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A patient with coccidioidal meningitis was treated with intrathecally administered amphotericin B, and an acute toxic delirium with EEG abnormalities developed. Clinical recovery followed discontinuation of therapy and paralleled EEG resolution. This complication was dose related and argues for caution when initiating intrathecal therapy with amphotericin B at doses greater than 0.025 mg.
Two patients with disulfiram-(Antabuse-)induced encephalopathy exhibited paranoid ideas, disorientation, impaired memory, ataxia, dysarthria, snout and grasp reflexes, and abnormal electroencephalograms. The first patient developed symptoms on two occasions, each time after disulfiram administration. The second patient experienced a generalized seizure followed by fulminant psychosis three weeks after starting disulfiram therapy. Spinal fluid examination in the latter patient revealed a low homovanillic acid (HVA) level. Since disulfiram inhibits dopamine oxidation, disulfiram-induced encephalopathy may be related to excess dopaminergic activity in the central nervous system.
We reviewed the use of physostigmine in the diagnosis and management of acute toxic psychosis due to drugs with anticholinergic properties. The syndrome of agitation and toxic confusional psychosis associated with peripheral signs of cholinergic blockade is produced by several plant toxins, antispasmodics, ophthalmic preparations, and certain proprietary sedatives, as well as antiparkinson medications, antidepressants, and some antipsychotic drugs. Physostigmine, uniquely among the available reversible anticholinesterase agents, can pass the blood-brain barrier to exert central as well as peripheral cholinomimetic actions to reverse this syndrome. Psychiatrists should make more use of this safe, specific, rapid, and effective treatment for anticholinergic drug toxicity, and should particularly be alert to reversible anticholinergic brain syndromes associated with antidepressants and antiparkinson medications, and even with antipsychotic medications.
Following chronic amphetamine pretreatment, guinea pigs demonstrate an increased sensitivity to both d-amphetamine sulfate- and apomorphine hydrochloride-induced stereotyped behavior. This observation suggests that chronic exposure to high doses of a dopamine agonist (d-amphetamine) alters the response of the brain to the subsequent administration of both indirect (d-amphetamine) and direct (apomorphine) dopamine agonists. This altered response may be due to the development of dopamine receptor site hypersensitivity. Clinical evidence suggests that a similar agonist-induced hypersensitivity may play a role in the development of dyskinetic movement disorders and psychoses in humans following the chronic use of such dopamine agonists as amphetamine and levodopa.
Injected intramuscularly, the enanthane and decanoate esters of the phenothiazine fluphenazine are an effective treatment of the disordered behavior and thinking of schizophrenia. The decanoate preparation is not only slightly longer-acting but also has a smaller incidence of side-effects that the enanthate. The major adverse effect of these medications is the high frequency of extrapyramidal system disturbance. Since the 50% rate of failure of schizophrenic outpatients to take prescribed oral medications decreases treatment failure to about 20% with the use of long-acting injectable phenothiazines, this route of administration offers an advantage in patient management particularly applicable to community mental health systems. Moreover, parenteral administration of long-acting fluphenazine may be useful for patients who do not attain effective serum levels with medication taken orally because of metabolic or absorption difficulties.
The initial clinical symptoms of 25 consecutive cases of cannabis psychosis of the paranoid type and 25 consecutive cases of paranoid schizophrenia were studied and compared, in order to delineate features that would enable a differentiation of the two conditions. It was observed that the patients with cannabis psychosis substantially differed in terms of behavioral manifestations. Most of these patients were violent and panicky and demonstrated bizzare behavior, but they possessed some insight into the nature of their illness. Schizophrenic patients manifested these disturbances and characteristics less frequently. Subjects with cannabis psychosis showed rapid ideation and flight of ideas, whereas the characteristic schizophrenic thought-disorder was found mostly in schizophrenic patients.
Fifteen patients who developed prolonged psychotic reactions following psychotomimetic drug use (probably primarily LSD) were followed up 1.9 to 5.8 years later. Two patients had committed suicide. Approximately half of the patients had a relatively good outcome and half did poorly. Aspects of the initial clinical picture that correlated with outcome measures are discussed. The possibility is considered that vulnerability to a prolonged psychotic reaction following psychotomimetic drug use may be related to a genetic vulnerability to illnesses in the manic-depressive/schizo-affective spectrum. In some instances this vulnerability may implicate central serotonergic neuronal systems.
