Addiction is a brain disease, and it matters

Scientific advances over the past 20 years have shown that drug addiction is a chronic, relapsing disease that results from the prolonged effects of drugs on the brain. As with many other brain diseases, addiction has embedded behavioral and social-context aspects that are important parts of the disorder itself. Therefore, the most effective treatment approaches will include biological, behavioral, and social-context components. Recognizing addiction as a chronic, relapsing brain disorder characterized by compulsive drug seeking and use can impact society's overall health and social policy strategies and help diminish the health and social costs associated with drug abuse and addiction.     

It''s time to adopt Internet technology

Human spermatozoal motility, viability and lipid peroxidation (LPO) have been assessed in Ringer-Tyrode supplemented with different concentrations of ascorbic acid (AA) ranging from 50 to 4000 microM. Ascorbic acid in concentrations below 1000 microM protects spermatozoa from free radical damage as evidenced from improvement in their motility and viability. Concomitantly, there is also witnessed depletion of malondialdehyde generation (an end product of LPO) following AA treatment. Ascorbic acid at 1000 microM concentration and above, however, is not protective, as evidenced by abrupt fall in sperm motility and viability and concomitant increase in LPO.     

"Tower vertebra": a new observation in sickle cell disease

PURPOSE: We studied the frequency of testicular microlithiasis (TM) in a select group of otherwise healthy infertile men with abnormal semen. METHODS: We reviewed scrotal sonography records of 180 consecutive patients with abnormal semen who were referred for evaluation of male infertility. The pampiniform plexus was evaluated for possible varicocele, and the testes were examined for the presence or absence of intratesticular calcifications and/or masses. Five patients with more than 5 echogenic foci per transducer field in either testis were identified. The medical records and sonograms of this subgroup of patients were analyzed. RESULTS: Of the 180 patients, 5 (2.8%) had TM. Three patients with TM had concomitant small varicoceles; 2 others had a history of testicular maldescent. Two patients eventually became fertile. CONCLUSIONS: Our results indicate a higher than expected frequency of TM in otherwise healthy infertile men. We speculate that the magnitude of hypospermatogenesis in patients with TM is variable and may relate to both the degree of testicular dysgenesis and the presence or absence of concomitant scrotal pathology (eg, scrotal varicocele and cryptorchidism).     

The enigma of "hidden" traumatic brain injury

OBJECTIVE: To examine individuals with "hidden" traumatic brain injury (TBI), defined in this study as those who sustained a blow to the head, with altered mental status, and experienced a substantial number of the cognitive, behavioral, and emotional sequelae typically associated with brain injury but did not make the causal connection between the injury and its consequences. DESIGN: Comparison of four groups of individuals matched for age, gender, years of education, and duration of loss of consciousness. SETTING: This study of hidden TBI followed the identification of 143 individuals who, within a larger study of people with TBI who live in the community, identified themselves as "nondisabled" (they were to be part of the comparison sample) but who had experienced a blow to the head that left them at minimum dazed and confused. PARTICIPANTS: 21 of these 143 individuals also reported large numbers of symptoms (eg, headaches, memory problems) associated with TBI. This group (Hidden TBI-High Symptoms group) was compared to three other matched samples: one with known TBI (Known Mild TBI group) and one with no disability (No Disability group) (both of which were drawn from the larger study), and one group of individuals who identified themselves as having no disability but who had experienced a blow to the head that resulted in a few symptoms (Head Trauma-Low Symptoms group). MAIN OUTCOME MEASURES: All study participants were administered an interview that incorporated several existing instruments documenting levels of reported symptoms, emotional well-being/distress, and vocational/social handicaps. RESULTS: The Hidden TBI-High Symptoms group was found to be similar to the Known Mild TBI group in terms of the number and types of symptoms experienced, whereas the Head Trauma-Low Symptoms group was similar in this respect to the No Disability group. The two former groups also evidenced high levels of emotional distress, whereas the two latter groups did not. However, on measures of handicap, the Hidden TBI-High Symptoms and Head Trauma-Low Symptoms groups were similar to the No Disability group and dissimilar from the Known Mild TBI group in that the last group experienced vocational handicap, in particular, whereas the other groups did not. Conclusions: We conclude that hidden TBI occurs at a nontrivial level (7% of our nondisabled sample). Also, individuals with hidden TBI (with persistent symptoms), unlike those with known mild TBI, are likely to experience emotional distress but not vocational handicap following injury.     

