Neurology MS

Multiple Sclerosis (MS)

Chronic, often disabling autoimmune demyelinating CNS disease with sclerotic plaques; fluctuates with exacerbations (relapses) and remissions. Known as the “great crippler of young adults.” Typical onset 20–40 yrs, more common in women and in White populations (rare in Blacks/Asians).

Charcot’s triad

Intention tremor, scanning speech, and nystagmus (classic MS signs).

Etiology (MS)

Idiopathic; immune-mediated attack on CNS myelin often triggered post-viral (measles, rubella, HHV-6). CSF often shows ↑IgG and oligoclonal bands. Family history in ~15%.

Pathophysiology

Immune activation (T & B lymphocytes, macrophages) → oligodendrocyte destruction → demyelination → impaired saltatory conduction → neural fatigue.

Exacerbation (relapse)

Period of new or worsening neurologic symptoms due to active inflammation/demyelination.

Remission

Partial recovery when inflammation subsides; may involve limited remyelination.

Chronic stage (gliosis)

Loss of oligodendrocytes → proliferation of astrocytes forming glial scars (plaques).

Gliosis

Astrocytic scarring replacing myelin in chronic MS.

Astrocyte

CNS support cell: BBB maintenance, repair, scar formation; drives gliosis.

Oligodendrocyte

CNS glial cell that forms myelin around CNS axons; target in MS.

Microglia

CNS immune cells clearing debris/pathogens.

Ependymal cell

Lines ventricles/central canal; produces and circulates CSF.

Schwann cell

PNS glial cell that forms myelin around PNS axons; not affected in MS.

Neuron signal flow

Dendrites → Soma → Axon → Terminals → Synapse → Next cell.

CNS tracts affected

Optic nerve (vision), subcortical white matter (cognition/behavior), corticospinal tracts (UMN signs), posterior columns (proprioception/vibration), cerebellar peduncles (balance/coordination).

Optic neuritis

Inflammation of optic nerve causing painful vision loss; common early sign.

Scotoma

Localized visual field defect.

Marcus Gunn pupil

Relative afferent pupillary defect due to optic nerve disease.

Nystagmus

Involuntary rhythmic eye movements; part of Charcot’s triad.

Paresthesia

Abnormal tingling “pins and needles”; frequent early symptom.

Dysesthesia

Burning/aching unpleasant sensation to normal stimuli.

Hyperpathia

Exaggerated pain response to mild stimuli.

Lhermitte’s sign

Electric-shock sensation down spine with neck flexion (posterior column lesion).

Trigeminal neuralgia (MS)

Severe stabbing facial pain from demyelination of CN V.

UMN signs (MS)

Spasticity, hyperreflexia, clonus, Babinski sign, spasms. Often more in LE.

Spasticity

Velocity-dependent ↑ tone with exaggerated reflexes.

Clonus

Rhythmic involuntary contractions indicating corticospinal lesion.

Babinski sign

Upgoing big toe on plantar stimulation; UMN lesion.

Ataxia

Incoordination; gait/limb dysmetria.

Dysmetria

Inaccurate movement range/force (past-pointing).

Dysdiadochokinesia

Impaired rapid alternating movements.

Dyssynergia

Poorly sequenced multi-joint movement.

Intention tremor

Tremor during goal-directed activity.

Postural tremor

Tremor with sustained posture.

Dysequilibrium

Balance impairment.

Vertigo/nausea

Spinning sensation from vestibular/brainstem involvement.

Dysarthria (scanning speech)

Slow, irregular, broken prosody due to cerebellar/brainstem lesion.

Dysphagia

Difficulty swallowing due to bulbar involvement.

Cognitive dysfunction

Deficits in memory, attention, processing speed, executive function.

Behavioral/emotional changes

Depression, anxiety, denial, anger, dependency, euphoria.

Fatigue (MS)

Disabling tiredness worsened by heat (Uhthoff’s), stress, exercise; improves with rest.

Uhthoff’s phenomenon

Heat-induced transient worsening of symptoms.

Bladder dysfunction types

Spastic (overactive): urgency/frequency. Flaccid (underactive). Dyssynergic sphincter: incoordination → incomplete emptying, incontinence.

