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Brain Lesions (brain + lesion)
Kinds of Brain Lesions Selected AbstractsDeviation of Fiber Tracts in the Vicinity of Brain Lesions: Evaluation by Diffusion Tensor ImagingISRAEL JOURNAL OF CHEMISTRY, Issue 1-2 2003Yaniv Assaf Diffusion Tensor Imaging (DTI) is used to characterize the diffusion properties of deviated white matter caused by brain tumors. DTI was recently shown to be very helpful in delineating white matter both within brain lesions and surrounding them. Displacement of white matter fibers may be one of the consequences of tumor growth adjacent to white matter. The combination of white matter mapping with DTI and gray matter mapping using functional MRI, in some cases, facilitated assessment of the relation between the shifted cortical areas and the corresponding white matter tracts. We found that the fractional anisotropy extracted from DTI is increased by 38% in areas of non-edematous shifted white matter fibers. By contrast, trace apparent diffusion coefficient (ADC) values in those areas were found to be similar to contralateral side and normal control values. Analysis of the three diffusion tensor eigenvalues revealed that the increase in the fractional anisotropy is a result of two processes. The first is the increase in the diffusion parallel to the fibers,,1 (by 18%), and the second is the decrease in the diffusion perpendicular to fibers,,3 (by 34%) as compared with the contralateral side. These opposing changes cause an increase in the diffusion anisotropy but no change in the trace ADC. It is suggested that the pressure caused by the tumor may lead to an increase in white matter fiber tension, thus causing an increase in ,1. On the other hand, the same pressure causes increased fiber density per unit area, leading to a higher degree of restricted diffusion in the extracellular space and, hence, a reduction in ,3. [source] MR peri-CSF lesions and CSF oligoclonal bands in Italian multiple sclerosis patientsACTA NEUROLOGICA SCANDINAVICA, Issue 4 2009A. Pichiecchio Objectives,,, We investigated the association between brain lesion distribution and the presence of oligoclonal IgG bands (OCBs) in Italian multiple sclerosis (MS) patients. Materials and methods,,, We retrospectively selected brain magnetic resonance imaging (MRI) uniformly performed in 56 relapsing patients (41 patients OCB positive). Results,,, Brain lesions in periventricular areas occurred in 92.86% of the patients (100% OCB+ and 73.33% OCB,) (P = 0.004), but we did not find a significant difference for their median volume (P = 0.553) and median number (P = 0.606) between the two groups. Parenchymal lesions occurred in 76.8% of the patients with a similar distribution (P = 1.00) and no significant difference in the median volume (P = 0.818) and number (P = 0.643) between the two groups. Conclusions,,, The present study on cohort of Italian MS patients demonstrated a lack of correlation between lesion distribution and OCBs, suggesting that B cells producing them could be localized both in meningeal niches and cerebral parenchyma. [source] Stereotactic biopsy and cytological diagnosis of solid and cystic intracranial lesionsCYTOPATHOLOGY, Issue 3 2003L. M. Collaço Cytological smears from 115 consecutive cases of stereotactic biopsies of intracranial lesions were reviewed. Ninety-five lesions were solid and 20 cystic. Material from 90 solid and 13 cystic lesions was sent both for cytological and histological examination. In 66 of the solid lesions, the cytological diagnosis was confirmed by histology (five were benign lesions and 61 malignant tumours: 56 primary brain tumours, three metastases and two lymphomas). In 24 cases with discrepant cytology and histology, the histology was inconclusive or insufficient in 14 cases, while cytology established the diagnosis of astrocytoma grade II (seven cases), metastases (two cases), gliosis (one case) and benign (four cases). Necrosis of tumour type was observed cytologically in six patients representing glioblastoma (two cases), anaplastic astrocytoma (one case), lymphoma (one case) and normal brain (two cases) histologically. Three cases reported cytologically as benign were primary brain tumour (two cases) and gliosis (one case). One smear of a glioblastoma was insufficient for cytological diagnosis. Cystic lesions were cytologically benign in 17 cases and malignant in three cases. Histology from the cyst wall confirmed the malignant diagnosis in three cases and showed tumour in six more cases, a benign process (two cases), changes induced by radiotherapy for arteriovenous malformation (one case) and insufficient material (one case). In conclusion, cytology from solid brain lesion allows an accurate diagnosis and subtyping of tumours in a majority of cases, and can thus be used to choose type of therapy. In cystic brain tumours, however, examination of the cystic fluid, is often inconclusive and a biopsy from the cyst wall should be performed if there is clinical or radiological suspicion of tumour. [source] The role of epilepsy in early language development in a child with a congenital lesion in the right hemisphereDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 11 2008C Mayor-Dubois MA Early epilepsy is known to worsen the developmental prognosis of young children with a congenital focal brain lesion, but its direct role is often very difficult to delineate from the other variables. This