MS and MG

I. Multiple Sclerosis (MS)

MS is a chronic inflammatory autoimmune disorder that affects the myelin sheath and nerve fibers of the Central Nervous System (CNS), including the brain and spinal cord.

  • Pathophysiology: Immune-mediated demyelination leads to slowed or blocked nerve impulses. As inflammation subsides, damaged tissue is replaced by scleroses (plaques).

  • Key Types to Know:

    • Clinically Isolated Syndrome (CIS): First episode, < 24-hour episode of neurological s/s attributed to MS; MRI may not show evidence of MS yet, will likely be diagnosed with MS within 10 years

    • Relapsing-Remitting (RRMS): Most common; symptoms develop and resolve in weeks/months, returning to baseline.

    • Primary Progressive (PPMS): Steady deterioration without remissions; typically onset at 40–60 years old.

    • Secondary Progressive (SPMS): Begins as RRMS but later becomes steadily progressive.

  • Assessment & Triggers:

    • Early Indicators: Vision changes (diplopia, nystagmus), mobility issues, and sensory disturbances (paresthesia).

    • Triggers: Fatigue, stress, overexertion, and heat (e.g., hot showers) can exacerbate symptoms.

    • Cognitive Changes: "MS hug" (dysesthesia), memory loss, and impaired judgment.

  • Pharmacology:

    • Disease-Modifying Drugs (DMDs): Interferon beta 1a/1b (immunomodulators) are used to reduce the frequency/severity of relapses. Side effects include flu-like symptoms, hepatotoxicity (monitor LFTs), and myelosuppression (monitor CBC).

    • Acute Relapse: Treated with short courses of high-dose IV glucocorticoids (Methylprednisolone) to suppress inflammation.

    • Spasticity: Managed with Baclofen or Diazepam.

II. Myasthenia Gravis (MG)

MG is a chronic autoimmune neuromuscular disorder characterized by fluctuating muscle weakness and rapid fatigue.

  • Pathophysiology: Antibodies attack nicotinic acetylcholine receptors at the neuromuscular junction (NMJ), reducing functional receptors by 70–90%.

  • Key Symptoms: Ptosis (drooping eyelids), diplopia, and difficulty swallowing (dysphagia) or breathing.

  • Pharmacology (Pyridostigmine):

    • The drug of choice is Pyridostigmine (Mestinon), a cholinesterase inhibitor that increases acetylcholine at the NMJ.

    • Patient Teaching: Dosing is individualized; patients should take the medication prior to exertion or eating to ensure muscle strength for swallowing.

    • Antidote: Atropine is used to treat excessive muscarinic responses (e.g., bradycardia).

III. Critical Comparison: Myasthenic vs. Cholinergic Crisis

Distinguishing between these two is a high-yield exam topic.

Feature

Myasthenic Crisis

Cholinergic Crisis

Cause

Undermedication (too little Ach)

Overdose of cholinesterase inhibitors

Symptoms

Extreme muscle weakness; respiratory paralysis

SLUDGE (Salivation, Lacrimation, Urination, Diaphoresis/Diarrhea, GI cramping, Emesis) & Killer Bs (Bradycardia, Bronchospasm)

Diagnosis

Tensilon Test: Symptoms improve with Edrophonium

Tensilon Test: Symptoms worsen or do not improve

Treatment

Neostigmine

Stop meds; Atropine; respiratory support

IV. Nursing Priorities & Collaborative Care

  • Safety & Aspiration: Perform a swallow screen before oral meds for MG or MS patients with dysphagia.

  • Vision Support: For diplopia (double vision), use an eye patch, alternating eyes every few hours.

  • Immunity: Many MS drugs are immunosuppressants; teach patients to avoid crowds and people with infections.

  • Mobility: Plan for periods of rest to manage fatigue and avoid overexertion which can trigger MS flare-ups