alcoholism and poor nutrition.
• The tempo of onset and the range of clinical symptoms vary.
  • Some patients present to the hospital with sudden onset of stupor or coma, and some present with seizures.
  • Other patients have acute, subacute, or chronic onset of dementia and/or gait problems. Spasticity often complicates the gait disorder.
  • Psychiatric disturbances, incontinence, hemiparesis, aphasia, and apraxia have been described.

Physical

Although the physical findings are typically nonspecific, good physical examination may offer clues to the diagnosis. Patients with severe alcoholism who have this syndrome frequently have other problems, such as subdural hemorrhage, Wernicke syndrome, and alcoholic liver disease. Therefore, the diagnosis is not often clear.

• General appearance and constitution: Patients later found to have MBD frequently present to an emergency department in a disheveled condition suggestive of chronic problems with alcohol.
• Mental status
  • Patients can be lethargic, stuporous, or even unconscious (coma or seizures).
  • If a patient is sufficiently alert for extensive neuropsychological testing, testing for ideomotor apraxia (ie, inability to perform motor activities that is not explainable by overt motor or sensory loss) may be revealing.
  • Apraxia of the left (or nondominant) hand suggests interhemispheric disconnection (ie, impaired transfer of information from the left hemisphere to the right hemisphere). Damage to the fibers of the corpus callosum is the cause.
  • Inability to retain new information (ie, Korsakoff syndrome) and delirium tremens should suggest alcoholism and prompt the examiner to consider other alcohol-related problems, such as MBD.
  • Dementia and aphasia have been noted in some patients with this disease.
• Cranial nerves: Disconjugate eye movements, together with confusion, may indicate Wernicke-Korsakoff syndrome, which should prompt the examiner to consider MBD.
• Motor function
  • Tremors, weakness, spasticity, and gait abnormalities, although nonspecific, have been seen in patients with MBD.
  • Delirium tremens is another alcohol-induced problem that patients with MBD may have. Currently, no evidence suggests that the presence of one is either positively or negatively correlated with the presence of the other.
• Sensory function: Sensory loss may suggest an alcoholic neuropathy.
• Cerebellar functions: Wide-based gait and truncal ataxia suggest alcoholism.
• Reflexes
  • Alcoholic neuropathy can cause a loss of deep tendon reflexes and therefore prompt the consideration of MBD in some patients.
  • The presence or absence of Babinski signs is not known to be specifically related to MBD.

Causes

• Alcoholism remains the greatest risk factor, although rare cases have occurred in individuals who did not drink alcohol.
• Nutritional factors have been suspected, but no specific nutrient has been identified.
• Electrolyte disturbances (as in central pontine myelinolysis) may be important.

Differential Diagnoses

Other Problems to Be Considered

The corpus callosum may also be affected in other diseases, such as ischemic stroke, contusion, or lymphoma. However, MBD is distinguished by callosal lesions that are usually symmetrical and located in the anterior portion of the callosum.

Workup

Laboratory Studies

• Because many patients with Marchiafava-Bignami disease (MBD) present with stupor or coma and seizures, the initial laboratory investigations should include measurements of serum electrolyte and glucose levels, a CBC count, and toxicology screening.
• Glucose and intravenous thiamine are frequently given in the emergency department immediately after blood is drawn.
• A spinal tap often is needed and usually performed after findings on a brain CT scan (see Imaging Studies below) have excluded an intracranial mass or hemorrhage.

Imaging Studies

• Findings on the initial CT scan may confirm the diagnosis.
  • If callosal damage is mild, it may go unnoticed until the radiologist carefully reviews the CT scan.
  • In some cases, the lesions may not be visible on a CT scan.
• MRI is currently the most sensitive diagnostic tool.
  • Fast spin-echo T2-weighted MRIs show hyperintensity of the lesions due to both edema and myelin damage.
  • Hypointensity on T1-weighted images (see Media file 1) is mainly related to a total loss of myelin with replacement of the region by a cyst. Neurons can also be lost, in a situation similar to that of multiple sclerosis. As reported by Sair et al in 2006, diffusion tensor imaging and the associated technique of fiber tracking can further increase the sensitivity of the MRI.⁹
  • 
    

    

    Callosal damage in Marchiafava-Bignami disease. Sagittal nonenhanced T1-weighted image (repetition time (milliseconds)/echo time (milliseconds), 500/16) demonstrates a small, well-defined, and hypointense lesion in the genu of the corpus callosum.

