Permanent Cognitive Impairment Research Articles

Driving restrictions post-stroke: Physicians' compliance with regulations

ABSTRACTObjective: Suffering a stroke might lead to permanent cognitive and/or physical impairment. It has been shown that these impairments could have an impact on an individual's fitness to drive. In Sweden, as in many other countries, there are regulations on driving cessation post-stroke. Information on driving cessation should be given to all patients and noted in the journal. The present study sought to determine physician's compliance to driving regulations post-stroke as well as follow-up and gender aspects.Method: A retrospective study of medical records on stroke patients was carried out. The study covered all of the medical records on stroke incidents (n = 342) during a year at a typical medium to large-sized hospital in Sweden.Results: A journal entry on driving cessation post-stroke was missing in 81% of the medical records. Only 2% of the patients were scheduled for a follow-up meeting specifically concerning fitness to drive. Significantly more men than women had an entry on driving in the journal.Conclusions: We conclude that the Swedish regulations on driving cessation post-stroke were not followed at the participating hospital. It is crucial that all stroke patients receive information on driving cessation because their condition might affect fitness to drive. Analysis of follow-up records showed that there was no consistent method for assessment of a patient's fitness to drive. There was also a gender difference in the material, which warrants further investigation.

Community reintegration postspinal cord injury: Indian scenario

Patients who suffer from spinal cord injury because of their permanent mobility and/or cognitive impairment will usually face difficulties in reentering into the community. The aim of this paper is to review the relevant architectural and attitudinal barrier, transportation difficulties in the current Indian scenario. MEDLINE®, Embase™, the Science Citation Index, and Google™ Scholar were used to look for relevant articles published in English literature. Rehabilitation should promote the full inclusion and participation of people with disabilities in the physical and psychosocial environment. The past two decades have seen a renewed interest in India to improve services for spinal injured. Although there are number of barriers to successful community reintegration in India; a holistic and empathetic approach to prioritize this issue is the need of the hour. Recent initiatives taken by the government, namely, “Sugamya Bharat Abhiyan - Accessible India” and Person with Disability Act 1995 are welcome steps in this direction.

Changes in the preferences of US physicians-in-training for medical interventions throughout medical education.

There exists a disparity between the views of physicians and the views of their patients on end-of-life decisions. However, the timing of when the end-of-life preferences of physicians and non-medically-trained individuals diverge is currently unknown. The objective of this paper is to characterise how preferences for medical interventions change throughout medical education and residency or fellowship training when confronted with scenarios of critical or terminal illness. This is a single-centre cross-sectional study that enrolled medical students at Sidney Kimmel Medical College and residents and fellows at Thomas Jefferson University Hospital. Through an online survey we determined the preferences of medical trainees for specific interventions throughout medical training when presented with different clinical scenarios. Interventions were organised into three categories: standard, intermediate and aggressive. We analysed responses to questions regarding different scenarios in separate repeated measures logistic regression models. The probability of declining medical interventions was modelled, and significant predictors of refusal of interventions were identified. Years of training was a significant predictor of declining interventions for several scenarios. When faced with permanent physical disability, increased years of training led to a higher rate of refusal of intermediate (OR = 1.14 [1.02-1.28], p = 0.02) and aggressive interventions (OR = 1.15 [1.03-1.28], p = 0.01). For the scenario of terminal illness with associated physical disability, years of training significantly influenced refusal of intermediate (OR = 1.14 [1.04-1.26], p = 0.006) and aggressive (OR = 1.20 [1.08-1.34], p = 0.001) interventions. For the scenario of permanent cognitive impairment, increased years of training led to a higher rate of refusal of standard (OR = 1.14 [1.01-1.29], p = 0.03), intermediate (OR = 1.30 [1.13-1.50], p < 0.001) and aggressive (OR = 1.38 [1.14-1.66], p = 0.001) interventions. Changes in end-of-life preferences occur throughout medical training. Years of training influenced the likelihood of declining medical interventions when faced with scenarios of terminal illness and physical or cognitive disability.

