Long-term outcomes after new onset seizure in children living with HIV: A cohort study.

OBJECTIVE: To determine the long-term outcomes, including mortality and recurrent seizures, among children living with HIV (CLWH) who present with new onset seizure. METHODS: Zambian CLWH and new onset seizure were enrolled prospectively to determine the risk of and risk factors for recurrent seizures. Demographic data, clinical profiles, index seizure etiology, and 30-day mortality outcomes were previously reported. After discharge, children were followed quarterly to identify recurrent seizures and death. Given the high risk of early death, risk factors for recurrent seizure were evaluated using a model that adjusted for mortality. RESULTS: Among 73 children enrolled, 28 died (38%), 22 within 30-days of the index seizure. Median follow-up was 533 days (IQR 18-957) with 5% (4/73) lost to follow-up. Seizure recurrence was 19% among the entire cohort. Among children surviving at least 30-days after the index seizure, 27% had a recurrent seizure. Median time from index seizure to recurrent seizure was 161 days (IQR 86-269). Central nervous system opportunistic infection (CNS OI), as the cause for the index seizure was protective against recurrent seizures and higher functional status was a risk factor for seizure recurrence. SIGNIFICANCE: Among CLWH presenting with new onset seizure, mortality risks remain elevated beyond the acute illness period. Recurrent seizures are common and are more likely in children with higher level of functioning even after adjusting for the outcome of death. Newer antiseizure medications appropriate for co-usage with antiretroviral therapies are needed for the care of these children. CNS OI may represent a potentially reversible provocation for the index seizure, while seizures in high functioning CLWH without a CNS OI may be the result of a prior brain injury or susceptibility to seizures unrelated to HIV and thus represent an ongoing predisposition to seizures. PLAIN LANGUAGE SUMMARY: This study followed CLWH who experienced a new onset seizure to find out how many go on to have more seizures and identify any patient characteristics associated with having more seizures. The study found that mortality rates continue to be high beyond the acute clinical presentation with new onset seizure. Children with a CNS OI causing the new onset seizure had a lower risk of later seizures, possibly because the trigger for the seizure can be treated. In contrast, high functioning children without a CNS OI were at higher risk of future seizures.

Early rise in brain damage markers and high ICOS expression in CD4+ and CD8+ T cells during checkpoint inhibitor-induced encephalomyelitis.

We report a case of rapid eradication of melanoma brain metastases and simultaneous near-fatal encephalomyelitis following double immune checkpoint blockade. Brain damage marker S-100B and C reactive protein increased before symptoms or signs of encephalomyelitis and peaked when the patient fell into a coma. At that point, additional brain damage markers and peripheral T cell phenotype was analyzed. The analyses were repeated four times during the patient's recovery. Axonal damage marker neurofilament light polypeptide (NFL) and astrocytic damage marker glial fibrillar acidic protein (GFAP) were very high in blood and cerebrospinal fluid and gradually normalized after immunosuppression and intensive care. The costimulatory receptor inducible T cell costimulatory receptor (ICOS) was expressed on a high proportion of CD4+ and CD8+T cells as encephalomyelitis symptoms peaked and then gradually decreased in parallel with clinical improvement. Both single and double immune checkpoint inhibitor-treated melanoma patients with other serious immune-related adverse events (irAE) (n=9) also expressed ICOS on a significantly higher proportion of CD4+ and CD8+T cells compared with controls without irAE (n=12). In conclusion, our results suggest a potential role for ICOS on CD4+ and CD8+T cells in mediating encephalomyelitis and other serious irAE. In addition, brain damage markers in blood could facilitate early diagnosis of encephalitis.

Limitations of periodical health examinations in detecting occupational chronic solvent encephalopathy.

