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Neurological Deficits (neurological + deficit)
Kinds of Neurological Deficits Selected AbstractsNEUROLOGICAL DEFICIT AS A PRESENTATION OF OCCULT METASTATIC THYROID CARCINOMAANZ JOURNAL OF SURGERY, Issue 10 2006Mark Izzard Three cases of occult metastatic thyroid carcinoma presenting with neurological deficits are reviewed. In each case the patient's initial presentation was with symptoms of neurological deficiency secondary to a spinal cord compression. All patients received a combination of surgery, external beam radiotherapy and postoperative thyroxine treatment. Two of the three patients are alive and well, able to mobilize with minor neurological dysfunction. The diagnosis and management of the patients, as well as their outcomes are reviewed, with a discussion on further management issues alongside a review of the current published work. [source] Neurological deficit after thoracic epidural catheter insertionACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 1 2009J. Antonio Aldrete No abstract is available for this article. [source] Cerebral vasospasm and ischaemic infarction in clipped and coiled intracranial aneurysm patientsEUROPEAN JOURNAL OF NEUROLOGY, Issue 4 2002M. Hohlrieder The influence of the treatment modalities (clipping/coiling) on the incidence of vasospasm and ischaemic infarction in aneurysm patients is still judged controversially. The purpose of this study was to analyse and compare retrospectively cerebral vasospasm and ischaemic infarction, as well as neurological deficits and outcome within a large population of clipped and coiled patients with ruptured and unruptured aneurysms. Within a 2-year period, a total of 144 interventions (53 clipping/91 coiling) entered the study. Daily bilateral transcranial Doppler sonographic monitoring was performed to observe vasospasm development. All cerebral computed tomography (cCT) and magnetic resonance imaging (MRI) scans were reviewed with respect to occurrence and localization of ischaemic infarctions. Focal neurological deficits were recorded and clinical outcome was evaluated using the Glasgow Outcome Scale. Statistical analysis included the use of multivariate logistic regression models to find determinants of vasospasm, ischaemic infarction and neurological deficits. Altogether, vasospasm was detected after 77 (53.5%) interventions, 61.8% in females (P < 0.01). Clipped patients significantly more often exhibited vasospasms (69.8 vs. 44.0%, P < 0.005) and were treated 1 week longer at the intensive care unit (P < 0.005). Seventy-seven patients (53.5%) developed ischaemic infarctions, 62.3% after clipping and 48.4% after coiling (P > 0.05). In the multivariate analysis, aneurysm-rupture was the strongest predictor for vasospasm and vasospasm was the strongest predictor for infarction. Neurological deficits at discharge (46.5%) were independent of treatment modality, the same applied for the mean Glasgow Outcome Scores. There was no significant difference in mortality between surgical and endovascular treatment (9.4 vs. 12.1%). Whilst the vasospasm incidence was significantly higher after surgical treatment, ischaemic infarctions were only slightly more frequent. The incidence of neurological deficits and clinical outcome was similar in both treatment groups. [source] Evaluation of predictors of mortality in Frontotemporal Dementia,methodological aspectsINTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, Issue 7 2003A. Gräsbeck Abstract Objectives To retrospectively evaluate pre-diagnostic clinical features (predictors) of mortality in frontotemporal dementia (FTD). The main aim was to investigate if there were indications against interpreting missing data as signs of absence. Material and methods 96 cases with FTD, here defined as Dementia in Pick's disease according to ICD-10. The predictors were behavioural/psychiatric features, language impairment and neurological deficits up to the date of diagnosis. Each predictor was rated as present (Yes), absent (No) or not recorded (Missing), and evaluated according to its distribution and mortality pattern: if a feature was not recorded because it was absent, the mortality of the Missing and the No-category should hypothetically be close. Statistical methods included Kaplan-Meier survival curves and Cox regression analyses. Results Neurological deficits and language impairments were frequently recorded as present or absent, while non-recordings were more prevalent among the behavioural/psychiatric features. Some features were excluded as predictors because they showed too little variation. Analyses of the survival pattern indicated that in some features, the observations of the Missing-category could be interpreted as absence of the symptoms. In other features these observations had to be regarded as truly missing. Conclusions In the retrospective evaluation of predictors of mortality a method for treating missing data was applied. The interpretation of non-recordings as signs of absence was supported by the analyses of the survival patterns in some of the studied features. However, the study underscores the importance of systematic estimations of pre-diagnostic clinical features in dementia. Copyright © 2003 John Wiley & Sons, Ltd. [source] Clinicopathological Conference: Case Report,A Case of Anorexia and Weak ArmACADEMIC EMERGENCY MEDICINE, Issue 1 2007Jennifer L. Wiler MD Abstract The authors present the case of a 49-year-old female who presented to the emergency department with a