The answer is B. Multiple sclerosis
Neurologic deficits separated in time and in space, in a young woman, with periventricular white matter lesions and CSF-restricted oligoclonal bands, is multiple sclerosis. MS is an immune-mediated demyelinating disease of the central nervous system: activated lymphocytes cross the blood-brain barrier and strip myelin from CNS axons, slowing or blocking conduction. Two words carry the diagnosis and are worth memorizing verbatim — dissemination in time and dissemination in space. Her optic neuritis two years ago, transverse myelitis six months ago, and brainstem-cerebellar syndrome now are three separate events (time) in three separate CNS locations (space), and the MRI showing simultaneously enhancing and non-enhancing lesions proves dissemination in time on a single scan, because enhancement marks a lesion less than about six weeks old. Epidemiology is high yield: women roughly two to three times more often than men, onset typically between 20 and 40, and incidence rising with distance from the equator, with low vitamin D and prior Epstein-Barr virus infection as the best-supported risk factors. Several findings in this stem are near-pathognomonic and should be recognized instantly. Internuclear ophthalmoplegia — impaired adduction of one eye with nystagmus of the abducting eye — comes from a lesion in the medial longitudinal fasciculus, and bilateral INO in a young adult is MS until proven otherwise. Lhermitte sign is an electric shock down the spine on neck flexion, from a demyelinated cervical cord. Uhthoff phenomenon is the transient worsening of existing deficits with heat — a hot shower, exercise, or fever — because conduction through partially demyelinated axons fails as temperature rises; note that it is a pseudo-relapse, not a true attack, and it resolves on cooling. Diagnosis rests on MRI of the brain and spinal cord with gadolinium, showing ovoid periventricular lesions perpendicular to the ventricles — Dawson fingers — plus juxtacortical, infratentorial, and cord lesions. Lumbar puncture is supportive rather than required: oligoclonal bands present in CSF but absent from serum indicate intrathecal immunoglobulin synthesis. Treatment splits cleanly into three questions. For an acute relapse, give high-dose intravenous methylprednisolone, with plasma exchange for steroid-refractory attacks; steroids shorten the attack but do not change long-term disability. For disease modification in relapsing-remitting disease, start therapy early — interferon beta, glatiramer acetate, dimethyl fumarate, fingolimod, teriflunomide, or monoclonal antibodies such as natalizumab and ocrelizumab — to reduce relapse rate and new lesion formation. For symptoms, treat spasticity with baclofen or tizanidine, fatigue with amantadine, neuropathic pain with gabapentin, and bladder dysfunction specifically, since urinary retention and recurrent infection drive much of the morbidity. Sorting the distractors: neuromyelitis optica spectrum disorder also pairs optic neuritis with myelitis, but the optic neuritis is often bilateral and severe, the cord lesion is longitudinally extensive spanning three or more vertebral segments, brain MRI is typically spared early, oligoclonal bands are usually absent, and aquaporin-4 IgG is positive — the distinction matters because interferon beta worsens NMOSD; acute disseminated encephalomyelitis is a monophasic postinfectious illness, usually in children, with encephalopathy and lesions that all enhance simultaneously, so it lacks dissemination in time; vitamin B12 deficiency causes subacute combined degeneration of the dorsal columns and corticospinal tracts with a macrocytic anemia and hypersegmented neutrophils, and it does not produce discrete relapsing attacks, optic neuritis, or oligoclonal bands; and Lyme neuroborreliosis follows an endemic tick exposure with facial nerve palsy, radiculopathy, and lymphocytic meningitis, and serology plus exposure history separate it.
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