Tardive dyskinesia in psychosis: are women really more at risk?

It is commonly held that women are more at risk of developing tardive dyskinesia (TD). However, recent evidence suggests that this may only be the case in samples of older patients, men being more at risk in the younger age groups. Abnormal movements were measured with the Abnormal Involuntary Movement Scale (AIMS) in a sample of 706 chronic psychotic patients aged not older than 65 years (median age 36 years). Female gender was associated with a lower risk of TD (OR, 0.5; 95% CI, 0.3-0.7). The effect of gender was independent of other risk factors such as older age, severity of negative symptoms and exposure to antipsychotic medication in the previous 2 years. There was no evidence that the effect of these risk factors differed between the sexes. In samples of relatively young patients with chronic psychotic illness, who typically represent the majority of patients in community programmes for the severely mentally ill, men are more at risk of TD than women.     

Partners of perinatal substance users: forgotten, failing, or fit to father?

The role fathers play in families affected by perinatal substance use largely has been unexamined. It is difficult to reconcile this peripheral role assigned to the fathers of substance-exposed infants as the importance of fathers in the lives of children and of partners in the lives of substance-using women has become better appreciated. In this article, case presentations of families in which both parents were substance users illustrate the complexities and diverse trajectories of relationships between perinatal substance users and their children's fathers. An examination of families' lives can be used to better understand the challenges they face, stimulate further discussion about how partners of perinatal substance users can be conceptualized as fathers, and consider the impact they have in the lives of their children and their children's mothers. Discussion of case studies can yield increased knowledge about the role of fathers in the lives of families affected by perinatal substance abuse. This will lead to better-informed treatment interventions, research, and public policy.     

Tardive dyskinesia is associated with impaired retrieval from long-term memory: the Curaçao Extrapyramidal Syndromes Study: IV

Tardive dyskinesia may be associated with cognitive dysfunction. It is not clear whether this dysfunction occurs in the form of a global or specific cognitive deficit. A cross-sectional study was conducted in a well-defined catchment area (Cura?ao, The Netherlands Antilles). All schizophrenic inpatients who had been taking neuroleptic medication for at least 3months and who were younger than 65years were included (n=53). Tardive dyskinesia was assessed with the Abnormal Involuntary Movement Scale. The neuropsychological assessment comprised tests of memory, executive function, and speed of information processing. Of the six cognitive measures, only delayed recall was significantly associated with orofacial dyskinesia. Limb-truncal dyskinesia was not associated with any of the cognitive measures. The pattern of memory impairment is consistent with there being a frontal-subcortical disturbance in orofacial dyskinesia. The results underscore the importance of using specific cognitive test procedures in the search for the cognitive correlates of dyskinesia.     

Motor Symptoms of Schizophrenia: Is Tardive Dyskinesia a Symptom or Side Effect? A Modern Treatment

Abnormal involuntary dyskinetic movements in schizophrenia patients have been documented for more than 140 years. Clinicians should distinguish between two kinds of disturbances—spontaneous dyskinetic movements and movements induced by psychotropic medications—which may look familiar clinically. As a modern term, tardive dyskinesia (TD) is a potentially permanent neurological hyperkinetic movement disorder that occurs after months or years of taking psychotropic drugs. Several distinct forms of TD exist, specifically tardive akathisia, tardive blepharospasm, tardive dystonia, tardive gait, tardive myoclonus, tardive tremor, and tardive tics, and they have different pathophysiologies and treatment. The pathogenesis of TD remains unclear, and the pathophysiology is complex and multifactorial. Moreover, there is solid evidence of a genetic predisposition to TD. This article summarizes recent relevant publications concerning TD and the most recent studies regarding treatment of this disorder with antioxidative agents.     

Psychiatry: mindless or brainless, both or neither?

After a period marked by one-sided emphasis on psychodynamics and social issues, or what could be called "brainless" psychiatry on account of its relative neglect of cerebral processes, we are witnessing an opposite trend towards extreme biologism or "mindless" psychiatry. The pendulum has swung periodically from one to the other of these reductionistic positions throughout the history of psychiatry. The author argues that neither brainless nor mindless psychiatry can do justice to the complexity of mental illness and to the treatment of patients. Psychiatry's distinguishing feature as a clinical discipline is its equal concern with subjective experience, or the mind, and with the body, including brain function, which together constitute a person, a psychiatrist's proper focus of inquiry and intervention. Moreover, a person, viewed as a mindbody complex, is in constant interaction with the environment. It follows that both study of mental illness and clinical practice need to take into account the psychological, the biological and the social aspects. These three aspects are not mutually reducible and are indispensable for the understanding and treatment of the individual patient. Such a comprehensive, biopsychosocial approach provides an antithesis to the reductionistic viewpoints and, in the writer's opinion, is both practically and theoretically most satisfying.     

Fundamental or forgotten? Is Pierre Paul Broca still relevant in modern neuroscience?

The ability to speak is a unique human capacity, but where is it located in our brains? This question is closely connected to the pioneering work of Pierre Paul Broca in the 1860s. Based on post-mortem observations of aphasic patients' brains, Broca located language production in the 3rd convolution of the left frontal lobe and thus reinitiated the localizationist view of brain functions. However, contemporary neuroscience has partially rejected this view in favor of a network-based perspective. This leads to the question, whether Broca's findings are still relevant today. In this mini-review, we discuss current and historical implications of Broca's work by focusing on his original contribution and contrasting it with contemporary knowledge. Borrowing from Broca's famous quote, our review shows that humans indeed “speak with the left hemisphere”– but Broca's area is not the sole “seat of articulatory language”.     

