Neurologic Sequelae (neurologic + sequelae)

Distribution by Scientific Domains


Selected Abstracts


Hyperbaric Oxygen Does Not Prevent Neurologic Sequelae after Carbon Monoxide Poisoning

ACADEMIC EMERGENCY MEDICINE, Issue 1 2002
Benjamin Gilmer MS
Abstract Delayed neurologic sequelae occur in up to 40% of severe carbon monoxide (CO) poisonings. Conflicting clinical data support the efficacy of hyperbaric oxygen (HBO) therapy in the acute treatment of CO poisoning. Objective: To determine whether oxygen therapy reduces neurologic sequelae after CO poisoning in mice. Methods: Male Swiss-Webster mice were exposed to CO at 1,000 ppm for 40 minutes and then 50,000 ppm until loss of consciousness (LOC) (4-9 additional minutes). Total time of both phases of CO exposure was 40-49 minutes. Treatment included HBO with 3 atmospheres (ATA) 100% oxygen, normobaric oxygen (NBO) with 1 ATA 100% oxygen, or ambient air 15 minutes after LOC. All animals underwent passive avoidance training and memory was assessed by measuring step-down latency (SDL) and step-up latency (SUL) seven days following CO exposure. Results: Carbon monoxide poisoning induced significant memory deficits (SDLCO= 156 sec; SULCO= 75%) compared with nonpoisoned (NP) animals (SDLNP= 272 sec; SULNP= 100%). Both HBO and NBO did not prevent these neurologic sequelae. Furthermore, no significant neurobehavioral differences were found between HBO and NBO. Histologic examination of the CA1 layer of the hippocampus for pyknotic cells showed significant damage from CO in the air-treated animals (9.6%) but not in the nonpoisoned animals (3.8%). No significant neuroprotection was seen histologically with NBO and HBO compared with ambient air. Conclusions: These results suggest that HBO is not effective in preventing neurologic sequelae in mice and that there is no benefit of HBO over NBO following severe CO neurotoxicity. [source]


Long-term neurological and functional outcome in Nipah virus infection

ANNALS OF NEUROLOGY, Issue 3 2007
James 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]


Delayed neurotoxicity associated with therapy for children with acute lymphoblastic leukemia

DEVELOPMENTAL DISABILITIES RESEARCH REVIEW, Issue 3 2006
Peter D. Cole
Abstract Most children diagnosed today with acute lymphoblastic leukemia (ALL) will be cured. However, treatment entails risk of neurotoxicity, causing deficits in neurocognitive function that can persist in the years after treatment is completed. Many of the components of leukemia therapy can contribute to adverse neurologic sequelae, including craniospinal irradiation, nucleoside analogs, corticosteroids, and antifolates. In this review, we describe the characteristic radiographic findings and neurocognitivie deficits seen among survivors of childhood ALL. We summarize what is known about the pathophysiology of delayed treatment-related neurotoxicity, with a focus on the toxicity resulting from pharmacologic disruption of folate physiology within the central nervous system. Finally, we suggest testable strategies to ameliorate the symptoms of treatment-related neurotoxicity or decrease its incidence. MRDD Research Reviews 2006;12:174,183. © 2006 Wiley-Liss, Inc. [source]


Hyperbaric Oxygen Does Not Prevent Neurologic Sequelae after Carbon Monoxide Poisoning

ACADEMIC EMERGENCY MEDICINE, Issue 1 2002
Benjamin Gilmer MS
Abstract Delayed neurologic sequelae occur in up to 40% of severe carbon monoxide (CO) poisonings. Conflicting clinical data support the efficacy of hyperbaric oxygen (HBO) therapy in the acute treatment of CO poisoning. Objective: To determine whether oxygen therapy reduces neurologic sequelae after CO poisoning in mice. Methods: Male Swiss-Webster mice were exposed to CO at 1,000 ppm for 40 minutes and then 50,000 ppm until loss of consciousness (LOC) (4-9 additional minutes). Total time of both phases of CO exposure was 40-49 minutes. Treatment included HBO with 3 atmospheres (ATA) 100% oxygen, normobaric oxygen (NBO) with 1 ATA 100% oxygen, or ambient air 15 minutes after LOC. All animals underwent passive avoidance training and memory was assessed by measuring step-down latency (SDL) and step-up latency (SUL) seven days following CO exposure. Results: Carbon monoxide poisoning induced significant memory deficits (SDLCO= 156 sec; SULCO= 75%) compared with nonpoisoned (NP) animals (SDLNP= 272 sec; SULNP= 100%). Both HBO and NBO did not prevent these neurologic sequelae. Furthermore, no significant neurobehavioral differences were found between HBO and NBO. Histologic examination of the CA1 layer of the hippocampus for pyknotic cells showed significant damage from CO in the air-treated animals (9.6%) but not in the nonpoisoned animals (3.8%). No significant neuroprotection was seen histologically with NBO and HBO compared with ambient air. Conclusions: These results suggest that HBO is not effective in preventing neurologic sequelae in mice and that there is no benefit of HBO over NBO following severe CO neurotoxicity. [source]


