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Epilepsy is a chronic brain dysfunction. Current antiepileptic medicines cannot prevent epileptogenesis. Increasing data have shown that microRNAs (miRNAs) are selectively altered within the epileptic hippocampi of experimental models and human tissues, and these alterations affect the genes that control epileptogenesis. Furthermore, manipulation of miRNAs in animal models can modify epileptogenesis. As a result, miRNAs have been proposed as promising targets for treating epilepsy. We searched PubMed using the terms "microRNAs/miRNAs AND epilepsy", "microRNAs/miRNAs AND epileptogenesis", and "microRNAs/miRNAs AND seizure". We selected the articles in which the relationship between miRNAs and target gene(s) was validated and manipulation of miRNAs in in vivo epilepsy models modified epileptogenesis during the chronic phase via gene regulation. A total of 13 miRNAs were found in the present review. Based on the current analysis of miRNAs and their target gene(s), each miRNA has limitations as a potential epilepsy target. Importantly, miR-211 or miR-128 transgenic mice displayed seizures. These findings highlight new developments for epileptogenesis prevention. Developing novel strategies to modify epileptogenesis will be effective in curing epilepsy patients. This article provides an overview of the clinical application of miRNAs as novel targets for epilepsy.

Sepiapterin reductase, a homodimer composed of two subunits, plays an important role in the biosynthesis of tetrahydrobiopterin. Furthermore, sepiapterin reductase exhibits a wide distribution in different tissues and is associated with many diseases, including brain dysfunction, chronic pain, cardiovascular disease and cancer. With regard to drugs targeting sepiapterin reductase, many compounds have been identified and provide potential methods to treat various diseases. However, the underlying mechanism of sepiapterin reductase in many biological processes is unclear. Therefore, this article summarized the structure, distribution and function of sepiapterin reductase, as well as the relationship between sepiapterin reductase and different diseases, with the aim of finding evidence to guide further studies on the molecular mechanisms and the potential clinical value of sepiapterin reductase. In particular, the different effects induced by the depletion of sepiapterin reductase or the inhibition of the enzyme suggest that the non‐enzymatic activity of sepiapterin reductase could function in certain biological processes, which also provides a possible direction for sepiapterin reductase research.

Sepsis occurs when a systemic infection induces an uncontrolled inflammatory response that results in generalized organ dysfunction. The exacerbated peripheral inflammation can induce, in turn, neuroinflammation which may result in severe impairment of the central nervous system (CNS). Indeed, the ensuing blood-brain barrier disruption associated with sepsis promotes glial activation and starts a storm of proinflammatory cytokines in the CNS that leads to brain dysfunction in sepsis survivors. Endotoxic shock induced in mice by peripheral injection of lipopolysaccharides closely resembles the peripheral and central inflammation observed in sepsis. In this review, we provide an overview of the neuroinflammatory features in sepsis and of recent progress toward the development of new anti-neuroinflammatory therapies seeking to reduce mortality and morbidity in sepsis survivors.

Anorexia nervosa is a chronic disorder of children, adolescents and young people typically characterised by self-starvation and resistance to interventions. Staff dealing with these young people frequently question patient motivations and the ethics of interventions that may be applied against the wishes of patients. The question of withdrawal of care in a subgroup of these patients has been raised. Futility is not an appropriate response to adolescent anorexia nervosa, and treatment withdrawal is not appropriate for a disorder in which most patients can be expected to recover, in which opposition to treatment is a characteristic of the disorder and in which brain dysfunction is precipitated by severe malnutrition.

