Psychiatric developments最新文献

Reduced speech activity is an important nonverbal symptom of retarded depressions. But speech patterns are also related to many other factors. Under an antidepressive drug treatment the speech behavior could be influenced not only by the therapeutic improvement but also by special pharmacological side effects. In a double-blind trial 21 endogenously depressed inpatients were treated with amitriptyline or pirlindol. Diagnostic interviews with the patients were recorded on TV-tapes on day 0, 4, 7, 14, 21 and 28. To investigate the psychopathological changes the tapes were analyzed under time-blind conditions. The AMP documented results of these ratings showed significantly better therapeutic effects in the amitriptyline-group than in the pirlindol-group. To study speech variables the tapes were computer analyzed. After 4 weeks the degree of improvement in the total group of patients was significantly correlated with the reduced length of speech pauses of both patients and interviewers. On the other hand remarkable drug influences in the course of speech variables were found. These could be interpreted as specific pharmacological effects.

When patients with panic disorders are divided into two groups, those that are without any signs of phobic avoidance and those that are frankly agoraphobic, we see a differential premorbid history of separation anxiety in childhood with school phobia. The former group we found to be without these problems, while the latter demonstrated a history of school phobia in the majority of cases (60 per cent). This may indicate that uncomplicated panic disorder and agoraphobia with panic attacks are not always differential cross-sections of the same disease process, or different levels of severity of the same psychopathological entity, but may represent illnesses best not conceptualized as lying on a continuum. Further research will be served by separating panic disorder (DSM-III 300.01) into two groups: uncomplicated panic disorder, and panic disorder with limited phobic avoidance, which will exist along with the present agoraphobia with panic attacks, perhaps best renamed panic disorder with extensive phobic avoidance.

A wide range of studies in man and other species suggest that early compromise of immunological tolerance (both maternal-fetal and self) may lead to severe and varied cognitive deficits. This article briefly reviews what is known of the genesis and maintenance of normal tolerance and current ideas on pathological deviances in tolerance. These ideas are discussed in relation to risk factor, family, twin, biochemical, anatomical, and immunological studies of pervasive developmental disorders (particularly infantile autism). A range of immunological injury hypotheses for the genesis of the pervasive developmental disorders are considered and technical problems in deciding among them are presented.

Depression appears to be a frequent complication of neoplastic disease. Recent surveys suggest that it is not only a common reason for psychiatric referral but that a substantial minority of hospitalized cancer patients suffer from an affective disturbance severe enough to warrant psychiatric intervention. In view of its reported prevalence it is likely that this complication adversely affects the quality of patients' lives and interferes with the management of their disease. Given the nature of this problem it is disturbing that so little systematic research has been done, especially in the area of treatment. In this article we critically review the literature concerned with the relationship of depression to cancer. We begin with comment on the nature of the association between cancer and depression and the question of whether depression is an etiologic factor in neoplastic disease. Before considering the prevalence of affective disorders among cancer patients, we examine the difficulty of diagnosing depression in seriously ill patients. Next, we explore the role of various psychological and biological factors in the etiology of this complication and, finally, we offer recommendations for treatment and suggest directions for future research.

The Dohrenwends have associated psychiatric screening instruments with Frank's concept of 'demoralization' through negative evidence of the criterion validity of the instruments for identifying 'diagnosable mental disorders'. New evidence from the Stirling County Study is given to suggest that absence of validity stems from symptom-enumerative scoring procedures and that concordance with clinical judgment is improved by employing diagnostic algorithms. The concepts of diagnosis and 'demoralization' are discussed, and the history of screening instruments is reviewed. It is suggested that, while 'demoralization' may be a useful concept for clinicians, it poses serious drawbacks for epidemiological research because of the assumptions it involves about etiology and outcome.