requires prolonged periods of follow-up with simultaneous serial electrophysiological and developmental assessments which are rarely obtained. We studied a male infant with a right prenatal infarct in the territory of the right middle cerebral artery resulting in a left spastic hemiparesis, and an epileptic disorder (infantile spasms with transient right hemihypsarrhythmia and focal seizures) from the age of 7 months until the age of 4 years. Pregnancy and delivery were normal. A dissociated delay of early language acquisition affecting mainly comprehension without any autistic features was documented. This delay was much more severe than usually expected in children with early focal lesions, and its evolution, with catch-up to normal, was correlated with the active phase of the epilepsy. We postulate that the epilepsy specifically amplified a pattern of delayed language emergence, mainly affecting lexical comprehension, reported in children with early right hemisphere damage. [source] EFNS guidelines on cognitive rehabilitation: report of an EFNS task forceEUROPEAN JOURNAL OF NEUROLOGY, Issue 9 2005Members of the Task Force on Cognitive Rehabilitation Disorders of language, spatial perception, attention, memory, calculation and praxis are a frequent consequence of acquired brain damage [in particular, stroke and traumatic brain injury (TBI)] and a major determinant of disability. The rehabilitation of aphasia and, more recently, of other cognitive disorders is an important area of neurological rehabilitation. We report here a review of the available evidence about effectiveness of cognitive rehabilitation. Given the limited number and generally low quality of randomized clinical trials (RCTs) in this area of therapeutic intervention, the Task Force considered, besides the available Cochrane reviews, evidence of lower classes which was critically analysed until a consensus was reached. In particular, we considered evidence from small group or single cases studies including an appropriate statistical evaluation of effect sizes. The general conclusion is that there is evidence to award a grade A, B or C recommendation to some forms of cognitive rehabilitation in patients with neuropsychological deficits in the post-acute stage after a focal brain lesion (stroke, TBI). These include aphasia therapy, rehabilitation of unilateral spatial neglect (ULN), attentional training in the post-acute stage after TBI, the use of electronic memory aids in memory disorders, and the treatment of apraxia with compensatory strategies. There is clearly a need for adequately designed studies in this area, which should take into account specific problems such as patient heterogeneity and treatment standardization. [source] Cortical lesions associated with transient neurological symptoms , not always a matter of cause and effectEUROPEAN JOURNAL OF NEUROLOGY, Issue 6 2003S. Kipervasser The occurrence of transient recurrent stereotypical neurological events mandates the exclusion of an underlying brain lesion. When imaging studies demonstrate the presence of a structural brain lesion, a cause and effect relationship between the two entities is assumed, and the decision for surgical intervention may then follow almost automatically. We describe five patients with transient neurological events suspected as being seizures that were referred for surgery because of an associated structural brain lesion. Video electroencephalographic recordings revealed that the events that brought these patients to neurosurgical attention were non-epileptic seizures. None of these patients underwent surgical intervention, and all were referred for behavioral therapy. Therefore, even in the presence of a confirmed brain lesion, the presenting paroxysmal events may be of a non-organic origin and should not necessarily be assumed to be caused by the concomitantly existing structural abnormality. [source] Anorexia nervosa associated with right frontal brain lesionINTERNATIONAL JOURNAL OF EATING DISORDERS, Issue 8 2007Emmanuelle Houy MD Abstract Objective: A causal association of brain lesion to the physiopathology of anorexia nervosa will be discussed. Method: The authors report the case of a female patient who developed anorexia nervosa. A cavernoma, located on the frontal side of the right sylvian, was discovered by chance after a seizure. Results: Surgical treatment of the lesion resulted in complete remission of the eating disorder at two years follow-up. Conclusion: Evidence for organic brain contribution to anorexia nervosa is strong and can be illustrated by this case report of anorexia nervosa associated with cerebral tumour. [source] Sleep Apnea, Delirium, Depressed Mood, Cognition, and ADL Ability After StrokeJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 4 2001Olov Sandberg MD OBJECTIVES: The incidence of sleep apnea and stroke increases with age. The aim of this study was to investigate the presence of sleep apnea after stroke and its relationship to delirium, depressed mood, cognitive functioning, ability to perform activities of daily living (ADLs), and psychiatric and behavior symptoms. DESIGN:Cross-sectional study. SETTING:Geriatric stroke rehabilitation unit. PARTICIPANTS:133 patients (78 women and 55 men, mean age 77.1 ± 7.7 years) consecutively admitted to a geriatric stroke rehabilitation unit. MEASUREMENTS: All patients underwent overnight respiratory sleep recordings at 23 ± 7 days (range 11 to 41 days) after suffering a stroke. The patients were assessed using the Organic Brain Syndrome Scale, Montgomery-Åsberg-Depression-Rating Scale, Mini-Mental State Examination (MMSE), and Barthel-ADL Index. Sleep apnea was defined as an apnea-hypopnea index (AHI) of 10 or more. RESULTS: The median of the AHI for the studied sample (N = 133) was 13 (range 0,79; interquartile range 6,28). Fifty-nine percent fulfilled the criteria for sleep apnea; 52% with first-ever stroke had sleep apnea. More patients with sleep apnea than without were delirious, depressed, or more ADL-dependent. Sleep apnea patients also had a higher frequency of ischemic heart disease and had more often suffered from an earlier cerebral infarction. Multivariate analysis showed that obesity, low ADL scores, ischemic heart disease, and depressed mood were independently associated with sleep apnea. Low ADL scores, apnea-related hypoxemia, body mass index ,27, and impaired vision were independently associated with delirium. The presence of sleep apnea was not associated with any specific type of stroke or location of the brain lesion. CONCLUSIONS:Sleep apnea is common in stroke patients and is associated with delirium, depressed mood, latency in reaction and in response to verbal stimuli, and impaired ADL ability. We suggest a trial investigating whether delirium, depressed mood, and ADL ability improve with nasal continuous positive airway pressure treatment of sleep apnea in stroke patients. [source] Chest physiotherapy and porencephalic brain lesions in very preterm infantsJOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 6 2001DB Knight Objective: National Women's Hospital is one of two hospitals to report a destructive brain lesion, namely encephaloclastic porencephaly (ECPE), in extremely preterm infants. It has been associated with non-cephalic presentation, early hypotension and the number of chest physiotherapy treatments in the first month. The aim of the present study was to determine the temporal relationship between ECPE and chest physiotherapy use in very low-birth weight (VLBW) infants in our unit. Methodology: Cerebral ultrasound scan reports, post-mortem reports, clinical and physiotherapy records and, if indicated, original ultrasound films were reviewed for all VLBW babies admitted between 1985 and 1998. Results: Over the 14 year period in question, 2219 babies with a birth weight , 1500 g were admitted. Encephaloclastic porencephaly was found in only the 13 previously reported babies born between 1992 and 1994. Encephaloclastic porencephaly was excluded in 1564 (70%) babies. In 621 (28%) babies who did not have late ultrasound scans, ECPE was thought to be unlikely either because the babies never had any chest physiotherapy (n = 479) or because they had chest physiotherapy but were known to be neurodevelopmentally normal on follow up (n = 142). Data were incomplete for 21 babies (0.9%). The number of chest physiotherapy treatments per baby decreased from a median of 95 prior to 1989 to 38 and the age of starting treatment increased from 5 to 8 days after 1990. The use of chest physiotherapy ceased in 1995. Conclusions: Encephaloclastic porencephaly emerged as a problem at a time when the use of chest physiotherapy had decreased. The cluster of cases seen between 1992 and 1994, although associated with the number of chest physiotherapy treatments given, began to appear because of some other factor. [source] Antineutrophil cytoplasmic antibody-associated glomerulonephritis in TaiwaneseNEPHROLOGY, Issue 5 2004PEIR-HAUR HUNG SUMMARY: Aims: This retrospective study defined the clinical features and outcome of antineutrophil cytoplasmic antibody-associated glomerulonephritis in 18 seropositive Taiwanese patients (11 male, seven female; median age 64 years; range 21,82 years) with biopsy-proven pauci-immune necrotizing crescentic glomerulonephritis. Results: Fourteen patients had a diagnosis of systemic vasculitis including 10 with microscopic polyangiitis and four with Wegener's granulomatosis; the remaining four had only glomerulonephritis. At onset, 100% of the systemic vasculitis patients had pulmonary lesions with or without haemoptysis, and 29% presented with seizure in the absence of a defined brain lesion. Median serum creatinine concentration was 362.4 µmol/L (range 61.9,857.5 µmol/L) and dialysis therapy was needed in six patients. During follow up (median 16.5 months; range 2,72 months), treatment included cyclophosphamide and corticosteroids (n = 8) or corticosteroids alone (n = 7). In some patients, treatment improved (n = 4) or stabilized (n = 4) renal function. But chronic dialysis was needed in the other 10 patients. Follow-up death occurred because of sepsis (n = 3) and haemorrhage (n = 2). Patient survival rates were 78% (1 year) and 72% (5 years). Renal survival rates were 56 and 39% at 1 and 5 years, respectively. Of the candidate clinical and pathological parameters, chronic glomerular lesions in renal biopsy were the only determinant of poor renal outcome (P = 0.006). Conclusion: Antineutrophil cytoplasmic antibody-associated glomerulonephritis should be considered in nephritic patients with extrarenal manifestations, especially pulmonary infiltrate, unexplained seizure, and fever of an unknown origin in Taiwanese patients. Renal biopsy should be performed before initiating immunosuppressive therapy because the most common cause of mortality was