Most mental pathologies are diagnosed on the sole basis of the symptoms reported by patients, such as "I'm feeling low." The thrust of this paper is the proposal to reconceptualize mental disorders as dysfunctions of brain subsystems. This shift from symptom to organ would bring psychiatry in line with the rest of medicine, and is analogous to the change in status of venereal infections from skin pathologies, such as chancres, to bacterial infections. The proposal in question is part of the reconceptualization of mental processes as brain processes, in line with the materialist conception of the mind as neural. A practical advantage of this conceptual change is that it suggests approaching mental disorders as brain dysfunctions treatable by biological and chemical means, in addition to social measures, such as accommodating mental patients in ordinary hospitals rather than in isolated "madhouses" at the mercy of amateurs or even charlatans. An additional advantage of the "embodiment" of mental diseases is that it suggests reframing some new research projects, such as explaining why the common cold causes mental fogginess, why hypertension can cause irritability, and why nicotine dependence can be even stronger than cocaine addiction. In other words, the present proposal is to complete the so-called "mapping of the mind onto the brain" by including the abnormal mental processes, which used to be treated by shamans at a time when the mind was conceived of as an immaterial entity detachable from the body.

Deoxynivalenol (DON) is one of the most important mycotoxins in cereal-based foods or other food productions, produced by Fusarium species. Because of the high occurrence of DON in food combined with vast consumption of cereals and grain worldwide, the DON-contaminated food is a very harmful factor for human and animal health. DON has been reported to induce anorexia at lower or chronic doses in animal models. However, further researches for DON-induced anorexia are limited. Previous publications demonstrated a close link between Bacteroidetes and Firmicutes, two kinds of gut microbiota, with weight loss and the effect of low administration of DON on neurotransmitters in the frontal cortex, cerebellum, hypothalamus, hippocampus and pons/medulla. These data are similar to other studies, which show selective 5HTα receptor agonists apparently causing hyperphagia whereas 5HT1β agonists appear to induce anorexia. Thus, the neurochemical effects of lower DON exposure can be as a result of peripheral toxicological events such as emesis, which overwhelmed its more subtle feed refusal activity. Besides, changes in the microbiota have an impact on stress-related behaviors like anxiety and depression, which can lead to weight loss through decreased feed intake. Gut dysbiosis is also associated with brain dysfunction and with behavioral changes. These conclusions illustrate as well a potential explanation for DON-induced anorexia.In this review, we summarize information about DON-induced anorexia from previous studies and provide our opinion for future investigations that could establish a link between gut microbiota, neurotransmitters, anorexia and weight loss under the DON exposure. Copyright © 2017 John Wiley & Sons, Ltd.

Schizophrenia research is providing an increasing number of studies and important insights into the condition's etiopathogenesis based on genetic, neuropsychological and cranial neuroimaging studies. However, research progress has not yet led to the incorporation of such findings into the revised classification criteria of mental disorders or everyday clinical practice. By 2020, schizophrenia will most likely still be a clinically defined primary psychotic disorder. While there is some hope that treatment will be improved with new antipsychotic drugs, drugs addressing negative symptoms, more refined psychotherapy approaches and the introduction of new treatment modalities like transcranial magnetic stimulation, an additional hope is to improve early detection and prevention. As the results of new research into the etiopathogenesis of schizophrenia are promising to improve diagnosis, classification and therapy in the future, a picture of complex brain dysfunction is currently emerging requiring sophisticated mathematical methods of analysis. The imminent clinical challenge will be to develop comprehensive diagnostic and treatment modules individually tailored to the time-variable needs of patients and their families.

The research for peripheral biological markers of schizophrenia, although abundant, has been unfruitful. In the last 2 decades, the S100B protein has made its own room in this area of research. S100B is a calcium-binding protein that has been proposed as a marker of astrocyte activation and brain dysfunction. Research results on S100B concentrations and schizophrenia clinical diagnosis are very consistent; patients with schizophrenia have higher S100B concentrations than healthy controls. The results regarding schizophrenia subtypes and clinical characteristics are not as conclusive. Age of patients, body mass index, illness duration and age at onset have been found to show no correlation, a positive correlation or a negative correlation with S100B levels. With respect to psychopathology, S100B data are inconclusive. Positive, negative and absence of correlation between S100B concentrations and positive and negative psychopathology have been reported. Methodological biases, such as day/night and seasonal variations, the use of anticoagulants to treat biological samples, the type of analytical technique to measure S100B and the different psychopathological scales to measure schizophrenia symptoms, are some of the factors that should be taken into account when researching into this area in order to reduce the variability of the reported results. The clinical implications of S100B changes in schizophrenia remain to be elucidated.

