Pathophysiology of delirium

Delirium is a syndrome with multiple etiologies comparable with conditions such as heart failure or renal insufficiency. Attempts to subdivide delirium based on different clinical presentations and to correlate them with objective measures have not been successful (Irzepacz.J994). Electroencephalography, studies of cerebral blood flow, modulation of neurotransmitter levels, and the study of hemispheric differences in the development of delirium are the principal methods used to understand the pathophysiology of delirium (TrzepaczJ994).

Electroencephalograph abnormalities are seen in virtually all delirious patients. Generalized slowing is typically seen in hypoactive states and in the majority of hyperactive states. Some hyperactive patients (e.g. those with delirium tremens) show low-voltage fast activity. Electroencephalograms can be read as normal if the patient demonstrates a baseline voltage above normal and only drops into the normal range during the delirious state.

Single-photon-emission CT and positron-emission tomography studies have shown globally increased cerebral blood flow in delirium tremens. Subclinical hepatic encephalopathy is associated with reduced cortical cerebral blood flow and with both increased and decreased subcortical cerebral blood flow.

Neurotransmitters have rarely been measured directly in delirious patients, but their involvement has been implied based on the effect of several drugs associated with delirium. Impaired cholinergic neurotransmission, induced by anticholinergic drugs or seen in elderly patients, can result in or facilitate delirium; physostigmine is effective in treating anticholinergic delirium. Reduction of dopaminergic neurotransmission at the dopamine D 2 receptor via typical neuroleptics is highly effective in the treatment of delirium. GABAergic neurotransmission has been found to be increased in hepatic encephalopathy and decreased during withdrawal from sedative agents. Benzodiazepines are effective in treating types of delirium. Increased serotonergic activity, as seen in the 'serotonin syndrome', leads to delirium.

Cerebrovascular accidents of the right hemisphere, particularly those involving the parietal and frontal lobes, are more likely to produce delirium than are insults to the left hemisphere. Recent anoxia or strokes of the basal ganglia and thalamus (again with a predilection for the right hemisphere) can also result in delirium.

Delirium can be conceptualized as an acute and often reversible alteration of consciousness (affecting primarily attention, orientation, and memory) resulting from temporary or permanent damage of (mainly right-sided) cortical and subcortical structures as well as from perturbations of several neurotransmitter systems.

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