chief complaint of "not eating well." She was found to have a heart murmur, a focal neurological deficit, and large mitral valve vegetation. The patient was later diagnosed with acute Pseudomonal endocarditis with septic emboli to the brain, liver, spleen, and kidneys. A discussion of the patient presentation, diagnostic evaluation, and outcome are reviewed. [source] Acute brain injury in hypoglycaemia-induced hemiplegiaDIABETIC MEDICINE, Issue 6 2004H. Shirayama Abstract Background The development of hemiplegia as a result of hypoglycaemia was first described in 1928. However, the mechanism remains unclear. Case report We report a case of a 58-year-old male with diabetes, who developed left hemiplegia during a severe hypoglycaemic event. Results Diffusion-weighted magnetic resonance imaging detected an increased signal intensity in the pons, indicating that the patient's hemiplegia resulted from acute brain injury. Conclusions This report provides evidence that acute brain injury may be a cause of the neurological deficit. [source] Migraine and delayed ischaemic neurological deficit after subarachnoid haemorrhage in women: a case,control studyEUROPEAN JOURNAL OF NEUROLOGY, Issue 12 2007J. P. Dreier The aim of the present case,control study was to investigate the role of migraine as a potential risk factor for a delayed ischaemic neurological deficit (DIND) after subarachnoid haemorrhage (SAH). A telephone interview was performed in patients or their relatives to determine the prevalence of migraine. Thirty-six women aged <60 years had SAH with Hunt & Hess grade I,III and DIND (group A). This group was compared with an age-matched group of 36 female SAH patients, Hunt & Hess grade I,III without DIND (group B). The two populations were also characterized regarding hypertension, smoking, diabetes mellitus and alcohol use. A significant difference was only found for the prevalence of migraine with 47% in group A and 25% in group B (P < 0.05; odds ratio: 2.68, confidence interval: 0.99,7.29). Migraineurs revealed similar prevalences of risk factors independently of the presence of DINDs. This retrospective study suggests that women with migraine have a higher risk to develop a DIND than women without migraine. [source] Coma after spinal anaesthesia in a patient with an unknown intracerebral tumourACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 9 2010T. METTERLEIN Spinal anaesthesia is contraindicated in patients with elevated intracranial pressure or space-occupying intracranial lesions. Drainage of the lumbar cerebrospinal fluid (CSF) can increase the pressure gradient between the spinal, supratentorial and infratentorial compartments. This can result in rapid herniation of the brain stem or occluding hydrocephalus. We present a case of a female patient with an occult brain tumour who received a spinal anaesthesia for an orthopaedic procedure. The primary course of anaesthesia was uneventful. Several hours after surgery, the patient became increasingly disoriented and agitated. The next day, she was found comatose. A computed tomogram of the head revealed herniation of the brain stem, resulting in an occluding hydrocephalus due to a prior not known infratentorial mass. By acute relieving of the intracranial pressure by external CSF drainage, the mass was removed 2 days later. The further post-operative course was uneventful and the patient was discharged from the hospital without neurological deficit 3 weeks after the primary surgery. [source] Bilateral common carotid occlusion without neurological deficitJOURNAL OF MEDICAL IMAGING AND RADIATION ONCOLOGY, Issue 4 2002Serdar Karaköse Summary A 40-year-old man presented with pain and numbness in his right arm. On his clinical examination, no neurological deficit was found. Bilateral common carotid artery duplex sonography scan demonstrated no flow in either lumen. No abnormality was recognized on brain CT. On cerebral digital substraction angiogram, total occlusion of the brachiocephalic trunk and left carotid artery were shown. There was a modest stenosis in the left vertebral artery. Collateral circulation feeding the intracranial carotid system mainly originated from the left vertebrobasilar system. Previous cases of bilateral carotid occlusion are reviewed and discussed. [source] Magnetic Resonance Imaging Monitoring of Multiple Sclerosis Lesion EvolutionJOURNAL OF NEUROIMAGING, Issue 2005Matilde Inglese MD ABSTRACT The characteristic feature of multiple sclerosis (MS) pathology is the demyelinated plaque distributed throughout the central nervous system. Although MS is a primary demyelinating disease, acute axonal injury is common in actively demyelinating MS lesions and it is considered one of the major determinants of neurological deficit. Magnetic resonance imaging (MRI) has had a dramatic impact on MS in both the clinical practice and basic science settings. Techniques such as T2-weighted and gadolinium-enhanced T1-weighted MRI are very sensitive in detecting lesions and, thus, increase the level of certainty of MS diagnosis. Conventional MRI has also improved our understanding of the pathogenesis of the disease and has provided objective and reliable measures to monitor the effect of experimental treatments in clinical trials. However, conventional MR,I does not provide specific information on the heterogeneous pathologic substrate of MS lesions. Advanced MRI techniques, such as magnetization transfer imaging, diffusion tensor imaging, and proton MR spectroscopy, offer the unprecedented ability