Aim To clarify the diagnosis and treatment of epilepsy with higher brain dysfunction (E-HBD). Methods Using neuropsychological testing we identified three cases. Results All three cases showed persistent aphasia, amnesia or attention deficits – possibly connected with epilepsy – and were treated with anti-epileptic drugs (AED). Although the AED proved effective, there were no findings of non-convulsive status epileptics. Conclusion The etiology of E-HBD is unclear, but treatment with AED alleviated the higher brain function deficits in our three patients.

We report on rare side effects of paroxetine. A 67-year-old female patient who had been suffering from prolonged depression for over a year but had not received appropriate treatment was administered 20-mg paroxetine daily. However, the patient required hospital admission after 16 days because of behavioural disturbances and delusions that she was being chased by evil persons from a religious group. The delusions were ultimately confirmed to be serial nightmares and an oneiroid state. The nightmares gradually disappeared following discontinuation of paroxetine. The Adverse Drug Reaction Probability Scale showed a score of 6 (probable). Reports on paroxetine-induced nightmares are rare, and there is a possibility that, in this case, parexetine caused the nightmares in association with depression and assumed underlying brain dysfunction due to ageing.

We measured ERPs of professional boxers in a Go/No-Go task, comparing them to fencers and non-athletes. Results showed that fencing improved attention and motor response control, but boxing did not. More strikingly, in boxers, as in brain trauma patients, the P3 component was delayed and reduced. The P3 delay of boxers was correlated with the amount of performed sport exercise. Furthermore, in terms of behavior, boxers showed increased intra-individual variability and switch cost. Results were consistent with the hypothesis of specific impairment at the level of response inhibition processing. We suggest that this impairment is derived from the cumulative effect of blows to the head. The changes found in boxers suggest that ERPs and reaction times may be a tool for early detection of specific brain dysfunction.

Our aim was to compare urinary ethylmalonic acid (EMA) levels in subjects who had no apparent clinical reason to have increased levels of this substance but were suffering from non-specific CNS impairment, and healthy controls. Urinary EMA concentrations detected by (1)H-NMR spectroscopy were studied in 130 subjects with CNS impairment of unknown origin (with no definite diagnosis, no specific symptoms or signs, and normal common biochemical and metabolic screening results) and 130 age- and sex-matched healthy subjects. EMA levels exceeding two standard deviations (SD) above normal (i.e. 8.1 mmol/molCn) were found in a subgroup of CNS-impaired patients and healthy controls. EMA levels exceeding 2 SD above normal were fourfold prevalent in the urine of patients with non-specific CNS impairment compared to from the EMA levels in healthy controls. Moreover, we found that the level exceeding > 8.1 mmol/molCn (i.e. > + 2 SD) had sufficient discrimination accuracy in identifying subjects with non-specific CNS impairment; the level exceeding 12 mmol/molCn (i.e. > + 6 SD) reaches suitable accuracy (i.e. 100% specificity and 78.6% sensitivity). These observations are of importance, as we found that subtle increases in urinary EMA levels are frequent in patients with non-specific CNS impairment. The reasons for this association remain unknown.

