Organic Brain Injury Research Articles

Neuroimaging alterations of the suicidal brain and its relevance to practice: an updated review of MRI studies.

Suicide is a leading cause of death in the United States. Historically, scientific inquiry has focused on psychological theory. However, more recent studies have started to shed light on complex biosignatures using MRI techniques, including task-based and resting-state functional MRI, brain morphometry, and diffusion tensor imaging. Here, we review recent research across these modalities, with a focus on participants with depression and Suicidal Thoughts and Behavior (STB). A PubMed search identified 149 articles specific to our population of study, and this was further refined to rule out more diffuse pathologies such as psychotic disorders and organic brain injury and illness. This left 69 articles which are reviewed in the current study. The collated articles reviewed point to a complex impairment showing atypical functional activation in areas associated with perception of reward, social/affective stimuli, top-down control, and reward-based learning. This is broadly supported by the atypical morphometric and diffusion-weighted alterations and, most significantly, in the network-based resting-state functional connectivity data that extrapolates network functions from well validated psychological paradigms using functional MRI analysis. We see an emerging picture of cognitive dysfunction evident in task-based and resting state fMRI and network neuroscience studies, likely preceded by structural changes best demonstrated in morphometric and diffusion-weighted studies. We propose a clinically-oriented chronology of the diathesis-stress model of suicide and link other areas of research that may be useful to the practicing clinician, while helping to advance the translational study of the neurobiology of suicide.

Challenges in the Borderline Personality Disorder diagnostic in clinical practice in community: results of a pilot study

IntroductionBorderline personality disorder (BPD) has a significant presence in outpatient psychiatric practice worldwide, but data on the clinical features of patients with BPD in Russia are limited. Clinicians experience a number of difficulties in diagnosing BPD, which is also due to the high comorbidity of BPD with other mental disorders (affective, anxiety, other personality and addictive disorders).ObjectivesThe aim of this pilot study was to investigate clinical characteristics of mental health care for patients с BPD in real clinical practice in community in Saint-Petersburg, Russia.MethodsFifty patients (72% female; n=36; mean age 22.4±4.3) who were treated in an outpatient community care were included in the study. Diagnosis was made according to the ICD-10 criteria (F60.31), as it does in clinical practice in Russia. Research methods included a clinical-catamnestic method.ResultsThe age of onset of BPD symptoms was 14.9±2.7. It was found that 50% of patients had previously received inpatient (20%, n=10) and outpatient (30%, n=15) psychiatric care unrelated to the current mental condition, that is, not due to the BPD. 16% of patients (n=8) referred for the first time for psychiatric care in adolescence. The vast majority of patients (86%; n=43) were not diagnosed with BPD when they first consulted a psychiatrist. Prior to the diagnosis of BPD, patients were diagnosed with mental disorders due to organic brain injury (4%), affective disorders (44%), schizophrenia spectrum disorders (12%), anxiety disorders (20%) and other personality disorders (6%). On average, it took 7.5±4.0 years from the date of first psychiatric assessment before the diagnosis of BPD was confirmed. At the time of inclusion in the study, patients were diagnosed with the following comorbid mental health conditions: affective disorders (12%), anxiety disorders (6%), eating disorders (4%), and addictive disorders (2%).ConclusionsThe hypodiagnosis of BPD in the early stages of the disorder has been identified, making it challenging to obtain high quality mental health care in a timely manner. The frequent comorbidity between BPD and other mental disorders has been confirmed. The study demonstrates the relevance of introducing programs (including education) to improve the diagnosis and study of comorbidity of BPD in real clinical practice. The pilot study results provide the basis for a project to investigate approaches to differential diagnosis and evaluation of treatment strategies for patients with BPD.Disclosure of InterestNone Declared

Hidden Truth in Cerebral Concussion-Traumatic Axonal Injury: A Narrative Mini-Review.

This study reviewed traumatic axonal injury (TAI) in patients with concussion. Concussion refers to transient changes in the neurological function of the brain resulting from head trauma that should not involve any organic brain injury. On the other hand, TAI has been reported in autopsy studies of the human brain and histopathological studies of animal brains following concussion before the development of diffusion tensor imaging (DTI). The diagnosis of TAI in live patients with concussion is limited because of the low resolution of conventional brain magnetic resonance imaging. Since the first study by Arfanakis et al. in 2002, several hundred studies have reported TAI in patients with concussion using DTI. Furthermore, dozens of studies have demonstrated TAI using diffusion tensor tractography for various neural tracts in individual patients with concussion. Hence, DTI provides valuable data for the diagnosis of TAI in patients with concussion. Nevertheless, the confirmation of TAI in live patients with concussion can be limited because a histopathological study via a brain biopsy is required to confirm TAI. Accordingly, further studies for a diagnostic approach to TAI using DTI without a histopathological test in individual patients with concussion will be necessary in the clinical field.