Neuroendocrine abnormalities in depression have been regarded, by many authors, as relatively specific markers of nosological subtypes of the disorder, e.g. primary vs. secondary, endogenous vs. non-endogenous or unipolar vs. bipolar depression. They should reflect the same changes in central neurotransmitters (e.g. noradrenergic insufficiency and/or cholinergic hyperactivity) that were hypothesized as the cause of clinical symptoms. This view is challenged on the basis of our own neuroendocrine investigations in 317 psychiatric patients and 103 normal controls. According to these studies the abnormalities are nosologically rather unspecific. They are induced by a large variety of factors, e.g. emotional stress associated with the clinical symptomatology, weight loss due to malnutrition as a consequence of reduced appetite, medication and drug withdrawal. Stress-induced hypercortisolism appears to be the most common abnormality that may trigger other neuroendocrine dysfunctions, such as a blunted TSH response to TRH. Differences in neuroendocrine abnormalities of depressives are probably due to variations in the manifold factors influencing the hormonal axes involved, to temporal changes in hormonal patterns (e.g. one abnormality triggering another) and to individual differences in the basic activity and the responsiveness of the various axes.

Two hundred and thirteen published case reports of acute lithium (Li) toxicity occurring between 1948 and 1984 are reviewed. Although chronic Li may cause toxic effects in a variety of organs, acute toxic effects are manifested mainly in the central nervous system (CNS). CNS depression is reflected in decreased upper motor neuron control, decreased level of consciousness, and slowing on the electroencephalogram. Permanent or long-lived neurological sequelae may occur in as much as a third of all cases. The outcome of toxicity is a function of maximum Li levels and promptness and efficacy of therapy.

The evidence in favour of a diagnosis of limbic epilepsy in the case of Dostoevsky is reviewed. Independent records from numerous biographical sources support the widely held view that Dostoevsky had frequent convulsive episodes, that the episodes began in childhood and continued throughout his life and that Dostoevsky himself was able accurately to record the premonitory aura and sequelae of such episodes. In addition the increasing memory impairment he suffered both for recent and remote events from the age of 40 supports the presence of progressive brain damage. This information renders implausible the analytic interpretations of Freud and his followers, that Dostoevsky's epilepsy was hysterical in origin, where epileptiform somatization was presumed to dispose of excessive psychic excitation, and that this process had its roots in Dostoevsky's unconscious hatred of his father and latent homosexuality. Nevertheless, Dostoevsky's neuroticism is clearly supported by his life-long hypochondriasis, obsessionality, paranoid traits, tendency to reactive depressions, and experience of quasi-hallucinatory episodes which were probably not epileptic in origin. Neither his epilepsy nor his neuroticism can explain or detract from the profundity and wisdom of the literary monuments which clearly attest Dostoevsky's ample genius.

The neuroleptic malignant syndrome (NMS) is an under-recognized yet sometimes fatal complication of antipsychotic drug therapy. NMS is comprised of hyperthermia, rigidity, autonomic disturbances, and altered consciousness. Until recently, there was no specific therapy for NMS other than discontinuing the offending neuroleptic and providing symptomatic treatment. However, 4 drugs (dantrolene and the dopamine agonists amantadine, bromocriptine, and carbidopa/levodopa) have clearly emerged to merit consideration in the therapy of NMS. The literature on their use in this disorder, either alone or in combination, is reviewed. The combination of dantrolene (a peripheral muscle relaxant) and post-synaptic dopamine agonists may prove the most effective in this condition.

Recent advances in brain imaging permit metabolic variables to be measured in psychiatric patients. These include regional cerebral blood flow, oxygen utilization, oxygen extraction and glucose utilization--all measures which reflect CNS energy utilization. The quantitative relationships between these metabolic parameters, neuronal activity, and higher cortical function are poorly understood. In evaluating the results of imaging studies, it is important to establish whether the reported changes correlate with episodic symptomatology or with a chronic disease process. Affective disorders exemplify conditions which are episodic, progress rapidly and respond to medication, making it difficult to identify consistent patterns of metabolic change. Thus unipolar subgroups have been described with both left and right metabolic predominance. On the other hand, imaging studies in dementia have consistently shown decreased glucose utilization, and more particularly poor verbal performance may go with reduced glucose uptake in the left temporal/parietal area. Although neuro-imaging studies are still at an early stage, the additional capacity to measure regional receptor distribution and kinetics using ligands tagged with positron emitters will open up new dimensions in the study of psycho-pathophysiology.