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Antipsychotic medication is the mainstay of treatment for the functional psychotic illnesses. Such drugs are also referred to as neuroleptics (meaning a drug with both antipsychotic effects and effects on movement) and major tranquillisers. The psychotic illnesses for which they are prescribed include schizophrenia, mania in the course of a bipolar mood disorder, and, more rarely, depression accompanied by psychotic symptoms. These are not uncommon illnesses. At some time during their lives approximately 1% of the population will suffer at least one episode of schizophrenia and a further 1% will suffer at least one episode of mania. During an episode some patients, but by no means all, suffer extreme changes in their thinking, mood and behaviour which can be very distressing to experience and which can make patients a danger to themselves or other people.
Regional cerebral blood flow was measured with H215O positron emission tomography in four patients with obsessive–compulsive disorder. Patients were scanned on 12 occasions in the same session, with each scan paired with brief exposure to one of a hierarchy of contaminants that elicited increasingly intense urges to ritualise. The relationship between symptom intensity and regional cerebral blood flow (rCBF; an index of neural activity) was subsequently examined in the group and in individual patients. The group showed significant positive correlations between symptom intensity and blood flow in the right inferior frontal gyrus, caudate nucleus, putamen, globus pallidus and thalamus, and the left hippocampus and posterior cingulate gyrus. Negative correlations were evident in the right superior prefrontal cortex, and the temporoparietal junction, particularly on the right side. The pattern in single subjects was broadly similar, although individual differences in neural response were also observed. A graded relationship between symptom intensity and regional brain activity can thus be identified in obsessive–compulsive disorder. It is hypothesised that the increases in rCBF in the orbitofrontal cortex, neostriatum, global pallidus and thalamus were related to urges to perform compulsive movements, while those in the hippocampus and posterior cingulate cortex corresponded to the anxiety that accompanied them.
The phenomenological features of 35 obsessive–compulsive disorder (OCD) patients with a lifetime history of tics were compared to 35 age- and sex-matched OCD patients without tics. Seven categories of obsessions and nine categories of compulsions were determined using the symptom checklist of the Yale–Brown Obsessive–Compulsive Scale (YBOCS). Discriminant function analysis revealed that, compared to their counterparts without tics, OCD patients with tics had more touching, tapping, rubbing, blinking and staring rituals, and fewer cleaning rituals, but did not differ on obsessions. These preliminary findings suggest that the types of compulsions present may help to discriminate between two putative subgroups of OCD, i.e. those with and without tics.
Previous studies have shown high rates of schizophrenia among the Afro-Caribbean population in Britain. In order to assess the role of genetic factors in the aetiology of this phenomenon, we have used a standardised family history method (FHRDC) to compare lifetime morbidity risks for first-degree relatives of Afro-Caribbean and white patients with RDC schizophrenia admitted in Central Manchester between 1982 and 1988. Lifetime morbidity risk for parents of Afro-Caribbean subjects was 8.9%, and for parents of white patients 8.4%. For the siblings of black probands, however, the risk was 15.9%, as compared with 1.8% for white siblings (P < 0.05). Among siblings of UK-born Afro-Caribbean probands, morbid risk was even higher at 27.3% (P = 0.001). High rates among siblings of younger Afro-Caribbean patients are consistent with previous reports of a higher incidence in the UK-born. These observations suggest that schizophrenia among Afro-Caribbeans is no less familial than for the remainder of the population, but that the increased frequency of the disorder is due to environmental factors which are most common in the Afro-Caribbean community, and capable of precipitating schizophrenia in those who are genetically predisposed.
Thirty-six consecutively admitted patients with schizophrenia and 20 with mania were studied for the morbid risk of psychosis in their first-degree relatives. Using the family history method of ascertainment, the morbid risk for schizophrenia in the relatives of schizophrenic probands was 4.12% compared with 1.42% in the relatives of manic probands. While this difference was not statistically significant, that between the morbid risk for affective psychoses in the relatives of manic patients (7.81%) was significantly higher than for the relatives of schizophrenic patients (0%).
This paper describes a prospective study of the relationship between non-psychotic prodromal symptoms and psychotic symptoms in 55 schizophrenic (DSM–III–R) out-patients. Once a month, a number of non-psychotic symptoms generally regarded as prodromal symptoms in schizophrenia were assessed, as well as psychotic symptoms, with standardised self-administered instruments and rating scales for a minimum of 12 months (range 12–29). The data were analysed for each patient using a longitudinal correlational design with a 1-month lag between the prodromal and psychotic symptoms over the total period. Results showed that in less than one-fifth of subjects did any of the prodromal symptoms, individually or in combination, show a significantly positive correlation with the subsequent level of psychotic symptoms. Such relationships were significant in an even smaller proportion of subjects when the confounding effect of concurrent psychotic symptoms on prodromal symptoms was partialled out. High levels of prodromal symptoms appeared to have adequate specificity but low sensitivity in their power to predict high levels of subsequent psychotic symptoms. There were no differences in age, gender, medication levels, and the number of previous admissions between the subjects who did or did not show a relationship between putative prodromal symptoms and psychotic symptoms.
The issue of progressive cognitive decline in patients with schizophrenia has been debated. We performed a cross-sectional study of patients with chronic schizophrenia, aged from 18 to 69 years, in order to address this issue. The patients included in this study passed a rigorous screen for any comorbid condition with an adverse impact on central nervous system function. We assessed intellectual deterioration with a battery of neuropsychological tests known to be sensitive to cognitive impairment in progressive dementia. No evidence of accelerated intellectual decline was found. No significant differences were found between the five age-derived cohorts (18–29, 30–39, 40–49, 50–59, and 60–69 years of age) on the Mini-Mental State Examination, Dementia Rating Scale, or other tests sensitive to dementia. While performance on the Boston Naming Test significantly declined with age, this was mainly due to age rather than duration of illness. However, it is important to note that mean performances on the majority of the tests were abnormal across all cohorts studied. These results suggest that intellectual function does not markedly decline during the adulthood of patients with schizophrenia. The course of schizophrenia is more consistent with a static encephalopathy than a dementing disorder.