OBJECTIVES: Occupational diseases (ODs) are globally underdetected, and chronic solvent encephalopathy (CSE) is no exception. The aim was to study how the recommended policies and protocols were followed in occupational health services (OHS) periodical health examinations where symptomatic CSE cases have remained undetected. METHODS: We retrospectively studied the medical records of occupational CSE cases (n=18) found in a screening project, which had not been detected in preceding OHS health examinations. We collected data from three sources: OHS units, the screening project and the Finnish Institute of Occupational Health. We analysed the health examinations conducted between symptom onset and the detection of CSE: regularity, content, use of recommended screening tools, exposure estimation and whether a physician was involved in the examinations, as recommended. RESULTS: The mean duration of symptoms before OD identification was 7.3 years (range 3-13), and 36 health examinations had been conducted. Fifteen workers had attended these (1-9 times each) while suffering from CSE symptoms, and two before symptoms. Only one had not had access to OHS. The recommended symptom screening questionnaire, Euroquest, was used in five (14%) examinations, and previous solvent exposure inquired once. A physician was involved in 24 (67%) examinations, whereas the rest were carried out by a nurse. CONCLUSIONS: Although health examinations are conducted, guidelines are not followed. This may be due to a lack of awareness concerning CSE, and may apply to other ODs. In addition to legislation and policies, OH professionals must be continuously educated to improve awareness, prevention and detection of ODs.

Chronic solvent-induced encephalopathy: course and prognostic factors of neuropsychological functioning.

PURPOSE: Working in conditions with daily exposure to organic solvents for many years can result in a disease known as chronic solvent-induced encephalopathy (CSE). The aims for this study were to describe the neuropsychological course of CSE after first diagnosis and to detect prognostic factors for neuropsychological impairment after diagnosis. METHODS: This prospective study follows a Dutch cohort of CSE patients who were first diagnosed between 2001 and 2011 and underwent a second neuropsychological assessment 1.5-2 years later. Cognitive subdomains were assessed and an overall cognitive impairment score was calculated. Paired t tests and multivariate linear regression analyses were performed to describe the neuropsychological course and to obtain prognostic factors for the neuropsychological functioning at follow-up. RESULTS: There was a significant improvement on neuropsychological subdomains at follow-up, with effect sizes between small and medium (Cohen's d 0.27-0.54) and a significant overall improvement of neuropsychological impairment with a medium effect size (Cohen's d 0.56). Prognostic variables for more neuropsychological impairment at follow-up were a higher level of neuropsychological impairment at diagnosis and having a comorbid diagnosis of a psychiatric disorder at diagnosis. CONCLUSIONS: Results are in line with previous research on the course of CSE, stating that CSE is a non-progressive disease after cessation of exposure. However, during follow-up the percentage patients with permanent work disability pension increased from 14 to 37%. Preventive action is needed in countries where exposure to organic solvents is still high to prevent new cases of CSE.

Work ability score of solvent-exposed workers.

PURPOSE: Occupational chronic solvent encephalopathy (CSE), characterized by neurocognitive dysfunction, often leads to early retirement. However, only the more severe cases are diagnosed with CSE, and little is known about the work ability of solvent-exposed workers in general. The aim was to study memory and concentration symptoms, work ability and the effect of both solvent-related and non-occupational factors on work ability, in an actively working solvent-exposed population. METHODS: A questionnaire on exposure and health was sent to 3640 workers in four solvent-exposed fields, i.e. painters and floor-layers, boat builders, printers, and metal workers. The total number of responses was 1730. We determined the work ability score (WAS), a single question item of the Work Ability Index, and studied solvent exposure, demographic factors, Euroquest memory and concentration symptoms, chronic diseases, and employment status using univariate and multivariate analyses. The findings were compared to those of a corresponding national blue-collar reference population (n = 221), and a small cohort of workers with CSE (n = 18). RESULTS: The proportion of workers with memory and concentration symptoms was significantly associated with solvent exposure. The WAS of solvent-exposed workers was lower than that of the national blue-collar reference group, and the difference was significant in the oldest age group (those aged over 60). Solvent-exposed worker's WAS were higher than those of workers diagnosed with CSE. The WAS were lowest among painters and floor-layers, followed by metal workers and printers, and highest among boat builders. The strongest explanatory factors for poor work ability were the number of chronic diseases, age and employment status. Solvent exposure was a weak independent risk factor for reduced WAS, comparable to a level of high alcohol consumption. CONCLUSIONS: Even if memory and concentration symptoms were associated with higher solvent exposure, the effect of solvents on self-experienced work ability was relatively weak. This in line with the improved occupational hygiene and reduced solvent exposure levels in industrialized countries, thus the effect may be stronger in high-level exposure environments. As a single question, WAS is easily included, applicable, and recommendable in occupational screening questionnaires.

