Blood tests ordered for muscle weakness
| Test | Normal Range | What weakness it detects |
|---|---|---|
| TSH | 0.4–4.0 mIU/L | Hypothyroidism: proximal muscle weakness |
| Vitamin D (25-OH) | 30–100 ng/mL | Deficiency causes muscle pain and weakness |
| Potassium | 3.5–5.0 mEq/L | Hypokalaemia: classic cause of muscle weakness |
| Calcium | 8.5–10.5 mg/dL | Hypocalcaemia: muscle cramps; hypercalcaemia, weakness |
| CK (Creatine Kinase) | Men: 55–170 U/L; Women: 30–135 U/L | Raised in myopathy, myositis, rhabdomyolysis |
| Aldolase | 1.0–7.5 U/L | Inflammatory myopathy (polymyositis/dermatomyositis) |
| Cortisol | AM: 6–23 mcg/dL | Adrenal insufficiency: fatigue and weakness |
What does a high CK mean with muscle weakness?
Creatine kinase and muscle damage
CK is an enzyme inside muscle cells. When muscle is damaged or inflamed, CK leaks into the blood. Mild-moderate elevation (2–10x normal): statin-induced myopathy, hypothyroidism, polymyositis. Marked elevation (>10x normal): rhabdomyolysis (muscle breakdown), can cause acute kidney failure from myoglobin in the urine. Very high CK with brown urine and muscle pain is a medical emergency.
Causes of proximal muscle weakness
| Cause | Key clue |
|---|---|
| Hypothyroidism | TSH raised; other thyroid symptoms |
| Vitamin D deficiency | 25-OH D <20 ng/mL; bone pain too |
| Polymyositis | CK very high; anti-Jo1 antibody positive |
| Statin myopathy | On statin medication; CK mildly raised |
| Cushing's syndrome | High cortisol; central obesity, easy bruising |
| Hypokalaemia | Potassium <3.5; often with fatigue |
Questions to ask your doctor
- Is my CK raised: could I have a muscle disease?
- Is my weakness from thyroid, Vitamin D, or electrolytes?
- Could my statin be causing muscle pain and weakness?
- Do I need a nerve conduction study or EMG?
Frequently Asked Questions
What's the difference between tiredness and true muscle weakness?
Which blood tests investigate muscle weakness?
When should muscle weakness be treated as urgent?
References
Sources cited on this page. PubMed links open the original abstract.
- Barohn RJ, Dimachkie MM, Jackson CE. A pattern recognition approach to patients with a suspected myopathy. Neurol Clin. 2014;32(3):569–593. PMID 25037082 · doi:10.1016/j.ncl.2014.04.008
Upper versus lower motor neuron weakness – a key clinical distinction
Neurological muscle weakness is classified by where in the nervous system the problem lies:
- Upper motor neuron (UMN) lesion (brain or spinal cord): Weakness with increased muscle tone (spasticity), brisk reflexes, and an upgoing plantar reflex (Babinski sign). Causes include stroke, multiple sclerosis, and spinal cord compression. Blood tests are often normal; MRI is the primary investigation.
- Lower motor neuron (LMN) lesion (nerve or neuromuscular junction): Weakness with reduced tone (flaccidity), diminished reflexes, and wasting. Causes include peripheral neuropathy, Guillain-Barré syndrome, and motor neuron disease. Nerve conduction studies and EMG are diagnostic.
- Muscle disease (myopathy): Weakness with normal or reduced reflexes, no sensory loss, typically proximal (difficulty rising from a chair or raising arms above head rather than fine hand weakness). Creatine kinase (CK) is often markedly elevated.
Blood tests that evaluate muscle weakness
When muscle weakness cannot be explained by a simple physical examination finding, blood tests identify treatable systemic causes:
- Creatine kinase (CK): The most sensitive marker of muscle cell damage. Elevated in inflammatory myopathies (dermatomyositis, polymyositis), rhabdomyolysis, muscular dystrophies, statin-induced myopathy, and hypothyroid myopathy. A CK more than 10 times the upper limit of normal is the threshold for considering inflammatory myopathy or toxic myopathy.
- Thyroid function (TSH): Both hypothyroidism and hyperthyroidism cause muscle weakness. Hypothyroid myopathy is characterised by proximal weakness, myalgia, delayed relaxation of reflexes, and a raised CK. It reverses completely with thyroxine replacement.
- Potassium and magnesium: Hypokalaemia (low potassium) and hypomagnesaemia cause profound muscle weakness and cramps. Causes include diuretic therapy, vomiting, diarrhoea, and primary hyperaldosteronism. Periodic paralysis (rare) is caused by episodic potassium shifts into cells.
- Calcium: Hypercalcaemia causes generalised weakness, fatigue, and confusion ("bones, groans, stones, and moans"). Hypocalcaemia causes muscle cramps and tetany (carpopedal spasm).
- ANA and myositis-specific antibodies (anti-Jo-1, anti-Mi-2, anti-MDA5): Autoimmune markers for inflammatory muscle diseases. Anti-Jo-1 in particular indicates antisynthetase syndrome – inflammatory myopathy with interstitial lung disease and a specific treatment approach.
- Aldolase: Another muscle enzyme, sometimes elevated in inflammatory myopathy when CK is only mildly raised.
- Vitamin D: Severe vitamin D deficiency causes proximal myopathy that closely mimics inflammatory muscle disease and is fully reversible with supplementation.
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