    
    
  • Acute or subacute lesions are characterized by edema and early myelin damage more than other changes. As lesions become chronic, cystic lesions are likely to develop. Cystic lesions are generally hyperintense around the rim on T2-weighted MRIs and hypointense in the actual cavity on T1-weighted MRIs.
  • Fluid-attenuated inversion recovery (FLAIR) images may be even more sensitive than those described above. Hyperintense rims and hypointense cores on FLAIR images probably represent damage to the myelin at the rim with a central necrotic area. Uniformly hyperintense lesions may contain a mixture of demyelination and edema. In acute lesions, the area of edema seen is frequently larger than the area of permanent damage.
  • Pathology may also be seen on diffusion-weighted imaging. Unlike stroke, however, in MBD, Hlaihel et al reported in 2005 that it is not uncommon for areas of restricted diffusion to resolve completely without apparent permanent damage.¹⁰
• In a 2004 review of acute and chronic cases, Heinrich et al separated most cases into 2 groups, which they labeled A and B.
  • Group A included the worst cases in which patients presented with coma or other severe impairment of consciousness. On MRIs, their lesions typically involved all or almost all of the corpus callosum. For example, in the acute phase, the entire corpus callosum was commonly hyperintense on T2-weighted MRIs. As the lesions evolved, considerable necrosis occurred, and cystic areas of necrosis were present in most or many regions of the corpus callosum. The death rate for patients with such presentations was high (21%), and those who lived frequently had severe deficits.
  • In group B, patients had little or no impairment of consciousness. Their deficits were subtle: various cognitive difficulties and signs of impaired interhemispheric information transfer, gait disturbances, dysarthria, limb hypotonia, and rare seizures or upper motor neuron signs. Initial hyperintense lesions on T2-weighted MRIs were limited to a few areas of the corpus callosum. Some cystic necrotic areas developed over time, but they were fewer and smaller than those in type A. No deaths occurred in this group, and patients frequently had good recoveries.
  • The authors did not attempt to correlate the severity of the cases with the presumed causes. Patients with the most severe alcoholism might have been in group A, but this is speculation. In both groups, the amount of early callosal edema in the acute phase often markedly exceeded the areas of ultimate cystic necrosis.
• Other radiologic studies have been reported in the literature.
  • In 2003, Gambini et al used magnetic resonance spectroscopy to suggest that an inflammatory reaction accompanies demyelination and necrosis.¹¹
  • SPECT scans have yielded interesting pathophysiologic data in persons with MBD. In one published case, SPECT scanning showed a bilateral reduction in cerebral blood flow. The patient had left hemispatial neglect in addition to the expected left-handed apraxia and agraphia
  • Although the callosal lesions are the hallmark of the disease, for years some cases of MBD were known to be associated with cortical damage in addition to damage to the white matter tracts of the corpus callosum. Generally, the cortical damage was in the lateral frontal and the temporal lobes mainly in the third (although sometimes also in the fourth) cortical layer. In these areas, the neurons degenerated and were replaced by glial cells. In 1939, Morel described this as cortical laminar sclerosis. Subsequently, this has been called Morel cortical laminar sclerosis.¹²
  • Although Morel did not report an association of cortical laminar sclerosis with MBD, many subsequent authors did, including Jequier and Wildi in 1956¹³ and Delay et al in 1959^14,15 . Indeed, Ropper et al stated in 2005¹⁶ in Adams and Victor's Principles of Neurology that Jequier and Adams (in an otherwise unpublished review) reexamined Morel's slides and found evidence of MBD in all of those cases. Thus, the prevailing view has generally been that Morel cortical laminar sclerosis is secondary to MBD. Nevertheless, in 1978, Naeije et al reported a case of Morel cortical laminar sclerosis in an alcoholic woman who did not have MBD.¹⁷ In addition, Okeda et al reported 3 cases of cortical laminar sclerosis in 1986 in patients who had various combinations of pontine and extrapontine myelinolysis but who did not have MBD.¹⁸ One of these patients had alcoholic cirrhosis and 2 had malignancies.
  • Prior to the MRI era, neuroradiological findings had little impact on the detection of cortical laminar sclerosis. Indeed, a prior version of this article stated that "Such lesions are rarely found with in vivo imaging" although a functional MRI demonstration by Ishii et al in 1999 was described as showing perfusion and metabolic effects on the cerebrum in a case of MBD.¹⁹ A 1996 article by Logak et al described cortical positron emission tomographic findings in a case of MBD.²⁰
  • In 2005, Johkura et al reported 2 cases in which lateral and frontal cortical lesions, in addition to corpus callosal lesions, were seen on FLAIR imaging.²¹
  • In 2006, Menegon et al reported 6 patients with MBD in whom (1) the entire corpus callosum appeared to be affected by a reduced apparent diffusion coefficient as seen on diffusion-weighted imaging studies and (2) lateral and frontal cortical lesions were also detected by diffusion-weighted imaging. Menegon et al suggested, on the basis of the outcomes of their patients, that such a combination of findings was a harbinger of a poor outcome both for survival and for cognitive recovery.²² However, as pointed out by Khaw et al in 2006²³ , the older literature, such as that by Brion from 1977²⁴ , does not support a correlation between laminar sclerosis and bad outcome. In addition, studies such as that by Hlaihel et al from 2006¹⁰ do not support a correlation between reduced apparent diffusion coefficient and poor prognosis or even with irreversibility of the lesion.
  • Finally, they note that cortical MRI findings have not been definitively correlated with the specific pathology of Morel cortical laminar sclerosis. However, if indeed they represent laminar sclerosis, the fact that this is present in the acute or subacute stages of MBD may force a reevaluation of the thought that the laminar sclerosis is a secondary consequence of the MBD.