Brain atrophy and white-matter hyperintensities are not significantly associated with incidence and severity of postoperative delirium in older persons without dementia

Postoperative delirium is a common complication in older people and is associated with increased mortality, morbidity, institutionalization, and caregiver burden. Although delirium is an acute confusional state characterized by global impairments in attention and cognition, it has been implicated in permanent cognitive impairment and dementia. The pathogenesis of delirium and the mechanisms leading to these disabling consequences remain unclear. The present study is the first to address the potential predisposing role of brain morphologic changes toward postoperative delirium in a large prospective cohort of patients undergoing elective surgery using state-of-the-art magnetic resonance imaging (MRI) techniques conducted before admission. We investigated the association of MRI-derived quantitative measures of white-matter damage, global brain, and hippocampal volume with the incidence and severity of delirium. Presurgical white-matter hyperintensities (WMHs), whole brain, and hippocampal volume were measured in 146 consecutively enrolled subjects, ≥70 years old, without dementia who were undergoing elective surgery. These 3 presurgical MRI indices were tested as predictors of incidence and severity of subsequent delirium. Out of 146 subjects, 32 (22%) developed delirium. We found no statistically significant differences in WMH, whole brain, or hippocampal volume between subjects with and without delirium. Both unadjusted and adjusted (age, gender, vascular comorbidity, and general cognitive performance) regression analyses demonstrated no statistically significant association between any of the MRI measures with respect to delirium incidence or severity. In persons without dementia, preexisting cerebral WMHs, general and hippocampal atrophy may not predispose to postoperative delirium or worsen its severity.

Life after cardiac arrest: A very long term follow up

AimTo describe survival and causes of death after cardiac arrest (CA) and the life situation of very long term survivors. MethodsIndividuals with successful resuscitation treated at the Sahlgrenska university hospital during 1995–1999 and presented in former CA publications were studied. Survival time and causes of death data were extracted from the individuals who had died's records. Very long term survivors were offered a follow up visit at home. Mini Mental State Examination (MMSE) used to describe cognitive abilities and EQ-5D to assess quality of life. The life situation was also explored. Results14 out of 104 possible participants had survived to follow up. The median time to follow up among the 8 who agreed to participation was 17 years. Out of the 8 participants, 4 failed to reach the cut off score of normal cognitive abilities in the MMSE and 7/8 participants did not reach the cut off score for normal cognitive function in the MoCA.Overall the participants were content with their life situation and QoL. However, a tendency towards lower scores on the cognitive testing and a lower self-reported QoL was observed. No depression, post-traumatic stress disorder or anxiety disorder were found. ConclusionsA CA may lead to permanent cognitive impairments and the risk of dementia may be higher because of the injuries sustained during the collapse. However, further studies with more participants are needed to fully determine the risk of cognitive impairment after a CA. Regarding life situation, there was a tendency of lower QoL with lower scores on the cognitive testing. With a new treatment paradigm, there is a need for long term studies regarding this new population.

Neuropsychological performance before and after partial or complete insulectomy in patients with epilepsy

Resection of the insular cortex is becoming more frequent as it is increasingly recognized that a nonnegligible proportion of surgical candidates with drug-resistant epilepsy have an epileptogenic zone that involves the insula. In the last decades, however, the insula has been proposed to be involved in several neuropsychological functions, and there is a lack of documentation on whether partial or complete insulectomy results in permanent cognitive impairments in this clinical population. In this study, we conducted standard preoperative and postoperative neuropsychological assessments in 18 patients undergoing epilepsy surgery that included the removal of the insula in the right (n=13) or the left (n=5) hemisphere. Postoperative testing was conducted at least five months after surgery. Cognitive impairments were common and heterogeneous prior to surgery, with language and verbal memory impairments being especially frequent among patients in whom epileptic seizures originated from the left hemisphere. After surgery, declines and improvements occurred on a variety of outcomes, although new deficits were relatively infrequent among patients who had obtained normal performance at baseline. Statistical comparisons between preoperative and postoperative assessments revealed significant deterioration of only one outcome – the color naming condition of the Stroop test – which relies on oro-motor speed and lexical access. These findings suggest that partial or complete resection of the insular cortex in patients with drug-refractory epilepsy can be conducted without major permanent neuropsychological impairments in a vast majority of patients. However, small decrements in specific cognitive functions can be expected, which should also be taken into account when considering the surgical option in this clinical population.

