Numbness, movement disorders and generalised weakness

Localisation before a diagnosis

Separate true loss of power from pain-limited movement, fatigue and reduced endurance. Determine onset, distribution, symmetry and progression, and ask about sensory change, gait, cranial symptoms and sphincter function. Examine power, tone, reflexes, sensation, coordination and cranial nerves, with a respiratory assessment when weakness is substantial. A sudden unilateral deficit suggests a central vascular process; a distal symmetrical sensory pattern suggests a peripheral neuropathy. Neither label should be applied from one symptom word such as “weak” or “tingling.”

Upper motor neuron disease can cause increased tone, brisk reflexes and an extensor plantar response, but acute central injury may initially lack the full pattern. Peripheral nerve or root disease more often reduces reflexes and produces an anatomical sensory/motor distribution. Proximal weakness without sensory loss raises myopathy; fatigable ocular or bulbar weakness raises neuromuscular-junction disease. Mixed patterns occur, especially in older people with multiple illnesses. Repeated examination and tempo often discriminate better than an indiscriminate panel of tests.

Peripheral neuropathy and urgent inflammatory disease

Common contributors to distal polyneuropathy include diabetes, alcohol exposure, B12 deficiency, kidney disease and medicines. Ask about nutrition, chemotherapy, toxins, family history and autonomic symptoms. Use targeted blood tests and consider nerve conduction studies for unexplained, asymmetric, rapidly progressive or motor-predominant disease. Diabetes should not become the explanation for every focal painful neuropathy. Carpal tunnel causes median-distribution symptoms, often at night; a cervical root lesion can mimic it but may have neck pain and reflex changes. Treat the cause and assess functional impairment.

Guillain–Barré syndrome can progress after infection with ascending weakness, reduced reflexes and autonomic instability. Respiratory failure may evolve before dramatic oxygen desaturation; assess respiratory mechanics, bulbar function and progression, with urgent hospital/neurology care. Monitor rhythm and blood pressure. CSF and nerve studies support diagnosis but may be unrevealing early; they should not delay treatment of a strongly concerning presentation. IV immunoglobulin or plasma exchange is specialist therapy. Corticosteroids are not routine effective treatment for GBS. Explain the need for monitored admission rather than reassurance from a single normal pulse oximetry result.

Neuromuscular junction and muscle disease

Myasthenia gravis causes fatigable weakness, ptosis, diplopia and sometimes dysphagia, without the typical sensory loss of neuropathy. New bulbar or respiratory weakness can be a crisis and requires urgent airway/neurology assessment. Infection, surgery and certain medicines can precipitate worsening. Specialist investigations include antibodies and neurophysiology; treatment combines symptom control and immune-directed therapy according to severity. Do not give a sedating drug to a breathless weak patient without considering ventilation. The apparent ability to speak a short sentence does not establish respiratory reserve.

Myopathy often produces proximal weakness: trouble climbing stairs, rising from a chair or lifting arms. Check medication exposures, thyroid disease, CK and systemic inflammatory features. CK can be normal in some muscle conditions and elevated after exercise or injury. Rhabdomyolysis with pain, weakness or dark urine needs potassium, renal, ECG and volume assessment, with fluids tailored to perfusion and overload risk. Distinguish steroid-related weakness from inflammatory myositis; the treatments differ. Rapid progression, dysphagia or respiratory symptoms merits urgent review.

Involuntary movements

A resting tremor with bradykinesia and rigidity supports parkinsonism. Essential tremor is usually postural/action-related and may involve the voice; medication, thyrotoxicosis and anxiety can amplify physiological tremor. Assess gait, falls, cognition, autonomic symptoms and drug-induced causes. Dopamine-blocking medicines can cause parkinsonism, akathisia or dystonia. Acute painful neck/eye deviation after such a drug suggests an acute dystonic reaction; stop the trigger and treat promptly under protocol. Akathisia can look like anxiety and can worsen distress or suicidal thoughts.

Parkinson treatment is individualised with neurology, balancing mobility, fluctuations, hallucinations and orthostatic symptoms. In hospital, time-critical dopaminergic medicines should not be casually omitted during fasting; arrange a safe administration plan. Sudden withdrawal can cause a dangerous rigid febrile syndrome. Chorea, tics and myoclonus have different phenomenology and causes; observe the movement, its suppressibility and relation to sleep or action. A family history can guide genetic evaluation, but consent, counselling and implications for relatives precede testing for inherited neurodegeneration.

Cases and practical management

A patient with tingling feet over years, absent ankle reflexes and reduced vibration needs a cause-focused neuropathy assessment and foot protection. A patient with new ascending weakness over two days, facial weakness and fluctuating pulse needs monitored urgent care for possible GBS. They should not share the same routine referral urgency. A third patient who develops inner restlessness after an antipsychotic dose increase needs an adverse-effect assessment, rather than automatic escalation for “agitation.” Review swallowing, falls, occupational safety and carers' capacity in every disabling neurological condition.

Australian stroke guidance for acute focal deficits and Medical Board code for limits of competence and coordinated care.

Review checkpoints

• Rapidly ascending weakness needs urgent respiratory and autonomic assessment.
• Fatigable weakness suggests a neuromuscular-junction disorder.
• Parkinsonism combines bradykinesia with other characteristic motor findings.