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Neurologic Dysfunction (neurologic + dysfunction)
Selected AbstractsNeurologic Dysfunction in Hypothyroid, Hyperlipidemic Labrador RetrieversJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 6 2007Christina L. Vitale Background: Hypothyroidism has been associated with a variety of neurologic signs, but the mechanism for this association is not completely understood. Hypothyroidism also is associated with hyperlipidemia that predisposes to atherosclerosis, increased blood viscosity, and thromboembolic events. Objective: The objective is to characterize neurologic signs potentially associated with hyperlipidemia and atherosclerosis in canine hypothyroidism. Animals: This study used dogs referred to North Carolina State University Veterinary Teaching Hospital for evaluation of neurologic signs. Materials and Methods: A retrospective study was conducted in which medical records of dogs with neurologic signs and a diagnosis of hypothyroidism and hyperlipidemia were reviewed. Details of the history, presenting signs, results of routine blood tests, thyroid tests, cerebrospinal fluid (CSF) analysis and diagnostic imaging, and response to therapy were compiled. Results: Three Labrador Retrievers and one Labrador Retriever cross fit the inclusion criteria. All dogs were hypothyroid and severely hyperlipidemic. Neurologic signs included tetraparesis, central and peripheral vestibular signs, facial paralysis, and paraparesis. Two dogs had an acute history and rapid resolution of signs consistent with an infarct, the presence of which was confirmed in 1 of the dogs by magnetic resonance imaging. Two dogs had chronic histories of cranial neuropathies and paraparesis. One of these dogs had evidence of iliac thrombosis and atherosclerosis on ultrasound examination. All dogs improved with thyroid hormone supplementation. Clinical Relevance: Labrador Retrievers may be predisposed to the development of severe hyperlipidemia in association with hypothyroidism. One possible consequence of severe hyperlipidemia is the development of neurologic signs due to atherosclerosis and thromboembolic events. [source] Long-term neurological and functional outcome in Nipah virus infectionANNALS OF NEUROLOGY, Issue 3 2007James J. Sejvar MD Objective Nipah virus (NiV) is an emerging zoonosis. Central nervous system disease frequently results in high case-fatality. Long-term neurological assessments of survivors are limited. We assessed long-term neurologic and functional outcomes of 22 patients surviving NiV illness in Bangladesh. Methods During August 2005 and May 2006, we administered a questionnaire on persistent symptoms and functional difficulties to 22 previously identified NiV infection survivors. We performed neurologic evaluations and brain magnetic resonance imaging (MRI). Results Twelve (55%) subjects were male; median age was 14.5 years (range 6,50). Seventeen (77%) survived encephalitis, and 5 survived febrile illness. All but 1 subject had disabling fatigue, with a median duration of 5 months (range, 8 days,8 months). Seven encephalitis patients (32% overall), but none with febrile illness had persistent neurologic dysfunction, including static encephalopathy (n = 4), ocular motor palsies (2), cervical dystonia (2), focal weakness (2), and facial paralysis (1). Four cases had delayed-onset neurologic abnormalities months after acute illness. Behavioral abnormalities were reported by caregivers of over 50% of subjects under age 16. MRI abnormalities were present in 15, and included multifocal hyperintensities, cerebral atrophy, and confluent cortical and subcortical signal changes. Interpretation Although delayed progression to neurologic illness following Nipah fever was not observed, persistent fatigue and functional impairment was frequent. Neurologic sequelae were frequent following Nipah encephalitis. Neurologic dysfunction may persist for years after acute infection, and new neurologic dysfunction may develop after acute illness. Survivors of NiV infection may experience substantial long-term neurologic and functional morbidity. Ann Neurol 2007 [source] Pseudomigraine With Lymphocytic Pleocytosis: A Calcium Channelopathy?HEADACHE, Issue 8 2003Clinical Description of 10 Cases, Genetic Analysis of the Familial Hemiplegic Migraine Gene CACNA1A Objective.,To report the clinical findings of 10 patients diagnosed with pseudomigraine with lymphocytic pleocytosis and the results of mutational analysis of the CACNA1A gene in 8 of these