Culture,Psychiatry, and the Written Word†

Pessimistic views about the course and outcome of schizophrenia have been replaced by a more hopeful perspective that emphasizes on providing opportunities for recovery. Recovery, from a provider perspective, means that priority is placed on providing access to treatments and community services that have been proven effective in both decreasing symptoms and assisting individuals to lead maximally productive and personally meaningful lives. In 2004, the Schizophrenia Patient Outcomes Research Team (PORT) published a consensus list of evidence-based practices (EBPs) that includes six psychosocial treatments. These psychosocial interventions in combination with access to pharmacotherapy are important components of comprehensive treatment programs for the seriously mentally ill. This paper summarizes and updates the research basis for the PORT psychosocial EBPs and discusses several additional issues and research topics to be considered in the future.     

To what ends? Psychotherapy goals and outcomes, the good life, and the principle of beneficence

Psychotherapists aim to benefit others, especially clients. The corresponding ethical principle, beneficence, is found in the aspirational, not enforceable, section of the American Psychological Association (2002) ethics code, is central to the idea of a professional, and is a crucial component of ethical excellence. Beneficence and related controversies (e.g., varying ideas about what it means to benefit others) are described, then linked to psychotherapy's goals and outcomes (which are, in part, the ethical ends toward which therapy aims and by which it is evaluated), especially through ideas about the good life. I conclude by discussing ways in which therapists can--through careful reflection and action aimed at benefiting others--move toward ethical excellence regarding beneficence. (PsycINFO Database Record (c) 2010 APA, all rights reserved).     

The deadly pleasures of the clitoris and the condom – a rebuttal of Brody,Costa and Hess (2012) 1

Brody, Costa and Hess (2012) have produced a critique containing errors both of commission and omission of my editorial (Levin 2012a) and review (Levin 2012b). This reply identifies a number of these and makes the appropriate rebuttals and vindications to correct both.     

Are child-, adolescent-, and adult-onset depression one and the same disorder?

This paper reviews prior research studies examining neurobiological correlates and treatment response of depression in children, adolescents, and adults. Although there are some similarities in research findings observed across the life cycle, both children and adolescents have been found to differ from depressed adults on measures of basal cortisol secretion, corticotropin stimulation post-corticotropin releasing hormone (CRH) infusion, response to several serotonergic probes, immunity indices, and efficacy of tricyclic medications. These differences are proposed to be due to 1) developmental factors, 2) stage of illness factors (e.g., number of episodes, total duration of illness), or 3) heterogeneity in clinical outcome (e.g., recurrent unipolar course vs. new-onset bipolar disorder). Relevant clinical and preclinical studies that provide support for these alternate explanations of the discrepant findings are reviewed, and directions for future research are discussed. To determine whether child-, adolescent-, and adult-onset depression represent the same condition, it is recommended that researchers 1) use the same neuroimaging paradigms in child, adolescent, and adult depressed cohorts; 2) carefully characterize subjects' stage of illness; and 3) conduct longitudinal clinical and repeat neurobiological assessments of patients of different ages at various stages of illness. In addition, careful attention to familial subtypes (e.g., depressive spectrum disorders vs. familial pure depressive disorders) and environmental factors (e.g., trauma history) are suggested for future investigations.     

Preliminary investigations on melatonin and 5-methoxytryptophol synthesis in the pineal,retina, and Harderian gland of the mole rat and in the pineal of the mouse “eyeless”

Summary Hydroxyindole-O-methyltransferase (HIOMT) activity for the synthesis of melatonin and 5-methoxytryptophol, both 5-methoxyindoles, was measured in the pineal, the Harderian gland and the retina of the mole rat and in the pineal of the mouse eyeless. In the pineal and the Harderian gland of the mole rat a larger amount of 5-methoxytryptophol than of melatonin is synthesized. 5-Methoxyindole synthesis is extremely high in the Harderian gland, whereas in the retina HIOMT activity is low and variable. In the pineal of the mouse eyeless, a low 5-methoxyindole synthesis showing no circadian rhythm is demonstrated. It is concluded that, besides the generally accepted regulation of the indole metabolism by light, in species with atrophied eyes having Harderian glands (mole rat) and in species without eyes other factors than light might be responsible for the indole metabolism in the pineal gland.     

Aβ1-16 can aggregate and induce the production of reactive oxygen species, nitric oxide, and inflammatory cytokines

Amyloid-β (Aβ40/42) aggregates containing the cross-β-sheet structure are associated with the pathogenesis of Alzheimer's disease (AD). It is generally accepted that the N-terminal peptide of Aβ40/42, Aβ1-16, does not aggregate, and is not cytotoxic. However, we here show that Aβ1-16 can aggregate, and form cytotoxic aggregates containing β-turns and regular non-amyloid β-sheet structures. Factors such as pH, ionic strength, and agitation were found to influence Aβ1-16 aggregation, and the amino acid residues Asp1, His6, Ser8, and Val12 in Aβ1-16 may play a role in this aggregation. Our MTT results showed that Aβ1-16 monomers or oligomers were toxic to SH-SY5Y cells, but Aβ1-16 fibrils exhibited less cytotoxicity. Our studies also indicate that Aβ1-16 aggregates can increase the formation of reactive oxygen species and nitric oxide, induce the loss of calcium homeostasis, and incur the microglial production of TNF-α and IL-4. Thus, our findings suggest that Aβ1-16 may contribute to AD pathogenesis.     

