Cranial imaging studies, such as CT or MRI, can assist in determining the etiology of the persistent vegetative state. Approximately 48 hr following a prolonged anoxic episode, hypodensities in the cerebral and cerebellar cortices and in the caudate and lenticular nuclei can occur. Days to weeks later, focal infarcts, edema, and atrophy may be evident.
PET and SPECT provide an alternative method of imaging that assesses cerebral function rather than brain anatomy. In vegetative patients, cerebral blood flow and metabolism are globally depressed. These procedures are useful in examining remaining cortical and brain stem function. In some cases, global reduction of cortical blood flow in the persistent vegetative state appears to be a consistent predictor of poor long-term outcome. Blood flow and metabolic studies can also be used as a diagnostic aide in differentiating individuals in the vegetative state from patients with the locked-in syndrome.
In patients with the persistent vegetative state, the EEG is useful in assessing cortical dysfunction and identifying the presence of occult seizure activity. The EEG may show a variety of changes. Some individuals in the persistent vegetative state have an isoelectric EEG or have periodic tracings consistent with REM sleep. If seizures develop and aggressive management is desired for the patient with the persistent vegetative state, then epileptic activity should be treated to reduce further neuronal cell loss in the cortex. Status epilepti-cus, status myoclonus, and myoclonic status epilepti-cus are associated with inability to recover consciousness in cardiac arrest survivors. In addition to issues of care, the EEG has been used to assess prognosis. In patients with terminal coma or persistent vegetative state, onset of abnormal EEG changes may be suggestive of a poor outcome.
Evoked potentials can provide information concerning the functional state of the cerebral cortex and brain stem. As previously described, patients with bilateral absence of cortical responses experience mortality rates between 73 and 98%. Brain stem auditory evoked potentials correlate with brain stem function. Simultaneous latency increase of all components can be consistent with progressive ischemia of the posterior fossa and a decrease in cerebral perfusion pressure. Loss of the brain stem auditory evoked potentials is usually suggestive of an incumbent deterioration and death. Although brain stem auditory evoked potentials are not usually modified by exogenous factors, brain stem auditory evoked potentials can be falsely altered by hypothermia, and combined use of anesthetics and barbiturates can induce latency and eventual abolition of brain stem auditory evoked potentials.
Management of the patient in the persistent vegetative state can raise several ethical concerns. The decision to assume an aggressive course or to gradually terminate care must be made after careful consideration of the patient's prior documented wishes. If the patient has not provided advance directive, then the course for further management should be decided between the patient's physician and health care surrogate (guardian, spouse, children, and family members). Decisions for care should focus on the utility of future treatment modalities, quality of life, and possible resource constraints.
Several therapeutic modalities have been proposed for the treatment of patients in persistent vegetative state. Sensory and electrical stimulation is a method that attempts to "increase arousal'' in vegetative patients. Deep brain stimulation of the mesencephalic reticular formation increases cerebral evoked potentials and EEG activity, whereas cervical cord spinal stimulation can activate cerebral glucose metabolism and blood flow. Pharmacological manipulation of the central nervous system has also been attempted in several cases of persistent vegetative state. Treatment with amantadine or Sinemet has been reported to improve the level of consciousness in some patients. However, these reports are anecdotal, and prospective, controlled trials with significant numbers of patients are required to determine the true efficacy of these treatment protocols. Nutrition should also be considered a component of the therapeutic regiment. The degree of nutritional support should correlate with the level of care selected.
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