Other Tests

• EEG is frequently performed to evaluate seizures. No specific or characteristic EEG findings are indicative of MBD.
• If the patient eventually recovers a reasonable level of consciousness, neuropsychological testing can demonstrate difficulties with information transfer between the right side of the brain and the left. Other aspects of the patient's dementia may also be elucidated.

Histologic Findings

In MBD, the middle portion (middle lamina) of the myelinated fiber tracts of the corpus callosum degenerates. The degeneration is frequently but not necessarily uniform. Degeneration of the corpus callosum is a cardinal feature. In some cases, the anterior portion is preferentially involved, with the most severe degeneration in the center of the lesion. The anterior and posterior commissures, the centrum semiovale, and the other white-matter tracts (eg, the long association fibers and the middle cerebral peduncles) may also be affected. However, the internal capsule and corona radiata, as well as the shorter arcuate subgyral association fibers, are typically spared. If the splenium of the corpus callosum is affected, the greatest degeneration most commonly occurs in the lateral portions of the middle segment.

With the advent of CT and MRI, more cases have been recognized than before. Analyses of such cases have revealed several patterns, including scattered lesions or cysts observed at intervals from the front to the back of the callosum. Nearby areas (eg, anterior commissure, posterior commissure, brachium pontis, other white-matter tracts) and the centrum semiovale are frequently involved.

Histopathologic studies reveal abundant macrophages in the areas of lesions. Otherwise, little inflammatory reaction is noted. Axons are demyelinated in the involved areas, but the axon cylinders are relatively spared, particularly in the peripheral portions of the lesions. Deep in the lesion, cavitation or cyst formation may be seen and corresponds to complete necrosis of all neural and glial elements.

Patients with MBD do not usually have midline lesions, which are typical in patients with Wernicke encephalopathy (of the medial thalamus or mamillary bodies).

Finally, as previously mentioned, cortical lesions are sometimes found on postmortem neuropathological studies. In these cases, neuronal degeneration of the third and fourth layers of the frontal and temporal cortices occurs, with replacement of the neuron by gliosis (ie, Morel cortical laminar sclerosis). As noted, controversy now exists regarding whether cortical MRI findings in MBD actual correlate with such pathological findings and whether they might have implications for prognosis. Whether the cortical findings are secondary to the callosal damage, whether both are caused by a similar process, or whether they are coincidental findings either of which may occur separately particularly in severe alcoholism, malnutrition, and/or other severely impairments remains unclear.

Treatment

Medical Care

Various treatments similar to those commonly administered Wernicke-Korsakoff syndrome, or for alcoholism in general, have been given to patients with Marchiafava-Bignami disease (MBD). Some have improved and some have not. The most common treatments are thiamine and other B vitamins (especially vitamin B-12 and folate, which is not a B vitamin but is commonly given with B-12). With regard to more unusual treatments, one case report by Staszewski et al from 2006 described amantadine given together with thiamine, vitamin B-12, and folate; the patient improved.⁸ In another case reported by Kikkawa et al from 2000, administration of high-dose corticosteroids was said to precede clinical improvement. In patients who improved, the CT and MRI findings also improved, at least somewhat.²⁵