Dementia and Cognitive Impairment Reduction after Laser Transcatheter Treatment of Alzheimer’s Disease

Reduced cerebral perfusion and microcirculation are found among AD causes, which should be considered in the development of new treatments for the disease. 165 patients with AD were examined. The examination plan included clinical assessment of dementia severity (CDR), cognitive function assessment (MMSE), laboratory examination, cerebral scintigraphy (SG), rheoencephalography (REG), cerebral CT and MRI, morphometric AD stages assessment (TDR) and cerebral multi-gated angiography (MUGA). 89 patients aged 34 - 79 (average age 67) were selected for the treatment: 31 (34.83%) male, 58 (65.17%) female patients. According to their AD stage, the patients were divided into: TDR-0 (preclinical stage)—10 (11.24%) patients, TDR-1 (early stage with mild dementia, mild cognitive impairment)—28 (31.46%) patients, TDR-2 (medium stage with moderate dementia, cognitive impairment sufficiently persistent)—34 (38.20%) patients, TDR-3 (late stage with sufficiently severe dementia and cognitive impairment)—17 (19.10%) patients. Test Group—46 (51.68%) patients—had transcatheter treatment with low-energy lasers. Control Group—43 (48.31%)—had conservative treatment with Memantin and Rivastigmine. The Test Group had cerebral microcirculation improvement leading to permanent dementia reduction and cognitive recovery which allowed transferring the patients to a lighter TDR group or withdrawing them from the scale. Control Group patients with earlier AD stages (TDR-0, TDR-1, TDR-2) obtained stabilization for a period of 6 months-3 years, with subsequent growth of dementia and cognitive impairment; patients with late AD stage (TDR-3) showed further increase of cognitive impairment and dementia. Transcatheter treatment allows reducing the effects of dyscirculatory angiopathy of Alzheimer’s type (DAAT) improving cerebral microcirculation and metabolism, which leads to permanent dementia regression and cognitive impairment reduction. These data show that AD treatment should be comprehensive and aimed at both the recovery of cerebral microcirculation and blood supply and the normalization of amyloid beta metabolism in the cerebral tissue.

Hypoglycaemia in diabetes mellitus: epidemiology and clinical implications.

Hypoglycaemia is a frequent adverse effect of treatment of diabetes mellitus with insulin and sulphonylureas. Fear of hypoglycaemia alters self-management of diabetes mellitus and prevents optimal glycaemic control. Mild (self-treated) and severe (requiring help) hypoglycaemia episodes are more common in type 1 diabetes mellitus but people with insulin-treated type 2 diabetes mellitus are also exposed to frequent hypoglycaemic events, many of which occur during sleep. Hypoglycaemia can disrupt many everyday activities such as driving, work performance and leisure pursuits. In addition to accidents and physical injury, the morbidity of hypoglycaemia involves the cardiovascular and central nervous systems. Whereas coma and seizures are well-recognized neurological sequelae of hypoglycaemia, much interest is currently focused on the potential for hypoglycaemia to cause dangerous and life-threatening cardiac complications, such as arrhythmias and myocardial ischaemia, and whether recurrent severe hypoglycaemia can cause permanent cognitive impairment or promote cognitive decline and accelerate the onset of dementia in middle-aged and elderly people with diabetes mellitus. Prevention of hypoglycaemia is an important part of diabetes mellitus management and strategies include patient education, glucose monitoring, appropriate adjustment of diet and medications in relation to everyday circumstances including physical exercise, and the application of new technologies such as real-time continuous glucose monitoring, modified insulin pumps and the artificial pancreas.

