In the endocrine encephalopathies described below, the clinical phenomena may take the form of a delirium. Confusional states may be combined with agitation, hallucinations, delusions, anxiety, and depression, and the time span of the illness may be in terms of weeks and months rather than days. Certain aspects of the endocrine psychoses are discussed further on.
Derangements of mental function that follow administration of adrenocorticotropic hormone (ACTH) and of corticosteroids have become the prototypes of iatrogenic psychoses. The same disturbances of mental function may accompany Cushing disease (see “Corticosteroid and Adrenocorticotropic Hormone Psychosis” in Chap. 49). Experience with this neuropsychiatric condition came originally from observations of patients receiving ACTH and later from those receiving prednisone for a variety of neurologic and medical diseases. With low doses there is usually no psychic effect other than a sense of well-being and decreased fatigability. At higher doses (equivalent to 60 to 100 mg/d of prednisone), approximately 10 to 15 percent of patients become overly active, emotionally labile, and unable to sleep. Unless the dose is promptly reduced, a progressive shift in mood follows, usually toward euphoria and hypomania, but sometimes toward depression and then inattentiveness, distractibility, and mild confusion. The EEG becomes less-well modulated and slower frequencies appear. A minority of patients experience frank hallucinations and delusions, giving the illness a truly psychotic stamp and raising the suspicion of schizophrenia or bipolar disease. In nearly all instances, there is a mixture of confusion and mood change, distinguishing the state from other mundane metabolic encephalopathies. Withdrawal of medication relieves the symptoms but full recovery may take several days to a few weeks, at which time, as with all confusional states and deliria, the patient has only a fragmentary recollection of events that occurred during the illness.
The neurologic basis of this condition is poorly understood. Its attribution to premorbid personality traits or a disposition to psychiatric illness is unconvincing. Critical studies of cellular or subcellular metabolism and morphologic changes are lacking. “Cerebral atrophy” (ventricular enlargement and sulcal widening) has been shown radiologically in patients with Cushing disease and after a prolonged period of corticosteroid therapy, but the basis of this change also is unclear (Momose et al). In most cases of brain shrinkage, withdrawal of steroids has led to a reduction in ventricular size, as documented on sequential imaging studies.
In patients with Cushing disease because of adrenal or basophilic pituitary tumors, mental changes suggestive of dementia and enlarged ventricles are unusual, especially by comparison to the incidence of these changes with exogenous corticosteroids. Here again, there is a peculiar combination of mood changes and impaired cognitive function. A frank psychosis may occur. This condition is described more completely in Chap. 49 and the attendant proximal myopathy, in Chap. 45.
Allusions to psychosis in thyrotoxic patients are frequent in the medical literature. Mental confusion, seizures, manic or depressive attacks, and delusions occur singly or in combination. Action tremor is almost universal, and chorea occurs occasionally in various combinations with proximal muscular weakness. In descriptions of abnormal movements, it is often not clear whether it was chorea, tremor, myoclonus, or just fidgetiness that was observed. Treatment of the hyperthyroidism gradually restores the mental state to normal, leaving one with no explanation of what had happened to the CNS. The separate and special associations of hyperthyroidism with periodic paralysis and myasthenia are discussed in later chapters.