Olfactory Changes After Military Deployment Are Associated With Emotional Distress but Not With Mild Traumatic Brain Injury History.

The aim of the study was to identify the impact of mild traumatic brain injury history and current emotional status on olfactory functioning. This was a cross-sectional study of 49 predominantly male, military veterans, reservists, and active duty service members with Operations Enduring Freedom, Iraqi Freedom, and New Dawn deployments and varying mild traumatic brain injury histories. Those with a positive history of mild traumatic brain injury (n = 32) endorsed significantly higher rates of self-reported olfactory disturbance. However, there were no differences between the mild traumatic brain injury and no mild traumatic brain injury groups for rates of objective odor identification dysfunction (none vs. microsmia or more severe) or overall accuracy of odor identification. In keeping with this, self-reported olfactory disturbance also failed to associate with odor identification dysfunction. In both groups, those self-reporting olfactory disturbance reported significantly greater emotional distress, severity of posttraumatic stress symptoms, and attentional impulsivity. However, self-reported olfactory disturbance was not associated with other behavioral factors frequently attributed to TBI, such as aggression, motor impulsiveness, poor planning, and cognitive flexibility. These findings indicate mild traumatic brain injury is not a risk factor for postacute microsomia among Operations Enduring Freedom, Iraqi Freedom, and New Dawn military veterans. Higher observed rates of self-reported olfactory disturbance in patients with mild traumatic brain injury may be a function of emotional distress rather than organic brain injury.

Sleep Electroencephalographic Response to Respiratory Events in Patients With Moderate Sleep Apnea-Hypopnea Syndrome.

Sleep apnea–hypopnea syndrome is a common breathing disorder that can lead to organic brain injury, prevent memory consolidation, and cause other adverse mental-related complications. Brain activity while sleeping during respiratory events is related to these dysfunctions. In this study, we analyzed variations in electroencephalography (EEG) signals before, during, and after such events. Absolute and relative powers, as well as symbolic transfer entropy (STE) of scalp EEG signals, were calculated to unveil the activity of brain regions and information interactions between them, respectively. During the respiratory events, only low-frequency power increased during rapid eye movement (REM) stage (δ-band absolute and relative power) and N1 (δ- and θ-band absolute power, δ-band relative power) sleep. But absolute power increased in low- and medium-frequency bands (δ, θ, α, and σ bands), and relative power increased mainly in the medium-frequency band (α and σ bands) during stage N2 sleep. After the respiratory events, absolute power increased in all frequency bands and sleep stages, but relative power increased in medium and high frequencies. Regarding information interactions, the β-band STE decreased during and after events. In the γ band, the intrahemispheric STE increased during events and decreased afterward. Moreover, the interhemisphere STE increased after events during REM and stage N1 sleep. The EEG changes throughout respiratory events are supporting evidence for previous EEG knowledge of the impact of sleep apnea on the brain. These findings may provide insights into the influence of the sleep apnea–hypopnea syndrome on cognitive function and neuropsychiatric defects.

Combat stress and organic brain injury: type of the dynamics of posttraumatic stress disorder

To study a role of traumatic brain injury (TBI) in the development of posttraumatic stress disorder (PTSD) in ex combatants. Eighty-seven ex combatants were studied. The duration of follow-up was 15-18 years. The diagnosis was established in accordance with ICD-10 criteria. Patients were stratified by diagnosis into main group (PTSD) and comparison group (organic brain injury with reduced symptoms of PTSD ). A psychopathological method and a battery of questionnaires and scales, including those adapted for assessment of consequences of combat trauma, were administered. Clinical presentations of both groups in posttraumatic period show the similarity and homogeneity of posttraumatic disorders in these groups. In the future, the pathogenetic role of TBI severity appears more clearly, which, depending on the severity, leads to the formation of an organic lesion of the brain or performs only a pathoplastic role, giving some features to the clinical picture of PTSD. It was found that the more severe the injury, the greater the likelihood of PTSD transition to organic brain damage. It is emphasized that PTSD treatment is a continuous, long-term, complex and graded process that includes pharmacotherapy, psychotherapy, psychosocial interventions.