Chronic "brain death": meta-analysis and conceptual consequences

OBJECTIVE: One rationale for equating "brain death" (BD) with death is that it reduces the body to a mere collection of organs, as evidenced by purported imminence of asystole despite maximal therapy. To test this hypothesis, cases of prolonged survival were collected and examined for factors influencing survival capacity. METHODS: Formal diagnosis of BD with survival of 1 week or longer. More than 12,200 sources yielded approximately 175 cases meeting selection criteria; 56 had sufficient information for meta-analysis. Diagnosis was judged reliable if standard criteria were described or physicians made formal declarations. Data were analyzed by means of Kaplan-Meier curves, with treatment withdrawals as "censored" data, compared by log-rank test. RESULTS: Survival probability over time decreased exponentially in two phases, with initial half-life of 2 to 3 months, followed at 1 year by slow decline to more than 14 years. Survival capacity correlated inversely with age. Independently, primary brain pathology was associated with longer survival than were multisystem etiologies. Initial hemodynamic instability tended to resolve gradually; some patients were successfully discharged on ventilators to nursing facilities or even to their homes. CONCLUSIONS: The tendency to asystole in BD can be transient and is attributable more to systemic factors than to absence of brain function per se. If BD is to be equated with death, it must be on some basis more plausible than loss of somatic integrative unity.     

Borna disease virus and the brain

Viruses with the ability to establish persistent infection in the central nervous system (CNS) can induce progressive neurologic disorders associated with diverse pathological manifestations. Clinical, epidemiological, and virological evidence supports the hypothesis that viruses contribute to human mental diseases whose etiology remains elusive. Therefore, the investigation of the mechanisms whereby viruses persist in the CNS and disturb normal brain function represents an area of research relevant to clinical and basic neurosciences. Borna disease virus (BDV) causes CNS disease in several vertebrate species characterized by behavioral abnormalities. Based on its unique features, BDV represents the prototype of a new virus family. BDV provides an important model for the investigation of the mechanisms and consequences of viral persistence in the CNS. The BDV paradigm is amenable to study virus-cell interactions in the CNS that can lead to neurodevelopmental abnormalities, immune-mediated damage, as well as alterations in cell differentiated functions that affect brain homeostasis. Moreover, seroepidemiological data and recent molecular studies indicate that BDV is associated with certain neuropsychiatric diseases. The potential role of BDV and of other yet to be uncovered BDV-related viruses in human mental health provides additional impetus for the investigation of this novel neurotropic infectious agent.     

Schizophrenia as a brain disease: Implications for psychologists and families.

Explains why families of persons with mental illness and members of the National Alliance for the Mentally Ill (NAMI) believe that schizophrenia is a brain disease, and presents evidence for the brain disease model. Etiological models of schizophrenia are discussed and the biopsychosocial model of G. W. Engel (see record 1978-01423-001) was found to be most comprehensive. The merits of different treatments for schizophrenia and rehabilitative models are considered. The concern of NAMI members is to obtain the best treatment possible for mentally ill individuals and that goal can only be achieved with the help of mental health professionals, including psychologists. It is therefore important that psychologists and NAMI members communicate and understand each other. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

"Loss of self" in the narratives of people with traumatic brain injuries: a qualitative analysis

To discover how people with traumatic brain injuries (TBI) experience themselves, narrative data from ten individuals with TBI were analyzed. The findings suggest that people with TBI experience loss of self in various forms although they may successfully use strategies to avoid or minimize the sense of loss. First, people with TBI find it difficult to develop clear self-knowledge about how they have become as they are and what they can and cannot do. Second, loss of self is conspicuous when they compare their present status with their past in many aspects of their lives. Third, their senses of self are threatened by labels that they feel the society imposes upon them. This categorization of loss of self can serve for rehabilitation counseling of this population. It may assist counselors to enhance their understanding of emotional distress after TBI and to make use of their clients' narratives for the intervention.     

"Follow-up" method for processing of brain function MR images

Human thrombopoietin (hTPO), a ligand for the protooncogene c-mpl, is the major humoral regulator of megakaryocytopoiesis and platelet production affecting the proliferation and maturation of committed cells. Recently the hTPO gene and cDNA were cloned from human genome and cDNA libraries. In this report, hTPO cDNA was synthesized by RT-PCR from a Chinese human fetal liver. The sequence of this cDNA showed a high homology with hTPO cDNA in the Genebank database (accession no. L36052) except that base substitution occurred at four sites (497, 595, 767, and 795 bp), which led to the change of three amino acid residues in the predicted protein.     