SUMMARY A total of 420 enuretic children aged between four and 15 years and 100 controls were examined by EEG in order to determine their hyperventilation response, which is considered to be a non-specific sign of brain dysfunction or of cortical instability as a result of delayed maturation. It was found that an increased hyperventilation response occurred mainly among children with primary enuresis (bed-wetters from birth). This was true even if the children had a ‘uropathy’. It was also commoner among the children with pathological EEGs at rest. The results for those with secondary enuresis (later onset) were similar to the controls. These findings indicate that disturbed cerebral control of the bladder is an important factor in primary enuresis. Psychological factors are thought to account for the occurrence of secondary enuresis. RESUME Enuresie et reponse a l'hyperpnee durante l'EEG 420 enfants enuretiques âges de quatre a 15 ans et cent controles ont beneficie d'un EEG dans le but de determiner leur reponse a l'hyperpnee, consideree comme un signe non specifique de dysfonction cerebrale ou d'instabilite corticale en raison d'un retard de maturation. II est apparu que la reponse exageree a l'hyperpnee s'observait principalement parmi les enfants aenuresie primaire (lit mouille depuisla naissance). Ceci restait vrai lorsque les enfants presentaient une ‘uropathie’. Le fait etait egalement plus frequent chez les enfants avec un EEG anormal durant le repos. Les resultats en casd'enuresie secondaire(debut tardif) etaient semblables a ceux des controles. Ces donnees indiquent que le controle cerebral de la vessie perturbe est un facteur important d'enuresie primaire. Les facteurs psychologiques jouent sans doute un role essentiel dans la survenue de l'enuresie secondaire. ZUSAMMENFASSUNG Enuresis und Hyperventilationszeichen im EEG Bei insgesamt 420 Kindern mit Enuresis im Alter von vier bis 15 Jahren und 100 Kontrollkindern wurden Elektroencephalogramme abgeleitet, um die Reaktion auf Hyperventilation zu untersuchen, die als unspezifisches Zeichen einer Hirndysfunktion oder einer kortikalen Instabilitat aufgrund einer verzogerten Reifung angesehen wird. Eine verstarkte Reaktion auf Hyperventilation trat hauptsachlich bei Kindern mit einer primaren Enuresis auf und dies traf selbst dann zu, wenn die Kinder eine ‘Uropathie’ hatten. Bei Kindern mit pathologischem Ruhe-EEG war dieser Befund ebenfalls haufiger. Die Ergebnisse der Kinder mit einer sekundaren Enuresis (spaterer Beginn) mit denen der Kontrollen vergleichbar waren. Die Befunde zeigen, das eine gestorte cerebrale Kontrolle der Blase bei der primaren Enuresis ein wichtiger Faktor ist. Psychologische Faktoren werden als Ursache fur die sekundare Enuresis angenommen. RESUMEN Enuresis y respuesta a la hiperventilacion en el EEG Un total de 420 ninos enureticos de cuatro a 15 anos de edad y 100 controles, fueron examinados con EEG con el objeto de determinar sus respuestas a la disfuncion, que se

Oxidative damage is believed to be an important cause of senescence. We have previously found that green tea catechins (GT-catechin), potent antioxidants, decrease oxidative damage to DNA and suppress brain dysfunction in aged senescence-accelerated mice (SAMP10) when ingested from the age of 1 month to the age of 12 months. To clarify the effect of GT-catechin on suppression of brain senescence, we investigated the effect of starting period to ingest GT-catechin. Six- or 9-month-old SAMP10 mice were allowed free access to water containing 0.02% GT-catechin. SAMP10 mice exhibit senescence characteristics such as shortened life span, atrophied forebrain and lowered learning and memory abilities. Learning ability was significantly higher in mice that ingested GT-catechin from the age of 6 months to 12 months when compared with same-aged control mice drank water without GT-catechin. Starting GT-catechin intake from the age of 9 months tended to improve learning ability. The ages of 6 and 9 months are thought to be adult and middle ages, respectively in SAMP10 mice. This result suggested that GT-catechin was helpful in suppressing brain dysfunction with aging even when ingestion started at the adult age.

Background: In the rare inborn autosomal recessive disorder maple syrup urine disease (MSUD) the accumulation of the branched-chain amino acids (BCAAs) and their metabolic products results in acute and chronic brain dysfunction. About 20% of the patients suffer from non-classic variant forms of MSUD of different clinical severity. Aim: Up to now variant cases have mostly been published as individual case reports; the aim of this study was to give a comparative description of 16 individuals (aged 6–30 years) with different forms of variant MSUD. Methods: Laboratory data, information on clinical course and treatment as well as aspects of developmental, intellectual and social outcome were obtained retrospectively. Data from in vitro and in vivo methods measuring the degree of enzyme deficiency were included. Results: In addition to a mild phenotype, which fits well into the so-called intermittent variant, and a more severe phenotype with a wider range from a mild variant to an almost classic form, which fits well into the so-called intermediate variant, we assume the existence of an asymptomatic, non-disease variant of MSUD. These clinical phenotypes are not unambiguously differentiable on the basis of biochemical parameters. Conclusion: A continuum of clinical severity from asymptomatic to very severe (border to classic) exists in variant MSUD. Apart from newborns with classic MSUD, also those with variant forms benefit from early diagnosis and start of adequate treatment.