Compensation neurosis: a too quickly forgotten concept?

There has been great debate concerning the existence and meaning of compensation neurosis. It is included in the International Classification of Diseases (ICD)-9 and -10 but not listed in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR). On the eve of publication of the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), we re-examine the history and concept of compensation neurosis and conceptually update the condition to reflect current psychiatric thought. We consider its utility as a diagnostic entity for forensic evaluations and its components as they relate to exaggeration in injury claims. We also discuss how compensation neurosis differs from malingering and factitious disorder.     

Levodopa-induced dyskinesia and rotational behavior in hemiparkinsonian rats: independent features or components of the same phenomenon?

Chronic daily administration of 6.25 mg/kg of levodopa in unilaterally 6-OHDA lesioned rats did not induce any observable behavioral effects for the first 12.5 ± 2.5 days. Thereafter, levodopa administration induced abnormal involuntary movements (AIMs), involving the contralateral limb, head, neck and trunk, along with the development of contralateral rotations. AIMs and rotations followed a progressively worsening, highly correlated, parallel course. We suggest that rotational behavior does not represent a pure antiparkinsonian response, but along with levodopa-induced dyskinesia is part of the levodopa-induced motor response complications syndrome.     

Right leisure: serious, casual, or project-based?

Leisure as a tool for rehabilitating people with neuro-disabilities is well established. Yet, despite significant progress in this area, problems remain in the way leisure is used for this purpose. One, as yet, unresolved problem is how to determine which leisure activity or activities will be attractive to people with particular disabilities. Another is how to counteract the persistent, dominant public view that real personal worth is measured according to the work people do rather than the leisure they pursue. The third is to inform practitioners, many of whom are unaware of recent advances in leisure theory, about these advances, which can help them solve the first problem and adapt to the second. The main body of this paper presents such a theory - the serious leisure perspective. It synthesizes three main forms of leisure, showing, at once, their distinctive features, similarities, and interrelationships. The forms are serious, casual, and project-based leisure. A review of the research on neuro-rehabilitation follows. Some implications of the Perspective for neuro-rehabilitation are then presented, including ways practitioners can introduce clients to certain types of leisure, encourage them to pursue the types chosen, and help them develop an optimal leisure lifestyle.     

Paroxysmal kinesigenic dyskinesia: a channelopathy? Study of 19 cases

INTRODUCTION: Paroxysmal kinesigenic dyskinesia (PKD) is characterized by brief episodes of dystonia and choreoathetosis triggered by sudden voluntary movements. Disease onset is seen in the first or second decade. The attacks typically last less than one minute. Three autosomal dominant PKD loci are identified: EKD1, EKD2 and EKD3. EKD1 has an overlap with the locus of the "Infantile Convulsion and Choreoathetosis (ICCA) syndrome". The favorable natural history, the episodic nature of the symptoms and their sensitivity to anticonvulsant therapy suggest channelopathy as a mechanism of PKD. PATIENTS AND METHODS: We reviewed the clinical features, the family history, the treatment response, the evolution and the technical investigations in 19 affected individuals. RESULTS: All cases were idiopathic. Ten patients had a positive familial history. Three patients suffered from ICCA syndrome. Some atypical features were seen, such as the association of kinesigenic and nonkinesigenic attacks and the presence of migraine, ataxia, seizures and myoclonus. Acetazolamide responsiveness was seen in two patients. CONCLUSION: The coexistence of PKD and nonkinesigenic dyskinesia in several patients confirms the earlier described presence of intermediary forms, nonrepresented in the current classification of paroxysmal dyskinesias. Our study results suggest channel dysfunction and basal ganglia involvement in the pathophysiology of PKD.     

Depression sub-typing: unitary, binary or arbitrary?

The strongest statistical support for the binary view of depression has been provided by factor (principal components) analytic studies which delineate a bipolar factor with features interpreted as reflecting "endogenous depression" and "neurotic depression" at opposing poles. We review the seminal studies to suggest instead that the bipolar factor has generally polarised depression and anxiety, and that no such entity or symptom complex of "neurotic depression" has been isolated. Instead "neurotic depression" has been defined principally by features of anxiety and personality style. We argue that the suggested entity is, in fact, a pseudo-entity, being no more than a residual group of non-depressive features without any significant intrinsic depressive characteristics. We support our interpretation by showing comparable solutions in published studies of depressives alone, contrasted with separate analyses of anxious and depressed patients. We also report two studies in which the "neurotic depressive" pole is made to appear and disappear by the inclusion and exclusion of anxiety items. As factor analytic studies have defined the "residual" pole so variably, we argue that some features held to distinguish neurotic depression are of no utility and that such a diagnosis is meaningless. We suggest that the clinician should not proceed (after excluding endogenous depression) to conclude that the default option is necessarily an entity "neurotic depression" and that instead a heterogeneous group of options (e.g. anxiety, personality disorder) require review. If the "neurotic depressive" type of the multivariate analytic studies is a pseudo-entity, then a modified unitary view of depression may be valid.     

Tau aggregates: toxic, inert, or protective species?

Alzheimer's disease brains are characterized by extracellular aggregates of the amyloid-beta peptide and intracellular neurofibrillary tangles, composed of aggregated hyperphosphorylated tau protein. The role of aggregated tau in neurodegeneration is still controversial, as evidence point to either a toxic or protective role in the disease. Here, we will first examine tau aggregation and its putative roles in Alzheimer's disease. We will then review the findings concerning different species of tau and their potential toxicity.