Weakness in adults can result from disorders of muscle, nerve, or neuromuscular transmission. The key challenge is distinguishing acute life-threatening conditions (e.g. Guillain-Barré, botulism, MG crisis) from chronic progressive diseases (e.g. ALS, muscular dystrophies). A systematic approach with careful history, examination, and time course analysis is essential.

🗣️ History

Onset: Sudden (vascular, GBS, botulism) vs insidious (ALS, dystrophies).
Progression: Hours–days (myasthenic crisis, GBS) vs weeks–months (CIDP, myopathies).
Distribution: Proximal (myopathies, LEMS) vs distal (neuropathy, MND).
Triggers: Infection, new drugs (steroids, statins), toxins, family history.
Associated features: Ptosis/diplopia (MG), sensory loss (GBS/CIDP), rash (dermatomyositis), bulbar symptoms.

🧑‍⚕️ Examination

Muscle bulk & tone: Wasting, fasciculations, spasticity.
Reflexes: Hyporeflexia/areflexia (GBS, CIDP), brisk reflexes (UMN in ALS).
Cranial nerves: Ptosis, diplopia, facial weakness, bulbar palsy.
Sensation: Usually spared in MG/myopathies, affected in neuropathies.
Respiratory effort: Always check vital capacity in suspected neuromuscular disease.

⏱️ Time Course & Causes

Time Course	Likely Causes
Acute (hours–days)	GBS, botulism, myasthenic crisis, stroke, electrolyte derangements (K+, Ca2+)
Subacute (weeks)	CIDP, inflammatory myopathies (polymyositis, dermatomyositis), drug-induced myopathy
Chronic (months–years)	ALS, muscular dystrophies, inherited neuropathies, metabolic myopathies

📊 Comparative Table – Causes of Weakness in Adults

Condition	Pathophysiology	Clinical Features	Diagnosis
💊 Myasthenia Gravis	Autoantibodies to post-synaptic ACh receptors → ↓ transmission	Fluctuating weakness, ptosis, diplopia, dysphagia, fatigability	Anti-AChR antibodies, EMG, CT/MRI for thymoma
⚡ Guillain-Barré Syndrome	Immune-mediated demyelination post-infection	Ascending symmetrical weakness, areflexia, respiratory failure risk	NCS, CSF (↑ protein, normal WCC)
🧠 Amyotrophic Lateral Sclerosis	Degeneration of UMN & LMN	Progressive weakness, wasting, fasciculations, spasticity, hyperreflexia	EMG, NCS, MRI (exclude mimics)
🧬 Muscular Dystrophies	Inherited dystrophin defects	Proximal weakness, pseudohypertrophy, progressive disability	Genetic testing, muscle biopsy, ↑ CK
☠️ Botulism	Toxin blocks presynaptic ACh release	Descending paralysis, CN palsies, respiratory weakness	Toxin assays, NCS, exposure history
🔥 Polymyositis / Dermatomyositis	Autoimmune inflammation & necrosis	Proximal weakness, dysphagia; dermato = heliotrope rash, Gottron’s papules	↑ CK, muscle biopsy, autoantibodies
🎯 Lambert-Eaton Syndrome	Antibodies to presynaptic VGCC (often paraneoplastic)	Proximal leg weakness, autonomic signs, improves with activity	Anti-VGCC Abs, EMG, cancer screening
🌀 CIDP	Chronic autoimmune demyelination	Symmetrical weakness + sensory loss ≥8 weeks	NCS/EMG, CSF (↑ protein)

🚨 Red Flags

Rapid progression (GBS, botulism, MG crisis) → airway/ventilation risk.
Bulbar symptoms: dysphagia, dysarthria → aspiration risk.
Respiratory weakness: orthopnoea, weak cough, reduced vital capacity.

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Weakness in Adults – Causes, Features, and Diagnosis 🧑‍⚕️

🗣️ History

🧑‍⚕️ Examination

⏱️ Time Course & Causes

📊 Comparative Table – Causes of Weakness in Adults

🚨 Red Flags

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