Treating inhalant abuse in adolescence: A recorded music expressive arts intervention.

Inhalant abuse is a significant public health problem that disproportionately affects adolescents (Garland, Howard, Vaughn, & Perron, 2011; Howard, Bowen, Garland, Perron, & Vaughn, 2011; Substance Abuse and Mental Health Services Administration, 2009). With an estimated one million adolescents in the United States aged 12 to 17 years (Substance Abuse and Mental Health Services Administration, 2010) and an average of 598,000 new initiates misusing inhalants each year (Substance Abuse and Mental Health Services Administration, 2008), inhalant abuse has emerged as the most widely misused substance among 12- and 13-year-olds, second to only marijuana as the most frequently abused drug among 8th graders (Johnston, O'Malley, Bachman & Schulenberg, 2005; Substance Abuse and Mental Health Services Administration, 2008; Wu, Pilowsky, & Schlenger, 2004). According to Monitoring the Future-a national survey on drug use, inhalants appear to be one of the few drugs whose prevalence has remained stable or even increased over the past decade for Americans aged 12 to 17 (Johnston et al., 2005, Johnston, O'Malley, Bachman, & Schulenberg, 2009).Inhalants and AdolescentsInhalants, or volatile substances, are a heterogeneous group of breathable chemical vapors such as organic solvents, nitrates, aerosols, and gases (e.g., fuels) that all produce psychoactive effects and potentially irreparable neurological damage when misused. Because most volatile substances are lipophilic, meaning they are absorbed by lipid-rich tissue, most notably the brain's white matter, they have rapid access to the brain and are particularly damaging to the central nervous system (Bowen, 2011).The appeal of inhalants to adolescents is likely due to a number of factors-they are widely available, easily accessible, legal to possess, and are low cost components of commonly used consumer products, such as household cleaners, aerosols, and dry erase markers. These substances also have a great abuse potential in impulsive adolescents because they have an immediate euphoric effect (Howard et al., 2011). Compared with other drugs of abuse, however, inhalants have a documented higher risk of permanent neurological damage (Lubman, Yucel, & Lawrence, 2008). The extreme neurotoxicity of volatile substances highlights that with just one misuse, inhalants can cause death or permanent neurological damage with lasting neuropsychological sequelae, from which individuals often do not recover (Dingwall & Caimey, 2011).Misuse of inhalants in early adolescence is especially deleterious because the brain is undergoing a critical stage of maturation through a process of synaptic pruning and myelination of neurons. Consequently, misuse of inhalants in adolescence may disrupt these normal developmental processes leading to potentially permanent cognitive and neuropsychological impairments. Inhalant abuse is also associated with a number of profound, potentially irreversible neuropsychological sequelae, such as suicidal ideation; psychosis; hallucinations; delusions; increased violent and aggressive behavior; impulsivity and fearlessness; elevated risk of mood, anxiety, and personality disorders; as well as dementia and organic brain syndrome (Byrne, Kirby, Zibin, & Ensminger, 1991; Freedenthal, Vaughn, Jenson, & Howard, 2007). Because the risk of devastating neurological sequelae is magnified by the preferred use of inhalants by younger teens whose brains are still developing and thus more vulnerable to the neurotoxic effects of volatile chemicals (Lubman, Yucel, & Hall, 2007; Lubman et al., 2008; Spear, 2000), it is critical to further research effective interventions to treat adolescents suffering from cognitive impairment secondary to inhalant abuse.Because inhalant abuse is well known to compromise neuropsychological functioning, learning, and memory (National Insthute on Drug Abuse, 2012a, 2012b; Takagi, Lubman, & Yucel, 2011; Yucel, Takagi, Walterfang, & Lubman, 2008), it creates unusual challenges for language-based psychotherapy, the primary modality common to most psychological treatments. …

Persistent cognitive impairment after transient ischemic attack.