Combat-related posttraumatic stress disorder: the historical evolution of concept from «irritable heart syndrome» to «psycho-organic disorder». Biological aspect

To study a role of traumatic brain injury (TBI) in the development of posttraumatic stress disorder (PTSD) in ex combatants. Eighty-seven ex combatants were studied. The duration of follow-up was 15-18 years. The diagnosis was established in accordance with ICD-10 criteria. Patients were stratified by diagnosis into main group (PTSD) and comparison group (organic brain injury with reduced symptoms of PTSD). A psychopathological method and a battery of questionnaires and scales, including those adapted for assessment of consequences of combat trauma, were administered. Clinical presentations of both groups in posttraumatic period show the similarity and homogeneity of posttraumatic disorders in these groups. In the future, the pathogenetic role of TBI severity appears more clearly, which, depending on the severity, leads to the formation of an organic lesion of the brain or performs only a pathoplastic role, giving some features to the clinical picture of PTSD. It was found that the more severe the injury, the greater the likelihood of PTSD transition to organic brain damage. It is emphasized that PTSD treatment is a continuous, long-term, complex and graded process that includes pharmacotherapy, psychopharmacotherapy, psychotherapy, psychosocial interventions.

P: 35 Hepatic Encephalopathy Is an Independent Risk Factor for the Occurrence of Infection in Cirrhotic Patients With Acute Decompensation

BACKGROUND: Hepatic encephalopathy (HE) in cirrhotic patients increases mortality with worsening of HE grade 1. Infection is important in the pathogenesis and a common reason for progression to HE and death in these patients 2. However, HE role as a predisposing factor to infection in patients with acute decompensation (AD) is not known. It's recently shown that CNS injury leads to secondary immunodeficiency, and significantly increases susceptibility to infection (Pneumonia is the commonest serious complication with stroke 3), with development of the so known CNS injury-induced immunodepression (CIDS). But those studies focused only on organic brain injuries, like stroke, TBI and SCI4. Our study aims to determine whether HE is associated with the development of new infections in cirrhotic patients with AD. METHODS: Patients were identified at two institutions (AIIMS & UCL) as part of ongoing prospective studies of AD. Culture positive Infections and severity of HE (classified by West Haven Criteria) were measured on the day of admission, and new culture positive infections were assessed for up to 28 days after admission. Organ failures were defined as CLIF-organ failure score. Cox-proportional hazard analysis was used to assess predictors of infection. RESULTS: 759 cirrhotic patients with AD were included with a median age of 45 years, and varying degrees of HE; grade 0/1 (n = 452), grade 2–4 (n = 307). On day 0, Patients classified into 4 groups; no HE no infection (n = 359), overt HE no infection (n = 222), no HE with infection (n = 93), overt HE with infection (n = 85). OFs (Liver, Renal, Brain, Coagulation, Respiratory, and Circulatory) and ACLF grades were measured on Day 0, with ACLF grade 0, 1, 2, and 3 (n = 242, 99, 206, and 212 respectively). On univariate and multivariate analyses, Overt HE (with no baseline infection) was independently predictive of new infections (1.639 and 1.608; P = 0.006, and 0.016 respectively). Furthermore, age and circulatory failure were also independent risk factors for infection (P = 0.001, and 0.017 respectively). Overall, HE was higher in non-survivors (n = 191) compared to survivors (n = 116). CONCLUSIONS: The results of this study show for the first time that, in AD patients, overt HE not only associated with higher mortality but is also an independent risk factor for infection. We also showed that Age and Circulatory failure are independent risk factors for infections. That would make them, after further studies, an indication for prophylactic antibiotics.

Language and alexithymia: Evidence for the role of the inferior frontal gyrus in acquired alexithymia

