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Acquired metabolic disorders and the nervous system 

Acquired metabolic disorders and the nervous system

Acquired metabolic disorders and the nervous system

Neil Scolding

and C.D. Marsden


Three relevant case histories from Neurological Case Histories: Case Histories in Acute Neurology and the Neurology of General Medicine have been added to this chapter.

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date: 30 March 2017

A very wide range of systemic disorders of metabolism can have neurological consequences. Conditions of particular note include the following:

Major organ diseases

Anoxic brain damage—cardiac arrest is a relatively common cause of global cerebral anoxia; other causes include suffocation, anaesthetic catastrophes, drowning, or acute carbon monoxide poisoning. The consequences depend on the duration of anoxia: (1) brief—manifests as syncope; (2) longer lasting (up to perhaps 5 min)—there is rapid loss of consciousness, generalized fits, dilated pupils, and bilateral extensor plantar responses; long-term course and prognosis are unpredictable; (3) more sustained (longer than a few minutes)—permanent or prolonged but reversible brain damage.

Other conditions—these include (1) hepatic failure—acute hepatic coma and chronic hepatic encephalopathy; (2) respiratory disease—chronic respiratory failure causing hypercarbic encephalopathy; obstructive sleep apnoea; (3) renal failure—neurological manifestations include uraemic encephalopathy, symmetrical sensorimotor polyneuropathy, myopathy, dialysis disequilibrium syndrome, dialysis dementia; (4) critical illness polyneuropathy.

Endocrine disorders

Many endocrine disorders can have neurological manifestations, including: (1) Phaeochromocytoma—anxiety, headache; complications of accelerated phase hypertension. (2) Cushing’s syndrome—proximal myopathy, psychiatric disorders, direct consequences of pituitary tumour. (3) Adrenal insufficiency—adrenal crisis may manifest with depressed consciousness and/or neurological complications of hypoglycaemia or hyponatraemia. (4) Thyroid disease—thyrotoxicosis can cause myopathy, chorea and mania; hypothyroidism can present with a confusional state or coma and is often associated with a myopathy. (5) Diabetes mellitus—complications include mononeuritis, diabetic amyotrophy, peripheral neuropathy, autonomic neuropathy, and those due to hypoglycaemia.

Ionic abnormalities

(1) Hyponatraemia—nonspecific symptoms may appear when the plasma sodium drops below about 120 mmol/litre; fits and coma are usually associated with plasma sodium values below 110 mmol/litre. The condition and its treatment (see Chapter 21.2.1) can be associated with central pontine myelinolysis. (2) Hypernatraemia—may cause drowsiness or (in severe cases) coma; (3) Hypercalcaemia—muscle weakness, lassitude, and a mild encephalopathy are common; (4) Hypocalcaemia—causes neuromuscular irritability, tetany with a Chvostek’s sign, and mild encephalopathy; severe hypocalcaemia may cause fits, psychosis, and coma.


Effects of alcohol on the nervous system, aside from those that are acute and transient, include (1) delirium tremens—an agitated confused state, with signs of sympathetic overactivity, that typically develops rapidly several days after ethanol abstinence in chronic abusers; (2) Wernicke–Korsakoff syndrome—classically manifesting with confusion, ophthalmoplegia and ataxia; treatment with thiamine should be given on suspicion; (3) peripheral neuropathy; (4) cerebellar degeneration; (5) dementia; (6) myopathy.

Acknowledgement: Much of the late Professor C D Marsden’s original chapter structure and text for the third edition has been retained.

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