sepsis. [source] Prediction for developmental delay on Neonatal Oral Motor Assessment Scale in preterm infants without brain lesionPEDIATRICS INTERNATIONAL, Issue 1 2010Sen-Wei Tsai Abstract Background:, Preterm infants often have difficulty in achieving a coordinated sucking pattern. To analyze the correlation between preterm infants with disorganized sucking and future development, weekly studies were performed of 27 preterm infants from initiation of bottle feeding until a normal sucking pattern was recognized. Methods:, A total of 27 preterm infants without brain lesion participated in the present study. Neonatal Oral Motor Assessment Scale (NOMAS) was utilized to evaluate the sucking pattern. Infants who were initially assessed as having disorganized sucking on NOMAS and regained a normal sucking pattern by 37 weeks old were assigned to group I; infants with a persistent disorganized sucking pattern after 37 weeks were assigned to group II. The mental (MDI) and psychomotor (PDI) developmental indices of Bayley Scales of Infant Development, second edition were used for follow-up tests to demonstrate neurodevelopment at 6 months and 12 months of corrected age. Results:, At 6 months follow up, subjects in group I had a significantly higher PDI score than group II infants (P= 0.04). At 12 months follow up, group I subjects had a significantly higher score on MDI (P= 0.03) and PDI (P= 0.04). There was also a higher rate for development delay in group II at 6 months (P= 0.05). Conclusion:, NOMAS-based assessment for neonatal feeding performance could be a helpful tool to predict neurodevelopmental outcome at 6 and 12 months. Close follow up and early intervention may be necessary for infants who present with a disorganized sucking pattern after 37 weeks post-conceptional age. [source] The Present State of Charles Bonnet SyndromePSYCHOGERIATRICS, Issue 1 2002Takeshi Terao Abstract: This review attempts to integrate the present, somewhat confusing, state of the research on Charles Bonnet syndrome (CBS). After a brief introduction giving the history of CBS and its diagnostic criteria, relevant case reports and studies are reviewed. As a result of this review, it is revealed that CBS may have heterogenous causes: peripheral (visual impairment), central (organic brain lesion), and both. The neuroimaging findings on CBS are inconsistent, but in the pharmacotherapy for CBS, it has been found that anticonvulsants may be effective, although randomized controlled studies are needed. Moreover, the time course of CBS seems to vary: remission, continuation, development into dementia, and so on. With respect to a possible association between CBS and dementia, it is suggested that clinicians follow such patients up longitudinally, because the available diagnostic criteria for CBS are almost exclusively based on cross-sectional observations. [source] Antibody-negative neuromyelitis optica with heavy B-cell infiltrationAPMIS, Issue 10 2009DANIEL BLACKBURN There are several distinct clinical phenotypes of inflammatory demyelinating diseases of the central nervous system. In classical multiple sclerosis (MS) there are varied pathological patterns, possibly with differences in pathogenesis. Neuromyelitis optica (NMO) is often associated with a specific antibody, suggesting a distinct pathogenesis. We report a case of a young Caucasian male who presented with right hemiparesis secondary to a left fronto-parietal inflammatory brain lesion, which improved over years leaving minimal deficit. Seventeen years later he re-presented with a progressive tetraparesis secondary to cervical myelitis that did not respond to treatment. The NMO antibody was not detected and neuropathological examination was unusual with evidence of a persistent B-cell inflammatory response in the cord. Although having some of the clinical features of NMO, this case presented novel clinico-pathological features that do not easily fit into current MS subtypes. [source] An ankle foot orthosis improves walking in the short-term but there is no evidence that an upper limb splint improves function, range of movement or reduces pain after a stroke or non-progressive brain lesionAUSTRALIAN OCCUPATIONAL THERAPY JOURNAL, Issue 3 2010Pip Logan No abstract is available for this article. [source] Neuroanatomical substrates of social cognition dysfunction in autismDEVELOPMENTAL DISABILITIES RESEARCH REVIEW, Issue 4 2004Kevin Pelphrey Abstract In this review article, we summarize recent progress toward understanding the neural structures and circuitry underlying dysfunctional social cognition in autism. We review selected studies from the growing literature that has used the functional neuroimaging techniques of cognitive neuroscience to map out the neuroanatomical substrates of social cognition in autism. We also draw upon functional neuroimaging studies with neurologically normal individuals and individuals with brain lesions to highlight the insights these studies offer that may help elucidate the search for the neural basis of social cognition deficits in autism. We organize this review around key brain structures that have been implicated in the social cognition deficits in autism: (1) the amygdala, (2) the superior temporal sulcus region, and (3) the fusiform gyrus. We review some of what is known about the contribution of each structure to social cognition and then review autism studies that implicate that particular structure. We conclude