The clinical relevance of alexithymia, a condition associated with difficulties identifying and describing one's own emotion, is becoming ever more apparent. Increased rates of alexithymia are observed in multiple psychiatric conditions, and also in neurological conditions resulting from both organic and traumatic brain injury. The presence of alexithymia in these conditions predicts poorer regulation of one's emotions, decreased treatment response, and increased burden on carers. While clinically important, the aetiology of alexithymia is still a matter of debate, with several authors arguing for multiple ‘routes’ to impaired understanding of one's own emotions, which may or may not result in distinct subtypes of alexithymia. While previous studies support the role of impaired interoception (perceiving bodily states) in the development of alexithymia, the current study assessed whether acquired language impairment following traumatic brain injury, and damage to language regions, may also be associated with an increased risk of alexithymia.Within a sample of 129 participants with penetrating brain injury and 33 healthy controls, neuropsychological testing revealed that deficits in a non-emotional language task, object naming, were associated with alexithymia, specifically with difficulty identifying one's own emotions. Both region-of-interest and whole-brain lesion analyses revealed that damage to language regions in the inferior frontal gyrus was associated with the presence of both this language impairment and alexithymia. These results are consistent with a framework for acquired alexithymia that incorporates both interoceptive and language processes, and support the idea that brain injury may result in alexithymia via impairment in any one of a number of more basic processes.

Disorder of Executive Function of the Brain after Head Injury and Mild Traumatic Brain Injury - Neuroimaging and Diagnostic Criteria for Implementation of Administrative Support in Japan.

The diagnotic criteria for disorder of the executive function of the brain (DEFB) as a syndrome of sequela were administratively established (ad-DEFB) in Japan in 2006 to support disabled patients whose impairment, limited to cognition (memory, attention, execution, and behavior), emerges after organic brain injuries regardless of physical deficits. However, some patients suffering from traumatic brain injury (TBI) have been excluded from receiving medico-social services. In particular, this tendency is more prominent in patients with mild TBI because no lesions are apparent on conventional computed tomography (CT) or magnetic resonance imaging (MRI) in the chronic phase. Recent development of new MRI neuroimaging modalities and positron emission tomography (PET) imaging makes it possible to detect regions of minute organic lesions and metabolic dysfunction in the brain where organic lesions may be absent or cannot be detected on conventional CT or MRI. In this review, we discuss diagnostic criteria for mild TBI and ad-DEFB, the relationship between the two disorders, characteristic neuroimaging [(MRI and 18F-fluorodeoxyglucose-positron emission tomography (FDG-PET)] of diffuse brain injury including cerebral concussion, which is the principal cause of mild TBI, and suggested pathological mechanisms of ad-DEFB in DBI.

Acute psychosis in an adolescent with cerebral palsy

IntroductionCerebral Palsy is a movement, posture or muscle toning disorder caused by an insult to the immature, developing brain, most often before birth. It is a leading cause for serious disabilities in childhood and a risk factor for the development of psychiatric disorders, particularly in adolescents. Moreover, according to DSM-5, a Brief psychotic disorder is a short-term illness with psychotic symptoms, which arise suddenly, but last for less than one month, after which the person recovers completely.Objectives/AimsThe authors aim to present a case of an adolescent with cerebral palsy who has developed secondary psychotic symptoms, a rare and sparsely understood phenomenon.MethodsA non-systematic review of English scientific literature was conducted through research in the PubMed search engine, using the keywords “Cerebral Palsy” and “Brief Psychotic Disorder”.ResultsA 16-year-old female adolescent with history of Cerebral Palsy (due to neonatal anoxia) was admitted in the paediatric ward due to behaviour disorder characterized by incoherent speech, full insomnia, agitation and auto/alo-aggression. A complete clinical investigation was performed, in which trauma, organic brain injury, degenerative and inflammatory diseases, infection or toxic ingestion were all excluded. The hypothesis of an acute psychotic disorder was considered and after antipsychotic treatment, a total remission of the symptoms was obtained.ConclusionsAlthough rare, the association between cerebral palsy and psychotic disorders should be considered in the diagnostic investigation of behavioural changes. Early identification allows a proper therapeutic intervention and a better quality of life.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Foreign Accent Syndrome, a Rare Presentation of Schizophrenia in a 34-Year-Old African American Female: A Case Report and Literature Review.

Foreign Accent Syndrome (FAS) is a rare phenomenon where speech is characterized by a new accent to the patient's native language. More than 100 cases with the syndrome have been published, the majority of which were associated with observed insults of the speech center. Some other cases have been described without identifiable organic brain injury, especially in patients with psychiatric illness. This paper presents a patient with schizophrenia and FAS, without any evidence of organic brain injury. FAS recurred during psychotic exacerbation and did not reverse before transfer to a long-term psychiatric facility. The case is discussed in the context of a brief review of the syndrome.

