Fasciitis, perimyositis, myositis, polymyositis, and eosinophilia

Several groups of cases of fasciitis and myositis with eosinophilia are reported. The common features are inflammation into fascia and/or perimysium, and/or muscle fibers; eosinophilia in blood and/or in muscle biopsy. The following classification of 24 cases is suggested: at one end of the spectrum are fasciitis with eosinophilia: diffuse fasciitis (Shulman syndrome): 10 cases (3 with hematological complications); 2 cases of diffuse fasciitis with muscle atrophy; 3 cases of restricted fasciitis. Relapsing perimyositis with eosinophilia belong to the same spectrum, either diffuse (5 cases) with myalgias, or localized (2 cases). Other cases are focal myositis or multiple myositis, polymyositis with eosinophilia. The relationship among these cases is discussed. There is a continuum among the different groups. The pathophysiology remains unknown.     

Diphenylhydantoin, Phenobarbital, and Primidone in Saliva, Plasma, and Cerebrospinal Fluid

Diphenylhydantoin, primidone, and phenobarbital were determined in saliva and plasma of 164 patients by gas-liquid chromatography. The saliva ratio was about one-tenth in patients on diphenylhydantoin, 0.32-0.38 on phenobarbital alone and with other drugs, 0.97 and 0.96 on primidone alone and with other drugs. The S/P ratio of phenobarbital was similar in patients treated with primidone alone or with co-medication. For diphenylhydantoin and primidone, the S/P and CSF/plasma ratio were similar; for phenobarbital the S/P ratio was lower due to the difference in pH of saliva and CSF. Thus the concentration in saliva serves as a measure of the nonprotein-bound or free concentration in plasma with the advantage that saliva is easy to obtain. Co-medication does not change the S/P ratio for the three drugs studied. The high correlation between levels in plasma and in saliva allows the plasma levels to be predicted from the concentration in saliva.     

Caspases, apoptosis, and Alzheimer disease: causation, correlation, and confusion

Extensive neuron loss occurs in Alzheimer disease (AD) brain and some authors have speculated that dysregulation of apoptotic death pathways is etiologically responsible for the disease. Apoptosis is regulated in mammalian cells by a family of cysteine proteases called caspases. At least 7 different caspases (caspases 1, 2, 3, 6, 8, 9, and 12) have been implicated in regulating neuronal cell death in response to amyloid beta (A beta) exposure in vitro, in animal models of neurodegenerative diseases, and in AD brain itself. Despite this seemingly impressive array of data implicating caspases and apoptosis as etiologic factors in AD, the direct involvement of caspase-dependent neuronal apoptosis in AD pathogenesis remains uncertain. Alternative explanations for some findings, contradictory experimental observations, and lack of morphologically convincing apoptotic neurons in the vast majority of AD brains has led to the revised hypothesis that apoptosis-associated molecular events cause neuronal dysfunction in the absence of, or prior to, neuronal death. Unfortunately, this new view renders the term "apoptosis-associated" functionally meaningless since it bears no relationship with apoptotic death and fails to focus scientific investigation on the molecular insults that trigger the "apoptosis-associated" response in AD neurons. On balance, an etiologic role for caspases in AD is far from proven. It remains possible, however, that caspase-dependent neuronal death contributes to AD neuron loss and thus, caspase inhibition offers some hope for extending AD neuron survival so that other agents, targeting upstream events, may delay or reverse primary AD pathology.     

Head size and intelligence, learning, nutritional status and brain development. Head, IQ, learning, nutrition and brain

This multifactorial study investigates the interrelationships between head circumference (HC) and intellectual quotient (IQ), learning, nutritional status and brain development in Chilean school-age children graduating from high school, of both sexes and with high and low IQ and socio-economic strata (SES). The sample consisted of 96 right-handed healthy students (mean age 18.0 +/- 0.9 years) born at term. HC was measured both in the children and their parents and was expressed as Z-score (Z-HC). In children, IQ was determined by means of the Wechsler Intelligence Scale for Adults-Revised (WAIS-R), scholastic achievement (SA) through the standard Spanish language and mathematics tests and the academic aptitude test (AAT) score, nutritional status was assessed through anthropometric indicators, brain development was determined by magnetic resonance imaging (MRI) and SES applying the Graffar modified method. Results showed that microcephalic children (Z-HC < or = 2 S.D.) had significantly lower values mainly for brain volume (BV), parental Z-HC, IQ, SA, AAT, birth length (BL) and a significantly higher incidence of undernutrition in the first year of life compared with their macrocephalic peers (Z-HC > 2S.D.). Multiple regression analysis revealed that BV, parental Z-HC and BL were the independent variables with the greatest explanatory power for child's Z-HC variance (r(2) = 0.727). These findings confirm the hypothesis formulated in this study: (1) independently of age, sex and SES, brain parameters, parental HC and prenatal nutritional indicators are the most important independent variables that determine HC and (2) microcephalic children present multiple disorders not only related to BV but also to IQ, SA and nutritional background.     

Cytokines, neurophysiology, neuropsychology, and psychiatric symptoms

Recent research has overcome the old paradigms of the brain as an immunologically privileged organ, and of the exclusive role of neurotransmitters and neuropeptides as signal transducers in the central nervous system. Growing evidence suggests that the signal proteins of the immune system - the cytokines - are also involved in modulation of behavior and induction of psychiatric symptoms. This article gives an overview on the nature of cytokines and the proposed mechanisms of immune-to-brain interaction. The role of cytokines in psychiatric symptoms, syndromes, and disorders like sickness behavior, major depression, and schizophrenia are discussed together with recent immunogenetic findings.     