Epigallocatechin-3-Gallate Protects against Homocysteine-Induced Brain Damage in Rats.

High levels of homocysteine are implicated in many neurovascular and neurodegeneration diseases. Epigallocatechin 3-gallate (EGCG), one of green tea polyphenols, has potential anti-oxidative and anti-inflammatory activities. However, it has not been explored whether EGCG has an effect on homocysteine-induced neuro-inflammation and neurodegeneration. In this study, we investigated the effects of EGCG on memory deficit, oxidative stress, neuro-inflammation, and neurodegeneration in hyper-homocysteinemic rats after a 2 wk homocysteine injection by vena caudalis. We found that supplementation of EGCG could rescue deficit of spatial memory induced by homocysteine. Treatment of EGCG significantly reduced the expression of malondialdehyde, glial fibrillary acidic protein, tumor necrosis factor-α, and interleukin-1ß and increased glutathione level in the homocysteine-treated group. In TdT-mediated dUTP nick end labeling (TUNEL) assay and Fluoro-Jade B staining, supplementation of EGCG could attenuate the apoptotic neurons and neurodegeneration. Interestingly, EGCG significantly ameliorated homocysteine-induced cerebrovascular injury. Our data suggest that EGCG could be a promising candidate for arresting homocysteine-induced neurodegeneration and neuro-inflammation in the brain.

Unusual complications from amitriptyline intoxication.

Althoughtricyclic antidepressants(TCAs) are frequently prescribed to patients with depression, these drugs can also be misused. A 21-year-old comatose patient was referred to our hospital presenting with ventricular tachycardia. Despite initial treatment including intravascular lipid emulsion, ventricular fibrillation occurred soon after arrival. Venoarterial extracorporeal membrane oxygenation and therapeutic hypothermia were administered. Refractory arrhythmia disappeared on the next day. A high concentration of amitriptyline was identified in his blood samples on arrival. Mechanical bowel obstruction followed after abdominal compartment syndrome caused by anticholinergic effects, and refractory seizure occurred due to TCA intoxication. Although seizure was brought under control with anticonvulsant agents, his Glasgow Coma Scale did not recover to the full score. MRI presented irreversible damage to the bilateral frontal lobe and insula. Amitriptyline has the potential to cause unusual serious complications, such as abdominal compartment syndrome, irreversible central nervous system disability and lethal arrhythmia.

Neurotoxicity of cyclosporine A in children with steroid-resistant nephrotic syndrome: is cytotoxic edema really an unfavorable predictor of permanent neurological damage?

BACKGROUND: Cyclosporine A-associated neurotoxicity has been reported mainly after organ transplantation. Only a small number of children with steroid-resistant nephrotic syndrome and cyclosporine A-associated neurotoxicity have been reported. PATIENTS: We report three children, aged 4, 11, and 15, with steroid-resistant nephrotic syndrome and cyclosporine A-associated neurotoxicity. In two of the patients, primary diagnosis was idiopathic nephrotic syndrome, and in one it was IgA nephropathy. Magnetic resonance with diffusion-weighted imaging, combined with quantification of apparent diffusion coefficient values, showed lesions caused by cytotoxic edema indicating irreversible brain damage. Nonetheless, the patients fully recovered clinically and radiologically after prompt discontinuation of cyclosporine A. CONCLUSIONS: Neurotoxic effects should be suspected in any child with nephrotic syndrome treated with cyclosporine A in whom sudden neurological symptoms occur. Cytotoxic edema is a rare finding in pediatric patients. However, even in such cases with seemingly irreversible brain damage, full recovery without permanent neurological sequels is possible with prompt cyclosporine A discontinuation and supportive therapy.

