Coma

Extract

[...] 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. [...]

[...] Tests Computed tomography or magnetic resonance imaging (MRI) is promptly performed whenever coma is unexplained. Unless meningitis is suspected and the patient is clinically deteriorating, imaging should precede lumbar puncture. If imaging is not readily available, a spinal tap is cautiously performed with a no.20 or no. If imaging reveals frank transtentorial or foramen magnum herniation, the comparative risks of performing a lumbar puncture or of treating for meningitis without CSF confirmation must be weighed individually for each patient. Other emergency laboratory studies include blood levels of glucose, sodium, calcium, and blood urea nitrogen (or creatinine); determination of arterial pH and partial pressures of oxygen and carbon dioxide; and blood or urine toxicology testing (including blood levels of sedative drugs and ethanol). [...]

[...] COMA FROM INFRATENTORIAL STRUCTURAL LESIONS Infratentorial structural lesions may compress or directly destroy the brainstem. Such lesions may also cause brain herniation, either transtentorially upward (with midbrain compression) or downward through the foramen magnum, with distortion of the medulla by the cerebellar tonsils. Abrupt tonsillar herniation causes apnea and circulatory collapse; coma is then secondary, for the medullary reticular formation has little direct role in arousal. In coma, primary infratentorial structural lesions are suggested by bilateral weakness or sensory loss, crossed cranial nerve and long tract signs, miosis, loss of lateral gaze with preserved vertical eye movements, dysconjugate gaze, ophthalmoplegia, short-cycle CSR, and apneustic or ataxic breathing. [...]

[...] VEGETATIVE STATE The terms akinetic mutism and coma vigil have been used to describe a variety of states, including coma with preserved eye movements following midbrain lesions, psychomotor bradykinesia with frontal lobe disease, and isolated diencephalic and brainstem function after massive cerebral damage. For this last condition, the term vegetative state is preferred to refer to patients with sleep–wake cycles, intact cardiorespiratory function, and primitive responses to stimuli, but without evidence of inner or outer awareness. Patients who survive coma usually show varying degrees of recovery within 2 to 4 weeks; those who enter the vegetative state may recover further, even fully. [...]