Late human cytomegalovirus (HCMV) proteins inhibit differentiation of human neural precursor cells into astrocytes

JOURNAL OF NEUROSCIENCE RESEARCH, Issue 3 2007
Jenny Odeberg
Abstract Human cytomegalovirus (HCMV) is the most common cause of congenital infections in developed countries, with an incidence varying between 0.5,2.2%. Such infection may be the consequence of either a primary infection or reactivation of a latent infection in the mother and the outcome may vary from asymptomatic to severe brain disorders. Moreover, infants that are asymptomatic at the time of birth may still develop neurologic sequelae at a later age. Our hypothesis is that infection of stem cells of the central nervous system by HCMV alters the proliferation, differentiation or migration of these cells, and thereby gives rise to the brain abnormalities observed. We show that infection of human neural precursor cells (NPCs) with the laboratory strain Towne or the clinical isolate TB40 of HCMV suppresses the differentiation of these cells into astrocytes even at an multiplicity of infection (MOI) as low as 0.1 (by 33% and 67%, respectively). This inhibition required active viral replication and the expression of late HCMV proteins. Infection as late as 24 hr after the onset of differentiation, but not after 72 hr, also prevented the maturation of infected cultures. Furthermore, in cultures infected with TB40 (at an MOI of 1), approximately 54% of the cells were apoptotic and cell proliferation was significantly attenuated. Clearly, HCMV can reduce the capacity of NPCs to differentiate into astrocytes and this effect may provide part of the explanation for the abnormalities in brain development associated with congenital HCMV infection. © 2006 Wiley-Liss, Inc. [source]


West Nile virus: lessons from the 21st century

JOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 1 2004
DACVECC, DACVIM, Pamela A. Wilkins DVM
Abstract Introduction: West Nile virus (WNV) first appeared in the United States in 1999, causing illness and death in birds, horses, and humans. While the initial outbreak of this sometimes deadly viral disease was limited to the northeastern United States, the virus had an inexorable migration across the continental United States over the next 3 years, causing huge losses among the affected species. The purpose of this review is to present currently available information regarding the epi-demiology, diagnosis, treatment, and prevention of WNV infection. Veterinarians, particularly those in an emergency practice, serve as an important source of reliable information regarding this disease for animal owners and the public in general. Data sources: Data sources used for the preparation of this review include computer-based searches of PubMed and Commonwealth Agricultural Bureaux (CAB) abstracts. A search in PubMed using ,West Nile' retrieved 1468 ,hits' or references, while a similar search in CAB abstracts produced 815 references. Additional information was obtained from various meeting proceedings, particularly data presented in abstract form, and from the Centers for Disease Control (CDC) website dedicated to WNV. Human data synthesis: Prior to the mid-1990s, reported large-scale epidemics of WNV infection in humans predominantly presented as acute, mild, febrile disease, sometimes associated with lymphadenopathy and skin rash. The recent large epidemic in the United States, in contrast, has prominently featured encephalitis, particularly among the elderly. Additionally, polio-encephalomyelitis-like complications resulting in long-term neurologic sequelae have been reported. There are many WNV-permissive native avian and mosquito hosts in the Unites States and there appear to be few limitations to the spread of the disease in the United States. It is expected that the virus will be identified in all 48 continental states, Mexico, and Canada by the end of 2003. Veterinary data synthesis: The horse is the animal species most affected by the recent WNV epidemic in the United States, and losses to the equine industry have been large and unprecedented. A United States Department of Agriculture (USDA)-approved vaccine against WNV has been in use in horses since 2001 and appears to be effective in limiting the incidence of disease in well-vaccinated populations. WNV infection has been documented in other species of mammals, including camelids (alpaca/llamas) and dogs, and veterinarians should include WNV as a differential diagnosis for animals presenting with clinical signs consistent with central nervous system infection. A large concern exists for endangered bird populations, particularly birds of prey, whether in zoos or in the wild. [source]


Delayed neuropsychologic dysfunction after liver transplantation for acute liver failure: A matched, case-controlled study

