Demyelinating diseases such as multiple sclerosis, ADEM, and optic neuritis are a mainstay of neurology, and as such are a very high-yield topic on neurology exams. The RITE® and board examinations ask numerous questions on this topic that command an understanding of diagnostic imaging and pathology as well as therapeutic approaches. Luckily, you will find all of that here! Use this chapter to review the most commonly tested demyelinating diseases, examine real patient pathology and radiology images, and test your retention with our Question Bank and flashcards.

Authors: Ryan Orie PA-C, James Eaton, MD
Editor: Brian Hanrahan MD

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Multiple sclerosis (MS)

  • Multiple sclerosis is a chronic inflammatory disorder characterized by progressive neurological decline that manifests in different clinical phenotypes.
  • Risk factors: Gender (female), family history, geographical latitude, low vitamin D levels. 
  • Patients can have a broad spectrum of acute focal neurological symptoms including but not limited to focal sensory or motor deficits, monocular visual loss, diplopia, and gait disturbance.
    • Patients with chronic MS or other demyelinating conditions tend to have fatigue exacerbated by heat (Uhthoff’s phenomenon) that improves with cooler temperatures.
    • Sleep disturbances, depression, euphoria, urinary retention, paroxysmal spasms and cognitive decline are also common.

    • Neuropsychological testing can show deficits in long term memory (most common), verbal fluency as well as speed and working memory.
    • Epilepsy is a rare complication, seen in only 2-5% of patients. 

Diagnosis

  • Comprehensive diagnostic criteria are outlined by the 2017 McDonald Criteria.
    • Diagnosis is based on patients that have evidence of demyelination with dissemination in space and time.
    • This can be based on clinical changes (relapse), features on imaging, and CSF findings.
      • Dissemination in space (DIS): Development of lesions in two distinct anatomical locations indicating a multifocal disease process.
      • Dissemination in time (DIT): Appearance of new CNS lesions on imaging over time, or lesions of different appearance (bright versus dark) indicating new and old.
        • Oligoclonal bands in CSF are now considered an indication of DIT as well.

Clinical Phenotypes

  • Relapsing-remitting MS (RRMS): Clearly defined attacks with neurologic recovery (complete or incomplete) between them.
  • Secondary progressive MS (SPMS): Seen in patients who initially had RRMS but now experiencing a gradual worsening regardless of occasional attacks. Early aggressive treatment may delay this progression.
  • Primary progressive MS (PPMS): Progressive decline of neurological function without clearly defined attacks over the course of at least 1 year.
Multiple Sclerosis Diagram showing relapsing-remitting and primary-progressive course for neurology resident board exam review

Clinically isolated syndrome (CIS)

  • Defined as a monophasic demyelinating episode in someone who otherwise has no clinical history of demyelinating disease. 
  • Initiating a disease-modifying therapy (DMT) after CIS can delay the time to a definitive diagnosis of multiple sclerosis (MS).

Radiologically isolated syndrome (RIS)

  • Diagnosed in a patient with an MRI that is consistent with MS but they have no clinical history of transient focal neurological deficits. 
  • When diagnosed patients have a 33% chance of having a clinical demyelinating attack over the following two years.
    • The risk of MS is higher if oligoclonal bands are present in the CSF.
cisris

Diagnostic studies

  • Typical findings in CSF include an elevated protein, elevated CSF IgG index, oligoclonal bands in the CSF which do not present in the serum, and possibly slight elevation of WBC count (lymphocytic predominant).
  • MRI imaging with contrast is the most important imaging modality in the workup of possible MS.
    • Demyelinating lesions related to MS are ovoid, >3 mm in diameter, and are typically located in particular regions: periventricular (Dawson’s fingers), juxtacortical, cortical, or spinal cord.

Typical demyelinating attacks

Optic Neuritis (ON)

  • Presents with monocular decreased visual acuity, loss of color vision, and an afferent pupillary defect (APD) due to a demyelinating lesion of the optic nerve.
    • Pain is also usually present with extraocular movements.
    • Children with ON are more likely to present with  headache and bilateral symptoms.
  • Can be the initial presentation of multiple sclerosis or neuromyelitis optica.
  • A funduscopic exam will show a swollen optic disc.
  • Optical coherence tomography (OCT) will show thinning of the retinal nerve fiber layer weeks to months after an acute attack.
  • Visual evoked potentials (VEPs) of the affected eye will show a prolonged P100 latency, even in patients with distant histories of ON with no residual visual deficits.

