Medical Conditions | Uncategorized


Condition of unconsciousness from which the patient cannot be roused, with various causes and varying degrees of depth. Normally consciousness is maintained by an activating centre in the brain stem which stimulates the rest of the brain. If this centre or a large part of the cerebral cortex fails, consciousness can no longer be maintained. Coma can occur in brain conditions such as stroke, encephalitis, meningitis , brain injury, brain tumour and serious attacks of epilepsy. Non-cerebral causes are a severe drop in blood pressure (through cardiac infarction or serious haemorrhage), metabolic disturbances (including inadequate blood sugar content or hypoglycaemia in diabetics) or serious liver and kidney disorders. Rare causes include Wernicke’s disease and thyroid hormone deficiency. Narcotic and carbon monoxide poisoning can also cause coma. The above-mentioned conditions cause coma through oxygen or glucose deficiency (the latter being the brain’s most important food), disturbance of enzyme systems (especially in poisoning or inflammation), disturbance of acid-base balance causing impairment of stimulus transfer (e.g. in liver and kidney disorders) and sudden disturbance of tissue metabolism. Depth of coma is determined by reaction to stimuli such as attempted communication and pain. If a coma leads to death, respiration fails first, then the heart. A patient in a coma must be admitted to hospital rapidly for investigation and observation, possibly blood tests and an EEG. Treatment is determined by the underlying cause. Good nursing and physiotherapy are important if complications such as pneumonia or bedsores are to be avoided. Usually short disturbance of brain function caused by a head injury. A distinction is made between ‘normal’ concussion and cerebral contusion, according to the seriousness of the injury. In the case of concussion the patient loses consciousness for a few minutes after the incident, and cannot remember the period immediately before it (retrograde amnesia). Nausea and vomiting often occur as a result of short-term lack of control of the central nervous system, possibly associated with headache. In contrast with cerebral contusion there are no faculty failures (such as paralysis or reflex disorders), because the brain is probably undamaged. Headache and dizziness may persist for days or weeks. Diagnosis is by the clinical picture just described; physical examination probably shows no abnormalities of cerebral function. The skull is usually X-rayed to exclude other types of brain injury. It is important to wake the patient every hour on the first night to discover possible complications in good time. Bed rest is advisable until any symptoms subside. Cerebral contusion is a form of brain damage; the blow causes extensive haemorrhage of the brain tissue, and fluid may accumulate (oedema). The patient loses consciousness (from a quarter of an hour to several days), followed by a period of unrest and confusion. Precisely as in ‘normal’ concussion there is loss of memory about the period before the injury, but the period is extended, and more than an entire day may be included. The memory also functions poorly afterwards, so that a number of days or even weeks may be lost. If this period lasts for less than a week, chances of recovery are good. Cerebral contusion is usually accompanied by failure symptoms, reflex disorders, unilateral paralysis or aphasia. Recovery is often complete, but in very serious cases a long period of coma may be followed by spastic paralysis and epilepsy. Sometimes the patient does not come out of the coma, and never regains consciousness. A number of patients die within a few hours or days of cerebral infarction. The brain is then damaged to the extent that accumulated fluid from the damaged cells puts pressure on previously undamaged cells.

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