Psychotic episodes

Some patients with parkinsonism communicate poorly and do not tell the primary health care provider or nurse that problems are occurring. The nurse observes the patient with parkinsonism for outward changes that may indicate one or more adverse reactions. For example a sudden change in the facial expression or changes in posture may indicate abdominal pain or discomfort, which may be caused by urinary retention, paralytic ileus, or constipation. Sudden changes in behavior may indicate hallucinations, depression, or other psychotic episodes. 

Antipsychotic, or neuroleptic drug Used in the treatment of schizophrenia. They are also used in the management of psychotic episodes associated with psychotropic drug toxicity and some neurodegenerative disorders. 

After the acute psychotic episode has resolved, the patient typically has residual features (e.g., anxiety, suspiciousness, lack of volition, lack of motivation, poor insight, impaired judgment, social withdrawal, difficulty in learning from experience, and poor self-care skills). Patients often have comorbid substance abuse and are nonadherent with medications. 

Medication should be continued for at least 12 months after remission of the first psychotic episode. Continuous treatment is necessary in most patients at the lowest effective dose. 

As noted above for the AEGL-1, chronic occupational exposure of adult males to >10 ppm produced symptoms of headache, weakness, changes in taste and smell, irritation of the throat, vomiting, and effort dyspnea (El Ghawabi et al. 1975 NIOSH 1976 Blanc et al. 1985). For a few individuals, chronic exposures occasionally produced more serious adverse effects, such as fainting and psychotic episodes. There was no evidence that these symptoms occurred after one exposure. A concentration of >25 ppm for 1 h resulted in numbness, weakness, vertigo, nausea, rapid pulse, and flushing of the face (Parmenter 1926). Only one individual was involved, and neither the exposure duration nor the concentration were measured. 

Neurological Effects. Neurological effects in hrnnans after acute inhalation exposure to chloroform are well documented because chloroform has been used as an anesthetic for surgery. Inhaled chloroform acts as a depressant on the central nervous system. Chronic inhalation exposure to chloroform resulted in exhaustion, lack of concentration, depression, and irritability in occupationally exposed people (Challen et al. 1958). In a case study, chloroform inhalation for 12 years resulted in psychotic episodes, hallucinations, and convulsions (Heilbmnn et al. 1945). Central nervous system toxicity was observed in humans after oral exposure to chloroform, which suggests that the effects of inhalation and oral exposure are similar. In case reports of patients who intentionally or accidentally ingested several ounces of chloroform, deep coma with abolished reflexes occurred within a few minutes (Piersol et al. 1933 Schroeder 1965 Storms 1973). 

Meanwhile, the wee bit of private practice I had engaged in, starting in late 1969, rekindled my interest in patient care. While cramming for Board exams, I immersed myself in clinical re-education. This fired me up even further. I began to recall my residency in psychiatry at Walter Reed Hospital with great fondness and remembered the satisfaction I had felt when patients under my care showed signs of recovery from a psychotic episode. 

Neurologic sequelae with vinblastine are much less common than those seen with vincristine and vindesine. Nonetheless, a causal relationship has been established for seizures, psychotic episodes, and confusional episodes. As common with other vinca agents, absence of reflexes and peripheral neuropathy are well described 23,24). 

Chronic abuse can lead to marked tolerance and psychic dependence with varying degrees of abnormal behavior. Frank psychotic episodes can occur, especially with parenteral abuse. Careful supervision is required during drug withdrawal because severe depression, as well as the effects of chronic overactivity, can be unmasked. Long-term follow-up may be required because of the patient s basic personality disturbances. 

Numerous mild to severe CNS and psychiatric disturbances may occur, including reduced attention span, anxiety, nightmares, daytime somnolence, euphoria, fatigue, paranoia, psychotic episodes, depression, and hallucinations. 

Overdose may produce agitation, tachycardia, palpitations, cardiac irregularities, chest pain, psychotic episode, seizures, and coma. 

Mental changes, such as paranoid ideation, psychotic episodes, and depression, maybe noted. 

Primary pulmonary hypertension (PPH), psychotic episodes, and valvular heart disease rarely occur. 

Shortly after iproniazid was shown to have antidepressant properties, imipramine was introduced as the first tricyclic antidepressant. These drugs received the name tricyclic because their structure contains three molecular rings. At first, imipramine was investigated as a possible treatment for the psychotic episodes associated with schizophrenia, a severe mental disorder that causes hallucinations and delusions, because it was chemically similar to another effective anti-schizophrenia drug. Imipramine did not reduce the severity of psychotic episodes, but it did elevate the mood of the patients who took it. In the late 1950s, it was released in the United States under the name Tofranil for the treatment of depression. 

Such men who are untrustworthy, soclopathlc, grossly disturbed or pathologic or have criminal history or a history of recurrent, severe or recent psychotic episodes should not be selected as volunteers and if they arrive at Edgewood, should be returned to their home station. This decision should ordinarily be made during the initial screening upon the basis of severe distortion of MMPI scores or very bizarre or unappropriate items on the history or questionnaire tests. 

Evidence indicates that the long-term outcome for a patient with schizophrenia is better when treatment of the acute episode is initiated rapidly. After a patient s first psychotic episode, treatment with the antipsychotic medication should be continued for at least 1 year after a full remission of psychotic symptoms. A trial period without medication may then be considered, except for patients with a history of serious suicide attempts or violent aggressive behavior... 

The risk of relapse in discontinuation trials depends on many non-pharmacological, often poorly controllable factors, notably the expectations of the patients, doctors and nurses, other environmental factors, the duration of hospitalization and prior treatment, and the time interval since the last acute psychotic episode. On the basis of an analysis of 14 discontinuation trials, Kane and Lieberman (1987) found that the relapse rate varied greatly from study to study depending on the trial, relapse rates of 30 86% with clustering around 60 70% have been reported in the first 12 months after placebo substitution. According to Kane and Lieberman, this scatter is a result of the different inclusion criteria applied and the different definitions of relapse . 

Anxiolytics are the treatment of choice for anxiety disorders, and antipsychotics should not be used for this purpose. Previously, psychotropics were classified as major (i.e., antipsychotics) and minor (i.e., anxiolytics) tranquilizers, a categorization we now know to be conceptually incorrect. There is evidence, however, that adding benzodiazepines (BZDs) to antipsychotics might improve the treatment of various acute psychotic episodes complicated by agitation, although this has not been well studied (see Chapter 5 and Chapter 10). 

Serious mental disorders fundamentally alter one s personality. Evidence from controlled studies demonstrates that antipsychotics can normalize thought processes. Some claim that the involuntary administration of these drugs violates a patient s freedom of speech. In fact, with the onset of a psychotic episode, patients normal mental processes become loose, rambling, illogical, circumstantial, incoherent, and inappropriately concrete and are often characterized by bizarre thought and speech patterns. Delusional ideas may dominate, with or without visual or auditory hallucinations. 

Drug intoxication. Cocaine and amphetamine intoxication may cause an agitated paranoid psychotic episode. Physical signs include dilated pupils, slurred speech, ataxia, hyperreflexia, and nystagmus, as well as evidence of drug use (e.g., needle tracks, nasal septum erosion). Vital signs, if obtainable, include elevated blood pressure, pulse rate, and temperature (see also the section The Alcoholic Patient in Chapter 14). 

This study provides significant evidence that antipsychotics and ECT positively alter the natural course of illness and that experiencing a psychotic episode without early definitive therapy is harmful. The precise mechanism involved in producing this harm is unknown, but we would assume that ... 

A psychotic episode may induce some lasting damage, making future episodes more likely. 

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