MRI estimations of cerebral blood volume (CBV), useful in mapping brain dysfunction, typically require intravenous (IV) injections of contrast agents. Transgenically engineered mice have emerged as the dominant animal model with which to investigate disorders of the brain and novel therapeutic agents. The difficulty in gaining IV access in mice prohibits repeated administration of contrast in the same animal, limiting the ability to map CBV changes over time. Here we address this limitation by first optimizing an approach for estimating CBV that relies on intraperitoneal (IP) rather than IV injections of the contrast agent gadodiamide. Next, we show that CBV maps generated with IP or IV injections are quantitatively comparable. Finally, we show that CBV maps generated with IP gadodiamide can be acquired repeatedly, reliably and safely over time. Although this approach has certain limitations, estimating CBV with IP injections is well-suited for mapping the spatiotemporal pattern of brain dysfunction in mice models of disease, and for testing pharmacological agents.

This article describes mothers' own reports of bringing up a son diagnosed with attention deficit hyperactivity disorder (ADHD). The effects of this widely misunderstood condition on the child, the family and the wider social network (including medical and education systems) are many and complex. Although there is evidence for a biological basis for this condition, ADHD symptoms are also seen in children of abusive or other disordered parenting. Children showing ADHD symptoms are often seen to be undisciplined, and their parents assumed to be either abusive or overindulgent. Many problems suffered by these families, particularly the mothers, may be due to the confusion of these two aetiologies. Rather than being seen as suffering from brain dysfunction, children are responded to with generalised social disapproval and ultimately ostracism. The article will describe the effects of the behavioural symptomatology as it influences the thinking, in accordance with the beliefs of casual observers, about its underlying causes. (author abstract)

The Halstead-Reitan Neuropsychological Test Battery consists of a series of individual neuropsychological measures that, in combination, permit a skilled examiner to make detailed inferences about the integrity of the cerebral hemispheres. Because the brain is the organ of adaptive behavior, brain dysfunction is typically observable in some behavioral aberrations. The tests included in the Halstead-Reitan Battery are designed to sample behavior across every possible sphere and assess all major cognitive, sensory, expressive, and motor functions. Keywords: halstead-reitan neuropsychological test battery; brain damage; neuropsychological impairment; brain-behavior relationships

We treated an 80-year-old man with vascular dementia who developed increased libido induced by fluvoxamine. Sexual stimulation associated with fluvoxamine administration has been rarely reported and the present findings suggest that organic brain dysfunction could be a risk factor for the development of the condition.

This paper describes a long-term art project. The programme has been developed and tested at Basic School, [1] Donovalska in Prague. We worked with the entire school population, including pupils with severe problems in areas of discipline, academic achievement and/or light brain dysfunction. The arts activities were based on a correlation between music and visual art.

Functional neuroimaging with SPET and PET offers the opportunity to visualize brain function either in terms of blood flow and metabolism or receptor function using specific ligands. SPET is a more widely available and cheaper technology than PET. Continuously developing and being refined, this technology will help the understanding of brain function generally and of brain dysfunction in psychiatric disorders specifically. SPET may also be used to study how these measures of brain function change with pharmacological intervention. Receptor imaging allows the study of drug-receptor interactions in vivo. As yet, the precise role and value of these techniques have not been established, but they do provide complementary tools to structural imaging and may ultimately provide prognostic information and facilitate refinement of the pharmacotherapeutic rationale underlying clinical practice.