Early outcomes of carotid endarterectomy without shunting in patients with complete occlusion of the contralateral internal carotid artery

Aim: Shunting in carotid endarterectomy (CEA) is a controversial issue, which remains to be clarified in patients with contralateral carotid occlusion (CCO). In our clinic, CEA is performed under general anesthesia and without shunting. The present study aimed to discuss 30-day mortality and morbidity outcomes of CEA performed without shunting on 53 CCO cases. Materials and Methods: In our clinic, 415 CEA procedures were performed on 376 patients between the years 2005 and 2013. Among these patients, 53 (39 males and 14 females) with CCO who underwent isolated CEA were included in the study. All patients were operated on without shunting and under general anesthesia. Results: Of the patients, 31 were symptomatic (mean age, 63.2 ΁ 5.1 years) and 22 were asymptomatic (mean age, 63.1 ΁ 6.7 years). One (1.9%) patient died of postoperative myocardial infarction. Another patient (1.9%) developed stroke due to intracranial hemorrhage on the postoperative 6 th day. Transient ischemic attack was observed in 2 (3.8%) patients. Eight (15.1%) patients developed ipsilateral transient peripheral nerve injury, 1 (1.9%) patient developed hoarseness, and 5 (9.4%) patients developed organic brain injury. Conclusion: It was observed that CEA without shunting could be performed with an acceptable risk ratio under general anesthesia in cases with CCO.

Of Mice and Men – or a Lack of Positive Effect of Enhanced Vegetative Nervous System Tonus on Mobilization of Hematopoietic Stem and Progenitor Cells – Results in Patients with Elevated Catecholamine Level in Peripheral Blood Suffering from Acute Psychotic and Anxiety Disorders

Background. It is well known that hematopoietic stem/progenitor cells (HSPCs) circulate under steady-state conditions at detectable levels in peripheral blood (PB), with their numbers increasing in response to stress, inflammation, and tissue and organ injury. Moreover, it has been demonstrated in mice that enhanced tonus of vegetative nervous system regulates mobilization of HSPCs into PB. Moreover, UDP-galactose:ceramide galactosyltransferase-deficient mice, which exhibit aberrant nerve conduction and do not release norepinephrine (NE) into the BM microenvironment, do not mobilize HSPCs in response to G-CSF. However, as recently reported modification of sympathetic output does not affect G-CSF-induced mobilization in humans, as would be predicted. Specifically, normal human HSPC volunteer donors who were receiving NE reuptake inhibitors (NRI) for depression or β2-blockers because of hypertension mobilize in a similar manner as normal controls (Leukemia 2013; 27:24-31). Mobilization in these patients was neither enhanced by NRI administration nor suppressed by β2-blockers, as one would expect based on murine data reported in the literature.Aim of the study. To address this intriguing issue and discrepancy between human and mice, we analyzed levels of circulating HSPCs in patients suffering from acute psychosis and anxiety disorders – clinical situations with elevated level of catecholamine in PB. Namely, these patients are under the influence of several neural mediators, and it is well known that the levels of NE and dopamine are elevated in peripheral tissues and blood.Material and Metods. Enrolled in this study were 30 unrelated individuals with a diagnosis of the first-episode psychosis and 30 patients suffering from acute anxiety disorders. The patients were compared with an ethnic- and gender-matched control group of 35 healthy volunteers without psychiatric disorders, which were excluded according to an examination by a specialist psychiatrist. Patients with a history of serious lifetime medical events, organic brain injuries, or drug/alcohol dependence were excluded from the study. Mobilization of HSPCs was evaluated by i) FACS to enumerate the number of CD34+, CD133+, CD34+CD45+Lin–, and CD133+CD45+Lin– cells circulating in PB, which are enriched for HSPCs, as well as by ii) functional in vitro assays to detect the number of CFU-GM and BFU-E clonogenic progenitors circulating in PB. In parallel we measured level of adrenaline, norepinephrine (NE) and dopamine in PB serum. Both cells and catecholamine levels were enumerated in acute psychotic and anxiety disorders patients before and after treatment and compared with age- and sex-matched controls.Results. We did not observe any significant differences in the numbers of circulating CD34+, CD133+, CD34+CD45+Lin–, and CD133+CD45+Lin– cells as well as clonogenic BFU-E and CFU-GM between normal controls and psychotic patients and patients with anxiety disorders. In particular number of circulating in PB HSPCs was not affected by increased level of adrenaline, norepinephrine and dopamine in PB of patients suffering from acute psychotic syndromes.Conclusions. Our data argue against an effect of enhanced vegetative nervous system tone on the number of HSPCs circulating in PB in humans. Our negative data performed on patients suffering from acute psychoses and anxiety disorders somewhat corroborate data reported for normal HSPC volunteer donors that were previously treated with NRI because of depression or with β2-blockers because of high blood pressure and mobilized with G-CSF (Leukemia 2013; 27:24-31). This finding suggests that there are some clear differences between rodents and humans in the effect of the vegetative nervous system on HSPCs mobilization. DisclosuresNo relevant conflicts of interest to declare.