patients. Background.,Pseudomigraine with lymphocytic pleocytosis, also referred to as headache with neurologic deficits and cerebrospinal fluid lymphocytosis (HaNDL), is characterized by episodic transient neurologic dysfunction associated with moderate to severe headache and cerebrospinal fluid lymphocytic pleocytosis. Episodes are recurrent and the condition is self-limiting. The etiology of this sporadic condition remains unknown, but the episodic nature and its ability to be triggered by angiography is somewhat reminiscent of the phenotypic features of familial hemiplegic migraine, a condition caused by mutations in the CACNA1A gene. Design/Methods.,Utilizing retrospective chart review, we describe the clinical features of pseudomigraine with lymphocytic pleocytosis in 10 patients. Whole blood was taken from 8 patients (2 were lost to follow-up) and used for DNA testing. The CACNA1A gene was screened for mutations using heteroduplex analysis and direct DNA sequencing. Results.,Clinical features of pseudomigraine with lymphocytic pleocytosis included transient episodes of weakness, sensory and visual symptoms, aphasia, and confusion lasting minutes up to 4 hours. Sensory symptoms, typically affecting the face and arm, were the most common presentation. Localization of symptoms did not conform to vascular territories. Headache was typically throbbing and most often bilateral. Genetic analysis did not identify any mutations in the CACNA1A gene. Conclusions.,Similarities between familial hemiplegic migraine and pseudomigraine with lymphocytic pleocytosis include recurrent headache with reversible neurologic deficit, cerebrospinal fluid lymphocytic pleocytosis, and triggers such as angiography. Even so, heteroduplex analysis and DNA sequencing failed to identify any sporadic mutations or shared polymorphisms in the exons or the intron/exon boundaries of the CACNA1A gene. These results do not support a role of the CACNA1A gene in the etiology of pseudomigraine with lymphocytic pleocytosis. [source] Vitamins E and C prevent the impairment of retention of an inhibitory avoidance task caused by arginine administrationJOURNAL OF NEUROCHEMISTRY, Issue 2002E. A. Reis Hyperargininemia is an inherited metabolic disease of urea cycle caused by the deficiency of arginase I activity, resulting in tissue accumulation of arginine (Arg). Patients affected by this disease usually develop spasticity, epilepsy and mental retardation as principal symptoms. Previous studies from our laboratory have showed that acute administration of Arg impairs retention of the inhibitory avoidance task and that l -NAME (NOS inhibitor) prevents this effect. In the present study, we investigated the effect of chronic treatment with antioxidants (vitamins E and C) on the retrieval of the inhibitory avoidance task in adults rats subjected to experimental model of acute hyperargininemia in order to investigate the participation of oxidative stress on this phenomenon. Sixty-day-old-rats were treated for one week with i.p. injection of saline (0.9%) or vitamins E and C (vit E 40 mg/kg and vit C 100 mg/kg). Twelve hours after the last injection Arg (0.8 g/kg) or an equivalent volume of saline were administered 1 h before training, 1 h before testing or immediately after training sessions. Memory was significantly impaired in Arg-treated group, whereas the rats chronically treated with vitamins E and C had this effect prevented. Present data strongly indicate that Arg administration impairs memory, an effect probably mediated by oxidative stress since treatment with vitamins E and C prevented amnesia. Assuming the possibility that this might occur in the human condition, reported results may be relevant to explain, at least in part, neurologic dysfunction associated with hyperargininemia. [source] The ubiquitous role of zinc in health and diseaseJOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 3 2009DACVIM, Julia E. Cummings DVM Abstract Objective , To review zinc physiology and pathophysiology and the importance of zinc toxicity and deficiency in veterinary patients. Data Sources , A review of human and veterinary medical literature. Human Data Synthesis , There is a significant amount of original research in humans and animals on the role of zinc in multiple organ systems. There is also significant data available on human patients with zinc abnormalities. Veterinary Data Synthesis , Zinc deficiency has been studied in dogs with genetic disease and dietary deficiency leading to dermatological disease and