to observe and quantify pathological changes in lesions and normal-appearing brain tissue over time. The present review will discuss the major contributions of conventional MRI and quantitative MRI techniques to understand how individual MS lesions evolve. [source] N-MYC Downstream-Regulated Gene 1 Is Mutated In Hereditary Motor And Sensory Neuropathy-LOMJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2001L Kalaydjieva Hereditary motor and sensory neuropathies, to which Charcot-Marie-Tooth (CMT) disease belongs, are a common cause of disability in adulthood. Growing awareness that axonal loss, rather than demyelination per se, is responsible for the neurological deficit in demyelinating CMT disease has focused research on the mechanisms of early development, cell differentiation, and cell-cell interactions in the peripheral nervous system. Autosomal recessive peripheral neuropathies are relatively rare but are clinically more severe than autosomal dominant forms of CMT, and understanding their molecular basis may provide a new perspective on these mechanisms. Here we report the identification of the gene responsible for hereditary motor and sensory neuropathy-Lom (HMSNL). HMSNL shows features of Schwann-cell dysfunction and a concomitant early axonal involvement, suggesting that impaired axon-glia interactions play a major role in its pathogenesis. The gene was previously mapped to 8q24.3, where conserved disease haplotypes suggested genetic homogeneity and a single founder mutation. We have reduced the HMSNL interval to 200 kb and have characterized it by means of large-scale genomic sequencing. Sequence analysis of two genes located in the critical region identified the founder HMSNL mutation: a premature-termination codon at position 148 of the N-myc downstream-regulated gene 1 (NDRG1). NDRG1 is ubiquitously expressed and has been proposed to play a role in growth arrest and cell differentiation, possibly as a signaling protein shuttling between the cytoplasm and the nucleus. We have studied expression in peripheral nerve and have detected particularly high levels in the Schwann cell. Taken together, these findings point to NDRG1 having a role in the peripheral nervous system, possibly in the Schwann-cell signaling necessary for axonal survival. [source] Brain structural damage in spinocerebellar ataxia type 2.MOVEMENT DISORDERS, Issue 6 2008A voxel-based morphometry study Abstract Voxel-based morphometry (VBM) enables an unbiased in-vivo whole-brain quantitative analysis of differences in gray matter (GM), white matter (WM) and cerebro-spinal fluid (CSF) volumes. We assessed with VBM 20 spinocerebellar ataxia Type 2 (SCA2) patients with mild or moderate cerebellar deficit and 20 age and sex-matched healthy controls. SCA2 patients showed a significant (P < 0.05 corrected for multiple comparison) symmetric loss of GM in the cerebellar vermis and hemispheres sparing lobules I,II, Crus II,VII, and X, and of the WM in the peridentate region, middle cerebellar peduncles, dorsal pons, and cerebral peduncles. The CSF volume was increased in the posterior cranial fossa. No GM, WM or CSF volume changes were observed in the supratentorial compartment. A mild (P < 0.05, >0.01) correlation was observed between the GM and WM loss and severity of the neurological deficit. In SCA2 patients with mild to moderate cerebellar deficit, GM and WM volume loss and CSF volume increase are confined to the posterior cranial fossa. © 2008 Movement Disorder Society [source] Intraoperative hyponatremia during craniofacial surgeryPEDIATRIC ANESTHESIA, Issue 4 2009K. RANDO MD Summary Background:, Hyponatremia is an important cause of morbidity in some groups of hospitalized children. Our aim is to describe the incidence and severity of intraoperative hyponatremia in children undergoing craniofacial surgery, and determine the associated risk factors. Methods:, A descriptive retrospective study of children who underwent primary craniofacial surgery between March 1994 and February 2008 was performed. All administered fluids contained a minimum sodium concentration of 140 mmol·l,1. Hyponatremia was classified as follows: severe ,125 mmol·l,1; moderate 126,130 mmol·l,1; and, mild 131,134 mmol·l,1. Results:, Hundred and seven cases are reported. Severe, moderate and mild intraoperative hyponatremia occurred in 14 (13%), 21 (19%) and 23 (22%) children respectively. Mannitol was given to 31 (29%) children, but was not associated with the development of hyponatremia. Neither the type nor duration of surgery, type of fluid replacement nor hourly urinary output, was associated with development of hyponatremia. Most episodes of significant intraoperative hyponatremia (44%) were detected between the 2nd and the 4th hour of surgery. There were no identified neurological sequelae (e.g. coma, neurological deficit) attributable to the hyponatremia. Conclusion:, Despite strict avoidance of low sodium solutions (<140 mmol·l,1), hyponatremia occurs frequently in children undergoing craniofacial surgery in our practice; and is unrelated to the administration of mannitol. Although the mechanisms are yet to be determined, anesthesiologists should be aware of this issue and be prepared to monitor and treat this potentially serious complication. [source] Epidural abscess following epidural analgesia in pediatric patientsPEDIATRIC ANESTHESIA, Issue 9 2005YUAN-CHI LIN MD MPH Summary Epidural abscess following epidural analgesia is an unusual event especially in pediatric patients. Two patients presented with