Muscle Weakness
- History to consider
- Pattern of onset – timing, areas, symmetry, proximal or distal
- Variations or fluctuations – fatiguability, diurnal changes
- Temporal spread
- Associated symptoms – pain/sensory, muscle wasting, cramps
- Medical history
- Family history
💥 Neurological causes
| Neuro-anatomical level | Key disorders | Diagnostic / bedside clues | Typical onset & tempo | Natural course / progression |
|---|---|---|---|---|
| Central nervous system / spinal cord | Multiple sclerosis | Focal neurological episodes (sensory, visual, cerebellar, sphincter); demyelinating plaques on MRI | Relapsing–remitting or progressive; first attack may be acute | Stepwise accumulation of disability; highly variable |
| Cervical myeloradiculopathy | Combination of upper- and lower-motor-neuron signs in limbs, radicular neck or arm pain; sphincter involvement; no bulbar signs | Subacute (weeks–months) or chronic | Slowly progressive unless surgically decompressed | |
| Motor nerve (peripheral) | Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) | Symmetrical, relapsing or steadily progressive weakness; distal sensory loss; slowed conduction on NCS | Subacute–chronic | May respond to IVIg / steroids / plasmapheresis |
| Peripheral nerve hyper-excitability (PNH) | Fasciculations and muscle cramps (calves common); little or no weakness/wasting; EMG: myokymia | Variable (often chronic) | Usually stable; treat underlying cause or symptomatic | |
| Multifocal motor neuropathy with conduction block | Unilateral or asymmetric distal upper-limb weakness (finger extensors); weakness > atrophy; NCS shows conduction block | Chronic | Slowly progressive; responds to IVIg | |
| Neuromuscular junction | Myasthenia gravis | Fluctuating fatigable weakness (ocular ± bulbar ± limb); AChR or MuSK antibodies; decrement on repetitive-stimulation EMG | Subacute–chronic, diurnal variation | Variable; controlled with immunotherapy & cholinesterase inhibition |
| Motor neurone | Motor neurone disease (ALS) | Asymmetric limb onset, fasciculations, mixed UMN/LMN signs; no sensory, bowel/bladder or ocular involvement | Insidious | Relentless progression over months–years |
| Post-polio syndrome | History of poliomyelitis; new asymmetric weakness, fatigue, pain | Very late (decades after initial infection) | Slowly progressive; supportive management | |
| Spinal muscular atrophy | Symmetric proximal weakness from childhood / early adulthood; genetic SMN1 deletion | Congenital or early onset | Variable; newer SMN-augmenting therapies modify course | |
| Muscle | Inclusion-body myositis | Distal finger-flexor & quadriceps weakness, often asymmetric; CK frequently > 1000 IU/L; biopsy with rimmed vacuoles | Very insidious (years) | Slowly progressive; refractory to immunosuppression |
💥 Idiopathic inflammatory myopathies
| Differential | Clinical pattern | Onset | Progression |
|---|---|---|---|
| Polymyositis | Symmetric proximal limb & neck flexor weakness, no rash | Subacute (wks–mths) | Progressive until immunotherapy |
| Dermatomyositis | As polymyositis + characteristic rash (heliotrope, Gottron papules) | Subacute | Similar; cancer-associated forms may be abrupt |
| Inclusion-body myositis | Proximal quadriceps and distal finger-flexor/asymmetric weakness; dysphagia common | Very insidious (yrs) | Slow, inexorable; poor response to immunosuppression |
| Juvenile dermatomyositis | Dermatomyositis pattern in children; calcinosis frequent | Subacute | Biphasic: active phase → remission or chronic |
