Coma is a state of unresponsiveness, with eyes closed, from which a patient cannot be roused by verbal or mechanical stimuli. It represents a greater degree of impairment of consciousness than stupor or obtundation, all three forming part of a continuum, rather than discrete stages, ranging from alert and comatose. This lack of precision prompts some authorities to prefer the description of the individual aspects of neurological function in unconscious patients, such as eye movements, limb movements, vocalization, and response to stimuli, since this conveys more information than the use of terms, such as coma, stupor or obtundation, or the use of a lumped "score", such as the Glasgow Coma Scale.

These signs should be documented serially to assess any progression of coma. Assessment of the depth of coma may be made by observing changes in eye movements and response to central noxious stimuli: roving eye movements are lost before oculocephalic responses; caloric responses are last to go. The switch from flexor to extensor posturing (decorticate vs. decerebrate rigidity) also indicates increasing depth of coma.

There are many causes of coma, which may be broadly categorized as structural or toxic-metabolic; the latter are generally more slowly progressive and produce symmetrical signs, whereas structural lesions more often have an abrupt onset and some focal asymmetric findings on examination, but these distinctions are not absolute. Recognized causes of coma include:

  • Structural:
    • Vascular insults (subarachnoid hemorrhage, cerebral infarction or hemorrhage);
      Trauma Tumor Hydrocephalus;
      Vasculitides, leukodystrophies, leukoencephalopathies.
  • Toxic-metabolic:
    • Drugs/toxins;
    • Metabolic causes: for example, hypoxia, hypercapnia, hypoglycemia Infections: for example, meningitis, encephalitis, sepsis;
    • Epilepsy.

Unrousability which results from psychiatric disease, or which is being feigned ("pseudocoma"), also needs to be differentiated.

A number of neurobehavioral states may be mistaken for coma, including abulia, akinetic mutism, catatonia, and the locked-in syndrome.

EEG features may assist in differential diagnosis: prominent rhythmic beta activity raises the possibility of drug intoxication.


Bates D. Medical coma. In: Hughes RAC (ed.). Neurological emergencies (2nd edition). London: BMJ Publishing, 1997: 1-28
Plum F, Posner JB. The diagnosis of stupor and coma (3rd edition). Philadelphia: FA Davis, 1980
Rubino FA. Approach to the comatose patient. In: Biller J (ed.). Practical neurology (2nd edition). Philadelphia: Lippincott Williams & Wilkins, 2002: 54-65
Teasdale G, Jennett B. Assessment of coma and impaired conscious-ness: a practical scale. Lancet 1974; 2: 81-84
Young GB, Ropper AH, Bolton CF (eds.). Coma and impaired consciousness: a clinical perspective. New York: McGraw-Hill, 1998 

Cross References

Abulia; Akinetic mutism; Caloric testing; Catatonia; Decerebrate rigidity; Decorticate rigidity; Locked-in syndrome; Obtundation; Oculocephalic response; Roving eye movements; Stupor; Vegetative states; Vestibuloocular reflexes