3 Patients appear incoherent, unable to direct and sustain lines of thought, and unable to understand abstract ideas and use appropriate judgment. Learning, retention, and recall may be impaired with consequences on recent and long-term memory. There may be confabulation and emotional lability. Patients are easily distractible and cannot sustain directed mental efforts. Tasks are left unfinished, and there may be perseveration in thoughts, speech, Inhibitors,research,lifescience,medical and action. Behavioral problems Hyperactive delirium frequently manifests as anxiety, agitation, or even anger.18-21 At the other end of the spectrum, lethargy, somnolence,

or even catatonia may occur. Patients Inhibitors,research,lifescience,medical may exhibit both ends of the spectrum. Limbs or facial jerks, tremors, and voluntary or involuntary limb and face movements can occur with fluctuating

intensity, making it difficult to differentiate from nonconvulsive status epilepticus (NCSE). It is the hypoactlve patient whose diagnosis may be overlooked. Prognosis Delirium is usually considered to be a transient disorder Inhibitors,research,lifescience,medical of the mind, but it typically appears in the setting of more serious underlying dysfunction. The morbidity and mortality, therefore, stem more from the underlying conditions engendering delirium, rather than from the delirium itself. Mortality appears to range from a quarter to a third of patients, whether assessed at the Inhibitors,research,lifescience,medical time of admission or over 3 or 6 months from diagnosis.22-24 Pathogenesis A number of causes for delirium have been identified (Table I). Risk factors include prior cognitive impairment,

advanced age, intercurrent infection, bone fracture, and medication use, particularly narcotics and neuroleptics. Postanesthesia delirium is common.25 Nonetheless, many delirious patients have no clear toxic or metabolic abnormality Some have attributed these states to environmental changes, particularly in the demented and elderly. Table I. Causes Inhibitors,research,lifescience,medical and of delirium. There are a number of mechanisms that may disrupt sleep-wake cycles and cognition. Arousal and cortical activation involves the ascending reticular activation system (ARAS), which modulates cortical excitability and wakefulness. Electrical stimulation of the ARAS may B-Raf cancer induce behavioral arousal in sleeping animals.26 Conversely, lesions of the reticular system can induce a sleep-like state.3,27 From such experiments, it appears that both sleep and coma are consequent to decreased inflow of tonic ascending impulses subserving wakefulness. A number of neurotransmitters have been suggested to be involved in this process.28-32 Serotonergic input modulates slow-wave sleep and initiates rapid eye movement (REM) sleep.