| Vasculitic myopathy | Painful muscles ± systemic vasculitis signs | Acute–subacute | May progress rapidly if untreated |
| Overlap syndromes (SLE, SSc, RA, Sjögren) | Proximal weakness ± arthralgia, rash, Raynaud, sicca, etc. | Variable | Depends on underlying CTD activity |
💥Endocrine & metabolic
| Differential | Pattern | Onset | Course |
|---|---|---|---|
| Hypothyroid myopathy | Proximal weakness, myalgia, delayed reflex relaxation | Gradual | Improves over months with thyroxine |
| Cushing (endogenous/exogenous) | Proximal weakness, steroid myopathy, wasting without pain | Subacute–chronic | Reversible with steroid reduction/control of cortisol |
| Electrolyte disorders (↓K⁺, ↓PO₄, ↓Ca²⁺, Na⁺ extremes) | Generalised flaccid weakness ± cramps, arrhythmia | Acute | Rapidly reversible when corrected |
| Vitamin B₁₂ deficiency | Mixed sensory ataxia + weakness (posterolateral cord, peripheral nerve) | Insidious | Improves partially with replacement |
💥Hereditary / metabolic myopathies
| Differential | Pattern | Onset | Course |
|---|---|---|---|
| Glycogen-storage (e.g. McArdle) | Exercise-induced cramps, episodic rhabdo | Childhood–young adult | Lifelong, non-progressive between episodes |
| Lipid-oxidation defects | Prolonged exercise/fasting triggers myalgia, rhabdo | Childhood–adult | Episodic; precipitated by stress, alcohol, fasting |
| Purine disorders (e.g. myoadenylate deaminase) | Early fatigue, myalgia after brief exertion | Adolescence | Stable course |
💥Drug- & toxin-induced
| Agent/class | Typical pattern | Onset after exposure | Progression |
|---|---|---|---|
| Alcohol (acute binge or chronic) | Generalised weakness, painful myopathy ± rhabdo | Hours–days | Resolves over days with abstinence |
| Corticosteroids | Painless proximal myopathy | Weeks–months | Gradually worsens; reversible if dose ↓ |
| Statins (HMG-CoA‐RI) | Myalgia ± proximal weakness; CK ↑ | Weeks | Improves within wks of cessation |
| Colchicine, antimalarials, zidovudine, penicillamine | Similar statin pattern; colchicine can cause axonal neuropathy | Weeks–months | Variable; often reversible |
| Illicit drugs (cocaine, heroin) | Focal or generalised rhabdo with severe pain | Hours | Self-limited if rhabdo managed |
💥Infective myopathies
| Pathogen & syndrome | Pattern | Onset | Course |
|---|---|---|---|
| Viral (influenza, Coxsackie, HIV, CMV, EBV) | Diffuse myalgia ± mild weakness; ↑CK | Acute | Resolves 1–3 wks; HIV chronic |
| Pyomyositis (Staph aureus) | Localised painful swelling, fever | Acute | May progress to abscess unless drained/IV ABx |
| Lyme myositis | Focal weakness, migratory pain | Subacute | Improves with doxy/ceftriaxone |
| Parasitic (Trichinella) | Myalgia, peri-orbital oedema, fever | Acute | Weeks; antiparasitic therapy helps |
| Fungal (rare, immunocomp.) | Focal pain, swelling | Subacute | Needs antifungal+debridement |
💥 Rhabdomyolysis triggers
| Trigger | Characteristic pattern | Onset | Progression |
|---|---|---|---|
| Crush trauma / compartment syndrome | Acute severe pain, weakness below injury | Immediate | CK peaks 24–72 h; risk AKI |
| Seizures | Generalised pain, transient weakness | Hours | Resolves over days |
| Delirium tremens / hyperkinesis | Generalised | Hours | Reversible with ethanol withdrawal care |
| Exertional (heat-related) | Painful proximal weakness ± hyperthermia | Hours | May progress to MODS if unrecognised |
| Malignant hyperthermia | Rigidity + weakness during GA | Minutes | Hyperacute; lethal without dantrolene |
| Post-vascular surgery / ischaemia-reperfusion | Limb swelling, weakness | Hours | Risk of reperfusion injury/AKI |
