Acute Neurological Signs Research Articles

The acute and chronic phases of chronic relapsing experimental autoimmune encephalomyelitis (CR EAE) are ameliorated by the peroxynitrite decomposition catalyst, 5,10,15,20-tetrakis(4-sulfonatophenyl)porphyrinatoiron (III) chloride, (FeTPPS)

There is increasing evidence that the oxidative radical, peroxynitrite (ONOO −), is involved in the pathogenesis of inflammatory diseases including multiple sclerosis and the animal counterpart, experimental autoimmune encephalomyelitis (EAE). Compounds that impede the actions of ONOO − have proved useful in the control of EAE. In particular, catalytic isomerisation of ONOO − to inactive nitrate, through the use of metalloporphyrins, curtails the cellular response to inflammatory stimuli and halts the progression of neuroinflammation during EAE. The present study examined the pharmacological effects of the metalloporphyrin and ONOO − decomposition catalyst 5,10,15,20-tetrakis(4-sulfonatophenyl)porphyrinatoiron(III)chloride (FeTPPS) on the acute and relapse phases of chronic relapsing (CR) EAE. Administration of FeTPPS to CR EAE-inoculated Biozzi mice commenced either therapeutically and immediately prior to the emergence of acute or relapse symptoms, or prophylactically, from the onset of remission of acute neurological signs. Drug therapy reduced acute and relapse symptoms but, and in contrast to the former phase, was of limited benefit in preventing histological changes during the latter stage of disease. In contrast, prophylactic FeTPPS was effective in limiting CNS pathology and neurological deficits. The findings confirm the inhibitory effects of FeTPPS on acute stage EAE. Moreover, the study extends previous observations by verifying compound efficacy on relapsing disease. Use of metalloporphyrins, such as FeTPPS, again highlights the important role played by ONOO − in the development of inflammatory diseases such as EAE.

Encephalopathy syndrome in children with hemato‐oncological disorders is not always posterior and reversible

Posterior reversible leukoencephalopathy (PRES) is a clinical-radiological event that can affect children undergoing chemotherapy regimen. Studies have shown that it is not always reversible, in spite of its original definition. We analyzed PRES cases which occurred during the last 10 years at our institute to focus on their clinical, radiological and EEG follow-up. We analyzed 12 cases of PRES in children who underwent intensive chemotherapy regimens, detailing the acute neurological presentation of the syndrome, their neuro-imaging characteristics (MRI) and EEG findings, in both an acute phase and during follow-up. All patients survived the acute event, showing a clinical recovery of the acute neurological signs in 1-3 days and normalization of the EEG pattern in a period ranging from 1 to 8 months. During long term follow-up, four patients developed either clinical impairment or EEG-MRI anomalies. We suggest that a long term follow-up is necessary to determine the reversibility of the neurological events. Clinical observation, as well as EEG and MRI should be included in follow-up evaluations.

Hormone Therapy for Treatment of Colonic Vascular Ectasia in 2 Dogs

Hormone Therapy for Treatment of Colonic Vascular Ectasia in 2 Dogs

Persistent Neurobehavioral Signs and Symptoms Following West Nile Fever

Persistent Neurobehavioral Signs and Symptoms Following West Nile Fever

Diagnosis of Anatoxin-a Poisoning in Dogs from North America

Anatoxin-a, a toxin produced by several genera of blue-green algae, is considered a potent neurotoxin. Ingestion of water contaminated with the toxin results in acute neurological signs and often death. This report describes fatal cases of anatoxin-a ingestion in 6 dogs, with confirmation of anatoxin-a exposure by liquid chromatography/tandem mass spectrometry (LC-MS/MS/MS). In 1 outbreak, 3 dogs developed seizures and died within an hour after swimming in a river in California, while the other outbreak involved 3 dogs that died within 1 hour after swimming in a pond in Ontario. Anatoxin-a poisoning is rarely reported in dogs as a cause of acute neurological signs and death. However, increased occurrences of blue-green algae blooms in North America make this neurotoxin an important consideration in the diagnosis of sudden death associated with environmental water exposure. This brief communication reports on the isolation and detection of anatoxin-a from environmental water sources and the stomach contents of North American dogs dying of acute neurotoxicosis. This demonstrates the first documented cases of anatoxin-a poisoning in dogs in North America and the importance of LC-MS/MS/MS in identifying neurotoxins responsible for sudden death in cases of suspected blue-green algae toxicosis; especially those cases showing no gross or histological lesions.