By definition, the symptoms of a transient ischemic attack (TIA) subside completely within 24 hours. Imaging studies show signs of persistent ischemic tissue damage in a substantial amount of patients with TIA. Cerebral infarction can cause permanent cognitive impairment. Whether permanent cognitive impairment occurs after TIA is unclear, as is its profile. Patients with TIA aged 45 to 65 years without prior stroke or dementia underwent comprehensive neuropsychological testing within 3 months. Z scores per cognitive domain were obtained, based on the mean of a control group within the same age range. Cognitive impairment was defined as a domain z score <-1.65. Patients underwent either computed tomography or MRI brain imaging. One hundred seven patients with TIA (63% women, mean age, 56.6 years) were included and compared with 81 controls (56% women, mean age, 52.9 years). Patients performed worse on all cognitive domains except episodic memory. Working memory (25%), attention (22%), and information processing speed (16%) were most frequently impaired and more often than in the control group (age- and sex-adjusted odds ratios, respectively, 22.5 [95% confidence interval, 2.9-174.3], 6.8 [1.9-24.3], 7.1 [1.5-32.5]). More than 35% of patients with TIA had impairment of ≥1 cognitive domain. Presence of silent brain infarcts was related to worse executive functioning but did not explain the whole relationship between TIA and cognitive impairment. More than a third of patients with TIA have impairment of ≥1 cognitive domain within 3 months after their TIA. The affected domains fit in the vascular cognitive impairment profile.

The development and implementation of a nurse practitioner sepsis screening team: Impact on transfer mortality

Background: Sepsis is a potentially deadly but treatable condition that occurs as a result of the systemic manifestations of infection. Despite large healthcare expenditures, patient outcomes can be poor, and survivors may still suffer from permanent organ damage, cognitive impairment, and physical disability. Failure to recognize and implement early goal-directed therapy leads to increased mortality. A review of hospital mortality identified that sepsis among inbound transfer patients to acute care units significantly contributed to the overall hospital mortality. As part of a multipronged, multidisciplinary approach, a nurse practitioner sepsis screening team was implemented to improve early diagnosis and treatment of sepsis and decrease mortality in this high-risk population. Methods: A large academic medical facility located in the Texas Medical Center in Houston accepts a significant number of transfer patients requiring a higher level of care from other institutions. A nurse practitioner sepsis screening team was created to focus on this highly vulnerable group. A validated, electronic screening tool was utilized to screen patients and facilitate early identification and treatment of sepsis. The nurse practitioner team screened and evaluated 3,268 inbound transfer patients from 10/01/2009 to 06/30/2012. When a high suspicion for sepsis was appreciated, or another acute condition was identified, the nurse practitioner collaborated with the attending physician and initiated appropriate treatment. The data analyzed were part of an Institutional Review Board (IRB) approved prospectively collected data set. The data were collected over a 57 month period spanning from 09/30/2007 through 06/30/2012 on all inbound transfer patients to the facility, which include pre-screening baseline statistics. Basic demographics including the patient’s age, gender, and race were collected. The outcome variable was status at discharge from the facility (alive or dead). After verifying assumptions of the chi-square test were met, a Pearson’s chi-square was run against the data set. All data were analyzed using IBM Corp. Released 2012. IBM SPSS Statistics for Windows, Version 21.0. Armonk, NY: IBM Corp. Results: There was a significant association between inbound transfer patients who were evaluated upon arrival at this institution by the nurse practitioner sepsis screening team and mortality in this population regardless of their diagnoses (χ 2 (1) 115.04, p &lt; .001). A patient not screened by the team was more likely to die during the hospitalization than a transfer patient that was screened. Conclusion: In this institution, the development and implementation of a nurse practitioner sepsis screening team has contributed to reducing mortality among the inbound acute care patient transfer population regardless of diagnoses. Further investigation is needed to understand the exact mechanisms that have contributed to this outcome.