Ventilatory effects of glial dysfunction in a rat brain stem chemoreceptor region"

Glia are thought to be important in brain extracellular fluid ion and pH regulation, but their role in brain stem sites that sense pH and stimulate breathing is unknown. Using a diffusion pipette, we administered the glial toxin, fluorocitrate (FC; 1 mM) into one such brain stem region, the retrotrapezoid nucleus (RTN) for 45-60 min. This dose and time period were chosen so that the effects of FC would be largely reversible. Within minutes, tissue pH decreased, and respiratory output increased. Both recovered almost completely after cessation of FC administration. The response to systemic CO2 stimulation was unaffected by FC treatment compared with that following control diffusion. Anatomic analysis showed, at the center of FC administration, some small (mean diameter = 5.1 micrometer) cells that stained for DEAD Red, a marker for altered cell membrane permeability, and some fragmented glia (glial fibrillary acidic protein immunohistochemistry). The average RTN tissue volume that contained such DEAD Red-positive cells was 271 nl, approximately 23% of the volume of one RTN region. Reversible disruption of glia in the RTN, a region known to contain central chemoreception, results in an acidic local pH and in stimulation of respiratory output.     

Increased brain concentrations of a neurotoxin, 3-hydroxykynurenine, in Huntington's disease

Concentrations of the neurotoxic tryptophan metabolite, 3-hydroxykynurenine, were determined in brain tissue taken post-mortem from patients with Huntington's disease and Alzheimer's disease. 3-Hydroxykynurenine was substantially and significantly increased in all three brain areas studied in Huntington's disease, but not significantly increased in the cortex in Alzheimer's disease, when compared to matched controls. These results demonstrate a possible dysfunction of tryptophan metabolism, via the kynurenine pathway, in Huntington's disease.     

"Near drowning" due to hydatid disease

Spontaneous rupture of a hydatid cyst is reported in a 19-year-old cattleman. Mechanical ventilation for respiratory failure and a right lower lobectomy were required for flooding of the airway with hydatid cyst fluid. The postoperative course was complicated by the development of acute respiratory distress syndrome. Complete recovery occurred with no recurrence following treatment with albendazole, praziquantel and partial hepatectomy.     

Stress echocardiography in "non-ischemic myocardial disease"

Stress echocardiography is nowadays an integral part of the diagnosis of ischaemic heart disease. In the submitted review the authors draw attention to the fact that ischaemic heart disease is no longer the domain of stress echocardiography. In recent years the interest of cardiologists in this method increased also in other cardiac diseases. Based on the appropriate pathophysiological mechanism of cardiac affection stress echocardiography is used to test left ventricular function after a dynamic or pharmacological stress, i.e. increased cardiac activity and cardiac minute volume in a number of heart diseases where we must know the extent of left ventricular affection and the functional reserve of the myocardium. These tests were also introduced to evaluate the impact of valvular disease and function of artificial grafts to evaluate left ventricular function in the transplanted heart. Stress echocardiograph holds its place also in paediatrics.     

Impaired brain microcirculation may trigger Alzheimer's disease

A working hypothesis on the pathogenesis of Alzheimer's disease (AD) is presented. The model is based on recent ultrastructural and classic histologic findings showing extensive and characteristic distortion of brain capillaries in Alzheimer brains. Brain capillary distortion induces normal laminar flow to become microturbulent or "disturbed", an outcome which over the course of many years can modify hemorheologic and hemodynamic flow patterns. As flow patterns become disturbed, micronutrient delivery to the brain is reduced thus compromising neurono-glial interaction. Catabolic outflow of CNS waste products is also depressed. When ischemic sensitive neurons, particularly in the CA1 sector, are unable to meet energy demands from lowered energy supply, they release astroglial mitogens signalling reactive astrocytes to proliferate. The resulting neuronal energy crisis is consequently complicated by the increased density of reactive astrocytes which ostensibly contribute to senile plaque development and neurofibrillary tangle formation as competition for nerve tissue space increases. The suboptimal delivery of glucose, oxygen, essential nutrients and protease regulators in AD brain becomes progressively unpredictable and in time yields to a linear decline of neurochemical, morphologic and cognitive functions.     

Fatty acid incorporation depicts brain activity in a rat model of Parkinson's disease

Following pulse labeling with [3H]arachidonic acid ([3H]AA), its incorporation pattern in brain reflects regional changes in neurotransmitter signal transduction using phospholipase A2, that is, functional activity. In a rat model of Parkinson's disease, unilateral 6-hydroxydopamine lesion in the substantia nigra, [3H]AA acid incorporation from blood was increased in cerebral cortex, caudate putamen, globus pallidus, entopeduncular nucleus, subthalamic nucleus and substantia nigra pars reticulata ipsilateral to the lesion. This increased [3H]AA incorporation likely reflects disinhibition of basal ganglia and cortical circuits secondary to absent inhibitory nigrostriatal dopaminergic input.