LIVER TRANSPLANTATION, Issue 10 2002
Elizabeth W. Jackson
Although several studies have identified posttransplant neurologic sequelae in patients with acute liver failure (ALF), the effects of these sequelae on neuropsychologic functioning after transplant is unknown. This study compared neuropsychologic functioning of ALF patients with chronic liver disease patients after liver transplantation. After liver transplantation, seven ALF patients were compared with a matched control group of patients who had been transplanted for chronic liver disease. The patients were matched by gender, age (within 5 years), and time since transplantation (within 2 years). Patients completed a 2-hour battery of tests, which included measures of attention, memory, motor performance, abstract conceptualization, and visuospatial perception. There were no significant differences between the groups on measures of socioeconomic status or education. Significant differences were found on three separate tests: WAIS-III Vocabulary, WAIS-III Similarities, and WMS-III Paired Associate Learning II. Although these tests measure distinct functions (vocabulary knowledge, abstract conceptualization, and delayed verbal recall), they may be influenced by broader verbal functions, such as verbal fluency, conceptualization, and the ability to articulate ideas. When patients were asked what functions had noticeably deteriorated since transplantation, nearly all complained of memory difficulties, and there was no difference between groups. However, more ALF than chronic liver disease (CLD) patients complained of concentration difficulties. The results of this study suggest that ALF patients may experience more neuropsychologic dysfunction after transplant. Further studies are required to expand on these initial observations with the potential to improve patient care and referral to appropriate rehabilitative services. [source]


Subarachnoid Hemorrhage as Complication of Phenylephrine Injection for the Treatment of Ischemic Priapism in a Sickle Cell Disease Patient

THE JOURNAL OF SEXUAL MEDICINE, Issue 4 2008
Hugo H. Davila MD
ABSTRACT Introduction., Ischemic priapism (IP) is a urologic condition, which necessitates prompt management. Intracavernosal injection of phenylephrine is a usual treatment modality utilized for the management of these patients. Aim., We present a case of subarachnoid hemorrhage following intracavernosal injection of phenylephrine for IP in a patient with sickle cell disease. Methods., We analyzed the degree of subarachnoid hemorrhage in our patient after intracavernosal injection of phenylephrine. The patient had an acute rise in blood pressure during corporal irrigation. This was followed by the onset of severe headache. Computed tomography (CT) scan confirmed the diagnosis of a subarachnoid hemorrhage. Main Outcome Measure., Subarachnoid hemorrhage associated with intracavernosal injection of phenylephrine. Result., A 23-year-old African American male with a history of sickle cell disease presented with a painful penile erection. The patient was started on intravenous fluids, oxygen by nasal canula, and analgesic medication. After this, a blood gas was obtained from his left corpora cavernosa. This was followed by normal saline irrigation and injection of phenylephrine. The patient complained of a sudden, severe "terrible headache" immediately following the last injection, and noncontrast CT scan of the head was obtained and a subarachnoid hemorrhage was noted. The patient was admitted for observation and no significant changes were noted. Conclusions., Intracavernosal injection of phenylephrine for the management of IP can be associated with several possible complications. We present our single case complicated with the formation of a subarachnoid hemorrhage. The patient was treated conservatively and had no long-term neurologic sequelae. Davila HH, Parker J, Webster JC, Lockhart JL, and Carrion RE. Subarachnoid hemorrhage as complication of phenylephrine injection for the treatment of ischemic priapism in a sickle cell disease patient. J Sex Med 2008;5:1025,1028. [source]


Spectrum of outcome in infants with extreme neonatal jaundice

ACTA PAEDIATRICA, Issue 7 2001
E HankÝ
The increasing number of case reports on neurologic sequelae related to hyperbilirubinaemia may represent a re-emergence of kernicterus in the industrialized world. However, not much has been written about infants who survived extreme levels of serum bilirubin without neurologic damage. We present three cases of extreme neonatal hyperbilirubinaemia, all with peak serum bilirubin levels >600 mmol/L. Two of the infants developed neurologic sequelae, but the third infant did not. In contrast to the two with sequelae, the infant without sequelae was female, had a positive Coombs' test, less clinical signs compatible with bilirubin encephalopathy, and a shorter exposure to serum bilirubin values >400 mmol/L. Conclusion: The basic mechanism of bilirubin neurotoxicity remains unknown, and it is not clear why some infants do not develop neurologic injury at serum bilirubin levels at which others do. We speculate that a comparison between patients with sequelate and those without may yield important information. [source]