This study explored the relationship between three indices of intersubtest scatter and level of cognitive deterioration in a sample of 104 patients with dementia of Alzheimer's type, who ranged in age between 52 and 84 years. Scatter was highly related to education and premorbid level of functioning. Advancement of dementia was shown to be associated with decrease in scatter, which suggests caution in interpretation of high magnitude of inter-subtest scatter as an indication of brain dysfunction. Easy-to-calculate range of scatter proved to be adequate measure of scatter. Calculation of more complex indices, such as PVI, provides only minimal incremental gain.

Neurological complications from cocaine use are well recognized. We propose that chronic cocaine use can also cause clinically silent brain dysfunction. We investigated brain glucose metabolism with positron emission tomography (PET) and 2-deoxy-2[18F] fluoro-D-glucose (FDG) in 21 neurologically intact chronic cocaine abusers (C) and 18 normal controls (N). The cocaine abusers were tested 1-6 weeks after the last use of cocaine and seven were retested after a 3 month drug-free period. Global cerebral glucose metabolism was not significantly different between controls and cocaine abusers (N = 38.4 +/- 3, C = 36.5 +/- 5 mumol/100 g of tissue, min). However, cocaine abusers had significantly (P less than 0.05) lower metabolic activity in 16 of the 21 left frontal regions and 8 of the 21 right frontal regions. These decreases persisted after 3-4 months of detoxification and were correlated with the dose (P less than or equal to 0.01) and the years of cocaine use (P less than or equal to 0.05). This study shows reduced rates of frontal metabolism in neurologically intact cocaine abusers that persist even after 3-4 months of detoxification.

Among a clinic sample of 6525 subjects, 61 males and 18 females with an ICD-9 diagnosis of the hyperkinetic syndrome of childhood were identified. Hyperactive girls had a lower IQ and significantly higher rates of language disorders and neurological disorders, suggesting a possible neurological basis for hyperactivity in females. In contrast, there was a population of male hyperactives with less evidence of brain dysfunction and a normal IQ, evidence compatible with the model of greater male constitutional variability. There was little evidence for the polygenetic multiple threshold model of sex inheritance.

Schneider F. Functional correlates of effect: the relevance of regional cerebral brain dysfunction. Bipolar Disord 2002: 4(Suppl. 1): 51. © Blackwell Munksgaard, 2002

It starts simply enough, with those memory failures that are common to everyone: losing keys, getting lost in an unfamiliar place, or forgetting the name of a new acquaintance. As months and years go by, however, people suffering from Alzheimer's disease have trouble recognizing where they are, have difficulty writing and spealdng, and forget how to perform routine daily tasks like washing their hands or getting dressed. Eventually, all sense of self seems to vanish, and the person becomes completely dependent on others for care. Alzheimer's affects up to 4 million people in the United States, with about 360,000 people developing the disease each year. The number of new cases will probably rise as the population ages. Although Alzheimer's becomes more common as people grow older, but it's not a normal part of aging (SN: 3/10/01, p.156). Alois Alzheimer first described the disease in 1907 after he examined the brains of people who had died of a severe dementia. The German psychiatrist noted the presence of abnormal protein deposits, or plaques, piled around nerve cells in the brain and tangled proteins inside the cells. These so-called beta-amyloid plaques and tau tangles have come to be considered the signature of Alzheimer's disease. Researchers have linked these plaques and tangles, which develop first in the area of the brain used for memory, to the decline in connections between nerve cells and the death of brain cellschanges presumed to be responsible for the brain dysfunctions of the disease. In the past few years, most scientists studying Alzheimer's have considered the beta-amyloid plaques to be the crucial factor underlying Alzheimer's disease. Yet some researchers now suggest that this so-called amyloid hypothesis is overstated and that other entities, including tau tangles, are as important as beta-amyloid.

