The diagnosis of concussion or of postictal coma depends on observation of the precipitating event or indirect evidence, as discussed in Chap. 34. Usually, a convulsive seizure is marked by a bitten tongue, urinary incontinence, and an elevated creatine kinase–skeletal muscle fraction; it may be followed by another seizure or burst of seizures. The presence of small clonic or myoclonic convulsive movements of a hand or foot or fluttering of the eyelids or eyes makes an EEG useful to determine whether underlying status epilepticus is the cause of coma. This state, nonconvulsive status epilepticus, described in Chap. 15, must be considered in the diagnosis of unexplained coma, especially in known epileptics (see Table 16-3).
With respect to the second group with signs primarily of meningeal irritation (head retraction, stiffness of neck on forward bending, Kernig and Brudzinski signs), bacterial meningitis and subarachnoid hemorrhage are the usual causes. However, if the coma is profound, stiff neck may be absent in both infants and adults. In such cases the spinal fluid must be examined in order to establish the diagnosis. In most cases of bacterial meningitis, the CSF pressure is elevated but is not exceptionally high (usually <400 mm H2O). However, in cases associated with brain swelling, the CSF pressure is greatly elevated; the pupils become fixed and dilated, and there may be signs of compression of the brainstem with arrest of respiration. Patients in coma from ruptured aneurysms also have high CSF pressure; the CSF is overtly bloody and the blood is invariably visible in the CT scan throughout the basal cisterns and ventricles if the bleeding has been severe enough to cause coma.
In the third group of patients, it is the focality of sensorimotor signs and the abnormal pupillary and ocular reflexes, postural states, and breathing patterns that provide the clues to serious structural lesions in the cerebral hemispheres and their pressure effects upon segmental brainstem functions. As the brainstem features become more prominent, they may obscure earlier signs of cerebral disease.
It is worth emphasizing once more that profound hepatic, hypoglycemic, hyperglycemic, and hypoxic states may resemble the coma due to a brainstem lesion in that asymmetrical motor signs, focal seizures, and decerebrate postures arise and deep coma from drug intoxication may obliterate reflex eye movements. Conversely, certain structural lesions of the cerebral hemispheres are so diffuse as to produce a picture that simulates a metabolic disturbance; TTP, fat embolism, vasculitis, intravascular lymphoma, acute disseminated encephalomyelitis, and the late effects of global ischemia–anoxia are examples of such states. At other times, they cause a diffuse encephalopathy with superimposed focal signs. The multifocal cerebral lesions, typified by TTP, are among the most difficult to detect as causes of coma, particularly because the structural damage may be combined with seizures.
Unilateral cerebral infarction because of anterior, middle, or posterior cerebral artery occlusion produces no more than drowsiness, as a rule; however, with massive unilateral infarction as a result of carotid artery occlusion, coma can occur if extensive brain edema and secondary tissue shift develop. There are exceptional cases wherein stupor results from massive infarction of the dominant (left) hemisphere. Edema of a degree serious enough to compress the brainstem and cause coma seldom develops before 12 or 24 h. Rapidly evolving hydrocephalus causes smallness of the pupils, rapid respiration, extensor rigidity of the legs, Babinski signs, and sometimes a loss of eye movements.