with a discussion of several potential future directions in the cognitive neuroscience of social deficits in autism. © 2004 Wiley-Liss, Inc. MRDD Research Reviews 2004;10:259,271. [source] Visual function in infants with brain lesions (1994)DEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 11 2008Eugenio Mercuri Another in our series of commentaries on notable papers from the DMCN archives. The full paper is available at http://www.mackeith.co.uk Pike MG, Holmstrom G, de Vries LS, Pennock JM, Drew KJ, Sonksen PM, Dubowitz LM. Patterns of visual impairment associated with lesions of the preterm infant brain. Dev Med Child Neurol 1994; 36: 849,62. [source] Development and lateralization of language in the presence of early brain lesionsDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 11 2005Karen Lidzba No abstract is available for this article. [source] Polymicrogyria in monozygous twins and an elder siblingDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 7 2003Po-Cheng Hung MD Monozygous twin births have been associated with brain lesions such as hydranencephaly, multicystic encephalomalacia, and porencephaly. Prenatal circulatory injury has been considered to be the cause. Polymicrogyria is rare but has been reported in autopsied cases. The sibship in this case report, comprising monozygotic male twins and their elder sister from the same non-consanguineous parents, all had global developmental delay. Brain MRI showed polymicrogyria. We suggest that, apart from circulatory compromise, genetic etiology must be implicated as the cause of polymicrogyria. [source] Early brain lesions and face-processing developmentDEVELOPMENTAL PSYCHOBIOLOGY, Issue 3 2005Scania de Schonen Abstract Studies of functional plasticity after pre- or perinatal brain damage can tell us whether the neural substrate normally involved in the development of a given ability is specific and, if so, when it becomes functionally specified and unique. Development of face processing was investigated in 5- to 17-year-old children who had a unilateral brain injury in the pre-, peri-, or postnatal period. In Studies 1 and 2, patients with a posterior injury involving the temporal regions exhibited a face-processing deficit that was independent of their age at test time. Even though differences were observed between the two hemispheres in face processing during infancy as well as in adults in cases of normal development, no clear differences between right and left injury were observed here in face-processing deficit. Poor postlesional face-processing plasticity seems to contrast with results of several studies on speech development after early unilateral injury. If the difference in the time window for postlesional plasticity between these two areas of competency is confirmed, it would suggest that the two kinds of abilities rely on neural cells which are sensitive to different plasticity factors. © 2005 Wiley Periodicals, Inc. Dev Psychobiol 46: 184,208, 2005. [source] Cognitive performance of male adolescents is lower than controls across psychiatric disorders: a population-based studyACTA PSYCHIATRICA SCANDINAVICA, Issue 6 2004M. Weiser Objective:, Psychiatric patients, as well as humans or experimental animals with brain lesions, often concurrently manifest behavioral deviations and subtle cognitive impairments. This study tested the hypothesis that as a group, adolescents suffering from psychiatric disorders score worse on cognitive tests compared with controls. Method:, As part of the assessment for eligibility to serve in the military, the entire, unselected population of 16,17-year old male Israelis undergo cognitive testing and screening for psychopathology by the Draft Board. We retrieved the cognitive test scores of 19 075 adolescents who were assigned any psychiatric diagnosis, and compared them with the scores of 243 507 adolescents without psychiatric diagnoses. Results:, Mean test scores of cases were significantly poorer then controls for all diagnostic groups, except for eating disorders. Effect sizes ranged from 0.3 to 1.6. Conclusion:, As group, adolescent males with psychiatric disorders manifest at least subtle impairments in cognitive functioning. [source] Aspiration biopsy cytomorphology of primary pulmonary germ cell tumor metastatic to the brainDIAGNOSTIC CYTOPATHOLOGY, Issue 10 2009Haitham Arabi M.D. Abstract Extragonadal germ cell tumors are uncommon and such tumors originating from the lung parenchyma are extremely rare. This is a case of 68-year-old female who was admitted with complaints of right-sided weakness, inability to maintain her balance, right-sided headache, and bloody sputum. Her workup revealed two enhancing brain lesions and large lung mass involving the left lower lobe. Fine-needle aspiration (FNA) of the lung followed by craniotomy was performed and the patient was initially diagnosed with lung adenocarcinoma metastatic to the brain based on the cytomorphology of the lung FNA and histology of the brain mass. However, retrospective investigation revealed markedly elevated alpha fetoprotein (AFP) of which the cytopathologist was unaware at the time of diagnosis. A review of the cytology and surgical specimen slides, as well as immunohistochemistry (IHC) on the brain tumor and FNA cell block were preformed. On the basis of the slides review, clinical findings, and immunostaining results, a diagnosis of primary pulmonary mixed germ cell tumor, containing choriocarcinoma and yolk sac elements, with brain metastases, was retrospectively made. Diagn. Cytopathol. 