The clinical features of coma vary both with the depth of coma and the etiology of coma. Coma speaks to the unresponsive state. However, there is a spectrum of signs within unresponsiveness that may point toward an etiology.
A variety of abnormal breathing patterns may be seen in the comatose patient. They are of interest but offer little information in the acute setting. Pupillary findings, the results of other cranial nerve evaluations, hemiparesis, and response to stimulation are all part of the clinical picture that needs to be assessed. These findings help the clinician sort the cause of the coma into a likely etiology—diffuse CNS dysfunction (toxic-metabolic coma) or structural coma. A further division of structural coma into hemispheric (supratentorial) and posterior fossa (hemispheric) coma is often possible at the bedside.
Toxic and metabolic causes of coma result from a wide range of clinical conditions. In general, the diffuse nature of the CNS dysfunction is reflected by the lack of physical examination findings that might point to a specific region of dysfunction within the brain. For example, in toxic-metabolic coma, if the patient is having either spontaneous movements or reflex posturing, the movements are symmetric without evidence of hemiparesis. Reflexes are symmetric. Pupillary response is generally preserved in toxic-metabolic coma, unless the toxin specifically affects pupillary function. Typically the pupils are small but reactive in nonspecific toxic-metabolic coma. If extraocular movements are present, again they are symmetric. However, if extraocular movements are absent, it is of no value in differentiating toxic-metabolic from structural coma. A notable exception is severe sedative poisoning as with barbiturates; the pupils may be large, extraocular movements absent, muscle tone flaccid, and the patient apneic, simulating the appearance of brain death.
Coma from lesions of the hemispheres, or supratentorial masses, may present with progressive hemiparesis; asymmetric muscle tone and reflexes may also be present. A patient in coma with a hemispheric hemorrhage may still have some muscle tone; careful examination may allow detection of decreased muscle tone on the side of the hemiparesis. The hemiparesis may be suspected with asymmetric responses to stimuli or asymmetric extensor or flexor postures. Additionally, there may be ocular signs of the eyes conjugately deviated toward the side of the hemorrhage. With expansion of the hemorrhage and surrounding edema, and increase in intracranial pressure or brainstem compression, the unresponsiveness may progress to a complete loss of motor tone, as well as loss of the ocular findings. Frequently, large acute supratentorial lesions are seen without the features consistent with temporal lobe herniation. Coma without lateralizing signs may result from decreased cerebral perfusion secondary to increased intracranial pressure. Reflex changes in blood pressure and heart rate may be observed with increased ICP or brainstem compression. Hypertension and bradycardia in a comatose patient may represent the Cushing reflex from increased ICP.
Posterior fossa or infratentorial lesions comprise another coma syndrome. An expanding mass, such as cerebellar hemorrhage or infarction, may cause abrupt coma, abnormal extensor posturing, loss of pupillary reflexes, and loss of extraocular movements. The anatomy of the posterior fossa leaves little room for accommodating an expanding mass. Early brainstem compression with loss of brainstem reflexes may develop rapidly. Another infratentorial cause of coma is pontine hemorrhage, which may present with the unique signs of pinpoint-sized, seemingly unreactive pupils. If magnification is used, these pinpoint pupils may be seen to be reactive.
Vertebrobasilar occlusion by thrombosis or embolism may cause the "locked-in" syndrome, which may readily be confused with coma. These patients have lost voluntary movement, except perhaps for vertical eye movement. Consciousness and understanding may well be intact; the patient cannot move, speak, or interact with the environment except, again, by vertical eye movements.21
Pseudocoma or psychogenic coma is occasionally encountered and may present a perplexing clinical problem. Adequate history and observation of responses to stimulation will reveal findings that differ from the syndromes described above. Pupillary responses, extraocular movements, muscle tone, and reflexes will be shown to be intact on careful examination. Tests of particular value are observing the response of the patient to manual eye opening (there should be little or no resistance in the truly unresponsive patient) and extraocular movements. Specifically, if avoidance of gaze is consistently seen with the patient always looking away from the examiner, or nystagmus is demonstrated on caloric testing, this is strong evidence for nonphysiologic or feigned unresponsiveness.
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