fever and local signs of infection without neurological deficit on day 4 after the initiation of epidural analgesia. Neuro-imaging studies revealed epidural abscess. Both pediatric patients were treated successfully with intravenous antibiotics. One of the patients' initial MRI was normal. However, the symptoms persisted and a followed-up scan revealed epidural abscess. The other patient presented with worsening local indurations over the epidural insertion site and positive blood culture with Hemolytic streptococcus. Our experience suggests that neuro-imaging study should be strongly considered to evaluate pediatric patients with suspicion of epidural abscess. [source] Management and outcome in prenatally diagnosed sacrococcygeal teratomasPEDIATRICS INTERNATIONAL, Issue 4 2008Tadao Okada Abstract Background: The aim of the present study was to retrospectively determine the clinical factors affecting the outcome after birth in prenatally diagnosed sacrococcygeal teratomas (SCT). Methods: Six cases of prenatal SCT were identified from January 1985 until August 2005. A retrospective review of case-notes and pathological reports was carried out. Clinical data during the perinatal period, operative findings, postoperative complications and follow up were evaluated in the patients with prenatally diagnosed SCT. Results: SCT presented as type I in two neonates and type III in four between 22 and 33 weeks' gestation. Fetal intervention was not performed for any fetus. Five of six were delivered by cesarean section and the other was delivered vaginally due to small tumor size. Patients were born at between 29 and 39 weeks' gestation and weighed from 1840 to 3500 g. All patients with type III SCT presented with related diseases, including bilateral hydronephrosis, neurological deficit of the communicating peroneal nerve such as paralytic talipes equines, bladder or bowel dysfunction, high-output cardiac failure, or fetal hydrops in one of a set of fraternal twins. A baby with high-output cardiac failure and fetal hydrops underwent urgent cesarean section at 29 weeks' gestation and died 8 days after birth despite intensive care due to multi-organ failure. In five cases, surgery was successful with good outcomes maintained at follow-up of between 8 months and 14 years. Conclusions: Detailed ultrasound should be performed to rule out associated anomalies, and determine the presence or absence of hydrops in prenatally diagnosed SCT. Fetal hydrops, orthopedic impairment such as lower extremity weakness and swelling, and urinary incontinence are important clinical factors affecting the outcome after birth in prenatally diagnosed SCT. In particular, the present study indicated that the association of a fraternal twin and fetal hydrops makes it very difficult to treat SCT perinatally. [source] Study of Japanese encephalitis and other viral encephalitis in Nepali childrenPEDIATRICS INTERNATIONAL, Issue 6 2007AJIT RAYAMAJHI Abstract Background: A hospital-based prospective cross-sectional study was conducted in children aged 1 month,14 years to identify the proportion of viral encephalitis due to Japanese encephalitis (JE) and compare the clinico-laboratory profile and outcome of JE with that of other viral encephalitis (non-JE). Methods: All probable cases of viral encephalitis on clinical and laboratory evaluation were confirmed as JE on anti-JE IgM in cerebrospinal fluid (CSF) and/or serum. Patients not having anti-JE IgM in CSF and/or serum were diagnosed as having non-JE. Results: Of 94 cases, 58 were JE and 36 non-JE. Although practice of rearing pigs at home was associated with JE (P = 0.0001), significantly higher serum creatinine, protein, aspartate aminotransferase and CSF protein levels were observed in non-JE. Longer duration of fever was associated with complete recovery in JE whereas shorter duration of fever was associated with recovery in non-JE. Risk of neurological sequelae (P = 0.01), especially hemiparesis (P = 0.03) was significantly more in JE. Sequelae were observed at 6 weeks follow up in 18.8% of JE and 13.9% of non-JE. Conclusion: JE was the most common cause of viral encephalitis in eastern Nepal and should be suspected in encephalitic patients having pig rearing at home and neurological sequelae. Although duration of hospitalization and complication were higher in JE, final outcome was similar to non-JE. Longer duration of fever in JE and shorter duration of fever in non-JE correlated with recovery, while altered sensorium and focal neurological deficit were independent predictors of sequelae at 6 weeks only in JE and not in non-JE. [source] Neuroprotective effects of Tanshinone IIA on permanent focal cerebral ischemia in mice,PHYTOTHERAPY RESEARCH, Issue 5 2009Kenan Dong Abstract The objective of this study was to evaluate whether Tanshinone IIA (TSA) was neuroprotective in permanent focal cerebral ischemia and to determine the possible mechanisms of its neuroprotection. Mice were subjected to permanent middle cerebral artery occlusion. The neuroprotection of TSA was investigated with respect to neurological deficit scores and infarct volume. Biochemical analyses for malondialdehyde (MDA) content and superoxide dismutase (SOD) activity in serum, and nitric oxide (NO) content and the inducible nitric oxide synthase (iNOS) activity in brain tissue were performed at 24 h after ischemia. Immunohistochemistry was used to measure the expression of iNOS. In vitro, the effects of TSA were tested in the cultured astrocytes exposed to hydrogen dioxide (H2O2). TSA (5, 10 and 20 mg/kg, i.p.) significantly reduced the infarct volume and improve neurological deficit. TSA also significantly increased the activity of SOD after 24 h of ischemia and decreased the MDA level, NO content, and iNOS expression. In vitro, the translocation of NF- ,B was inhibited by TSA and the survival rate of astrocytes was markedly increased and the NO production was decreased. In conclusion, these results illustrated that TSA protected the brain from ischemic injury by suppressing the oxidative stress and the radical-mediated inflammatory insult. Copyright © 2008 John Wiley & Sons, Ltd. [source] Unawareness in schizophrenia: Neuropsychological and neuroanatomical findingsPSYCHIATRY AND CLINICAL NEUROSCIENCES, Issue 5 2006LORENZO PIA phd Abstract, The lack of insight in schizophrenia has so far been interpreted as a primary symptom of the illness, namely a defensive mechanism rather than a neurologically-based condition. However, recent findings have emphasized its relationship with damage to specific brain areas as well as the domain specificity in which it may occur. This supports a neuropsychological interpretation of the lack of insight in schizophrenia. The present article reviews the foregoing data, and takes into account the most relevant anatomo-clinical results. There is evidence that the lack of insight in schizophrenia may occur as a neurological disease per se following brain damage that seems related to frontal lobe areas. Additionally, it could either be related to all aspects of the disease or be domain-specific, occurring for one kind of symptom but not for others. These data indicate several analogies with the phenomenon called anosognosia for a neurological deficit. [source] Recurrent spreading depolarizations after subarachnoid hemorrhage decreases oxygen availability in human cerebral cortexANNALS OF NEUROLOGY, Issue 5 2010Bert Bosche MD Objective Delayed ischemic neurological deficit (DIND) contributes to poor outcome in subarachnoid hemorrhage (SAH) patients. Because there is continuing uncertainty as to whether proximal cerebral artery vasospasm is the only cause of DIND, other processes should be considered. A potential candidate is cortical spreading depolarization (CSD)-induced hypoxia. We hypothesized that recurrent CSDs influence cortical oxygen availability. Methods Centers in the Cooperative Study of Brain Injury Depolarizations (COSBID) recruited 9 patients with severe SAH, who underwent open neurosurgery. We used simultaneous, colocalized recordings of electrocorticography and tissue oxygen pressure (ptiO2) in human cerebral cortex. We screened for delayed cortical infarcts by using sequential brain imaging and investigated cerebral vasospasm by angiography or time-of-flight magnetic resonance imaging. Results In a total recording time of 850 hours, 120 CSDs were found in 8 of 9 patients. Fifty-five CSDs (,46%) were found in only 2 of 9 patients, who later developed DIND. Eighty-nine (,75%) of all CSDs occurred between the 5th and 7th day after SAH, and 96 (80%) arose within temporal clusters of recurrent CSD. Clusters of CSD occurred simultaneously, with mainly biphasic CSD-associated ptiO2 responses comprising a primary hypoxic and a secondary hyperoxic phase. The frequency of CSD correlated positively with the duration of the hypoxic phase and negatively with that of the hyperoxic phase. Hypoxic phases significantly increased stepwise within CSD clusters; particularly in DIND patients, biphasic ptiO2 responses changed to monophasic ptiO2 decreases within these clusters. Monophasic hypoxic ptiO2 responses to CSD were found predominantly in DIND patients. Interpretation We attribute these clinical ptiO2 findings mainly to changes in local blood flow in the cortical microcirculation but also to augmented metabolism. Besides classical contributors like proximal cerebral vasospasm, CSD clusters may reduce O2 supply and increase O2 consumption, and thereby promote DIND. ANN NEUROL 2010;67:607,617 [source] Primary central nervous system vasculitis: analysis of 101 patientsANNALS OF NEUROLOGY, Issue 5 2007Carlo Salvarani MD Objective To analyze the clinical findings, response to therapy, outcome, and incidence of primary central nervous system vasculitis (PCNSV) in a large cohort from a single center Methods We retrospectively studied 101 patients with PCNSV, selected by predetermined diagnostic criteria, who were seen during a 21-year period. This was a collaborative study by five departments at a large multispecialty clinic. Clinical findings and outcomes were compared among patients categorized by method of diagnosis, response to therapy, survival, and degree of disability. An annual incidence rate was calculated Results Seventy patients were diagnosed by angiography and 31 by central nervous system biopsy. Three histological patterns were observed during biopsy. Although most patients responded to therapy, an increased mortality rate was observed. Relapses occurred in one fourth of patients. Mortality rate and disability at last follow-up were greater in those who presented with a focal neurological deficit, cognitive impairment, cerebral infarctions, and angiographic large-vessel involvement but were lower in those with prominent gadolinium-enhanced lesions when evaluated by magnetic resonance imaging. The annual incidence rate of PCNSV was 2.4 cases per 1,000,000 person-years Interpretation PCNSV is a rare disease that may result in serious neurological outcomes or death. Angiography and brain biopsy may complement