2009. © 2009 Wiley-Liss, Inc. [source] Role of cortical dysplasia in epileptogenesis following prolonged febrile seizureEPILEPSIA, Issue 9 2010Kyung-Il Park Summary Purpose:, Hippocampal sclerosis, characterized by prominent neuronal loss and reactive gliosis, is the most common pathology in human temporal lobe epilepsy (TLE). Although prolonged febrile convulsion (FC) is a risk factor of TLE, it is not clear whether FC provokes hippocampal sclerosis and subsequent TLE. Given that underlying brain lesions, such as cortical dysplasia (CD), in the immature brain predispose patients to FC, CD may link FC and TLE. However, the role of CD in epileptogenesis after FC is also unclear. Here, we investigated whether inborn CD increases the risk of later epilepsy induced by prolonged FC using a rat model. Methods:, Experimental CD was induced by in utero exposure of methylazoxymethanol (MAM). Rat pups from MAM-treated or control rats were then subjected to prolonged FC. We examined morphologic changes in the hippocampi with respect to neuronal loss, reactive gliosis, and synaptogenesis, and evaluated spontaneous recurrent seizures (SRS) by long-term video-EEG (electroencephalography). Results:, The MAM+FC group had a significantly lower hippocampal neuronal density in the CA1 and dentate hilus than other control groups. A robust increase in glial cells and synaptic reorganization was also detected in the MAM+FC groups. Furthermore, later SRS occurred in all rats in the MAM+FC group and in 50% and 25% of the rats in the FC-only and MAM-only group, respectively. The frequency and total duration of SRS was highest in the MAM+FC group. Discussion:, Our results suggest that preexisting CD in the immature brain augments the proepileptogenic effects of prolonged FC, leading to TLE. [source] Cognitive outcome of status epilepticus in adultsEPILEPSIA, Issue 2007Christoph Helmstaedter Summary There is no doubt that structural morphological brain lesions and malformations in epilepsy represent major etiological factors for the cognitive impairments seen in this disease. The role of epileptic activity and seizures for cognition and cognitive development, however, is less easily determined. Epileptic dysfunction ranges from interictal and periictal activity over self-terminating seizures to non-convulsive and convulsive status epilepticus, which appear the most severe conditions along this continuum. The decisive question in this regard is as to whether cognitive impairments observed in the acute epileptic condition are reversible or not. Impairments from interictal or postictal epileptic dysfunction are reversible and may interfere at most with brain maturation and cognitive development in the young patient. Seizures and ictal dysfunction in contrast, even when reversible, can leave a permanent trace which extends the phase of postictal recovery. As for status epilepticus and subsequent cognitive decline it often remains open whether the epileptic condition itself or the underlying clinical condition is causative for the aftermath. While there is evidence for both possibilities, group data from neuropsychological cross sectional and longitudinal studies indicate that more severe mental impairments, which in turn indicate more severe clinical conditions, appear to be a risk factor for sustaining status epilepticus, rather than that status epilepticus causes the cognitive decline. Reviewing the literature the cognitive condition in patients with status epilepticus varies with the type of epilepsy, the etiology of epilepsy, severity of the status, and the age of the patient. [source] Symptomatic Epilepsies Imitating Idiopathic Generalized EpilepsiesEPILEPSIA, Issue 2005Hirokazu Oguni Summary:, The diagnosis of idiopathic generalized epilepsies (IGEs) is not generally difficult if one follows the clinical and electroencephalogram (EEG) definitions of each subsyndrome that constitutes IGEs. In contrast, symptomatic epilepsies develop based on organic brain lesions and are easily diagnosed by the presence of developmental delay, neurologic abnormalities, and a characteristic seizure and EEG pattern. However, in clinical practice, it is sometimes difficult to differentiate IGEs from symptomatic epilepsies, especially when the clinical course from the onset of epilepsy is too short to exhibit typical clinical and EEG findings of either epilepsy type, or when patients with symptomatic epilepsies have atypical features that imitate the clinical characteristics of IGEs. The neurodegenerative or metabolic disorders at times start during the clinical course with epileptic seizures and later show typical neurologic abnormalities. The newly recognized metabolic disorder of glucose transporter type 1 deficiency syndrome (Glut-1 DS) may start with myoclonic seizures at an age of less than 1 year and imitate benign myoclonic epilepsy in infancy early in the clinical course. Progressive myoclonus epilepsies (PMEs) that develop at 1,4 years of age at times imitate epilepsy with myoclonic-astatic seizures with respect to the presence of astatic seizures and an epileptic encephalopathic EEG pattern. In addition, young children with focal cortical dysplasia may also have similar clinical and EEG patterns, although the latter may become localized after treatment. Approximately 15% of patients with juvenile