Transverse myelitis (TM)

  • Presents with myelopathic findings (weakness, hyperreflexia, sensory symptoms, and occasionally bladder/bowel dysfunction).
    • Lhermitte’s sign, an electric shock sensation down the neck/spine with neck flexion or extension) may also be present.  
  • MRI will show a T2/FLAIR hyperintense lesion involving the spine +/- contrast enhancement based on the lesion’s acuity.
  • TM can be the initial presentation of demyelinating disease. However, it is also important to exclude infectious, rheumatologic, postvaccination/postinfectious, and nutritional mimics of demyelinating disease.
  • If felt to be truly inflammatory or idiopathic TM once other etiologies are ruled out, then initiation of steroids is indicated.
Transverse Myelitis
Transverse myelitis

Pathology

  • On gross anatomy, there will be grey plaques within white matter representing the loss of myelinated tissue.

  • Microscopic analysis can gauge the chronicity of a demyelinating plaque.
    • Active plaques will have a destruction of oligodendroglia while sparing neurons and their axons, inflammatory infiltrates of the parenchyma and in the perivascular space, as well as macrophages containing myelin debris.

    • During the recovery phase, recruited oligodendrocyte precursor cells remyelinate active plaques leading to reduced myelin density and thin myelin sheaths.
      • Almost half of chronic MS plaques will show some degree of remyelination.
      • Remyelinated plaques are also known as “shadow plaques”.
    • Chronic inactive plaques have sharply demarcated hypocellular plaques with myelin loss and glial scar formation via astrocytes.

Acute treatment:

  • High dose steroid therapy: IV methylprednisolone (1 gm per day for 3-5 days) +/- prednisone taper.
    • Although IV steroids are typically identified as first-line for acute MS exacerbations, oral steroids have also been shown to have an equal benefit, and thus can be used as first-line. This approach might be preferred by some providers for some patients.
  • If IV steroids fail to improve symptoms, providers can try plasma exchange (PLEX).
    • PLEX has more established data for acute MS exacerbation treatment than does IVIG.
  • Disease-modifying therapies are not recommended as the sole treatment for acute MS exacerbations.

Disease-modifying therapies (DMTs):

Oral medications:

  • Fingolimod:

    • Moderate to high efficacy.
    • Mechanism of action:
      • Sequesters lymphocytes in lymph nodes, thereby reducing the number of lymphocytes in peripheral circulation and the central nervous system.

Mnemonic: Think of FINGolimod using its long FINGers to sequester lymphocytes .

Injectables:

  • Interferons

    • Mild effectiveness
    • Mechanism of action: Nonselective immunomodulation
    • Side effects: Myalgias, flu-like symptoms, injection site reactions
    • Has a risk of decreased effectiveness over time due to the formation of neutralizing antibodies with prolonged use.

  • Glatiramer acetate

    • Moderate effectiveness
    • Mechanism of action: Selective immunomodulation
    • Tends to be better tolerated than interferons.
    • Side effects: Lipoatrophy at injection sites
    • No risk for the formation of neutralizing antibodies, unlike beta-interferons or natalizumab.

Ofatumumab

  • Mechanism of action: monoclonal antibody to CD20 B-cells.
  • Proven to be more effective than teriflunomide in randomized drug trials.
  • Side effects: Injection site irritation, upper respiratory tract infections, headache
  •  Screening for hepatitis B and low immunoglobulins should be done prior to initiating therapy.

Infusions:

  • Natalizumab

    • A highly effective medication.
    • Mechanism of action: Monoclonal antibody targeting of alpha 4-integrin which is expressed on activated T-lymphocytes. This blocks the transmigration of T-cells across the blood-brain barrier.
    • Side effects:
      • Progressive multifocal leukoencephalopathy (PML).
        • A usually fatal opportunistic infection of the central nervous system within oligodendrocytes due to reactivation of latent JC polyomavirus infection.
        • Risks for the development of natalizumab-associated PML include positive anti-JC virus antibodies before initiating therapy, prior use of immunosuppressive therapy, and more than 24 months of natalizumab therapy.
          • Patients on natalizumab have their JCV titers checked before starting therapy. JC viral positive patients can still undergo treatment, however the risk for PML increases when the duration of therapy is greater than 2 years.
        • Treatment for PML requires discontinuation of natalizumab. PLEX is often used to accelerate drug clearance.
          • Restoration of immune function may result in immune reconstitution inflammatory syndrome (IRIS).
        • Sudden cessation without transition to another therapy can lead to worsening of symptoms.

MS variants

  • Tumefactive MS (TMS):

    • Presents with a large (>2 cm) demyelinating lesion with incomplete ring enhancement, mass effect, minimal surrounding edema, and low cerebral blood volume.
      • Imaging may be difficult to differentiate from a brain tumor, ADEM, or abscess.
        • Tumors will often have more significant surrounding edema and higher cerebral blood volume than TMS. 
      • A biopsy is sometimes required to confirm the diagnosis.
    • Pathology: Foamy macrophages containing phagocytosed myelin debris.