Obstetric Anesthesia Liability Concerns.

Obstetric practice carries a high risk of medical liability and involves both obstetricians and anesthesiologists. Analysis of data from the Anesthesia Closed Claims Project database shows an increase in the proportion of anesthesia claims for maternal death and brain damage between the 1990s and 2000 and later, primarily due to hemorrhage. The proportion of claims for newborn brain damage remained unchanged while those for maternal nerve injury and minor injuries decreased. Use of massive transfusion protocols and clinical drills have been shown to improve outcomes from hemorrhage. Good communication and teamwork are critical for reducing obstetric liability.

Unusually Prolonged Presentation of Designer Drug Encephalopathy Responsive to Steroids.

The availability and use of novel psychoactive substances has risen dramatically over the last decade. The unpredictability of their toxicity constitutes a real challenge. We report a case of an adolescent who developed prolonged encephalopathy after ingesting "Hot Molly," which was found to contain the novel psychoactive substance, methylenedioxybenzylpiperazine when analyzed by high resolution mass spectrometry assay. This is the first case of human toxicity from methylenedioxybenzylpiperazine ingestion in the medical literature confirmed by body fluid analysis presenting with significant and prolonged encephalopathy. The prolonged course may be due to CYP2D6 inhibition from a combination of the methylenedioxyphenyl moiety and the patient's ultrarapid metabolizer pharmacokinetics. The response to high dose corticosteroids suggests a possible inflammatory effect that warrants further investigation.

Beraprost sodium protects against chronic brain injury in aluminum-overload rats.

BACKGROUND: Aluminum overload can cause severe brain injury and neurodegeneration. Previous studies suggest that prostacyclin synthase (PGIS) expression and prostacyclin receptor (IP) activation are beneficial for treatment of acute traumatic and ischemic brain injury. However, the potential value of PGIS/IP signaling pathway to chronic brain injury is still unclear. In this study, we investigated the change of PGIS/IP signaling pathway and the effect of beraprost sodium (BPS) on chronic brain injury in chronic aluminum-overload rats. METHODS: Rat model of chronic cerebral injury was established by chronic intragastric administration of aluminum gluconate(Al3+ 200 mg/kg per day,5d a week for 20 weeks). The methods of ELISA, qRT-PCR and Western blotting were used to detect the PGI2 level and the PGIS and IP mRNA and protein levels in hippocampi of chronic aluminum-overload rats, respectively. Rat hippocampal superoxide dismutase (SOD) activity and malondialdehyde (MDA) content also were measured. The effects of BPS (6, 12 and 24 µg⋅kg(-1)) on brain injury in chronic aluminum-overload rats were evaluated. RESULTS: Compared with the control group, PGIS mRNA expression, PGI2 level, and the IP mRNA and protein expressions significantly increased in hippocampi of chronic aluminum-overload rats. Administration of BPS significantly improved spatial learning and memory function impairment and hippocampal neuron injury induced by chronic aluminum overload in rats. Meanwhile, administration of BPS resulted in a decrease of PGI2 level and downregulation of PGIS and IP expressions in a dose-dependent manner. Aluminum overload also caused a decrease of SOD activity and an increase of MDA content. Administration of BPS significantly blunted the decrease of SOD activity and the increase of MDA content induced by aluminum overload in rats. CONCLUSIONS: BPS has a significant neuroprotective effect on chronic brain injury induced by aluminum overload in rats. Remodeling the balance of PGIS/IP signaling pathway and inhibition of oxidative stress involve in the neuroprotective mechanism of BPS in aluminum-overload rats. The PGIS/IP signaling pathway is a potential therapeutic strategy for chronic brain injury patients.