myoclonic epilepsy (JME) are resistant to antiepileptic drugs (AEDs) and may require extensive study to make a differential diagnosis from symptomatic epilepsies. PMEs that develop during adolescence may imitate JME early in the clinical course; however, a detailed history and the differentiation between myoclonic seizures and myoclonus would help to distinguish both conditions. The diagnosis of IGEs is very demanding for patients with atypical features with regard to seizure type, EEG findings, and response to appropriate AEDs. [source] Drug Resistance in Epilepsy: Putative Neurobiologic and Clinical MechanismsEPILEPSIA, Issue 6 2005Dieter Schmidt Summary:, Drug-resistant epilepsy with uncontrolled severe seizures despite state-of-the-art medical treatment continues to be a major clinical problem for up to one in three patients with epilepsy. Although drug resistance may emerge or remit in the course of epilepsy or its treatment, in most patients, drug resistance seems to be continuous and to occur de novo. Unfortunately, current antiepileptic drugs (AEDs) do not seem to prevent or to reverse drug resistance in most patients, but add-on therapy with novel AEDs is able to exert a modest seizure reduction in as many as 50% of patients in short-term clinical trials, and a few become seizure free during the trial. It is not known why and how epilepsy becomes drug resistant, while other patients with seemingly identical seizure types can achieve seizure control with medication. Several putative mechanisms underlying drug resistance in epilepsy have been identified in recent years. Based on experimental and clinical studies, two major neurobiologic theories have been put forward: (a) removal of AEDs from the epileptogenic tissue through excessive expression of multidrug transporters, and (b) reduced drug-target sensitivity in epileptogenic brain tissue. On the clinical side, genetic and clinical features and structural brain lesions have been associated with drug resistance in epilepsy. In this article, we review the laboratory and clinical evidence to date supporting the drug-transport and the drug-target hypotheses and provide directions for future research, to define more clearly the role of these hypotheses in the clinical spectrum of drug-resistant epilepsy. [source] Visual Function in Infants with West Syndrome: Correlation with EEG PatternsEPILEPSIA, Issue 7 2004Teresa Randò Summary:,Purpose: Several studies have reported behavioral and electrophysiological evidence of visual impairment during the active stage of West syndrome. The underlying mechanisms are, however, poorly understood, and little has been reported about the correlation between visual impairment, EEG patterns, and brain lesions. The aim of the study was to assess visual function at the onset of spasm and 2 months thereafter and relate visual findings to brain lesions and EEG features. Methods: Twenty-five infants with West syndrome were enrolled and studied with (a) a full clinical assessment including a battery of tests specifically designed to assess visual function, (b) a video-polygraphic study, and (c) brain magnetic resonance imaging (MRI). Besides brain neuroimaging and EEG comparison with visual function, an intra-EEG analysis was performed to investigate the possible relation of EEG patterns to fluctuating visual behavior (fixation and following). Results: Twenty-two children had at least one abnormal result on one or more of the tests assessing visual function at T0. Visual impairment at the spasm onset was related to the sleep disorganization rather than to the hypsarrhythmic pattern in awake EEG. After 2 months, both EEG features become significantly linked to visual function. Visual function improved in several cases after 2 months, in parallel with the seizure regression. No relation was found between EEG patterns and fluctuating visual behavior. Conclusions: The study supplies new evidence of the involvement of visual function in West syndrome. The presence of abnormal visual findings in infants without lesions on brain MRI suggests that visual abnormalities are due not only to brain injury but also to epileptic disorder per se. New insight is also provided into the possible mechanisms underlying clinical and EEG abnormalities. [source] Effects of Male Vocal Learning on Female Behavior in the Budgerigar, Melopsittacus undulatusETHOLOGY, Issue 10 2005Arla G. Hile Parrots are unusual among birds and animals in general in the extent of their ability to learn new vocalizations throughout life and irrespective of season. The budgerigar (Melopsittacus undulatus), a small parrot that is well suited for laboratory studies, has been the subject of numerous studies investigating the neurobiology of vocal learning. To date, few studies have focused on the function of vocal imitation by parrots. Previous work from our research group has shown that vocal imitation in budgerigars is sex-biased, as males paired with females learn vocalizations from their new mates, but not vice versa. This bias led us to hypothesize that vocal learning has a reproductive function. To test this hypothesis, we conducted two experiments. In the first experiment, we tutored males so that they could produce a call similar to one shared by a group of experimental females. The experimental females were then presented with one of the tutored males and another, equally unfamiliar, male that had not been tutored. We found that the