• No specific proven treatment is available.
• Seizures and coma are treated as described in the various eMedicine articles on these topics (eg, see Seizures in the Emergency Department).
• Thiamine is administered for Wernicke-Korsakoff syndrome, although no significant evidence suggests that thiamine is a specific treatment for MBD. Vitamin B-12, folate, and other B vitamins (and sometimes multivitamins) are also frequently given to sick alcoholic patients admitted to the hospital; the authors deem administering the same protocol of vitamin therapy that would be given to patients with possible Wernicke-Korsakoff syndrome justified.
• The fact that the brain pathology can now be observed repeatedly via serial MRI scans raises the question of whether to try other treatments mentioned in the literature and then monitor the appearance of the brain. A course of high-dose intravenous corticosteroids (eg, 250 mg methylprednisolone q6h) could be tried if the attending physician believes the possible benefits outweigh the risks. Likewise, a standard dose of amantadine (100 mg bid) could be considered if the patient can safely take it orally or through a tube. However, remember that no method exists to calculate a risk-to-reward ratio from isolated case reports and the improvement seen in the small number of individual patients who received such treatments may have occurred anyway with the passage of time.
• Patients who survive should receive rehabilitation and, if appropriate, alcohol and nutritional counseling.
• Patients are usually admitted because they present with stupor, coma, and, frequently, seizures.

Consultations

Depending on the specific presentation and course, the patient may require consultation with a neurologist for seizure control, a critical care specialist for coma management, a neuropsychologist for workup of the dementia, a neurorehabilitation specialist, and a psychiatrist or psychologist for treatment of the alcoholism.

Medication

The goals of pharmacotherapy in Marchiafava-Bignami disease (MBD) are to reduce morbidity and prevent complications.

Vitamin, water-soluble

Improvement has been seen in the small number of individual patients who received treatments that included at least 1 agent in this drug category.

Thiamine (Thiamilate)

Water-soluble vitamin that combines with adenosine triphosphate to form the coenzyme thiamine pyrophosphate, which is necessary for carbohydrate metabolism. The B vitamins are readily absorbed from the GI tract (except in cases of malabsorption syndromes). Alcohol inhibits absorption of thiamine, which occurs primarily in the duodenum.

Dosing

Adult

50-100 mg/d PO/IV/IM

Pediatric

Not established

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Sensitivity reactions can occur (intradermal test-dose recommended in suspected sensitivity); deaths have resulted from IV use; sudden onset or worsening of Wernicke encephalopathy, following glucose, may occur in thiamine-deficient patients; administer before or together with dextrose-containing fluids in suspected thiamine-deficiency

Immunosuppressant agents

Improvement has been seen in the small number of individual patients who received treatments that included at least 1 agent in this drug category.

Methylprednisolone (Adlone, Depo-Medrol, Depopred, Medrol, Methylone, Solu-Medrol)

May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

Dosing

Adult

250 mg PO/IV/IM q6h

Pediatric

Not established

Interactions

Coadministration with digoxin, may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels of methylprednisolone; phenobarbital, phenytoin, and rifampin may decrease levels of methylprednisolone (adjust dose); monitor patients for hypokalemia when taking medication concurrently with diuretics; grapefruit juice increases prednisolone concentrations; methylprednisolone and cyclosporine mutually inhibit one another resulting in increased plasma levels of each drug

Contraindications

Documented hypersensitivity; viral, fungal or tubercular skin infections

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections are possible complications of glucocorticoid use
Depo-Medrol contains benzyl alcohol, which is potentially toxic when administered locally to neural tissue; administration of Depo-Medrol by routes other than indicated routes, including the epidural route, has been associated with reports of serious medical events including arachnoiditis, meningitis, paraparesis/paraplegia, sensory disturbances, bowel/bladder dysfunction, seizures, visual impairment including blindness, ocular and periocular inflammation, and residue or slough at injection site

Antiparkinson agents

Improvement has been seen in the small number of individual patients who received treatments that included at least 1 agent in this drug category.

Amantadine (Symmetrel)

Inhibits N-methyl-D-aspartic acid (NMDA) receptor-mediated stimulation of acetylcholine release in rat striatum. May enhance dopamine release, inhibit dopamine reuptake, stimulate postsynaptic dopamine receptors, or enhance dopamine receptor sensitivity.