Hippocampal neuronal cyclooxygenase-2 downstream signaling imbalance in a rat model of chronic aluminium gluconate administration.

BACKGROUND: Acute and chronic brain damages including neurodegenerative diseases are a group of neuroinflammation-associated diseases characterized by cognitive function defect and progressive neuron loss. The pathophysiological procession of brain damages involves the overexpression of cyclooxygenase (COX)-2. Owing to the limited benefit to chronic brain damage and the late adverse effect of COX-2 inhibitors, the COX downstream signaling pathway has become a focus in neurological research. In order to explore the mechanism of aluminum neurotoxicity and the importance of COX2 downstream signaling pathways to chronic brain damage, the present study was designed to simultaneously observe the prostaglandin (PG) contents, and the expressions of PG synthases and PG receptors of hippocampus in a rat model induced by chronic administration of aluminium gluconate. METHODS: A rat model of chronic brain damage was established by chronic intragastric administration of aluminium gluconate (Al3+ 200 mg/kg per day, 5d a week for 20 weeks). PG contents, the expressions of PG synthases, and the expressions of PG receptors in rats were measured by ELISA, RT-PCR and Western blotting, respectively. RESULTS: Chronic aluminium gluconate administration resulted in hippocampal neuron injury and learning and memory disorders in rats. Aluminium gluconate administration also resulted in increased levels of PGE2, PGD2, TXA2, PGI2, and PGF2α in rat hippocampus. The DP1, EP2, IP, mPGES-1, EP4, PGIS and TXAS mRNA expressions, and the DP1, EP2 and IP protein expressions significantly increased in the Al-treated hippocampus, while the EP3 and FP mRNA and protein expressions and the TP mRNA expression decreased. CONCLUSIONS: The PGS/PGs/PG receptors signaling pathway in chronic aluminium gluconate-overloaded rat hippocampus is disturbed, which may be involved in the mechanism of aluminium neurotoxicity.

Chemobrain: ¿podemos hablar de un daño cerebral adquirido por quimioterapia? / Chemobrain: can we consider an acquired brain injury from chemotherapy?

Objetivo: Conocer el deterioro cognitivo producido por la quimioterapia en una muestra de pacientes con cáncer de mama frente a los controles y frente a sí mismas, antes y después del tratamiento. Pacientes y método: Estudio de corte longitudinal prospectivo. Se administró la Mini International Neuropsychiatric Interview, se evaluó depresión, ansiedad, función sexual, calidad de vida y sueño. Se midió memoria, atención, velocidad de procesamiento, memoria de trabajo, función ejecutiva y fluidez. Tanto la muestra inicial como la final fue de 19 pacientes y 19 controles. Resultados: Las pacientes presentaron diferencias en depresión, ansiedad, calidad de vida, función sexual y calidad de sueño frente al grupo control en el momento basal y a los seis meses. Se encontraron diferencias neurocognitivas entre pacientes y controles antes del tratamiento en memoria y en función ejecutiva y después del tratamiento en memoria, función ejecutiva e índice de función prefrontal. Conclusiones: Encontramos diferencias entre pacientes y controles antes de comenzar el tratamiento, síntomas de ansiedad, depresión, calidad de vida y sueño, en función sexual y en las variables neurocognitivas de memoria y función ejecutiva. Tras la quimioterapia, se observó declive en las pacientes respecto a los controles en: ansiedad, depresión, calidad de vida, calidad de sueño y función sexual y los dominios cognitivo de atención, memoria, función ejecutiva e índice de función prefrontal (AU)