PKC in developmental hypothyroid rat brain

Thyroid hormone (TH) is essential for the proper development of mammalian central nervous system. TH deficiency during the critical period of brain development results in permanent cognitive and neurological impairments. Members of the protein kinase C (PKC) family play a key role in the regulation of cellular functions in the nervous system. Alteration of PKC can be involved in the pathogenesis of neuronal disorders. This review details recent progress made in determining the roles played by PKC isoforms in developing hypothyroid rat brain. Evidence indicates that hippocampus down-regulation of PKCβ and PKCγ may be related to impaired learning and memory observed in perinatal hypothyroid rats. Enhanced PKCα activity in neonatal hypothyroid brain may bring about oxidative stress and cause brain damage. The activated pro-apoptotic PKCs including PKCδ can cause extensive apoptosis in the hypothyroid rat brain.

Prevalence of iron deficiency anaemia in anaemic under-5 children in Enugu South East Nigeria

Background: Iron deficiency anaemia has been described as the commonest type of nutritional anaemia in infancy and childhood. The associated adverse health sequelae include permanent behavioural and cognitive impairments. Early detection and prompt treatment are necessary to prevent these complications.Aim: To determine the prevalence and socio-demographic distribution of iron deficiency anaemia among anaemic under five children in Enugu.Subjects and methods: Under-five children presenting at a tertiary hospital were consecutively enrolled and screened for iron deficiency anaemia using haematocrit and serum ferritin levels. Iron deficiency anaemia was defined as haematocrit level &lt;30% and ferritin level &lt;12ng/ml.Results: Three hundred and twelve children (187 males, 125 females) aged below 60 months had a PCV check out of which 178 (57.1%) were anaemic (PCV&lt; 30%). Of the anaemic group, 61(34.3%) had iron deficiency anaemia. Prevalence of iron deficiency anaemia was higher among the males (38.0%) [p=0.235], age group 13- 23months (40.0%) [p=0.575] and children from lower socioeconomic class (43.5%)[p=0.158]. There is a positive but weak correlation between serum ferritin and haematocrit levels [r= 0.11 p=0.130].Conclusion: The prevalence of iron deficiency anaemia in the study population was high and varies with the child’s age group, gender and parental socioeconomic class.Keywords: iron deficiency anaemia, serum ferritin, haemtocrit, Enugu.

Miswiring the brain: Δ9-tetrahydrocannabinol disrupts cortical development by inducing an SCG10/stathmin-2 degradation pathway.

Children exposed in utero to cannabis present permanent neurobehavioral and cognitive impairments. Psychoactive constituents from Cannabis spp., particularly Δ(9)-tetrahydrocannabinol (THC), bind to cannabinoid receptors in the fetal brain. However, it is unknown whether THC can trigger a cannabinoid receptor-driven molecular cascade to disrupt neuronal specification. Here, we show that repeated THC exposure disrupts endocannabinoid signaling, particularly the temporal dynamics of CB1 cannabinoid receptor, to rewire the fetal cortical circuitry. By interrogating the THC-sensitive neuronal proteome we identify Superior Cervical Ganglion 10 (SCG10)/stathmin-2, a microtubule-binding protein in axons, as a substrate of altered neuronal connectivity. We find SCG10 mRNA and protein reduced in the hippocampus of midgestational human cannabis-exposed fetuses, defining SCG10 as the first cannabis-driven molecular effector in the developing cerebrum. CB1 cannabinoid receptor activation recruits c-Jun N-terminal kinases to phosphorylate SCG10, promoting its rapid degradation in situ in motile axons and microtubule stabilization. Thus, THC enables ectopic formation of filopodia and alters axon morphology. These data highlight the maintenance of cytoskeletal dynamics as a molecular target for cannabis, whose imbalance can limit the computational power of neuronal circuitries in affected offspring.

Type 2 diabetes mellitus and Alzheimer's disease.