Cerebral Gas Embolism Caused by Pleural Fibrinolytic Treatment

Intrapleural fibrinolytic therapy is a technique used to treat empyemas and parapneumonic effusions. Cerebral air embolism is an unusual potentially severe complication of this technique. Summary of Case- A patient with parapneumonic pleural effusion underwent pleural lavage with streptokinase when he suddenly demonstrated focal neurological signs and seizures. The CT revealed multiple air-isodense spots in right hemisphere of the brain, suggesting cerebral air embolism. As a result of early diagnosis and emergency hyperbaric oxygenation, the patient recovered without delayed sequelae. Air embolism is a potentially severe complication which can occur during fibrinolytic pleural lavage, and clinicians should be aware of this risk. In this context, the onset of acute focal neurological signs or seizures should suggest the possibility of air embolism and lead to the transfer of the patient close to a hyperbaric facility within a few hours.

Both Epsilon-Toxin and Beta-Toxin Are Important for the Lethal Properties of Clostridium perfringens Type B Isolates in the Mouse Intravenous Injection Model

Clostridium perfringens is capable of producing up to 15 toxins, including alpha-toxin (CPA), beta-toxin (CPB), epsilon-toxin (ETX), enterotoxin, beta2-toxin (CPB2), and perfringolysin O. Type B isolates, which must produce CPA, CPB, and ETX, are associated with animal illnesses characterized by sudden death or acute neurological signs, with or without intestinal damage. Type B pathogenesis in ruminants is poorly understood, with some animals showing lesions and clinical signs similar to those caused by either type C or type D infections. It is unknown whether host or environmental conditions are dominant for determining the outcome of type B disease or if disease outcomes are determined by variable characteristics of type B isolates. To help clarify this issue, 19 type B isolates were evaluated for toxin production during late-log-phase growth via quantitative Western blotting and by biological activity assays. Most type B isolates produced CPB levels similar to those produced by type C isolates in vitro and have the potential to produce genotype C-like disease. The lethality of type B isolate supernatants administered intravenously to mice was evaluated with or without prior trypsin treatment, and monoclonal antibody neutralization studies also were performed. Correlation analyses comparing toxin levels in type B supernatants versus lethality and neutralization studies both found that the main contributor to lethality without pretreatment with trypsin was CPB, whereas neutralization studies indicated that CPB and ETX were both important after trypsin pretreatment. At least part of the CPB produced by type B isolates remained active after trypsin treatment. However, the overall lethalities of most supernatants were lower after trypsin pretreatment. Also, there was a significant association between ETX, CPB2, and CPA production in vitro among type B isolates. However, our results suggest that both CPB and ETX are likely the most important contributors to the pathogenesis of C. perfringens type B infections in domestic animals.

Pituitary Apoplexy-Like Disease in 4 Dogs

Pituitary apoplexy in humans is a clinical syndrome resulting from sudden infarction, hemorrhage, or both in a normal or an adenomatous pituitary gland. Describe a clinical syndrome in dogs similar to pituitary apoplexy in humans. Four dogs exhibiting a sudden onset of neurologic signs. A retrospective study was used, including clinical examination, computed tomography (CT), postmortem examination, and histopathology of the brain. Pituitary tissue from 3 of the dogs was subjected to immunocytochemistry. Four dogs (2 Mongrels, 1 Bordeaux Dog, and 1 Cocker Spaniel; median age, 11 years; median body weight, 20.5 kg) presented with acute neurologic signs including depression (n = 3), behavioral changes (n = 1), vision loss (n = 1), seizures (n = 1), and collapse (n = 1). CT disclosed suprasellar infarction, hemorrhage, or both associated with a pituitary macroadenoma in 3 dogs and a frank hemorrhage in a nonadenomatous pituitary gland in 1 dog. CT findings were correlated with postmortem findings, and pituitary apoplexy was confirmed by histopathology and immunocytochemistry of the pituitary tissue. This study provides histopathologic evidence of pituitary apoplexy in dogs. The results are relevant for future diagnosis and treatment of pituitary disease in dogs.