Objective: To meet the cognitive impairment caused by chemotherapy in a sample of patients with breast cancer versus controls and themselves, before and after treatment. Patients and methods: Prospective longitudinal study. The Mini International Neuropsychiatric Interview was administered and other emotional symptoms like depression, anxiety, sexual function, quality of life and sleep was assessed. Memory, attention, processing speed, working memory, executive function and flow were measured. Both the initial and the final sample were 19 patients and 19 controls. Results: Patients differ in depression, anxiety, quality of life, sexual function, and quality of sleep versus controls at baseline and 6-month. Neurocognitive differences between patients and control group were found in memory before treatment and executive function. After treatment the differences were in memory, executive function and index of prefrontal function. Conclusion: There are significant differences between patients and control group before starting treatment, symptoms of anxiety, depression, quality of life and sleep, sexual function and neurocognitive variables in memory and executive function. After chemotherapy, decline was seen in patients respect control group in: anxiety, depression, and quality of life, quality of sleep and sexual function and cognitive domains of attention, memory, executive function and index of prefrontal function (AU)

Comparison of neurodegeneration and cognitive impairment in neonatal mice exposed to propofol or isoflurane.

BACKGROUND: While previous studies have demonstrated neuronal apoptosis and associated cognitive impairment after isoflurane or propofol exposure in neonatal rodents, the effects of these two anesthetics have not been directly compared. Here, we compare and contrast the effectiveness of isoflurane and propofol to cause neurodegeneration in the developing brain and associated cognitive dysfunction. METHODS: Seven-day-old mice were used. Mice in the isoflurane treatment group received 6 h of 1.5% isoflurane, while mice in propofol treatment group received one peritoneal injection (150 mg/kg), which produced persistent anesthesia with loss of righting for at least 6 h. Mice in control groups received carrying gas or a peritoneal injection of vehicle (intralipid). At 6 h after anesthetic treatment, a subset of each group was sacrificed and examined for evidence of neurodegeneration, using plasma levels of S100ß, and apoptosis using caspase-3 immunohistochemistry in the cerebral cortex and hippocampus and Western blot assays of the cortex. In addition, biomarkers for inflammation (interleukin-1, interleukin-6, and tumor necrosis factor alpha) were examined with Western blot analyses of the cortex. In another subset of mice, learning and memory were assessed 32 days after the anesthetic exposures using the Morris water maze. RESULTS: Isoflurane significantly increased plasma S100ß levels compared to controls and propofol. Both isoflurane and propofol significantly increased caspase-3 levels in the cortex and hippocampus, though isoflurane was significantly more potent than propofol. However, there were no significant differences in the inflammatory biomarkers in the cortex or in subsequent learning and memory between the experimental groups. CONCLUSION: Both isoflurane and propofol caused significant apoptosis in the mouse developing brain, with isoflurane being more potent. Isoflurane significantly increased levels of the plasma neurodegenerative biomarker, S100ß. However, these neurodegenerative effects of isoflurane and propofol in the developing brain were not associated with effects on inflammation or with cognitive dysfunction in later life.

Protective effects of selenium on cadmium-induced brain damage in chickens.

Selenium (Se) is an important dietary micronutrient with antioxidative roles. Cadmium (Cd), a ubiquitous environmental pollutant, is known to cause brain lesion in rats and humans. However, little is reported about the deleterious effects of subchronic Cd exposure on the brain of poultry and the protective roles on the brain by Se against Cd. The aim of this study was to investigate the protective effects of Se on Cd-induced brain damage in chickens. One hundred twenty 100-day-old chickens were randomly assigned to four groups and were fed a basal diet, or Se (as 10 mg Na2SeO3/kg dry weight of feed), Cd (as 150 mg CdCl2/kg dry weight of feed), or Cd + Se in their basic diets for 60 days. Then, concentrations of Cd and Se, production of nitric oxide (NO), messenger RNA (mRNA) level and activity of inducible NO synthase (iNOS), level of oxidative stress, and histological and ultrastructural changes of the cerebrum and cerebellum were examined. The results showed that Cd exposure significantly increased Cd accumulation, NO production, iNOS activities, iNOS mRNA level, and MDA content in the cerebrum and cerebellum. Cd treatment obviously decreased Se content and antioxidase activities and caused histopathological changes in the cerebrum and cerebellum. Se supplementation during dietary Cd obviously reduced Cd accumulation, NO production, mRNA level and activity of iNOS, oxidative stress, and histopathological damage in the cerebrum and cerebellum of chickens. It indicated that Se ameliorates Cd-induced brain damage in chickens by regulating iNOS-NO system changes, and oxidative stress induced by Cd and Se can serve as a potential therapeutic for Cd-induced brain lesion of chickens.

