Causes of coma

Consciousness depends upon an intact ascending reticular activating substance (ARAS) in the brain stem acting as the alerting or awakening element of consciousness, together with a functioning cerebral cortex of both hemispheres which determines the content of that consciousness. The ARAS is a continuous isodendritic core, extending from the medulla through the pons to the midbrain which is continuous caudally with the reticular intermediate grey lamina of the spinal cord and rostrally with the subthalamus, the hypothalamus, and the thalamus (Figure 1.1).3 The functions and interconnections of the ARAS are considerable and its role greater than that of a simple cortical arousal system. There are named nuclei throughout the reticular formation. Although it was originally considered that cortical arousal depended upon projections from the reticular formation via the midline thalamic nuclei to the thalamic reticular nucleus and cortex, it now seems unlikely that the thalamic reticular nucleus is the final relay. The specific role of the various links from the reticular formation to the thalamus has yet to be identified.

Similarly the neurotransmitters involved in this arousal system are not fully determined though it seems likely that, in addition to cholinergic and monoaminergic systems, gamma aminobutyric acid (GABA) may be important in controlling consciousness.4-6

It follows from the anatomy and pharmacology of the ARAS that structural damage to this pathway or chemical

Midbrain ri formation

Midbrain ri formation

Figure 1.1 The anatomy of consciousness


Figure 1.1 The anatomy of consciousness derangement of the neurotransmitters involved are mechanisms whereby consciousness may be impaired. Such conditions will occur with focal lesions in the brain stem, mass lesions in the posterior fossa impinging directly on the brain stem, or mass lesions involving the cerebral hemispheres causing tentorial pressure coning and consequently compromising the ARAS either by direct pressure or by ischaemia (Figure 1.2). In addition toxins, including most commonly ingested drugs, may have a significant depressant effect upon the brain stem ARAS and thereby result in loss of consciousness.

The content of consciousness resides in the cerebral cortex of both hemispheres. Unlike those discrete cortical functions such as language or vision which are focally located within the cortex, the content of consciousness can best be regarded as the amalgam of all cognitive functions. Coma arising from disruption of cortical activity requires a diffuse pathology such as generalised anoxia or ischaemia, commonly seen after cardiac arrest or anaesthetic accidents, or cortical vasospasm seen in infective meningitis, or subarachnoid haemorrhage, where generalised cortical ischaemia is believed to be the cause of disruption of function.

The physician attempting to diagnose the cause of coma should consider the following.

herniation causing third nerve palsy herniation causing third nerve palsy

Figure 1.2 Causes of coma. (a) Focal brain stem lesions; (b) mass lesions; (c) diffuse cortical pathology

1. Supratentorial or infratentorial mass lesions. Typically these will provide evidence of raised intracranial pressure and commonly produce focal signs. Processes such as neoplasm or haematoma, infarction with cerebral oedema, abscess, focal encephalitis, and venous sinus thrombosis must all be considered.

2. Subtentorial destructive lesions or the local effect of toxin. These processes will directly damage the ARAS in brain stem infarction, rhombencephalitis, brain stem demyelination, and the more common effects of self-poisoning with sedative drugs.

3. Diffuse damage to the cerebral cortex. Bilateral cortical injury is most commonly seen following hypoxia and ischaemia but may be mimicked by hypoglycaemia, ketoacidosis, electrolyte abnormalities, bacterial meningitis, viral encephalitis, and diffuse postinfective encephalomyelitis. It is also the likely pathology of coma following subarachnoid haemorrhage.

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