each other when determining the diagnosis. Early recognition and treatment may reduce poor outcomes. PCNSV is a variable syndrome that appears to consist of several subsets of heterogeneous diseases. Ann Neurol 2007 [source] Symptoms associated with malignancy of peripheral nerve sheath tumours: a retrospective study of 69 patients with neurofibromatosis 1BRITISH JOURNAL OF DERMATOLOGY, Issue 1 2005L. Valeyrie-Allanore Summary Background, Neurofibromatosis 1 (NF1) is a common genetic disorder with variable clinical manifestations and an unpredictable course. Plexiform neurofibromas are common complications of NF1. Their malignant transformation is the main cause of mortality in adult patients with NF1. Objectives, To identify clinical factors associated with malignant transformation of plexiform neurofibromas. Methods, Using the database of our neurofibromatosis clinic we included in a retrospective study all patients with NF1 having at least one peripheral nerve sheath tumour for which they underwent surgery or surgical biopsy. Predictive values for malignant transformation of three clinical symptoms, i.e. pain, enlargement of mass and neurological symptoms, were evaluated in association with histological parameters. Results, Of 69 patients studied, 48 had at least one plexiform neurofibroma and 21 had a malignant peripheral nerve sheath tumour. Only enlargement of the tumour had high negative and positive predictive values for malignant transformation: 0·92 and 0·95, respectively. In multivariate analysis, tumour enlargement was independently associated with malignant transformation (odds ratio 167·8, 95% confidence interval 14·0,2012·1). Conclusions, From a practical point of view, pain, neurological deficit and enlargement of a pre-existing peripheral nerve sheath tumour in NF1 must lead to deep surgical biopsy to rule out malignant transformation. [source] Transcranial Doppler ultrasonography-directed intravenous glycoprotein IIb/IIIa receptor antagonist therapy to control transient cerebral microemboli before and after carotid endarterectomy,BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 6 2008D. van Dellen Background: Patients with a transient focal neurological deficit, critical carotid stenosis and/or microemboli detected by transcranial Doppler ultrasonography (TCD) have a significant risk of stroke. The effect of tirofiban, a selective glycoprotein IIb/IIIa inhibitor, was assessed in patients with microembolic signals on TCD after transient ischaemic attacks or carotid endarterectomy (CEA). Methods: Thirty-three patients with microemboli on TCD (13 symptomatic preoperative, 19 postoperative, one both) were treated with tirofiban between 2002 and 2007. All patients had carotid stenosis greater than 70 per cent. TCD monitoring was used during and after tirofiban therapy. Results: The median (range) rate of microemboli decreased from 22 (4,260) per h before surgery and 81 (44,216) per h after surgery to 0 (0,9) per h in both groups (P < 0·001, Mann,Whitney U test). This occurred rapidly (preoperative median 30 min; postoperative median 45 min) and was well tolerated in all patients, with no serious adverse effects. Conclusion: Cerebral microemboli were controlled by tirofiban both before and after CEA. Further study is required to compare the relative efficacy of tirofiban and dextran. Copyright © 2008 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source] Why ischemic stroke patients do not receive thrombolytic treatment: results from a general hospitalACTA NEUROLOGICA SCANDINAVICA, Issue 3 2009J. S. P. Van Den Berg Objectives,,, To determine the proportion of patients with an ischemic stroke that received intravenous (IV) thrombolytic treatment, and reasons why patients are not treated. Methods,,, A prospective registry of all patients with an ischemic stroke admitted to our emergency department (ED). Results,,, A total of 286 patients with an ischemic stroke were admitted. Eighty-one patients were admitted within 3 h of onset of neurological deficit, of which 28 received IV thrombolysis. In 25 patients no thrombolytic treatment was given because of the presence of the National Institute of Neurological Disorders and Stroke (NINDS) exclusion criteria, and one patient refused treatment. No thrombolytic treatment was given to 27 patients because of mild neurological deficit or rapid clinical improvement, and after 3 months all these patients were independently living at home without nursing help. Despite a public campaign to gain awareness concerning stroke, the majority of the patients arrived too late at the ED for thrombolytic treatment. Conclusions,,, A large proportion of the patients with an ischemic stroke are admitted too late to receive IV thrombolysis. More needs to be done to increase both public and medical awareness of stroke as a treatable emergency. [source] Vascular cognitive syndromes: relation to stroke etiology and topographyACTA NEUROLOGICA SCANDINAVICA, Issue 3 2009M. Hoffmann Background,,, Cognitive syndromes (CS) after stroke may be important to measure and monitor for management and emerging therapies. Aim,,, To describe the spectrum and frequency of CSs in the first month after stroke and to relate these to stroke etiology and topopgraphy. Methods,,, A validated cognitive examination was administered during the first month of stroke presentation and analyzed according to five large-scale networks for cognition and correlated with neuropsychological tests. A multivariate analysis was performed to determine