eMedicine Specialties > Neurology > Inflammatory and Demyelinating Diseases

Marchiafava-Bignami Disease: Differential Diagnoses & Workup

Author: Jennifer Ault, DO, DPT, Resident Physician, Department of Neurology, Dartmouth-Hitchcock Medical Center
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; 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
Contributor Information and Disclosures

Updated: Nov 16, 2009

Differential Diagnoses

Alzheimer Disease
Herpes Simplex Encephalitis
Alzheimer Disease in Individuals With Down Syndrome
Multiple Sclerosis
Aphasia
Paraneoplastic Encephalomyelitis
Ataxia with Identified Genetic and Biochemical Defects
Pick Disease
Central Pontine Myelinolysis
Status Epilepticus
Complex Partial Seizures
Tonic-Clonic Seizures
Cortical Basal Ganglionic Degeneration
Frontal and Temporal Lobe Dementia
Frontal Lobe Syndromes

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. S...

      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.

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      Callosal damage in Marchiafava-Bignami disease. S...

      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 195914,15 . 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.

More on Marchiafava-Bignami Disease

Overview: Marchiafava-Bignami Disease
Differential Diagnoses & Workup: Marchiafava-Bignami Disease
Treatment & Medication: Marchiafava-Bignami Disease
Follow-up: Marchiafava-Bignami Disease
Multimedia: Marchiafava-Bignami Disease
References
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References

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Further Reading

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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

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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 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
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