Sponsored by the Oasi Institute for Research on Mental Retardation and Brain Aging Genetics is a rapidly growing field of medical science, which reveals molecular mechanisms of biological phenomena in health and disease. For this reason, we selected the topic ‘Neurogenetic Disease: From Molecule to Patient’, for the 4th International Symposium on Brain Dysfunction to be held September 1997. Various aspects of neurogenetic diseases: phenotype, pathology, pharmacology, biochemistry, genetics, animal models, and treatment will be discussed. We hope that this international meeting will further promote research in this field in order to understand pathogenesis as well as to develop new therapeutic approaches to genetic diseases affecting the nervous system.

Investigated the relationship between the Halstead Category Test and the Wisconsin Card Sorting Test. A correlational analysis revealed a statistically significant but modest relationship between the two variables in separate samples of brain-damaged and non-brain-damaged individuals (N = 156). Thus, in spite of the apparent similarity of the two measures, their relationship is not sufficiently close to suggest that in fact they are measuring the same abilities. However, the combination of hit rates of the two measures and the high base rate of brain dysfunction in the present sample yielded good diagnostic accuracy for decisions with regard to the presence of brain damage.

In assessing behavioral problems of the elderly there is a need for procedures which reliably indicate the presence and extent of impaired brain function. In this study, the relation of two mental status measures [the Mental Status Questionnaire (MSQ) and the Face-Hand test] to intellectual performance and education was evaluated. The sample consisted of 153 consecutive inpatients and outpatients referred to a gerontology clinic. Intellectual performance was assessed with 8 tests of learning and memory, such as Paired Associates and Babcock Story Recall. The findings indicate that positive ratings for impaired brain function on either mental status test were related to lower intellectual performance at each of three levels of education - grade school, high school, and college. Subjects with more education and mental status scores indicating mild impairment performed better on intellectual tests than did less educated persons with no brain dysfunction, but they showed significant deficits compared to other subjects with similar education and intact brain function. Larger intellectual deficits were found when the patient made more test errors and when both tests gave positive ratings. These results confirm the importance of the MSQ and Face-Hand tests as screening devices for the intellectual deficits associated with impaired brain function in a clinically heterogeneous population.

Investigated the Weigl's diagnostic significance by correlating it with several psychometric and personal variables, including degree of brain dysfunction. Forty-three male, veteran, psychiatric patients were administered the complete WAIS, Hooper, Benton, and Weigl, and their ward psychiatrist estimated presence and degree of brain dysfunction. Although uncorrelated with brain dysfunction, the Weigl did correlate significantly with 13 of the 19 study variables involved in assessment of brain function. Factor-analytic studies showed that the Weigl loaded significantly on the factor associated with neurological function. It was discovered that when a patient who is being screened can perform the conceptual requirements of the Weigl, then additional conceptual-verbal tests (e. g., Similarities) are less useful in discriminating organicity than perceptual tests (e. g., Object Assembly). When a patient cannot shift on the Weigl, then further conceptual tests will be useful.

Summary: Three questions are dealt with in this paper. (1) Do patients with epilepsy differ behaviorally from normal control groups and from persons with other medical and neurological conditions with respect to emotional adjustment, and if so, in what ways? (2) Are patients with temporal lobe epilepsy different emotionally or behaviorally from patients with other types of epilepsy? (3) To what degree does underlying brain dysfunction create a substrate for abnormal and maladaptive behavior? A review of the literature reveals the following. (1) Persons with epilepsy demonstrate more emotional and psychiatric problems than normal individuals and more difficulties than other patient groups having nonneurological disorders, but have about the same incidence of these problems as persons with other neurological disorders. (2) Increased emotional and psychiatric problems are not found among patients with temporal lobe epilepsy in comparison to patients with other types of epilepsy, although there are some behavioral peculiarities which appear in a small proportion of these patients. (3) There is a mild tendency for impairment on neuropsychological tests to be associated with emotional and psychiatric problems in epilepsy.