Risk Factors for Post-Traumatic Epilepsy in Adults

Craniocerebral trauma (CCT) is the cause of 20% ofsymptomatic and 5% of all cases of epilepsy [23]. In Russia,CCT is the main cause (27.7%) of location-dependentepilepsy in adults [1, 18].Post-traumatic epilepsy (PTE) is one of the late and mostserious complications of CCT. CCT and, hence, the possiblerisk of PTE, is most common in the age range 15–34 years,where the number of cases is about 30% [30]. The mostimportant cause of CCT consists of transport accidents (most-ly traffic accidents), as well as domestic, sporting, and indus-trial accidents, as well as military injuries.Assessment of the morbidity of PTE involves use of var-ious definitions of CCT itself and PTE [17], as well as dif-ferent durations of studies. This is because the developmentof PTE requires a stably developed focus of epileptic activityresulting from organic brain injury [1, 29]. The mechanismsof epileptogenesis are tightly linked with the course of recov-ery processes after CCT or the occurrence of aberrant plas-ticity. The most important are changes in neurotransmitterprocesses, sprouting, the various mechanisms of neurondeath, changes in membrane and receptor properties, and theformation of hyperexcitable neuronal systems [19]. Whileepileptic activity during the acute phase of traumatic braininjuries results from cortical injury and the nonspecificresponse to intense physical actions (the mechanisms of pri-mary brain damage), in the later period of trauma, the harm-ful actions of free radicals and excitotoxicity due to gluta-mate accumulation (the mechanism of delayed secondarybrain damage) are probably more important [30]. An impor-tant role here is played by impairments to cellular andhumoral immunity and disintegration of the functions ofautonomic and humoral-endocrine regulation [1]. In allcases, genetic predisposition factors are of undoubted impor-tance, though they are complex and heterogeneous [17, 21].PTE should also be discriminated from post-traumaticseizures. PTE includes repeated, late (i.e., onset more thanone week after CCT) post-traumatic seizures [15, 23, 51].Post-traumatic epileptic seizures include any epilepticseizure developing as a result of CCT [21, 34, 35]. Epilepticseizures can develop at different times after CCT. In assess-ing the periods of onset of epileptic seizures, most authorsuse the Barolin et al. classification [5], initially developedfor epileptic seizures in cerebrovascular diseases. This clas-sification identifies the following types of epileptic seizures:immediate, developing within the first 24 h; early, develop-ing at 1–7 days from onset of illness; and late, starting atseven or more days.The time of onset and the frequency of development ofepileptic seizures depend on the type, location, and volumeof the focus of brain damage and the state of the premorbidbackground of the patient (presence of cerebrovascular dis-ease, repeated CCT in the history, genetic predisposition,chronic alcoholism, etc.) [1]. The incidence of early post-traumatic seizures is 3–5%, compared with an incidence of

Executive function in children with intellectual disability – the effects of sex, level and aetiology of intellectual disability

Executive function is very important in the children's overall development. The goal of this study was to assess the executive function in children with intellectual disability (ID) through the use of the Behavior Rating Inventory of Executive Function (BRIEF) teacher version. An additional goal was to examine the differences in executive function in relation to child's sex, level and aetiology of ID. The sample consisted of 90 children with ID attending two special education schools in Sarajevo, Bosnia and Herzegovina. There were 42 children with mild ID and 48 children with moderate ID. Of those, 54 were boys and 36 were girls. Children were classified into three etiological categories: 30 children with Down syndrome, 30 children with other genetic cause or organic brain injury and 30 children with unknown aetiology of ID. Special education teachers, who knew the children for at least 6 months filled the BRIEF. Children with ID had a significant deficit in executive function as measured by the BRIEF. There were no statistically significant differences in executive function in relation to the child's sex. Level of ID had a significant effect on executive function. In relation to the aetiology of ID, the only significant difference was on the Shift scale of the BRIEF. Knowing what executive function is most impaired in children with ID will help professionals design better intervention strategies. More attention needs to be given to the assessment of executive function and its subsequent intervention in the school settings.

