Posturing in response to noxious stimulation indicates moreserious neurologic conditions. Decorticate posturing consists of rigid extension of the legs and feet, flexion and supinationof the arms, and fisting of the hands. It indicates bilateral cortical or subcortical abnormalities or herniation, with preservedbrainstem function. Decerebrate posturing (rigid extensionand internal rotation of legs and arms) indicates a midbrainabnormality and is classically associated with herniation ortoxic-metabolic abnormalities. These postures may be exhibitedunilaterally or bilaterally. A structural cause is likely when posturing is asymmetric, whereas symmetric posturing may bemore likely with underlying toxic-metabolic etiologies.
The evolution of change in consciousness is an important clue to the etiology. A detailed history and physical examination usually provide sufficient clues to differentiate among the three major diagnostic categories producing coma: metabolic/toxic, infectious, and structural. In most clinical situations, the cause of coma is readily identified.
Metabolic derangements are common causes of altered mental status. Disturbances of blood chemistries (glucose, sodium, calcium, bicarbonate, blood urea nitrogen, ammonia) may produce depressed mental status. Metabolic causes of acute coma are suggested by spontaneous fluctuations in the level of consciousness, tremors, myoclonus, asterixis, visual and tactile hallucinations, and deep coma with preservation of pupillary light reflexes. Acute metabolic or toxic disorders usually produce a hypotonic, limp state, but hypertonia, rigidity, and decorticate and decerebrate posturing are sometimes observed in coma caused by hypoglycemia, hepatic encephalopathy, and short-acting barbiturates. A subacute course of somnolence progressing to difficulty arousing from a deep sleep (stupor) over hours suggests drug intoxication or organ system failure (kidney, liver) producing a metabolic encephalopathy. Care must be taken to investigate background medical conditions that may produce a decline in consciousness (e.g., diabetes mellitus, leukemia, kidney failure, liver disease). Intoxication and ingestion are common causes of acute alteration of consciousness, and a thorough history must be taken to search for the offending agent (Chapter 45). A history of social and emotional difficulties, drug abuse, or depression raises concern for self-inflicted injury or toxic ingestion.
Central nervous system infection, such as meningitis or encephalitis, usually causes abrupt alteration of mental status, althoughviral meningoencephalitis (particularly herpes simplex virus) canpresent with subacute alterations in mental status. The presenceof fever, petechiae, chills, and sweats suggests infection. Prodromal photophobia and pain on movement of the head or eyes aresymptoms of meningeal irritation. Premonitory symptoms, suchas abdominal pain, diarrhea, sore throat, conjunctivitis, cough, orrash, point toward viral encephalitis or a postinfectious syndromeas the cause of the altered consciousness.
Structural processes, such as hemorrhage, infarction, or acute hydrocephalus, can cause sudden depressed consciousness in children. An evolution of headache and morning vomiting suggests increased intracranial pressure (ICP). A gradual fading of alertness or declining school performance over preceding weeks suggests an expanding intracranial mass, subdural hematoma, or chronic infection (e.g., tuberculous meningitis, human immunodeficiency virus). Deprivation of oxygen to the brain, caused by either deficient oxygen in the blood (hypoxemia) or deficient delivery of blood to the brain (ischemia), impairs consciousness.