association of CSs with etiology (TOAST classification), topography and neurological deficit by National Institute of Health Stroke Score (NIHSS). Results,,, Of a total of 2105 patients, one or more patients with CS was present in 1569/1796 (87%) stroke patients vs 112/309 (36%, P , 0.001) transient ischemic attack (TIA) patients. The frequency of frontal network syndromes (FNS) was 908/1796 (51%), left hemisphere network (LH) syndromes 646/1796 (36%), right hemisphere (RH) network syndromes 275/1796 (15.3%), occipitotemporal network (OT) syndromes 107/1796 (6%), hippocampal limbic (HL) network syndromes 397/1796 (22%) and miscellaneous (M) syndromes 481/1796 (27%). Stroke etiology and their signature CS by multivariate analyses revealed significant associations for LH with cardioembolism (OR 1.61, P = 0.0029), FNS and ,other' etiology (OR 1.96, P , 0.0001) and HL also for ,other' etiology (OR 1.57, P = 0.0026). Coma (OR 2.95, P , 0.0001) and encephalopathy (OR 2.82, P , 0.0001) were both associated significantly with hemorrhage. A left hemisphere lesion was associated with LH CSs (OR 9.26, P , 0.0001). An FNS was associated with frontal lesions (OR 5.19, <0.0001) as well as subcortical lesions (OR 1.91, P , 0.0001). The M group of CS was associated with subtentorial (OR 1.86, P = 0.0283) and right hemisphere lesions (OR 2.47, P , 0.0001). The LH and RH syndromes had the highest NIHSS and differed significantly from all others. Conclusions,,, (1) CSs are present in the vast majority of stroke patients. (2) Particular stroke etiological subtypes are associated with specific CS. (3) Certain signature CS results from lesions that relate to the major anatomical cognitive networks. [source] Investigation Of AM-36: A Novel Neuroprotective AgentCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 11 2001Jk Callaway SUMMARY 1. The neurochemical sequelae following cerebral ischaemia are complex, involving excess release of excitatory amino acids, particularly glutamate, disruption of ionic homeostasis due to Na+ and Ca2+ influx and generation of toxic free radicals, ultimately leading to cell death by both necrosis and apoptosis. 2. Drugs that block components of this biochemical cascade, such as glutamate receptor antagonists, sodium channel blockers and free radical scavengers, have been investigated as putative neuroprotective agents. The knowledge that multiple mechanisms contribute to neuronal injury in ischaemia have led to the general recognition that a single drug treatment is unlikely to be beneficial in the treatment of cerebral ischaemia. 3. AM-36 [1-(2-(4-chlorophenyl)-2-hydroxy)ethyl-4-(3,5-bis(1,1-dimethyl)-4-hydroxyphenyl)methylpiperazine] is one of a series of hybrid molecules designed to incorporate multiple neuroprotective mechanisms within the one structure. Primary screening tests demonstrated that AM-36 inhibited binding to the polyamine site of glutamate receptors, blocked neuronal sodium channels and had potent anti-oxidant activity. In neuronal cell cultures, AM-36 inhibited toxicity induced by N -methyl- D -aspartate (NMDA) and the sodium channel opener veratridine and, in addition, inhibited veratridine-induced apoptosis. 4. In a middle cerebral artery occlusion model of stroke in conscious rats, systemic administration of AM-36 markedly reduced both cortical and striatal infarct volume and significantly improved functional outcome in motor performance, neurological deficit and sensorimotor neglect tests. AM-36 was neuroprotective even when administration was delayed until 3 h systemically, or 5 h intravenously, after induction of stroke. 5. These studies indicate that AM-36 is a unique neuroprotective agent with multiple modes of action, making it an attractive candidate for the treatment of acute stroke in humans. [source] Spondylodiscitis due to Propionibacterium acnes: report of twenty-nine cases and a review of the literatureCLINICAL MICROBIOLOGY AND INFECTION, Issue 4 2010I. Uçkay Clin Microbiol Infect 2010; 16: 353,358 Abstract Propionibacterium acnes is the most frequent anaerobic pathogen found in spondylodiscitis. A documented case required microbiological proof of P. acnes with clinical and radiological confirmation of inflammation in a localized region of the spine. Microbiological samplings were obtained by surgery or aspiration under radiological control. Twelve males and 17 females (median age, 42 years) with spondylodiscitis due to P. acnes were diagnosed within the last 15 years. Three patients were immunosuppressed. All patients reported back pain as the main symptom, and most were afebrile. Three patients had a peripheral neurological deficit, one a motor deficit, and two a sensory deficit attributable to the infection; and six patients had an epidural abscess. The most frequent risk factor was surgery, which was present in the history 28 of 29 (97%) patients. The mean delay between spinal surgery and onset of disease was 34 months, with a wide range of 0,156 months. Osteosynthesis material was present in twenty-two cases (76%). In 24 (83%) patients, additional surgery, such as débridement or spondylodesis, was performed. Previous osteosynthesis material was removed in 17 of the 22 (77%) patients where it was present. Total cure was reported in all patients, except one, after a mean duration of antibiotic therapy of 10.5 weeks (range, 2,28 weeks). In conclusion, spondylodiscitis due to P. acnes is an acute infection closely related to previous surgery. The most prominent clinical feature is pain, whereas fever is rare, and