Sleep disorders in mental diseases and their correction

The authors analyze the data available in the literature on sleep disorders and their correction in the population and in patients with mental disorders and give their experience in using zolpidem (sanval) to treat insomnia in different mental diseases. The clinical features of sleep disorders are characterized in neurotic and affective disorders, schizophrenia, and organic brain injuries. Indications for the use of sanval both alone and in combination with other psychotropic drugs (antidepressants and antipsychotics with a sedative effect) for the therapy of sleep disorders within the framework of mental disorders are discussed. Sanval is shown to be highly effective and well tolerated in 100psychiatric in- and outpatients. No dependence on this drug and withdrawal syndrome permit sanval to be used as long-term courses in patients with chronic permanent insomnia and at an old age.

Capgras Syndrome Related to Left-Hemisphere Injury

Back to table of contents Previous article Next article LettersFull AccessCapgras Syndrome Related to Left-Hemisphere InjuryJean M. Fils, M.D., and Jonathan T. Stewart, M.D.Jean M. FilsSearch for more papers by this author, M.D., and Jonathan T. StewartSearch for more papers by this author, M.D.Published Online:1 Jul 2011AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To the Editor: Capgras syndrome (CS) was first described in 19231 and is characterized by the belief that someone, often a close relative, has been replaced by an imposter. Although initially reported in schizophrenia, a substantial proportion of cases are related to neurologic pathology, noted almost invariably in the right hemisphere.2 We present a patient who developed CS in the context of a left-hemisphere traumatic brain injury (TBI).Case ReportA 72-year-old, right-handed man with no previous psychiatric or cognitive problems suffered a motorcycle accident resulting in intraparenchymal, subdural, and subarachnoid hemorrhages. He had a difficult hospitalization but ultimately returned home. Neuropsychiatric sequelae reportedly included memory and executive impairment and paranoia, the latter responding well to quetiapine. CT scan showed encephalomalacia limited to the left inferior frontal lobe.About 2 months after discharge, he was seen in our clinic. His wife reported his having discontinued his quetiapine 1 month earlier because of worries about potential side effects. Since that time, she reported paranoid ideation about neighbors stealing from him, but also episodes of his misidentifying her as someone impersonating his wife in order to steal. During these episodes, the patient would become agitated, but would generally respond to reassurance. He was oriented to person and place but not to date, and denied the episodes of misidentification. He often perseverated about his sailing experience in the Navy.Over the next 5 months, the episodes of misidentification continued; his wife ultimately agreed to a trial of risperidone, but he again quickly stopped the medication because of worries about potential side effect. At the last visit, she reported the episodes of misidentification as gradually decreasing and responding better to reassurance. She declined any further medication trials.CS has been reported frequently in neurodegenerative diseases, stroke, and TBI, and the right hemisphere has generally been implicated in its genesis.2 Our patient's injury, however, was to the left frontal lobe, and it is difficult to reconcile this with previously reported cases. Several potential explanations come to mind. Although neuroimaging showed encephalomalacia limited exclusively to the left frontal lobe, there may conceivably have been a covert right-hemisphere contre-coup injury, as well; possibly, an MRI scan would have been helpful.Alternatively, Joseph3 has hypothesized that CS and other misidentification syndromes may arise from a disconnection between right and left cortical areas that decode afferent sensory information. Finally, seizure disorders are common complications of TBI and may be associated with delusions and other psychiatric symptoms,4 although an association between CS and seizures has not been suggested. Unfortunately, no EEG was performed. Our patient's CS seemed to improve at least modestly with time; it is not clear what his course would have been with consistent antipsychotic treatment.Our understanding of the neuropathology of CS remains limited. This case suggests that CS after left hemisphere damage may occasionally occur, although potential mechanisms are elusive.James A Haley VA Hospital, University of South Florida College of Medicine, Tampa, FLCorrespondence: jonathan.[email protected]govThis work was presented at the American Neuropsychiatric Association annual meeting in Tampa, FL, March 2010.1. Capgras J , Reboul-Lachaux J : L'illusion des “sosies” dans un delire systematise chronique. Bull Soc Clin Med Ment 1923; 11:6–16Google Scholar2. Feineberg TE , Roane DM : Delusional misidentification. Psychiatr Clin North Am 2005; 28:665–683Crossref, Medline, Google Scholar3. Joseph AB : Focal central nervous system abnormalities in patients with misidentification syndromes. Bibl Psychiatry 1986; 164:68–79Medline, Google Scholar4. Fujii D , Ahmed I : Characteristics of psychotic disorder due to traumatic brain injury: an analysis of case studies in the literature. J Neuropsychiatry Clin Neurosci 2002; 14:130–140Link, Google Scholar FiguresReferencesCited byDetailsCited ByCapgras Syndrome With Left Hemisphere Neurological DamageCarlos Peña-Salazar, M.D. Pere Cendrós, M.D. Santiago Escoté, M.D. Teresa Romero, B.Sc.(Psych) Juan García-Barrionuevo, M.D. Pere Roura-Poch*, M.D., M.P.H. Francesc Arrufat, Ph.D.1 January 2014 | The Journal of Neuropsychiatry and Clinical Neurosciences, Vol. 26, No. 4Management of Auditory Hallucinations as a Sequela of Traumatic Brain InjuryAmerican Journal of Therapeutics, Vol. 21, No. 1Paranoid Personality Disorder and Organic Brain Injury: A Case ReportSøren Fryd Birkeland, M.D.1 January 2013 | The Journal of Neuropsychiatry and Clinical Neurosciences, Vol. 25, No. 1 Volume 23Issue 3 Summer 2011Pages E6-E6 Metrics This work was presented at the American Neuropsychiatric Association annual meeting in Tampa, FL, March 2010.PDF download History Published online 1 July 2011 Published in print 1 July 2011