Bowel dysfunction

Constipation common due to inactivity, ↓fluids, meds.

Sexual dysfunction

↓libido, vaginal dryness, orgasm difficulty (♀); ED (♂).

Relapsing–Remitting MS (RRMS)

Most common; relapses with recovery, no progression between.

Primary Progressive MS (PPMS)

Steady worsening from onset.

Secondary Progressive MS (SPMS)

Initially RRMS → progressive decline.

Progressive–Relapsing MS (PRMS)

Progressive course with relapses.

Benign MS

Minimal disability ≥15 yrs after onset.

Malignant MS

Rare, rapidly progressive, severe disability/death.

Prognosis (favorable)

Younger onset, monosymptomatic onset, RRMS.

Prognosis (poor)

Older onset, progressive from start, multiple system involvement.

MRI in MS

T2/FLAIR hyperintense plaques in brain/spinal cord.

Evoked potentials

Prolonged visual/somatosensory/motor latencies.

CSF profile

Normal/mild ↑ protein/cell count; ↑IgG index; oligoclonal bands.

Disease-modifying therapy

Interferon-β, other immunomodulators to reduce relapses/new lesions.

Spasticity medications

Baclofen, tizanidine, dantrolene; botulinum toxin for focal spasticity.

Bladder management

Anticholinergics (spastic), alpha-blockers (dyssynergic), Credé maneuver (flaccid).

Pain medications

Carbamazepine, phenytoin, amitriptyline.

Fatigue medications

Amantadine, pemoline.

Tremor medications

Isoniazid, clonazepam.

Vertigo meds

Meclizine.

Mood management

Antidepressants.

PT assessment

Cognition/affect, sensory integrity, vision, cranial nerves, pain, ROM, strength, fatigue, heat sensitivity, coordination, posture, gait/balance, aerobic capacity, skin, environment.

Vision strategies (PT)

Contrast, lighting, tinted glasses, eye patch, reduce clutter.

Sensory strategies (PT)

Verbal/tactile cues, biofeedback, proprioceptive loading.

Pain strategies (PT)

Massage, stretching, ultrasound, lukewarm hydrotherapy, compression.

Spasticity strategies (PT)

Cold packs, stretching, antagonist activation, positioning.

Fatigue strategies (PT)

Pacing, energy conservation, morning/low-impact exercise.

Ataxia strategies (PT)

Mat work, joint approximation, alternating isometrics, rhythmic stabilization, dynamic balance, aquatic (29–30 °C).

Mobility interventions

Orthoses, gait training, wheelchair training.

Cardiorespiratory fitness

Low-impact aerobics, seated calisthenics/zumba.

Skin care

Turn q2h in bed; pressure relief q15 min in wheelchair.

Posterior column signs

Loss of vibration/position sense; positive Lhermitte’s sign.

Corticospinal tract signs

Weakness with spasticity, hyperreflexia, pathological reflexes.

Cerebellar peduncle involvement

Limb/gait ataxia, intention tremor.

Subcortical white matter involvement

Cognitive/behavioral changes, slowed processing.

Heat sensitivity in MS

Worsening of conduction with ↑temperature.

Neural conduction block

Failure of impulse across demyelinated segments.

Nodes of Ranvier

Gaps in myelin where AP regenerates; essential for saltatory conduction.

Sclerotic plaques

Chronic demyelinated/gliotic areas seen on MRI.

Monosymptomatic onset

Single neuro symptom at onset; better prognosis.

Executive dysfunction

Poor planning, sequencing, problem-solving, self-monitoring.

Energy conservation

Task simplification, pacing, scheduled rest to manage fatigue.

Detrusor–sphincter dyssynergia

Bladder-sphincter discoordination → incomplete emptying.

Credé maneuver

Manual abdominal pressure technique for voiding in flaccid bladder.

Diplopia (MS)

Double vision from internuclear/brainstem lesion.

Gait ataxia

Wide-based, irregular stepping.

Sensory ataxia

Ataxia from posterior column loss; worse eyes closed (Romberg +).