  • Marburg variant disease (Acute/fulminant Multiple Sclerosis)

    • A fulminant form of MS with large tumefactive lesions, associated with a high mortality rate.
      • It is relatively unresponsive to therapy but high-dose steroids and PLEX may help.
    • Pathology will show more macrophage infiltrates and necrosis than typical MS.

  • Balo’s concentric MS

    • Imaging will show concentric alternating bands of preserved myelination with alternating areas of demyelination. This is also described as “onion bulbs” when seen pathologically.
Balos Concentric Sclerosis MS Variant
Luxol fast blue stain, low power view shows a large plaque with alternating (concentric) bands of severely demyelinated tissue and rings of myelin.

  • Schilder’s disease:

    • Seen primarily in childhood.
    • Lesions will be large in size, contrast-enhancing, and usually involve the centrum semiovale.

Pregnancy with MS

  • Pregnancy is generally safe in patients with MS.
    • Children born from parents with MS have a 3-5% risk of developing MS themselves.
  • The relapse rates decrease over the duration of pregnancy and increase postpartum.
  • Pregnancy and breastfeeding have no effect on overall disease progression.
  • Although not universal, DMTs should be discontinued or avoided if possible during pregnancy , especially if the patient is taking teriflunomide or mitoxantrone[/pms-restrict].
  • Glatiramer acetate and interferon beta are felt to be the safest options to use during pregnancy.
  • High-dose corticosteroids can be used for acute relapses during pregnancy and are not teratogenic.

Multiple sclerosis mimics

Neuromyelitis optica spectrum disorder (NMOSD)

  • Formally known as Devic disease, NMOSD is an inflammatory CNS disorder distinct from MS, most commonly associated with antibodies to aquaporin-4 (APQ4). 
  • Core clinical characteristics:
    • Optic neuritis (longitudinal/chiasmal lesion)
    • Longitudinally extensive transverse myelitis (LETM) is defined by a single lesion involving 3 or more vertebral segments.
    • Brainstem/diencephalic lesions.
    • Area postrema syndrome: Hiccups, nausea, and vomiting

  • Antibodies for aquaporin-4 (AQP4) and myelin oligodendrocyte glycoprotein (MOG) should be checked in any patient when NMO is suspected.
    • AQP4 is a water channel localized in the CNS at the endfeet of astrocytes. 
    • MOG is found on oligodendrocytes.
  • Unlike MS, oligoclonal bands are often absent from the CSF.
  • Pathologic findings include perivenous infiltration of lymphocytes, inflammation, and demyelination. 
  • Treatment:
    • Acute therapy: High dose steroids, then PLEX or IVIG if symptoms are steroid-resistant.
    • Long-term management:
      • IVIG
      • Immunosuppressants (azathioprine, mycophenolate)
      • Monoclonal antibodies (if anti-AQP4 antibody positive)

    • The disease-modifying agents for multiple sclerosis have not demonstrated effectiveness for NMOSD.

Acute disseminated encephalomyelitis (ADEM)

  • Also known as postinfectious encephalomyelitis.
  • A monophasic autoimmune illness that presents abruptly with headaches, fever, and widespread CNS demyelination and occurs primarily in children and young adults.
    • Symptoms usually resolve within a week without residual neurologic deficits. Children are more likely to make a complete recovery than adults.
  • Disease onset is 7 to 14 days after environmental exposure.
    • Most commonly occurs after viral upper respiratory infections but can occur after immunizations as well.
  • MRI brain with contrast will show multiple bilateral hyperintense T2-weighted lesions with poor margins and variable enhancement.
Acute Disseminated Encephalomyelitis (ADEM)
Acute Disseminated Encephalomyelitis (ADEM)

Swollen white matter with widely scattered hemorrhagic foci in the white matter.
  • Pathologic findings include perivenous infiltration of lymphocytes, inflammation, and demyelination.

Progressive multifocal leukoencephalopathy (PML)

  • Usually fatal infection of oligodendrocytes caused by reactivation of latent JC polyomavirus.
  • Patients will present with subacute progressions of encephalopathy, focal motor deficits, ataxia, diplopia, and/or hemianopia.
  • The CNS infection is established via hematogenous dissemination of the latent virus in the kidneys which then crosses the blood-brain barrier.
  • Occurs in patients with impaired immune systems: HIV, leukemia, and those on immunosuppressive agents (chemotherapy/monoclonal antibodies).
    • For JC-positive patients, natalizumab has a high risk of causing PML when treatment is greater than 2 years.
    • Patients on immunosuppressive medications at the time of diagnosis should have their medications discontinued and then consider plasma exchange to remove the drug from the circulation.
    • Patients with HIV-related PML should be started on HAART therapy.
      • Restoration of immune function may result in immune reconstitution inflammatory syndrome (IRIS), which presents with worsening neurologic symptoms and contrast enhancing cerebral edema .
        • IRIS occurs 3-6 weeks after treatment for PML and should be treated with high-dose IV steroids followed by an oral slow taper regimen.
  • Imaging will show non-enhancing FLAIR lesions preferentially involving the white matter without mass effect.