To test further the highly successful outcomes of a controlled study of in-home behavioural family management (BFM) for schizophrenic patients, a clinic-based version of this intervention was compared with customary care alone for 41 schizophrenic patients in a Veterans Administration (VA) mental health clinic. Monthly Brief Psychiatric Rating Scale (BPRS) ratings, conducted by clinic psychiatrists who were ‘blind’ to the patients' assignment, revealed that 3 (14%) patients who received behavioural family management as well as customary care, as compared with 11 (55%) patients who received customary care alone, had symptomatic exacerbations during the first year of treatment.
Chromosomal abnormalities associated with bipolar disorder may help in the localisation of susceptibility genes for bipolar illness by pinpointing ‘candidate’ regions of the genome for further study using molecular genetic methods. We review descriptions of chromosomal abnormalities in association with bipolar and related affective disorders and evaluate their relevance for localising susceptibility genes for bipolar disorder, using standardised criteria. We found 28 reports. We identified four genomic regions of potential interest: 11q21-25; 15q11-13; chromosome 21; Xq28. It is important that clinicians are able to recognise patients who may have chromosome abnormalities which could help in the localisation of susceptibility genes for psychiatric disorders. We suggest referral for specialist investigation and karyotyping, to a psychiatric genetics research group, of any patient with functional psychosis and one or more of the following: (a) a strong family history of functional psychosis; (b) mental retardation; (c) another disease known to be caused by a single gene; or (d) congenital abnormalities.
All new attenders at the Menopause Clinic in Edinburgh over six months were interviewed to detect current depressive disorder (MADRS) and past psychiatric disorders (SADS-L), to find out whether women who were depressed at the time of clinic attendance had a history of depression. Of the 95 subjects who entered the study, 78 had gone through a natural menopause and 17 had undergone hysterectomy with or without oophorectomy. Of the 78 who had experienced a natural menopause, 35 were found to be depressed at the time of clinic attendance and 43 were not. A strong association was found between current and past depressive illness, 29 of the patients depressed at the time of clinic attendance having had depression previously. However, a clear peak of illness was seen in the perimenopausal period (four years either side of the last menstrual period): 35% of all patients with past or current depressive illness experienced their first episode of illness in this period.
About 10% of women show elation and associated features of hypomania in the first 5 days following childbirth. These symptoms can be detected using a self-rating scale (the ‘Highs’) based on SADS-L criteria. This phenomenon has been confirmed using the observer-rated Comprehensive Psychopathological Rating Scale, which also revealed a high degree of related irritability. Significantly more women scoring ⩾ 8 on the Highs scale at 3 days postpartum went on to manifest depression at 6 weeks than did subjects with no psychopathology in the early puerperium. It is suggested that the ‘highs’ followed by depression may be a mild and common form of bipolar disorder.
The construction of a semi-structured interview depression scale that is sensitive to change for use in the elderly is described. Depression items from a well validated diagnostic instrument, the Geriatric Mental State Schedule (GMSS), were used as the core items in the development of the instrument. Improvement in depression in 80 elderly patients was independently assessed with two standard rating scales for depression, the Hamilton Rating Scale for Depression and the Beck Depression Inventory, and by an independent clinician's judgement before and after standard antidepressant treatment. Depression items that were sensitive to change were retained from the core items to form the new instrument. Results indicate that this scale is reliable and valid, shows better correlation with both the clinician's and the patient's judgement of improvement than the standard instruments, and is sparing of the rater's time.
The aim of this study was to establish the prevalence of epilepsy in persons with Down's syndrome aged 19 years and over. A total of 191 adults with Down's syndrome were identified, giving a prevalence of 0.76/1000 (95% CI 0.75 to 0.77). Of these, 18 had epilepsy, giving a prevalence of 9.4% (95% CI 5.3% to 13.5%). The prevalence of epilepsy increased with age, reaching 46% in those over 50. The neurophysiological (EEG) findings of the epilepsy group were compared with those of a control group of Down's syndrome adults without epilepsy. Paroxysmal abnormalities consistent with a diagnosis of epilepsy were found in 80% of the epilepsy group, compared with only 13% of controls (P < 0.001). Epilepsy of late onset was associated with diffuse EEG abnormalities and clinical evidence of dementia. The age distribution and EEG findings suggest two independent processes in the causation of epilepsy: late-onset epilepsy associated with clinical evidence of dementia, and early-onset epilepsy in the absence of dementia.
A novel approach is described for the treatment of post-traumatic stress disorder (PTSD). Eye-movement desensitisation (EMD) requires the patient to generate images of the trauma in the mind and define physiological and emotional arousal states. While concentrating on these states, lateral multisaccardic eye movements are induced. Ten consecutive cases are reported who presented with symptoms originating from a range of traumas. The effectiveness of EMD in reducing symptoms outlined by DSM–III–R is described. An independent rater indicated that eight of the ten cases showed considerable improvement in PTSD symptoms following EMD, which was maintained at follow-up. Particular reference is given to the ‘specificity’ of EMD in treating symptoms and the changing pattern of effect at follow-up.
In a study of 100 institutionalised patients with psychosis and an equal number of age- and sex-matched healthy controls from the same regional background, the prevalence of Australia antigen (HBsAg) was 11 and 2, respectively. Institutionalised psychotic patients are a high-risk group for hepatitis B virus infection.