Dosing

Adult

100 mg PO bid

Pediatric

Not established

Interactions

Drugs with anticholinergic or CNS stimulant activity increase amantadine toxicity; the concurrent administration of hydrochlorothiazide plus triamterene with amantadine may increase plasma concentrations of amantadine

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in liver disease, uncontrolled psychosis, eczematoid dermatitis, seizures, and those receiving CNS stimulant drugs; reduce dose in renal disease when treating Parkinson disease; do not discontinue this medication abruptly

Follow-up

Prognosis

• No systematic study has been conducted to assess the prognosis of patients with MBD. In the pre-CT era, almost all patients were discovered at autopsy. They usually died from the effects of alcoholism and typically had severe neuropsychological deficits before death.
• Modern CT scanning and MRI allow the detection of mild cases, and some patients have recovered with minimal deficits.
• If the underlying cause is alcoholism, the prognosis is poor unless the patient adheres to an alcohol treatment program.
• Recent data suggest an improved overall prognosis, which is correlated with the subtype, as follows:
  • Type A has a long-term disability rate of 86% and a mortality rate of 21%.
  • Type B has a long-term disability rate of 19% and a mortality rate of 0%.
• As Helenius et al reported in 2004, of the approximately 250 reported patients, 200 died, 30 remained severely demented or bedridden, and only 20 had a favorable outcome.
  • Alcohol abuse is such a common problem that underdiagnosis of MBD seems likely.
  • Many cases may be diagnosed but not reported, and autopsies are largely not performed.
  • Hence, the disease may be more common than thought, and the overall outcome may be better than previously believed.

Multimedia

Media file 1: Callosal damage in Marchiafava-Bignami disease. Sagittal nonenhanced T1-weighted image (repetition time (milliseconds)/echo time (milliseconds), 500/16) demonstrates a small, well-defined, and hypointense lesion in the genu of the corpus callosum.

References

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Keywords

Marchiafava-Bignami syndrome, MBD, MBS, primary degeneration of the corpus callosum, symmetrical demyelination or necrosis of the middle portion of the corpus callosum and adjacent subcortical tissue, occurring predominantly in malnourished alcoholics

Contributor Information and Disclosures

Author

Jennifer Ault, DO, DPT, Resident Physician, Department of Neurology, Dartmouth-Hitchcock Medical Center
Jennifer Ault, DO, DPT is a member of the following medical societies: American Academy of Neurology, American Academy of Osteopathy, American Medical Association, and American Physical Therapy Association
Disclosure: Nothing to disclose.

Coauthor(s)

Stephen A Berman, MD, PhD, Professor, Department of Internal Medicine, Section of Neurology, Dartmouth Medical School; Chief, Neurology Service, White River Junction Veterans Medical Center
Stephen A Berman, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Mardjohan Hardjasudarma, MD, Chief of Neuroradiology, Program Director, Professor, Departments of Clinical Radiology and Ophthalmology, Louisiana State University Health Sciences Center
Mardjohan Hardjasudarma, MD is a member of the following medical societies: American College of Radiology, American Medical Association, American Society of Neuroradiology, Canadian Medical Association, Ontario Medical Association, Pennsylvania Medical Society, and Southern Medical Association
Disclosure: Nothing to disclose.

Eric Dinnerstein, MD, Consulting Staff Neurologist, Maine Neurology
Eric Dinnerstein, MD is a member of the following medical societies: American Academy of Neurology and American Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Jonathan S Rutchik, MD, MPH, Assistant Professor, Department of Occupational and Environmental Medicine, University of California at San Francisco
Jonathan S Rutchik, MD, MPH is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American College of Occupational and Environmental Medicine, and Society of Toxicology
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Florian P Thomas, MD, MA, PhD, Drmed, Director, Spinal Cord Injury Unit, St Louis Veterans Affairs Medical Center; Director, National MS Society Multiple Sclerosis Center; Professor, Department of Neurology and Psychiatry, Associate Professor, Institute for Molecular Virology, and Department of Molecular Microbiology and Immunology, St Louis University
Florian P Thomas, MD, MA, PhD, Drmed is a member of the following medical societies: American Academy of Neurology, American Paraplegia Society, and National Multiple Sclerosis Society
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Chief Editor

B Mark Keegan, MD, FRCPC, Assistant Professor of Neurology, College of Medicine, Mayo Clinic; Master's Faculty, Mayo Graduate School; Consultant, Department of Neurology, Mayo Clinic, Rochester
B Mark Keegan, MD, FRCPC is a member of the following medical societies: American Academy of Neurology, American Medical Association, and Minnesota Medical Association
Disclosure: Neurology (Journal of the American Academy of Neurology)  Honoraria Section Editor

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