Pharmacological effects of venlafaxine, a new antidepressant, given repeatedly, on the α1-adrenergic, dopamine and serotonin systems

Summary. Venlafaxine (VEN) is a representative of a new class of antidepressants (SNRIs) which inhibit selectively the uptake of serotonin and noradrenaline, but – in contrast to tricyclics – show no affinity for neurotransmitter receptors. The present study was aimed at determining whether repeated VEN (given twice daily for 14 days) induced adaptive changes in the α₁-adrenergic, dopamine and serotonin systems, similar to those reported by us earlier for tricyclic antidepressants. The results indicate that VEN potentiates the clonidine-induced aggressiveness and the methoxamine-induced exploratory hyperactivity, both these effects being mediated by α₁-adrenoceptors. VEN increased the hyperlocomotion induced by D-amphetamine and (±)-7-OH-DPAT. Neither the apomorphine and quinpirole hyperlocomotion, nor the apomorphine and D-amphetamine stereotypies were changed. VEN did not affect the behavioural syndrome induced by 8-OH-DPAT (a 5-HT_1A effect), and decreased both the head twitch reaction induced by L-5-HTP or (±)DOI and the hyperthermia induced by trifluoromethylphenylpiperazine, all those effects being mediated by 5-HT₂ receptors. Repeated VEN did not change the hypothermia evoked by oxotremorine (a central cholinergic agonist). The above results indicate that repeated VEN increases – as do tricyclics – the responsiveness of α₁-adrenergic and dopaminergic (mainly D₃) systems and decreases the responsiveness of the 5-HT₂ system. It may be concluded that the lack of affinity for neurotransmitter receptors is of no importance to the development of adaptive changes in the studied systems, observed after repeated treatment. Received April 20, 1998; accepted July 22, 1998     

Trump,Freud, the Puzzle of Femininity—and #MeToo

Abstract

Beneath Donald Trump’s repudiation of democratic values and practically all vestiges of Obama’s legacy (which has spurred a clamor to repudiate Trump) lies a repudiation of the feminine. It underwrites Trump’s cult of hypermasculinity and enables his exploitation of masculine insecurity, along with the gutting of climate protections and reproductive rights. Freud believed the repudiation of femininity was “psychological bedrock” (for both sexes); this article argues that, on the contrary, we have no fundamental need to repudiate the feminine. In fact, to embrace the feminine, in both material and symbolic ways, would be to open an important space for a more democratic polity. But claiming the feminine is so threatening that some, perhaps most, would prefer to lock it up and deny its vast and elemental erotic power and democratizing possibility. #MeToo unleashes the feminine potential for an emancipatory politics beyond patriarchy.     

Effects of interferon-γ, interleukin-1β, and tumor necrosis factor-α on the serotonin metabolism in the nucleus raphe dorsalis of the rat

Summary The effects of the cytokines interferon (IFN)-, interleukin (IL)-1, and tumor necrosis factor (TNF)- on the serotoninergic transmission in the nucleus raphe dorsalis (NRD) were studied after peripheral and central application. The studies were performed in the freely moving rat using differential pulse voltammetry with multicarbon fibre electrodes to study the extracellular levels of the serotonin (5-HT) metabolite 5-hydroxyindoleacetic acid (5-HIAA). The extracellular 5-HIAA levels were not changed in the NRD after peripheral application of rat recombinant IFN-, but elevated by the cytokines IL-1 and TNF-. After intracerebroventricular (i.c.v.) application the cytokines IFN-, IL-1 and TNF- stimulated the serotoninergic transmission in the NRD. Our data suggest that the effect of peripherally elevated cytokine concentrations on the serotonin metabolism in the NRD of the rat is cytokine-dependent. In this respect the T-cell and NK-cell cytokine IFN- acts clearly different when compared to the mainly macrophage-derived cytokines IL-1 and TNF-, and plays a different role in the communication between immune and central nervous system.     

What are the computations of the cerebellum,the basal ganglia and the cerebral cortex?

