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weakness
- 2. Conditions that causeGeneralized Weakness Medical Conditions that Cause Fatigue and Weakness Asthenia, Fatigue, and Weakness of non-Neurologic Origin Generalized Weakness in Cancer Generalized Weakness with AIDS Generalized Weakness Due to Drugs or Toxins Generalized Weakness of CNS origin
- 3. Conditions that causeGeneralized Weakness Medical Conditions that Cause Fatigue and Weakness Generalized Weakness Due to Drugs or Toxins Generalized Weakness in Cancer Generalized Weakness with AIDS
- 4. Weakness of non-NeurologicOrigin Psychiatric illness – Patients with depression and other illnesses may interpret their fatigue and lack of motivation as global weakness – They may present with functional weakness (preferred term instead of "psychogenic weakness") – There is often a mental, affective, or "psychic" component accompanying the weakness – Don't let a strong psychiatric history pre-empt investigation of neurologic symptoms – It is entirely reasonable to consult Neurology if you are unsure!
- 6. _Cardiovascular: congestive heartfailure – * Hematologic: anemia, leukemia, lymphoma – * Renal: uremia, electrolyte abnormalities – * Pulmonary: COPD – * Endocrine (may cause true neuromuscular weakness as well): hypothyroidism, hyperthyroidism, hyperparathyroidism, hypogonadism, Addison disease, aldosterone deficiency, Cushing disease, hypercalcemia......and many, many more ! Medical Conditions that Cause Fatigue and Weakness
- 7. – * Erythrocytesedimentation rate (ESR) – * Complete blood cell count (CBC) – *"Complete metabolic panel" (electrolytes including Ca2+, Mg2+, PO4 3-, glucose, creatinine, urea) – * Liver function tests and liver enzymes – * Thyroid function tests – * Creatine kinase (CK) level – * Chest x-ray WeaknessRoutine laboratory evaluation for fatigue
- 8. Generalized Weakness Dueto Drugs or Toxins • Muscle is very sensitive to drugs and toxins because of its high metabolic activity – a daunting list of medications may produce muscle toxicity – they can interfere with muscle metabolism at many different sites – it is not useful to remember all of the drugs that can cause myopathy – but there are a few common offenders: • steroids • alcohol • statins • colchicine • Symptoms range from cramps and myalgias to rhabdomyolysis with severe muscle weakness and renal failure • Patients less able to clear drugs are at greater risk – Elderly, infants, ICU patients, liver and renal failure
- 9. Statin Myopathy • Statinscause a toxic necrotizing myopathy • Symptoms of toxic necrotizing myopathy: – myalgias – weakness – hyper CK-emia – myoglobinuria • The mechanism of toxicity is unknown • Muscle toxicity is rare with statin use – myalgias in 2% to 7% of statin users – elevated transaminases (assumed to come from muscle breakdown) in 0.5% to 2% – weakness and hyper CK-emia in 0.1% to 1% – severe myopathies in 0.08% – fatal rhabdomyolysis - 0.15 deaths per million prescriptions
- 10. • There isa newly-described immune myopathy associated with statin use – Immune-mediated necrotizing myopathy (INEM) – Statin somehow triggers an immune- mediated myopathy – It appears to be rare – Patients develop proximal muscle weakness and hyper CK-emia that persists after statin discontinuation
- 11. Steroid Myopathy • Causedby endogenous (Cushing's) or exogenous chronic excess corticosteroid – risk increased with doses of prednisone >30 mg/day – risk seems greater with fluorinated glucocorticoids (triamcinolone > betamethasone > dexamethasone) • Unknown mechanism of toxicity • Causes proximal limb weakness and atrophy (spares cranial muscles) • Sometimes called a "bland myopathy": – CK level is usually normal – EMG studies tend to be normal – Muscle biopsy tends to be normal or have only mild non-specific abnormalities (e.g. type IIb fibre atrophy)
- 12. Alcoholic Myopathy • Alcoholmore often causes neuropathy than myopathy • It causes several distinct muscle disorders: – acute necrotizing myopathy – acute hypokalemic myopathy – chronic alcoholic myopathy – asymptomatic alcoholic myopathy – alcoholic cardiomyopathy • Pathologic mechanisms are unknown • What you need to know: – alcohol can cause acute or chronic myopathy – the CK may be elevated, or normal – there is often a co-existing neuropathy – alcoholics have many other reasons to be weak (nutritional, metabolic, etc)
- 13. Colchicine Neuromyopathy • Colchicineinhibits polymerization of tubulin into microtubular structures • It is toxic to nerves and muscle (neuromyopathy) • Neuromyopathy can develop with acute intoxication, or long-term use at normal doses – patients with chronic renal failure are at higher risk of toxicity • Symptoms improve with discontinuation of colchicine – but may take 4 to 6 months to recover
- 14. Inflammatory Myopathies • Manymyopathies have an inflammatory component, secondary to... – toxic (e.g. immune-mediated necrotizing myopathy) – metabolic abnormalities – other connective tissue diseases (scleroderma, Sjögren syndrome, RA, SLE, mixed CTD) – ...PMR is not a myopathy (it is a vasculitis), but it produces muscle pain and weakness • Three "primary" inflammatory myopathies – Dermatomyositis – Polymyositis – Inclusion Body Myositis • They are pathologically distinct – DM is not "PM with a rash" – IBM is not "PM with inclusion bodies and rimmed vacuoles" – They differ in their response to treatment and prognosis
- 15. Polymyositis • PM probablyisn't a single disease entity • PM is better defined by what it isn't, than what it is • Clinical presentation: – Symmetric weakness, proximal > distal – Tender, aching muscles may be present, but usually pain isn't severe • "the more severe the pain, the less likely the diagnosis of polymyositis" -- Bradley's NICP – Cranial muscles are usually spared • ocular muscles are not involved • bulbar muscles may be involved in severe cases (dysphagia, dysarthria) – Tendon reflexes diminished in proportion to muscle weakness • which means that even patients with severe weakness should have DTRs • areflexia is more suggestive of neuropathy
- 16. • Associated features: –all of these occur in DM, too – Cardiomyopathy – Interstitial Lung Disease – Polyarthritis – Malignancy • PM and DM both may develop as a paraneoplastic syndrome • association with malingnancy may be stronger in DM Polymyositis
- 17. Dermatomyositis • More thanjust "PM with a rash" • Clinical presentation: – Symmetric weakness, proximal > distal – Unlike PM, DM occurs in children – Unique skin manifestations in DM – Heliotrope (violet-colored) rash and periorbital edema – Gottron's papules – Photosensitivity rash (shawl sign, V sign, etc) – Dilate nail bed capillary loops – Cutaneous calcinosis (more common in children) • skin manifestations usually accompany, or precede the onset of weakness • except when they lag behind the onset of weakness by months, or don't occur at all! • DM can still be diagnosed in the absence of rash, because of distinct findings on muscle biopsy • Associated features: – (as previous)
- 18. Inclusion Body Myositis •Pathology is uncertain, but seems to be an inflammatory myopathy • More common in men than women, tends to occur after 50 years • Unique clinical features: • Patients progress slowly over months/years – Most patients remain ambulatory – May become wheelchair or bed-bound • Doesn't respond to typical immunomodulatory therapy – some cases of "refractory" PM turn out to be IBM • Associated features – Not associated with cardiomyopathy, ILD, or malignancy – Autoimmune disorders coexist in up to 15% of IBM patients • SLE • Sjören syndrome • Scleroderma • Thrombocytopenia • Sarcoidosis