Epidemiological and biological evidences support a link between type 2 diabetes mellitus (DM2) and Alzheimer's disease (AD). Persons with diabetes have a higher incidence of cognitive decline and an increased risk of developing all types of dementia. Cognitive deficits in persons with diabetes mainly affect the areas of psychomotor efficiency, attention, learning and memory, mental flexibility and speed, and executive function. The strong epidemiological association has suggested the existence of a physiopathological link. The determinants of the accelerated cognitive decline in DM2, however, are less clear. Increased cortical and subcortical atrophy have been evidenced after controlling for diabetic vascular disease and inadequate cerebral circulation. Most recent studies have focused on the role of insulin and insulin resistance as possible links between diabetes and AD. Disturbances in brain insulin signaling mechanisms may contribute to the molecular, biochemical, and histopathological lesions in AD. Hyperglycemia itself is a risk factor for cognitive dysfunction and dementia. Hypoglycemia may also have deleterious effects on cognitive function. Recurrent symptomatic and asymptomatic hypoglycemic episodes have been suggested to cause sub-clinical brain damage, and permanent cognitive impairment. Future trials are required to clarify the mechanistic link, to address the question whether cognitive decline may be prevented by an adequate metabolic control, and to elucidate the role of drugs that may cause hypoglycemic episodes.

Clinical characteristics and outcome of children with electrical status epilepticus during slow wave sleep.

Background:Electrical status epilepticus in slow wave sleep (ESES) is a rare, age-related, self-limited disorder characterized as epilepsy with different seizure types, neuropsychological impairment in the form of global or selective regression of cognitive functions, motor impairment, and typical electroencephalographic (EEG) findings of continuous epileptic activity occupying 85% of nonrapid eye movement sleep.Aims:The aim is to examine the clinical and electrophysiological findings and treatment modalities of children with ESES and to evaluate the outcome of the disorder.Materials and Methods:Fourteen patients with a diagnosis of electrical status epilepticus during slow wave sleep and followed-up at least 2 years were included.Statistical Analysis:Pearson correlation test was used in the study.Results:Among the 14 patients, eight of them had normal mental development before ESES. Twelve of the patients mentioned cognitive impairment and decline in school performance during ESES. After ESES, seven patients had mental retardation in different severity. One of these patients was diagnosed with benign partial epilepsy of childhood with centrotemporal spikes and had normal intelligence quotient level prior to ESES. The diagnosis of ESES was made after newly occurred different seizure types in four of the patients while two of the previously known epileptic patients presented with only severe psychiatric impairment. Valproic acid and carbamazepine were the mostly frequently used drugs before the onset of ESES. After at least 2 years of follow-up, seven patients were seizure free, but still taking antiepileptic treatment. Five patients were seizure free, while two of them had ongoing seizures despite antiepileptic therapy.Conclusion:ESES should be kept in mind in children with unexplained regression or stagnation of development associated with seizures or not. Sleep EEGs should be performed for timely diagnosis, proper treatment and prevention of permanent cognitive impairment.

Long‐term evolution of neuropsychological competences in encephalopathy with status epilepticus during sleep: A variable prognosis

The aim of this study was to evaluate the long-term cognitive outcome in children with continuous spikes and waves during slow wave sleep (CSWS syndrome). We reviewed the neuropsychological tests of 25 children diagnosed with CSWS between 1987 and 2010 and with a mean follow-up of 13.5 years. Cognitive performances worsened during CSWS in virtually all patients. Seven patients (28%) with nonlesional epilepsy had a positive outcome; three patients (12%) showed persistence of motor deficit without involvement of cognitive functions; and seven patients (28%) who presented a long duration of CSWS (mean = 28.1 months) had a negative cognitive outcome. In 6 patients (24%) with structural or metabolic disorders before CSWS onset cognitive outcomes did not change; 2 patients (8%) had a negative outcome irrespective of the duration or presence of other neurologic disorders before CSWS onset. Forty-four percent of children with CSWS demonstrated permanent cognitive impairment. The long-term outcome of CSWS syndrome is variable and seems to depend on treatment response, disease duration, and underlying etiology.