The classical notion that the cerebellum and the basal ganglia are dedicated to motor control is under dispute given increasing evidence of their involvement in non-motor functions. Is it then impossible to characterize the functions of the cerebellum, the basal ganglia and the cerebral cortex in a simplistic manner? This paper presents a novel view that their computational roles can be characterized not by asking what are the “goals” of their computation, such as motor or sensory, but by asking what are the “methods” of their computation, specifically, their learning algorithms. There is currently enough anatomical, physiological, and theoretical evidence to support the hypotheses that the cerebellum is a specialized organism for supervised learning, the basal ganglia are for reinforcement learning, and the cerebral cortex is for unsupervised learning.This paper investigates how the learning modules specialized for these three kinds of learning can be assembled into goal-oriented behaving systems. In general, supervised learning modules in the cerebellum can be utilized as “internal models” of the environment. Reinforcement learning modules in the basal ganglia enable action selection by an “evaluation” of environmental states. Unsupervised learning modules in the cerebral cortex can provide statistically efficient representation of the states of the environment and the behaving system. Two basic action selection architectures are shown, namely, reactive action selection and predictive action selection. They can be implemented within the anatomical constraint of the network linking these structures. Furthermore, the use of the cerebellar supervised learning modules for state estimation, behavioral simulation, and encapsulation of learned skill is considered. Finally, the usefulness of such theoretical frameworks in interpreting brain imaging data is demonstrated in the paradigm of procedural learning.     

Missionaries with the hopeless? Inebriety,mental deficiency and the Burdens

The late nineteenth‐ and early twentieth‐century campaign for the treatment of ‘inebriates’ used many of the themes used by campaigners for the care of the ‘feeble‐minded’. The inebriate reformatories admitted mainly women, and their low rate of success was blamed on the inmates being ‘mental defectives’, rather than a result of the methods used. When the reformatories closed, these were reused as institutions under the Mental Deficiency Act of 1913. Having been missionaries, the Reverend H. N. Burden and his wives managed inebriate reformatories and then switched to running colonies for ‘mental defectives’. The present article examines some of the links between the two movements.     

Seizures and electroencephalography in the intensive care unit—new insights,challenges, and concerns

Clinical Epileptology -     

General practitioners’ knowledge,practices, and obstacles in the diagnosis and management of dementia

Objectives: To identify general practitioners’ (GPs) knowledge, practices, and obstacles with regard to the diagnosis and management of dementia.

Methods: Standardized questionnaires covering knowledge, practices, and obstacles were distributed among a purposive sample of GPs in Kathmandu, Nepal. Three hundred and eighty GPs responded (response rate = 89%).

Results: Knowledge of practitioners’ with regard to the diagnosis and management of dementia was unsatisfactory (<50%). Diagnosis and management barriers are presented with regard to GP, patient, and carer factors. Specifically, the results address the following issues: communicating the diagnosis, negative views of dementia, difficulty diagnosing early-stage dementia, acceptability of specialists, responsibility for extra issues, knowledge of dementia and aging, less awareness of declining abilities, diminished resources to handle care, lack of specific guidelines, and poor awareness of epidemiology.

Conclusions: Demographic changes mean that dementia will represent a significant problem in the future. The following paper outlines the problems and solutions that the Nepalese medical community needs to adopt to deal effectively with diagnosis, care, and management of dementia.     

Bioethics, Assisted Suicide, and the “Right to Die”

Physician-assisted suicide is much talked about. But confusion remains as to what precisely it is, and debate continues about its ethical implications. Is physician-assisted suicide distinguishable from refusal of treatment? Is there a “right to die?” Does assisted suicide necessarily have to mean physician-assisted suicide? What is the relationship of physician-assisted suicide to end-of-life care? How should physicians deal with a request for assisted suicide? These issues are explored in this paper, along with a review of the ethical arguments for and against physician-assisted suicide. The paper concludes that society should encourage individuals not to see assisted suicide as their best option. A better policy than widespread legalization of physician-assisted suicide is to provide the necessary social support, health care including mental health care, hospice care, and compassion to those who feel they face an undignified life, or an undignified painful death. This paper is based on a presentation made at the AACP 2000 Annual Meeting, October 14, 2000.     

Are the effects of the antidepressants amitriptyline, maprotiline, and fluoxetine on inhibitory avoidance state-dependent?

State-dependent learning (SDL) is a phenomenon in which the retrieval of newly acquired information is possible if the subject is in the same physiological state as during the encoding phase. SDL makes it possible to separate the effects of drugs per se on learning from the effects due to changes in drug state during the task. The present work was designed to investigate whether the antidepressants amitriptyline (30 mg/kg), maprotiline (25 mg/kg), and fluoxetine (15 mg/kg) produce SDL of the inhibitory avoidance conditioning in male and female CD1 mice. In three separate experiments, independent groups were used for each pharmacological treatment and for each sex using a 2 x 2 experimental design. The results do not show SDL in any of the drugs. In the case of amitriptilyline, the data can be attributed to a memorization deficit, while the maprotiline results are interpreted as simultaneously influenced by memorization deficit and performance facilitation due to motor impairment. Fluoxetine treatment did not produce any deteriorating effect on the conditioning. Drugs had some different effects on the performance of males and females, males showing a slightly higher deterioration than females with administration of amitriptyline and maprotiline. This study shows that these antidepressants affect the acquisition/consolidation but not the retrieval process in the inhibitory avoidance learning.