The term altered mental status refers to an aberration of a patient’s level of consciousness. It always implies serious pathology and mandates an aggressive search for the underlying disorder. More precise terminology describes the degree of altered mental status and has important implications for differential diagnosis and management:

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  Lethargy is a state of reduced wakefulness in which the patient displays disinterest in the environment and is easily distracted but is easily aroused and can communicate.

  
  
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  Delirium is characterized by agitation, disorientation, delusions, hallucinations, fearful responses, irritability, and sensory misperception.

  
  
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  Obtundation is severe blunting of alertness with a decreased response to stimuli.

  
  
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  Stupor exists when the patient can only be aroused by extremely vigorous and repeated stimulation.

  
  
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  Coma occurs when a profound reduction in neuronal function results in unresponsiveness to sensory stimuli. It constitutes the most severe manifestation of altered mental status. Coma is further categorized depending on the area of the brain affected.^1–3 Several scoring systems exist that permit objective and reproducible assessment of the degree of altered mental status and allow effective communication among health care providers. The most widely used is the Glasgow Coma Scale (GCS), which scores three responses with a range from 3 to 15.^2,4 The GCS has been modified so that it can be applied to infants and children. The main difference is the verbal response (Table 6-1).^2,5

In general, patients with altered mental status have suffered a diffuse insult to the brain. For patients with no history of trauma, the most common causes are metabolic abnormalities, poisonings, and infectious etiologies such as meningitis and encephalitis. For coma to occur, the underlying abnormality must be either damage or dysfunction to both cerebral hemispheres or to the ascending reticular activating system, which transverses the brain stem through the upper pons, midbrain, and diencephalon, and plays a fundamental role in arousal. Coma can result from structural damage to tissue, infectious processes, metabolic derangements, poisonings, or inadequate cerebral perfusion. Metabolic, infectious, and toxic etiologies tend to produce diffuse but symmetric deficits, such as confusion, that precede other abnormalities, such as motor deficits. Structural lesions result in focal deficits that progress in a predictable pattern. Supratentorial lesions produce focal findings that progress in a rostral–caudal fashion, whereas subtentorial lesions result in brain stem dysfunction followed by a sudden onset of coma, cranial nerve palsies, and respiratory disturbances. The causes of coma are listed in Tables 6-2 and 6-3.^6,7