These initial symptoms rapidly give way to a clinical picture that is one of the most colorful in medicine. The patient is inattentive and unable to perceive the elements of his situation. He may talk incessantly and incoherently, and look distressed and perplexed; his expression may be in keeping with vague notions of being annoyed or threatened by someone. From his manner and the content of speech, it is evident that he misinterprets the meaning of ordinary objects and sounds, misidentifies the people around him, and is experiencing vivid visual, auditory, and tactile hallucinations, often of a most unpleasant type. At first the patient can be brought into touch with reality and may identify the examiner and answer other questions correctly; but almost at once he relapses into a preoccupied, confused state, giving incorrect answers and being unable to think coherently. As the process evolves, the patient cannot shake off his hallucinations and is unable to make meaningful responses to the simplest questions and is profoundly distracted and disoriented. Sleep is impossible or occurs only in brief naps. Speech is reduced to unintelligible muttering.
The signs of overactivity of the autonomic nervous system, more than any others, distinguish delirium from other confusional states. Tremor of fast frequency and jerky restless movements are practically always present and may be of high amplitude. The face is flushed, the pupils are dilated, and the conjunctivae are injected; the pulse is rapid, blood pressure elevated, and the temperature may be raised. There is excessive sweating. Most of these signs are reflections of overactivity of the sympathetic nervous system.
The most certain indication of the subsidence of the attack is the occurrence of lucid intervals of increasing length and sound sleep. Recovery is usually complete. In retrospect, the patient has only a few vague memories of his illness or none at all. Single seizures may punctuate the syndrome at any time, including before its development.
Fragments of the full syndrome are common. Brief disorientation, isolated hallucinations, or restlessness with mild hypersympathetic features all occur in withdrawal states from sedative medications, febrile illnesses, and with various intoxications as well as with the syndrome associated with antibodies to the NMDA receptor of the type associated with ovarian teratoma, with overdosage from sympathetic drugs such as the selective serotonin reuptake inhibitors or those with atropinic effects (see below), and from ingestion of psychoactive substances such as phencyclidine (PCP). Delirium may also occur in association with a number of recognizable cerebral diseases, such as viral (herpes) encephalitis or meningoencephalitis, cerebral trauma, cerebral hemorrhage after surgery for craniopharyngioma or other tumors in the same region, or multiple embolic strokes caused by subacute bacterial endocarditis, cholesterol or fat embolism, or following cardiac or other surgery.
The brains of patients who have died in delirium tremens from alcohol withdrawal without associated disease or injury usually show no pathologic changes of significance. The topography of the lesions in most of the deliriums that are symptomatic of underlying destructive processes is of interest; they tend to be localized in the rostral midbrain and hypothalamus or in the temporal lobes, where they involve the reticular activating and limbic systems. Involvement of the hypothalamus perhaps accounts for the autonomic hyperactivity that characterizes delirium in some cases of cerebral disease and the autoantibody condition. That these are not the only sites implicated is emphasized by the observations that an acute agitated delirium has occurred, albeit infrequently, with lesions involving the fusiform and lingual gyri and the calcarine cortex (Horenstein et al); the hippocampal and lingual gyri (Medina et al); or the middle temporal gyrus (Mori and Yamadori).