females spent a greater proportion of time in proximity of, and made more affiliative displays toward, the tutored males. In the second experiment, seven males received small bilateral brain lesions that disrupt vocal learning. These males and an equal number of control males were then released into an aviary containing females and reproductive resources. We found that lesioned and control males were equally successful in obtaining social mates, but females mated to lesioned males were more likely to engage in extra-pair activities. These experiments indicate that a male's ability to imitate a female's call can influence the sexual behavior of the female even though lack of imitation ability does not appear to influence social pairing. We hypothesize that mate choice in budgerigars has multiple stages. Upon meeting a strange male, a female quickly assesses its ability for social acquisition of calls by the presence or absence of a call type similar to its own in its repertoire. As courtship proceeds into pair formation, the female assesses the ability of male to learn more directly by the extent of the male's perfection of imitation. [source] A CIITA-independent pathway that promotes expression of endogenous rather than exogenous peptides in immune-privileged sitesEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 2 2004Carolina Abstract A CIITA-independent pathway of MHC class II expression has been found in the eye and the brain, both immune-privileged sites. Although corneal endothelial cells were unable to express MHC class,II in response to IFN-, alone, these cells readily expressed MHC class,II molecules via a CIITA-independent pathway when triggered by simultaneous exposure to IFN-, and TNF-,. CIITA-independent expression of MHCclass,II molecules enabled corneal endothelial cells to present cytosolic, but not endosomal, ovalbumin (OVA) to OVA-primed T,cells. To determine whether CIITA-independentexpression of MHC class,II is relevant in vivo, minor,H-only-incompatible corneal allografts prepared from CIITA knockout (KO) mice, MHC class,II KO mice or wild-type donors were placed ineyes of normal mice. Cornea allografts from wild-type and CIITA KO mice suffered similar rejection fates, whereas far fewer class,II-deficient corneas were rejected. In addition, MHC class,II-bearing macrophages were observed in cuprizone-induced inflammatory and demyelinating brain lesions of CIITA KO mice. We conclude that class,II expression via the CIITA-independent pathway enhances the vulnerability to rejection of corneal grafts expressing minor antigens. The potential relevance of CIITA-independent MHC class,II expression at immune-privileged sites is discussed in relation to tolerance to strong autoantigens. [source] Recombinant human interferon beta in relapsing,remitting multiple sclerosis: a review of the major clinical trialsEUROPEAN JOURNAL OF NEUROLOGY, Issue 4 2000M. Chofflon The beneficial effects of interferon beta (IFN-,) on disease activity in relapsing,remitting multiple sclerosis (RRMS) have been confirmed in several clinical trials. Three IFN-, products are currently available and licensed for use in RRMS at different dosages and with different routes of administration. For the prescribing physician, therefore, questions remain about the effect these differences may have on the success of therapy. This paper reviews the four large placebo-controlled clinical trials that have been conducted with IFN-, in patients with RRMS. The evidence available indicates that optimal results are likely to be achieved with the highest tolerable dosage of IFN-,. Furthermore, as inflammatory brain lesions in MS have been shown to exhibit more extensive and early axonal damage than previously suspected, early treatment may be advisable in order to delay disease progression in RRMS. [source] Induction of bilateral plasticity in sensory cortical maps by small unilateral cortical infarcts in ratsEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2003S. Reinecke Abstract Behavioural impairments caused by brain lesions show a considerable, though often incomplete, recovery. It is hypothesized that cortical and subcortical plasticity of sensory representations contribute to this recovery. In the hindpaw representation of somatosensory cortex of adult rats we investigated the effects of focal unilateral cortical lesions on remote areas. Cortical lesions with a diameter of ,,2 mm were induced in the parietal cortex by photothrombosis with the photosensitive dye Rose Bengal. Subsequently, animals were kept in standard cages for 7 days. On day seven, animals were anaesthetized and cutaneous receptive fields in the cortical hindpaw representations ipsi- and contralateral to the lesion were constructed from extracellular recordings of neurons in layer IV using glass microelectrodes. Receptive fields in the lesioned animals were compared to receptive fields measured in nonlesioned animals serving as controls. Quantitative analysis of receptive fields revealed a significant increase in size in the lesioned animals. This doubling in receptive field size was observed equally in the hemispheres ipsi- and contralateral to the lesion. The results indicate that the functional consequences of restricted cortical lesions are not limited to the area surrounding the lesion, but affect the cortical maps on the contralateral, nonlesioned hemisphere. [source] | |||||||||||||||||||||||||||||||||||||||||||