Isolation of Vibrio Cholerae from the Brain of a Feedlot Heifer with Meningoencephalitis

A 700-pound, 9-month-old Angus heifer from a feedlot presented with acute neurologic signs, characterized by circling, posterior weakness, and nonresponsiveness, followed by death. Histologically, the frontal lobe and the thalamus contained multiple foci of liquefaction that contained numerous degenerative neutrophils and foamy macrophages. Some of these foci were centered on blood vessels that contained fibrin thrombi and exhibited varying degrees of fibrinoid necrosis of the vessel wall. There was adjacent axonal degeneration and neuronal necrosis characterized by pronounced cytoplasmic eosinophilia, peripheralization of the nuclei, and loss of Nissl substance. Aerobic culture of the brain yielded moderate growth of Vibrio species, which was determined to be Vibrio cholerae by polymerase chain reaction analysis of a 438-base pair fragment of the 16 S ribosomal RNA gene. V. cholerae are motile, gram-negative, curved rod-shaped bacteria. Some strains of V. cholerae are important food- and water-borne bacterial pathogens that produce an often fatal diarrhea in humans. This is the first known case report of V. cholerae meningoencephalitis and cerebral abscessation in a bovine.

Predation as a Cause of Neurologic Signs and Acute Mortality in a Pheasant Flock

A flock of approximately 15,000 ring-necked pheasants (Phasianus colchicus) was evaluated for a sudden increase in mortality and acute neurological signs after having been previously diagnosed 3 wk earlier with a chronic respiratory disease of undetermined etiology. Approximately 25 live birds were displaying neurological signs including circling, ataxia, and obtunded behavior and 50 birds were dead. Three birds with neurological signs were submitted for evaluation. Extensive subcutaneous hemorrhage over the head and penetrating puncture wounds through the skull and into the brain were found. Trauma from a wild predatory mammal, most likely the long-tailed weasel (Mustela frenata) that had invaded the pheasant house and expressed surplus killing behavior was determined to be the cause of the acute neurological signs and mortality. The relationship of the chronic respiratory disease to the predation episode was not determined but it is possible that pheasants with severe respiratory disease may have had increased susceptibility to predation.

Hypoxic adaptation during development: relation to pattern of neurological presentation and cognitive disability

Children with acute hypoxic-ischaemic events (e.g. stroke) and chronic neurological conditions associated with hypoxia frequently present to paediatric neurologists. Failure to adapt to hypoxia may be a common pathophysiological pathway linking a number of other conditions of childhood with cognitive deficit. There is evidence that congenital cardiac disease, asthma and sleep disordered breathing, for example, are associated with cognitive deficit, but little is known about the mechanism and whether there is any structural change. This review describes what is known about how the brain reacts and adapts to hypoxia, focusing on epilepsy and sickle cell disease (SCD). We prospectively recorded overnight oxyhaemoglobin saturation (SpO2) in 18 children with intractable epilepsy, six of whom were currently or recently in minor status (MS). Children with MS were more likely to have an abnormal sleep study defined as either mean baseline SpO2 <94% or >4 dips of >4% in SpO2/hour (p = .04). In our series of prospectively followed patients with SCD who subsequently developed acute neurological symptoms and signs, mean overnight SpO2 was lower in those with cerebrovascular disease on magnetic resonance angiography (Mann-Whitney, p = .01). Acute, intermittent and chronic hypoxia may have detrimental effects on the brain, the clinical manifestations perhaps depending on rapidity of presentation and prior exposure.

