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  1. Introduction
  2. Examination and major diagnostic procedures
    1. Fever
    2. Asymmetry of muscle tone
    3. Respiration
    4. Pupils
    5. Eyelids and eye movements
    6. Tests
    7. The electroencephalogram
  3. Coma from supratentorial structural lesions
    1. Aqueductal obstruction
    2. The downward course of transtentorial herniation
  4. Coma from infratentorial structural lesions
  5. Coma from metabolic or diffuse brain disease
  6. Hysteria and catatonia
  7. Locked in syndrome
  8. Vegitative state
  9. Brain death
  10. Conclusion
  11. Bibliography

Consciousness, the awareness of self and environment, requires both arousal and mental content; the anatomic substrate includes both reticular activating system and cerebral cortex. Coma is a state of unconsciousness that differs from syncope in being sustained and from sleep in being less easily reversed. Cerebral oxygen uptake (cerebral metabolic rate of oxygen [CMRO2]) is normal in sleep or actually increases during the rapid eye movement stage, but CMRO2 is abnormally reduced in coma.

[...] Coma is a state of unconsciousness that differs from syncope in being sustained and from sleep in being less easily reversed. Cerebral oxygen uptake (cerebral metabolic rate of oxygen [CMRO2]) is normal in sleep or actually increases during the rapid eye movement stage, but CMRO2 is abnormally reduced in coma. Coma is clinically defined by the neurologic examination, especially responses to external stimuli. Terms such as lethargy, obtundation, stupor, and coma usually depend on the patient's response to normal verbal stimuli, shouting, shaking, or pain. [...]


[...] Pupils Pupillary abnormalities in coma may reflect an imbalance between input from the parasympathetic and sympathetic nervous systems or lesions of both. Although many people have slight pupillary inequality, anisocoria should be considered pathologic in a comatose patient. Retinal or optic nerve damage does not cause anisocoria, even though there is an afferent pupillary defect. Parasympathetic lesions (e.g., oculomotor nerve compression in uncal herniation or after rupture of an internal carotid artery aneurysm) cause pupillary enlargement and ultimately full dilatation with loss of reactivity to light. [...]


[...] The electroencephalogram (EEG) can distinguish coma from psychic unresponsiveness or locked-in state, although alphalike activity in coma after brainstem infarction or cardiopulmonary arrest may make the distinction difficult. In metabolic coma, the EEG is always abnormal, and early in the course, it may be a more sensitive indicator of abnormality than the clinical state of the patient. The EEG may also reveal asymmetries or evidence of clinically unsuspected seizure activity. Infrequently, patients without clinical seizures demonstrate repetitive electrographic seizures or continuous spike-and-wave activity; conversely, patients with subtle motor manifestations of seizures sometimes display only diffuse electrographic slowing. [...]

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