the prognosis is very good. [source] Activity-based restorative therapies: Concepts and applications in spinal cord injury-related neurorehabilitationDEVELOPMENTAL DISABILITIES RESEARCH REVIEW, Issue 2 2009Cristina L. Sadowsky Abstract Physical rehabilitation following spinal cord injury-related paralysis has traditionally focused on teaching compensatory techniques, thus enabling the individual to achieve day-to-day function despite significant neurological deficits. But the concept of an irreparable central nervous system (CNS) is slowly being replaced with evidence related to CNS plasticity, repair, and regeneration, all related to persistently maintaining appropriate levels of neurological activity both below and above the area where the damage occurred. It is now possible to envision functional repair of the nervous system by implementing rehabilitative interventions. Making the transition from "bench to bedside" requires careful analysis of existing basic science evidence, strategic focus of clinical research, and pragmatic implementation of new therapeutic tools. Activity, defined as both function specific motor task and exercise appears to be a necessity for optimization of functional, metabolic, and neurological status in chronic paralysis. Crafting a comprehensive rehabilitative intervention focused on functional improvement through neurological gains seems logical. The terms activity-based restorative therapies, activity-based therapies, and activity-based rehabilitation have been coined in the last 10 years to describe a new fundamental approach to deficits induced by neurological paralysis. The goal of this approach is to achieve activation of the neurological levels located both above and below the injury level using rehabilitation therapies. This article reviews basic and clinical science evidence pertaining to implementation of physical activity and exercise as a therapeutic tool in the management of chronic spinal cord-related neurological paralysis. © 2009 Wiley-Liss, Inc. Dev Disabil Res Rev 2009;15:112,116. [source] Sturge,Weber syndrome and paroxysmal hemiparesis: epilepsy or ischaemia?DEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 11 2004Floor E Jansen MD Transient neurological deficits experienced by patients with Sturge,Weber syndrome can be caused by epilepsy, or may result from temporary ischaemia of the cortex underlying the vascular malformation. To show the difficulty in distinguishing seizures from ischaemic symptoms, two male children with episodes of acute unilateral weakness are presented here as well as a review of the literature. The first child presented at 2 years of age with a sudden increase in his pre-existing right hemiparesis accompanied by screaming. Ictal epileptiform activity was recorded at the moment of the attack, and subsequent seizures were controlled by adjustment of antiepileptic drug treatment. The second child presented at 4 years of age with attacks of vomiting and a coinciding increase in the pre-existing paresis of the left leg. Electroencephalogram (EEG) recording did not show ictal epileptiform activity. The origin was presumed to be vascular. Treatment with aspirin led to control of these transient ischaemic attacks. Ictal EEG is needed to differentiate between an epileptic and an ischaemic origin of transient focal deficit. Treatment with aspirin should be considered if an ischaemic origin cannot be excluded. [source] Cognitive Deficits during Status Epilepticus and Time Course of Recovery: A Case ReportEPILEPSIA, Issue 10 2007Wim Van Paesschen Summary:, We describe a young woman with progressive cognitive and neurological deficits during a parietal lobe status epilepticus (SE). Ictal FDG-PET showed left parietal lobe hypermetabolism and frontal lobe hypometabolism with concomitant EEG slowing. Cognitive and neurological deficits fully reversed more than 1 year after seizure remission, and were associated with normalization of FDG-PET and EEG. Our findings suggest that ictal hypometabolism and EEG delta activity at a distance from the epileptic focus were seizure-related phenomena, possibly representing inhibition in seizure propagation pathways, which could be responsible for the epileptic encephalopathy. [source] Adult-Onset Rasmussen's Encephalitis: Anatomical-Electrographic-Clinical Features of 7 Italian CasesEPILEPSIA, Issue 2006Flavio Villani Summary:,Purpose: A limited number of cases of adult-onset Rasmussen's encephalitis (A-RE) have been reported, but the features of the syndrome are still unclear. The aim of this study was to verify the clinical features of A-RE, and outline a noninvasive approach that may allow its early diagnosis and treatment. Methods: Retrospective evaluation of extensive noninvasive work-up of seven patients with A-RE, including repeat clinical, neurophysiological, and neuroimaging investigations. Results: The study identified two distinct patterns of disease presentation, one characterized by focal motor epilepsy (the "epileptic" phenotype), and the other by focal cortical myoclonus (the "myoclonic" phenotype). Unilateral neurological deficits and brain atrophy were progressive in both phenotypes, but they were more prominent and were detected earlier in the "epileptic" phenotype. Conclusions: The anatomo-electroclinical features of these patients allowed a noninvasive diagnosis of A-RE and identification of two distinct disease phenotypes. Early noninvasive diagnosis can allow faster initiation of treatment. [source] | ||||||||||||||||||||||||||||||||||||||||