Cost of detecting a chronic solvent encephalopathy case by screening.

BACKGROUND: Stepwise screening of chronic solvent encephalopathy (CSE), using a postal survey followed by clinical examinations, has been shown to detect symptomatic exposed workers with an occupational disease even in industrialized countries with long-term, but relatively low dose exposure. Previous studies have suggested under-detection and late recognition of CSE, when work ability is already markedly reduced. AIMS: The aim was to estimate the cost of detecting one new CSE case by screening and diagnostics, to estimate the career extension needed to cover the cost of screening, and to study the work ability of the CSE cases. METHODS: A financial analysis of stepwise postal CSE screening followed by clinical examinations (SPC screening) was carried out, and the results were compared to those of the group of CSE cases referred to the Finnish Institute of Occupational Health (FIOH) by the existing national practice of occupational health services (OHS screening). The work ability of the SPC screened CSE cases was studied in relation to the retirement rate and the Work Ability Index (WAI). RESULTS: An analysis of the costs of detecting a new verified CSE case revealed them to be approximately 16,500 USD. Using the mean monthly wages in the fields concerned, we showed that if a worker is able to continue working for four months longer, the screening covers these costs. The cost for detecting a CSE case was twenty times higher with the existing OHS routine, when actualized according to the national guidelines. A CSE case detected at an early stage enables occupational rehabilitation or measures to decrease solvent exposure. The retirement rate of the SPC screened CSE cases was significantly lower than that of the OHS screened cases (6.7% vs. 74%). The results suggest that SPC screening detects patients at an earlier stage of the disease, when they are still capable of working. Their WAI sores were nevertheless lower than those of the general population, implying a greater risk of becoming excluded from the labor market. CONCLUSION: Stepwise screening of CSE using a postal survey followed by clinical examinations detected new CSE cases at lower costs than existing OHS screening routines. Detecting CSE at an early stage prevents early retirement.

Monkeys that voluntarily and chronically drink alcohol damage their brains: a longitudinal MRI study.

Neuroimaging has consistently documented reductions in the brain tissue of alcoholics. Inability to control comorbidity, environmental insult, and nutritional deficiency, however, confound the ability to assess whether ethanol itself is neurotoxic. Here we report monkey oral ethanol self-administration combined with MR imaging to characterize brain changes over 15 months in 18 well-nourished rhesus macaques. Significant brain volume shrinkage occurred in the cerebral cortices of monkeys drinking ≥ 3 g/kg ethanol/day (12 alcoholic drinks) at 6 months, and this persisted throughout the period of continuous access to ethanol. Correlation analyses revealed a cerebral cortical volumetric loss of ~0.11% of the intracranial vault for each daily drink (0.25 g/kg), and selective vulnerability of cortical and non-cortical brain regions. These results demonstrate for the first time a direct relation between oral ethanol intake and measures of decreased brain gray matter volume in vivo in primates. Notably, greater volume shrinkage occurred in monkeys with younger drinking onset that ultimately became heavier drinkers than monkeys with older drinking onset. The pattern of volumetric changes observed in nonhuman primates following 15 months of drinking suggests that cerebral cortical gray matter changes are the first macroscopic manifestation of chronic ethanol exposure in the brain.

Daño cerebral relacionado con el alcohol. Situación actual y llamada a la acción / Alcohol related brain damage. State of the art and a call for action

No disponible