immune deficiency. Zinc toxicity has been described after ingestion of metallic foreign bodies containing zinc. Conclusions , Historically, the role of zinc in health and disease has been studied through patients with toxicity or severe deficiency with obvious clinical signs. As the ubiquitous contribution of zinc to structure and function in biological systems was discovered, clinically significant but subtle deficiency states have been revealed. In human medicine, mild zinc deficiencies are currently thought to cause chronic metabolic derangement leading to or exacerbating immune deficiency, gastrointestinal problems, endocrine disorders, neurologic dysfunction, cancer, accelerated aging, degenerative disease, and more. Determining the causal relationships between mild zinc deficiency and concurrent disease is complicated by the lack of sensitive or specific tests for zinc deficiency. The prevalence of zinc deficiency and its contribution to disease in veterinary patients is not well known. Continued research is warranted to develop more sensitive and specific tests to assess zinc status, to determine which patients are at risk for deficiency, and to optimize supplementation in health and disease. [source] Depression in multiple system atrophy: A case reportPSYCHIATRY AND CLINICAL NEUROSCIENCES, Issue 4 2000Kyoko Goto MD Abstract A 53-year-old woman who developed depression as the first symptom of multiple system atrophy was treated. Depression was followed successively by autonomic failure, parkinsonism and cerebellar ataxia. Treatment with L -DOPA, L -threo-DOPS, and thyroid releasing hormone was associated with improvement of autonomic failure and parkinsonism. As for depression, scores on the Zung scale and the Hamilton scale improved from 58 to 49 and from 30 to 22, respectively. This case is remarkable in that depression preceded neurologic dysfunction and was managed successfully by antiparkinsonian medication. A common underlying disturbance may be responsible for the depression and neurologic dysfunction in multiple system atrophy. [source] Long-term neurological and functional outcome in Nipah virus infectionANNALS OF NEUROLOGY, Issue 3 2007James J. Sejvar MD Objective Nipah virus (NiV) is an emerging zoonosis. Central nervous system disease frequently results in high case-fatality. Long-term neurological assessments of survivors are limited. We assessed long-term neurologic and functional outcomes of 22 patients surviving NiV illness in Bangladesh. Methods During August 2005 and May 2006, we administered a questionnaire on persistent symptoms and functional difficulties to 22 previously identified NiV infection survivors. We performed neurologic evaluations and brain magnetic resonance imaging (MRI). Results Twelve (55%) subjects were male; median age was 14.5 years (range 6,50). Seventeen (77%) survived encephalitis, and 5 survived febrile illness. All but 1 subject had disabling fatigue, with a median duration of 5 months (range, 8 days,8 months). Seven encephalitis patients (32% overall), but none with febrile illness had persistent neurologic dysfunction, including static encephalopathy (n = 4), ocular motor palsies (2), cervical dystonia (2), focal weakness (2), and facial paralysis (1). Four cases had delayed-onset neurologic abnormalities months after acute illness. Behavioral abnormalities were reported by caregivers of over 50% of subjects under age 16. MRI abnormalities were present in 15, and included multifocal hyperintensities, cerebral atrophy, and confluent cortical and subcortical signal changes. Interpretation Although delayed progression to neurologic illness following Nipah fever was not observed, persistent fatigue and functional impairment was frequent. Neurologic sequelae were frequent following Nipah encephalitis. Neurologic dysfunction may persist for years after acute infection, and new neurologic dysfunction may develop after acute illness. Survivors of NiV infection may experience substantial long-term neurologic and functional morbidity. Ann Neurol 2007 [source] Can Patients with Brain Herniation on Cranial Computed Tomography Have a Normal Neurologic Exam?ACADEMIC EMERGENCY MEDICINE, Issue 2 2009Marc A. Probst MD Abstract Objectives:, Herniation of the brain outside of its normal intracranial spaces is assumed to be accompanied by clinically apparent neurologic dysfunction. The authors sought to determine if some patients with brain herniation or significant brain shift diagnosed by cranial computed tomography (CT) might have