The accuracy of prediction of brain dysfunction for three neuropsychological tests-the Weigl, the Hooper, and the Benton-was compared. Sixty-six male, veteran, psychiatric inpatients were administered all three tests, and diagnoses of brain dysfunction or intactness were made by their ward psychiatrist, who used neurodiagnostic techniques. The results disclosed that each test alone can predict brain dysfunction significantly better than chance. All chi 2 tests were significant at the .025 level or better. When the Weigl was used as a moderator variable with the Hooper and also with the Benton, the p values for each test were somewhat reduced (p = .005 and .01), an indication of improvement in predictive power. When the percentage of predictive accuracy (hit rates) for the three tests used alone and in combination was analyzed, it was shown that the hit rate is increased by combining the Weigl with the Hooper and also with the Benton. It is increased further by combining all three tests into a predictive index.

The effectiveness of the Wechsler Memory Scale as a screening test for brain dysfunction when used with "new" scoring procedures was assessed in this cross-validation study. The scoring procedures studied were those reported by Bachrach and Mintz (1974) and Kljajic (1975). In general, these procedures were found to be unreliable methods to separate brain dysfunctional patients from psychiatric patients. While the Wechsler Memory Scale may be a good test of short-term verbal memory, it samples too narrow a band of behaviors to be a reliable screening instrument of brain dysfunction in a large range of patients.

Digit repetition was investigated in samples of unilaterally (N = 87) and bilaterally (N = 75) brain-damaged adults. The study was designed to investigate the hemispheric and neuropsychological factors that underlie performance on these two dissimilar tasks. Digit repetition was disproportionately depressed in such patients, especially those with left hemisphere lesions. The incidence of individually impaired digit repetition performance, especially of digits backward, was significantly higher than in normals, again particularly within the left hemisphere sample. However, impaired digit repetition was not invariably associated with brain dysfunction. The data suggest, but do not confirm, a differential function hypothesis, as well as a unilateral hemispheric hypothesis that underlies the ability to repeat forward and backward digits; this finding is consistent with some previous literature. Group performance showed considerable overlap, which limited the possibility of demonstrating a double dissociation between digits forward and verbal measures, and digits backward and nonverbal factors. Digit repetition in brain-damaged patients appears to have some theoretical value, but limited clinical utility.

Reviewed evidence for the validity of the Background Interference Procedure (BIP) version of the Bender-Gestalt test as a screening test for organic brain dysfunction. Low reliability and shortcomings in BIP validation studies suggest that the diagnostic validity of the BIP is lower than previously reported. A study was conducted in which the BIP was used to determine the presence or absence of brain dysfunction in groups of 45 brain-damaged and 39 nonimpaired male inpatients who were equated for age and education. Both the hit rate (61%) and relative accuracy of the BIP, compared with the EEG and neuroradiological procedures, were lower than in most earlier reports. The results are seen as limiting the usefulness of the BIP as a screening test for brain damage. A potential role for the BIP as a measure of constructional praxis is discussed.

Investigated two problem areas: (a) difficulty in the diagnoses of some types of organic brain dysfunctions; and (b) lack of accuracy in the differentiation of patients with organic disorders from patients with nonorganic disorders. Hospitalized male Ss (N = 152) were selected by diagnoses to form one nonorganic and three organic groups. For each group, data from Ss' MMPI protocols were analyzed via Cattel's Coefficient of Profile Similarity and discriminant analysis. Both MMPI factor scales (Barker, Fowler, & Peterson, 1971) and the usual clinical scales were used and compared in all analyses. Statistically significant differences among groups were found on both scales, with a greater separation of the groups provided by the factor scales. Results suggest that the MMPI, through the use of regression formulas derived from discriminant analysis of multiple groups, may be of diagnostic utility in organic brain dysfunction.

Thirty-four social drinkers who had referred themselves to the Regional Brain Damage Unit for assessment of the effects of drinking alcohol were compared with 42 volunteer control subjects of equivalent age but with low alcohol intake, using two ‘learning’ tests — the Rey Auditory Verbal Learning Test (RAVLT) and the Austin Button Maze. The Maze Test gave no evidence of disorder, but the two groups were significantly different on the RAVLT. No abnormalities in standard cognitive tests were apparent. These results suggest that a deficit in learning ability may be an early feature of the brain dysfunction associated with excessive alcohol consumption.