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Neurology · Additional Topics

Sclerosis in neurology

Sclerosis multiplex

In neurological practice, the term "sclerosis" is most commonly associated with demyelinating pathologies in which the myelin sheath of nerve fibers is destroyed. Classic examples include multiple sclerosis and acute disseminated encephalomyelitis (ADEM), which require careful differential diagnosis with infections affecting the nervous system.

Active lesionContrast enhancement on T1-weighted MRI indicates recent inflammation.
ADEM courseThe active phase lasts no more than 3 months, followed by improvement.
Vision in MSA lesion in the optic tract causes homonymous hemianopsia.
MS mimicEncephalomyelitis in borreliosis requires differential diagnosis with MS.
3 min readFor medical studentsUpdated 10.10.2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesPending instructor review

Multiple sclerosis and optic pathway lesions

The onset of multiple sclerosis is often associated with visual disturbances due to focal fiber demyelination. The clinical picture depends on the localization of the pathological process:

  • Optic neuritis: accompanied by decreased visual acuity, loss of parts of the visual fields, pain upon eye movement, and impaired pupillary light reflex.
  • Optic tract lesion: leads to homonymous hemianopsia (loss of corresponding halves of the visual fields). For example, with a lesion in the left optic tract (tractus opticus sinister) or left optic radiation (radiatio optica), the right half of the visual field is affected.

Brain MRI is performed to confirm the diagnosis. Hyperintense demyelinating lesions are visualized on T2-weighted images. If the lesion enhances contrast on T1-weighted scans, it indicates recent (active) inflammation. Timely corticosteroid therapy in such cases allows for rapid regression of symptoms.

Acute disseminated encephalomyelitis (ADEM)

ADEM is a diagnosis of exclusion. According to IPMSSG (2012) criteria, its diagnosis requires the simultaneous presence of several factors:

  1. First episode of encephalopathy (alteration in consciousness or behavior not attributable to fever) with polyfocal neurological deficits.
  2. Presumed inflammatory demyelinating nature.
  3. Characteristic MRI changes within the first 3 months.
  4. No new symptoms or lesions after 3 months.

MRI findings in ADEM differ from multiple sclerosis. Lesions are usually large (greater than 1–2 cm), diffuse, with indistinct borders, predominantly in the white matter. T1-hypointense lesions are absent. In children, deep gray matter (thalamus, basal ganglia) is frequently involved.

The disease typically has a monophasic course. If new lesions appear on follow-up MRI (up to 6 months), a relapsing demyelinating disease (multiple sclerosis or neuromyelitis optica spectrum disorder) should be suspected.

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Neuroborreliosis as a differential diagnosis

Nervous system involvement in tick-borne borreliosis can mimic demyelinating diseases. Progressive encephalomyelitis in neuroborreliosis presents with spastic paraparesis, ataxia, cranial nerve palsies, and psychiatric disorders.

MRI reveals a multi-focal lesion pattern resembling demyelination. A pathognomonic sign that allows differentiation of neuroborreliosis from multiple sclerosis is the combination of encephalomyelitis with arthropathies (joint involvement).

Additionally, neuroborreliosis causes hemodynamic disturbances: the tone of small and medium arteries increases, vascular resistance rises, and venous outflow is impaired, leading to cerebral ischemia.

Topical diagnosis of visual impairments

In addition to demyelination, visual disturbances are caused by other neurological pathologies. Topical diagnosis is established based on specific symptoms:

  • Retina: acute ischemia (embolism, thrombosis) causes scotoma or amaurosis. Transient blindness can be a sign of a transient ischemic attack.
  • Chiasm and optic tracts: most commonly affected due to compression by pituitary tumors. Visual field defects, papilledema, and neuroendocrine disorders are characteristic.
  • Geniculate body: symptoms are identical to an optic tract lesion (hemianopsia), but pupillary light reflexes are preserved. The cause is isolated ischemia of this area.
  • Optic radiation: affected in strokes or temporal and parietal lobe tumor compression.
How to memorize

How to distinguish an optic tract lesion from a geniculate body lesion? In a tract lesion, pupillary reactions are impaired. The geniculate body is located "further" along the pathway, so the reflex arc of the pupillary reaction remains intact (light reflex is preserved).

Class and exam questions

How to distinguish a fresh demyelinating lesion from an old one on MRI?

A recent (active) inflammatory lesion enhances contrast agent on T1-weighted images.

What is the main difference in the course of ADEM versus multiple sclerosis?

ADEM typically has a monophasic course: the active phase lasts up to 3 months, after which improvement occurs and no new lesions appear.

Which symptom helps distinguish encephalomyelitis in borreliosis from multiple sclerosis?

A pathognomonic feature of neuroborreliosis is the combination of signs of multifocal CNS demyelination with arthropathies (joint involvement).

What does prolonged papilledema lead to?

It causes irreversible fiber damage, optic disc atrophy, and persistent decrease in visual acuity up to complete blindness (amaurosis).

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What else to study on this topic

  • Slowly progressive optic neuropathies (intoxications, hypovitaminosis, Leber's disease)
  • Multiphasic form of ADEM and criteria for transition of the diagnosis to multiple sclerosis
  • Peripheral nervous system involvement in neuroborreliosis (radiculoneuritis)
  • Differential diagnosis of neuroborreliosis and tick-borne encephalitis
  • Hemodynamic disturbances and cortical ischemia in tick-borne borreliosis

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