a normal neurologic examination. Methods:, This is a secondary analysis of the National Emergency X-Radiography Utilization Study (NEXUS) II cranial CT database compiled from a multicenter, prospective, observational study of all patients for whom cranial CT scanning was ordered in the emergency department (ED). Clinical information including neurologic examination was prospectively collected on all patients prior to CT scanning. Using the final cranial CT radiology reports from participating centers, all CT scans were classified into three categories: frank herniation, significant shift without frank herniation, and minimal or no shift, based on predetermined explicit criteria. These reports were concatenated with clinical information to form the final study database. Results:, A total of 161 patients had CT-diagnosed frank herniation; 3 (1.9%) had no neurologic deficit. Of 91 patients with significant brain shift but no herniation, 4 (4.4%) had no neurologic deficit. Conclusions:, A small number of patients may have normal neurologic status while harboring significant brain shift or brain herniation on cranial CT. [source] 3164: Post-concussive syndromeACTA OPHTHALMOLOGICA, Issue 2010V PURVIN Purpose Over 85% of traumatic brain injuries (TBI) are considered "mild", also referred to as "concussion". Mild TBI is increasingly recognized as an important public health problem. Despite their designation as "mild", adverse outcomes from such injuries are significant, with 25% of patients still impaired at one year. Visual difficulties are common, reported by two-thirds of patients in a Veterans Administration study. Methods Visual symptoms of mild TBI typically include blurring, light sensitivity, eyestrain, difficulty with near focus, trouble tracking, seeing haloes around lights, and diplopia (monocular and binocular). Results Despite the high incidence of visual symptoms, results of standard eye examination and neuro-ophthalmic testing are typically normal. Conventional neuro-imaging also fails to demonstrate objective evidence of neurologic dysfunction in most cases. Recent developments in neuroimaging (particularly diffusion tensor imaging) and serologic testing (S-100B) have provided some correlates of such injury. Conclusion New information from neuroimaging and serologic testing has helped to provide some objective markers for post-concussive syndromes. The diagnosis of such post-traumatic syndromes remains largely clinical. [source] Induced hypothermia following out-of-hospital cardiac arrest; initial experience in a community hospitalCLINICAL CARDIOLOGY, Issue 12 2006Brook D. Scott M.D. Abstract Background Successful resuscitation from sudden cardiac death is frequently accompanied by severe and often fatal neurologic injury. Induced hypothermia (IH) may attenuate the neurologic damage observed in patients after cardiac arrest. Hypothesis This study examined a population of nonselected patients presenting to a community hospital following successful resuscitation of sudden cardiac death. We sought to determine whether a program of induced hypothermia would improve the clinical outcome of these critically ill patients. Methods We initiated a protocol of IH at the Oklahoma Heart Hospital in August of 2003. Study patients were consecutive adults admitted following successful resuscitation of out-of-hospital cardiac arrest. Moderate hypothermia was induced by surface cooling and maintained for 24 to 36 h in the Intensive Care Unit with passive rewarming over 8 h. Results Forty-nine patients who were resuscitated and had the return of spontaneous circulation completed the hypothermia protocol. The cause of cardiac arrest was acute myocardial infarction in 24 patients and cardiac arrhythmias in 19 patients. Nineteen patients (39%) survived and were discharged. Sixteen of the patients discharged had no or minimal residual neurologic dysfunction and 3 patients had clinically significant residual neurologic injury. Conclusion A program of induced hypothermia based in a community hospital is feasible, practical, and requires limited additional financial and nursing resources. Survival and neurologic recovery compare favorably with clinical trial outcomes. Copyright © 2006 Wiley Periodicals, Inc. Wiley Periodicals, Inc. [source] BK virus infection and neurologic dysfunctions in a patient with lymphoma treated with chemotherapy and rituximabEUROPEAN JOURNAL OF HAEMATOLOGY, Issue 3 2008Angela Ferrari No abstract is available for this article. [source] | ||||||||||||||||||||||