  • Pathology:
    • Demyelination . Immunohistochemistry staining for the JC virus is considered the gold standard for diagnosis.
  • JC virus PCR titers can also be used for diagnostic purposes and should be performed before biopsy if clinical suspicion is high.

Central pontine myelinolysis

  • Also known as osmotic demyelination syndrome, this disease is due to the rapid correction of hyponatremia.
    • This rapid correction leads to the demyelination of the base of the pons.
    • Extrapontine demyelinating lesions are infrequent but when present they are seen at cortical gray-white matter junctions.
  • Seen in alcoholics, end-stage renal disease, chronically malnourished patients, and patients undergoing a hepatic transplant.
  • Patients present acutely with AMS, hypotension, and hypoventilation with progression to pseudobulbar palsy and quadriparesis. Severe cases can progress to a “locked-in” syndrome.
  • While there are no available therapies, many patients improve over time.
Central Pontine Myelinolysis
Central Pontine Myelinolysis

Inherited Leukodystrophies

  • Inherited leukodystrophies are a heterogeneous group of inherited, metabolic demyelinating neurodegenerative diseases of the central nervous system.
  • Patients with leukodystrophy commonly have an initial period of normal development followed by progressive neurological deterioration. Common symptoms include bilateral and symmetric spasticity, weakness, and ataxia.
    • Cases can present at any age, ranging from infancy to adulthood.
    • Some leukodystrophies also present with demyelination of peripheral nerves; such as Metachromatic leukodystrophy and Krabbe disease.
  • MRI imaging can be variable but it will universally show changes in the cortical white matter, appreciated as T2 sequence hyperintensity. Particular dystrophies may also have white matter contrast enhancement. If only particular regions are involved, this can point you in the right direction to a particular disease.
  • Treatment: Adrenoleukodystrophy, metachromatic leukodystrophy, and Krabbe’s disease can be treated with stem cell transplantation.

Metachromatic leukodystrophy

  • An autosomal recessive disease due to a deficiency of arylsulfatase A enzyme from a mutation in the ARSA gene.
  • Can present in infancy, childhood/juvenile, or adulthood depending on the severity of the gene dysfunction.
    • Infants present with vision loss, spastic ataxia, and seizures. Death usually occurs in 2-4 years after disease onset.
    • Juvenile onset has similar symptoms but a slower rate of progression.
    • Adults present with behavioral change, psychosis, and dementia.
  • Imaging will show extensive white matter demyelination
  • A demyelinating sensorimotor polyneuropathy is also present in almost all cases.

X-linked Adrenoleukodystrophy

  • Due to an X-linked mutation in the gene ABCD1, which is responsible for the function of peroxisomes. The mutation leads to impaired very-long-chain fatty acid (VLCFA) oxidation.
    • Blood and urine studies can show increased levels of VLCFAs.
    • Within the same family, the same genetic mutation can have variable phenotypes.
  • Presents with adrenal failure, testicular atrophy, hyperactivity, ataxia, vision/hearing loss, and seizures. 
  • Adrenal insufficiency is seen in 50-80% of patients and can cause hyperpigmentation.
    • Intermittent adrenal testing may be needed as well as corticosteroid supplementation during times of stress/illness.
  • Imaging will show posterior predominant white matter demyelination with sparing the frontal lobes and contrast enhancement.
  • Adrenomyeloneuropathy (AMN) variant:
    •  Primarily affects the spinal cord leading to lower extremity weakness and spasticity. 
Axial T2 FLAIR MRI showing posterior-predominant white matter hyperintensities consistent with adrenoleukodystrophy
Axial T2 FLAIR MRI showing posterior predominant white matter hyperintensities consistent with X-linked adrenoleukodystrophy

Krabbe disease

  • Due to a deficiency of the enzyme galactocerebrosidase.
  • The infantile form will present with an exaggerated startle, fevers, behavioral regression, optic atrophy, and hypertonicity. Death usually occurs within a few years of diagnosis. There are juvenile and adult forms as well which are less progressive than the infantile form.
    • Seizures are frequent.
  • Imaging will show white matter changes .
  • Pathology will show large globoid cells which are PAS-positive multinucleated macrophages with galactocerebroside present.

Axial T2 sequences showing hyperintensity of the cortical white matter consistent with leukodystrophy

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