Agressive behavior after traumatic brain injury

Introduction In cases of agitation and aggressive behavior after severe traumatic brain injury (TBI), the benefits/risks ratio of pharmacological treatments remains unclear. A qualitative analysis of clinical situations could highlight the relevance of psychotherapy care. Case report In January 2005, this 24-year-old patient sustained severe traumatic brain injury (Glasgow at 4/15), with bilateral frontotemporal injury and temporal extradural hematoma. On the third day, a temporal lobectomy was performed. The patient's evolution showed severe neurobehavioral disorders, with agitation and aggressive behavior towards family members and medical caregivers. Maximum doses of antipsychotic drugs brought no improvement. Antidepressant medication improved social contact. Several stays in the psychiatric unit, where institutionalized and psychotherapy care were implemented, showed systematically a real improvement of the behavioral disorders, increased participation in group activities and the ability to walk around alone in a closed environment. Discussion/conclusion Aggressive behavior can unveil organic brain injuries, depressive syndrome as well as iatrogenic nature of the environment. This clinical case is based on the fact that antipsychotic drugs, aside from their sedative effect, are not the proper treatment for agitation following traumatic brain injury. This case also highlights how management of behavioral disorders following TBI should not be based on pharmacological treatments only but instead should focus on multidisciplinary strategies of care.

Impaired cerebral autoregulation in primary biliary cirrhosis: implications for the pathogenesis of cognitive decline

Cognitive impairment is recognised in the early stages of primary biliary cirrhosis (PBC). To determine the mechanisms that underlie the cognitive dysfunction that can occur in early-stage PBC, with a particular focus on the role of autonomic dysfunction and altered cerebral autoregulation. Early-stage PBC patients, and age- and sex-matched controls. Brain magnetic resonance imaging to determine the relationship between structural brain abnormalities (T(2)) and cerebral vasculature responsiveness assessed using the Valsalva manoeuvre. Dynamic assessment of cerebral vascular flow using transcranial Doppler was also performed in PBC subjects to derive the pulsatility index (a marker of cerebral resistance) and the autoregulatory slope index [ASI; ratio between the cerebral blood flow velocity and blood pressure (BP)]. Cerebral resistance was increased (P=0.04), and cerebral autoregulation in response to the Valsalva was significantly impaired in the PBC group with markedly lower mean ASI values compared with the controls (7.8+/-7.0 vs -8.5+/-8.4; P=0.002). All controls had normal cerebral autoregulation compared with only 20% of the PBC group. Indicators of sympathetic failure (BP change between Valsalva phases III-IV and low-frequency heart rate variability) correlated with increasing globus pallidus (GP) T(2) values (P<0.05), beyond the effect of age. This study demonstrates the presence of increased cerebral vascular resistance and abnormal cerebral autoregulation in PBC patients, and identifies a potentially important association between the degree of abnormality in structural changes in the GP. These findings suggest that organic brain injury in PBC is directly related to autonomic dysfunction.