Activities of arginase, transamidinase, and ornithine aminotransferase in glia, neurons, and synaptosomes

The regional, cellular, and subcellular distribution of some enzymes of the urea cycle in brain is not clearly known. Glia, neurons, and synaptosomes have been prepared from rat cerebral cortex and arginase (EC 3.5.3.1), transamidinase (EC 2.1.4.1), and ornithine aminotransferase (EC 2.6.1.13) have been estimated in order to understand the metabolic and functional role of these enzymes. It has been observed that arginase is predominantly localized in synaptosomes and neurons. The ornithine aminotransferase was found to be high in glial cells and very high in synaptosomes (higher than arginase). Transamidinase was mostly localized in glial cells. The implication of these results has been discussed in relation to a possible role of ornithine acting as a precursor of glutamate in glutametargic nerve endings and its possible participation in the glutamate-glutamine cycle.     

Alcohol, nicotine, caffeine, and mental disorders

Alcohol, nicotine, and caffeine are the most widely consumed psychotropic drugs worldwide. They are largely consumed by normal individuals, but their use is even more frequent in psychiatric patients, Thus, patients with schizophrenia tend to abuse all three substances. The interrelationships between depression and alcohol are complex. These drugs can all create dependence, as understood in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV). Alcohol abuse is clearly deleterious to the brain, provoking acute and chronic mental disorders, ranging from intoxication with impairment of cognition, to delirium tremens, halluosis, and dementia. In contrast, the main health consequences of nicotine, notably cancer and cardiovascular disases, lie outside the realm of psychiatry However, the mes of nicotine dependence and motivation to smoke or quit are of concern to psychiatrists.     

Locked-in Syndrome,BCI, and a Confusion about Embodied,Embedded, Extended,and Enacted Cognition

In a recent contribution to this journal, Andrew Fenton and Sheri Alpert have argued that the so-called “extended mind hypothesis” allows us to understand why Brain Computer Interfaces (BCIs) have the potential to change the self of patients suffering from Locked-in syndrome (LIS) by extending their minds beyond their bodies. I deny that this can shed any light on the theoretical, or philosophical, underpinnings of BCIs as a tool for enabling communication with, or bodily action by, patients with LIS: BCIs are not a case of cognitive extension. I argue that Fenton and Alpert’s claim to the contrary is the result of a widespread confusion about some related, but significantly different, approaches to cognition that all fall under the heading of “situated cognition.” I first provide a short taxonomy of various situated approaches to cognition, highlighting (some of) their important commonalities and differences, which should dissolve some of the confusions surrounding them. Then I show why the extended mind hypothesis is unsuitable as a model of BCI enhancements of LIS patients’ capacity to interact with their surroundings, and I argue that the situated approach with obvious bearings on the sort of questions that were driving Fenton and Alpert is not the idea that cognition is extended, but the idea that cognition is enacted.     

Reality,Dream, and Trauma

Comparing various psychoanalytic perspectives on envy and malignant envy, the author argues for a developmental reconsideration of envy that locates its emergence in the breakdown of intersubjectivity. This breakdown is connected with the inability of the mother/analyst to hold and contain the child's/patient's affective states such that the child/patient is deprived of being recognized as a subject. Moreover, the dyad is unable to experience fully the pleasure and enjoyment of a reciprocal, mutual, and intimate relationship. This developmental failure interferes with the patient's capacity to experience and act on her desire. Unable to to sustain a link with the other's mind, the child cannot take in and then hold on to good, pleasurable experiences. The author illustrates his argument with two clinical examples, those of a child patient and of an adult patient. The child case highlights the breakdown of intersubjectivity as a developmental precursor to envy, whereas the adult vignette emphasizes the relationship between destructive envy and the perversion of desire.     

Research,Curriculum, and Diversity

The ideal psychoanalytic institute will prepare outstanding clinicians of varied backgrounds, who can exchange insights about how each culture produces different conditions for mental health. The ideal institute will also do clinical outcome research, to insure the survival of the psychoanalytic field. Candidates would not only learn psychoanalytic ideas, but also see them in the context of findings from other fields, including experimental psychology, neuroscience, anthropology, sociology, philosophy, sexology, and literature.     

Epilepsy, psychiatry, and neurology

This article reviews the relationship between the psychiatry and neurology of epilepsy, especially in the last 100 years. Throughout most of its recorded history of 3 to 4 millennia epilepsy has been viewed as a supernatural or mental disorder. Although first suggested by Hippocrates in the 5th century B.C., the concept of epilepsy as a brain disorder only began to take root in the 17th and 18th centuries. The discipline of neurology emerged from "nervous disorders" or neuropsychiatry in the late 19th century, when vascular theories of epilepsy predominated. By the turn of the 19th century psychiatry and neurology were diverging and epilepsy remained to some extent in both disciplines. It was only in the middle of the 20th century with the development of electromagnetic theories of epilepsy that the concept of epilepsy per se as a neurological disorder was finally adopted in international classifications of disease. This was associated with a refined definition of the ictal, pre-, post-, and interictal psychological disorders of epilepsy, which have contributed to a renaissance of neuropsychiatry. At the beginning of the 21st century and the centenary of the ILAE psychiatry and neurology have been converging again, led in some respects by epilepsy, which has provided several useful models of mental illness and a bridge between the two disciplines.