Use of Evidence-based Practice in Rehabilitation Counseling: Facilitating Recovery and Community Integration for Persons with Schizophrenia

Schizophrenia is a chronic and debilitating psychiatric disorder that affects 1% of the population worldwide. Symptoms of schizophrenia can add to or take away from a person's normal range of behavior, may cause permanent cognitive impairments, and may vary greatly from one individual to another. The course of the illness is variable, precluding an accurate summary of long-term outcomes. However, many professionals still deny that stability and remission are possible. Providing hope of recovery is at the core of rehabilitation counseling. Every client with schizophrenia should be instilled with hope that he or she may become stable or experience complete remission. Through empirical research, multiple pharmacological and psychosocial evidence-based treatments have emerge for people with schizophrenia. Better clinical and vocational outcomes are associated with the use of these treatments. This paper offers a thorough explanation of schizophrenia and provides rehabilitation counselors with information about the best evidence-based practices to use when working with clients who have schizophrenia.

A clinical study of the effects of lead poisoning on the intelligence and neurobehavioral abilities of children

BackgroundLead is a heavy metal and important environmental toxicant and nerve poison that can destruction many functions of the nervous system. Lead poisoning is a medical condition caused by increased levels of lead in the body. Lead interferes with a variety of body processes and is toxic to many organs and issues, including the central nervous system. It interferes with the development of the nervous system, and is therefore particularly toxic to children, causing potentially permanent neural and cognitive impairments. In this study, we investigated the relationship between lead poisoning and the intellectual and neurobehavioral capabilities of children.MethodsThe background characteristics of the research subjects were collected by questionnaire survey. Blood lead levels were detected by differential potentiometric stripping analysis (DPSA). Intelligence was assessed using the Gesell Developmental Scale. The Achenbach Child Behavior Checklist (CBCL) was used to evaluate each child’s behavior.ResultsBlood lead levels were significantly negatively correlated with the developmental quotients of adaptive behavior, gross motor performance, fine motor performance, language development, and individual social behavior (P < 0.01). Compared with healthy children, more children with lead poisoning had abnormal behaviors, especially social withdrawal, depression, and atypical body movements, aggressions and destruction.ConclusionLead poisoning has adverse effects on the behavior and mental development of 2–4-year-old children, prescribing positive and effective precautionary measures.

The 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) pathway regulates developmental cerebral-vascular stability via prenylation-dependent signalling pathway

Spontaneous intracranial hemorrhage is a debilitating form of stroke, often leading to death or permanent cognitive impairment. Many of the causative genes and the underlying mechanisms implicated in developmental cerebral-vascular malformations are unknown. Recent in vitro and in vivo studies in mice have shown inhibition of the 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) pathway to be effective in stabilizing cranial vessels. Using a combination of pharmacological and genetic approaches to specifically inhibit the HMGCR pathway in zebrafish (Danio rerio), we demonstrate a requirement for this metabolic pathway in developmental vascular stability. Here we report that inhibition of HMGCR function perturbs cerebral-vascular stability, resulting in progressive dilation of blood vessels, followed by vessel rupture, mimicking cerebral cavernous malformation (CCM)-like lesions in humans and murine models. The hemorrhages in the brain are rescued by prior exogenous supplementation with geranylgeranyl pyrophosphate (GGPP), a 20-carbon metabolite of the HMGCR pathway, required for the membrane localization and activation of Rho GTPases. Consistent with this observation, morpholino-induced depletion of the β-subunit of geranylgeranyltransferase I (GGTase I), an enzyme that facilitates the post-translational transfer of the GGPP moiety to the C-terminus of Rho family of GTPases, mimics the cerebral hemorrhaging induced by the pharmacological and genetic ablation of HMGCR. In embryos with cerebral hemorrhage, the endothelial-specific expression of cdc42, a Rho GTPase involved in the regulation of vascular permeability, was significantly reduced. Taken together, our data reveal a metabolic contribution to the stabilization of nascent cranial vessels, requiring protein geranylgeranylation acting downstream of the HMGCR pathway.