While mania usually occurs as a phase of manic-depressive disease, it can occur in association with organic dysfunction--medical and pharmacological--in patients with no history of affective disorder. In reviewing the literature, we have found that mania occurs secondary to drugs, infection, neoplasm, epilepsy, and metabolic disturbances. These cases are best considered secondary manias. They suggest that mania--like, for example, hypertension--is a syndrome with multiple causes and that with further research many manic syndromes currently considered primary will be shifted into the secondary category. Furthermore, the concept of secondary mania casts doubt on any unitary or single-agent hypothesis of the etiology of mania and supports the notion of a continuum of psychopathologic syndromes. Clinicians are alerted to the existence of this syndrome and are urged to screen for it when conditions warrant.
Delirium has been defined as a condition of cerebral insufficiency consisting of impairment of cognitive processes, with a characteristic slowing of the electroencephalographic pattern. Present also is a global "clouding" of consciousness, resulting from a potentially reversible impairment of ability to maintain attention. In these states there is usually a simultaneous diminution of the ability to think, perceive, and remember. Although drowsiness may be a part of this state, patients can be awake and yet delirious, with diminished consciousness of their surroundings. Postoperative delirium is seen more often in patients over 50 years of age, in those who are "vigilant" or overalert, and in those undergoing more complex surgery. Adverse influences in the postoperative period are certain drugs and the psychological stresses engendered by the ICU environment. Appropriate management obtains from attention to the impact of the strange enviornment on the patient.
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Psychosis secondary to dopaminergic therapy can limit the ability to manage motor symptoms of advanced Parkinson's disease (PD). We report the results of an open label 3-month trial that evaluated the antipsychotic effects of clozapine in eight PD patients with drug-induced psychosis. Response was quantified using a simplified brief psychiatric rating scale and two PD scales. Clozapine significantly improved psychiatric scores at low doses. The use of every other day regimens (not previously utilized) led to good control of symptoms and minimized side effects. Clozapine also had a positive sleep effect in four patients and improved dyskinesia in one. Finally, this treatment prevented recurrence of psychosis while levodopa doses were significantly increased and while other antiparkinsonian medications were added. Motor disability related to PD improved as a result of these treatment adjustments. We conclude that clozapine is effective in treating drug-induced psychosis in PD and allows for safe optimization of antiparkinsonian therapy.
Follow-up study of 6 workers, who after survival of an acute arsine poisoning, developed psychopathologic and neurologic abnormalities. The symptoms appeared after a latency of 1 to 6 months indicating a toxic polyneuropathy and a mild psycho-organic syndrome. The severity of these reversible manifestations was directly related to the period of time of exposure to arsine. The clinical picture of arsine polyneuropathy was similar to that observed in arsenic poisoning, suggesting that arsine polyneuropathy is due to the action of arsenic. The psychopathologic syndrome corresponds to the so-called "Vergiftungsspätfolgesyndrom" and therefore does not appear to be a specific sequel of arsine poisoning.
A case of bromide psychosis is described. A course of repeated measurements of the regional cerebral blood flow (rCBF) was followed, using the 133Xe inhalation method. At the first examination, when the serum bromide level was 45 mmol/1, the cerebral blood flow was reduced to about one-third of the normal. The regional flow pattern was also abnormal with low flows in frontal and parieto-occipital regions. Hemodialysis was performed with an overall improvement of the condition and a successive normalization of rCBF. The pronounced decrease of the cerebral blood flow, together with the positive effects of hemodialysis, seems to indicate that bromide psychosis is of a toxic origin and not an abstinence phenomenon.
Function psychosis is the most frequently observed response of the brain to disturbances in general practice and in hospital. A complete test system is presented for measuring grades of severity of function psychoses. It is possible to trace the course of the function psychosis in a curve similar to pulse and temperature curves.
No organic substrate is known for endogenous psychoses, neuroses and behaviour disorders. Therefore genetic studies have to depart from the behavioural level. This approach has yielded the empirical risk figures which depend on genetic and environmental factors. Beyond this level behaviour genetics endeavours to clarify the genetic mechanisms underlying normal and abnormal behaviour. In the schizophrenias f.i. several stretegies have been developed to approach the genetic basis: Mathematial models as to the mode of inheritance; use of modified classificatory and diagnostic criteria for genetic analysis; search for phenomena representing steps between genotype and phenotype and showing a clear mode of inheritance, f.i. biochemical or electrophysiological characters. In case the neurotransmitters are not changed in quality or total quantity but in compartmentation in the genetic defect might be localized in the pre- or postsynaptic membranes or receptors. Genetic factors are also involved in nonpsychotic behaviour disorders but to a lesser degree. They can be demonstrated even in psychoses with somatic background.
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