A Case of Fat Embolism Syndrome of Fat Globules Found in BAL Fluid after Recovery from Acute Respiratory Failure

Fat embolism syndrome is a rare clinical diagnosis of dyspnea with acute respiratory failure and neurological signs caused by a traumatic long bone fracture. We report a case of fat embolism in a 22 year-old man after a traffic accident. Dyspnea and stuporous mental changes developed on the day after the external fixation operation of a left metaphyseal femur fracture. On the following day, he was transferred from a hospital to this one because of acute respiratory failure. After recovery, macrophages with fat droplets were found in the bronchoalveolar lavage fluid 1. It is important to diagnose a fat embolism as the correct cause of acute respiratory failure through the BAL in the acute state of fat embolism syndrome It is believed that clinically apparent or sometimes hidden fat embolism syndrome can be diagnosed from the BAL during the recovery state.

MAGNETIC RESONANCE IMAGING APPEARANCE OF SUSPECTED ISCHEMIC MYELOPATHY IN DOGS

Ischemia and infarction of the spinal cord is a known cause of acute spinal injury in dogs. Currently, the diagnosis of spinal cord infarction in small animals is based on history, clinical signs, and the exclusion of other differentials with radiography and myelography. It is a diagnosis only confirmed through necropsy examination of the spinal cord. The aim of this paper is to describe the Magnetic resonance imaging (MRI) findings of the spinal cord of dogs with suspected spinal cord infarcts to utilize this technology for antemortem support of this diagnosis. This retrospective study evaluated the spinal MR examinations of 11 dogs with acute onset of asymmetric nonpainful myelopathies. All patients except one (imaged at 2 months) were imaged within 1 week of clinical signs and managed conservatively with minimal medical and no surgical intervention. They were followed clinically for a minimum of 4 months after discharge. MR findings in all dogs were characterized by focal, intramedullary, hyperintense lesions on T2-weighted images with variable contrast enhancement similar to what is reported in humans. Though it could not be used to diagnose spinal cord infarction definitively, MRI was useful in excluding extramedullary spinal lesions and supporting intramedullary infarction as a cause of the acute neurologic signs. Together with the history and clinical examination findings, MRI is supportive of a diagnosis of spinal cord infarction.

Respiratory Syncytial Virus Infection and Neurologic Abnormalities: Retrospective Cohort Study

Respiratory syncytial virus is a common cause of acute respiratory infection in children. Previous reports have associated respiratory syncytial virus infection and acute neurologic symptoms, including apnea and seizures. This study examined the prevalence of acute neurologic symptoms associated with respiratory syncytial virus and non-respiratory syncytial virus respiratory infections in children requiring admission to a pediatric intensive care unit. We screened all admissions over a 4-year period at a single center, identifying children between birth and 2 years of age with bronchiolitis or acute upper respiratory infection. Children with a history of prematurity, preexisting medical conditions, or prior neurologic problems were excluded. Retrospective chart review of 236 admissions was conducted, identifying the etiology of respiratory infection and the presence or absence of acute neurologic signs or symptoms. This study demonstrated a prevalence of acute neurologic signs or symptoms in 36.4% of respiratory syncytial virus-negative patients (n = 115) and 39.1% in the respiratory syncytial virus-positive group (n = 121). Apnea, the most common symptom, was observed in 19.8% of respiratory syncytial virus-positive cases and 16.5% of negative patients. Seizures were reported in 6.6% of the positive cases and in 12.2% of the negative cohort. These differences showed no statistical significance. Although neurologic signs and symptoms are common in this population of children with acute respiratory infection, there was no significant difference in the prevalence of neurologic problems between respiratory syncytial virus-positive and -negative patients.

Giant Cell Arteritis.

Patients with a suspected diagnosis of giant cell arteritis (GCA) should be started on high-dose corticosteroid therapy without delay. A temporal artery biopsy should be performed after initiation of therapy to confirm the diagnosis. Patients with acute visual or neurologic symptoms present a neuro-ophthalmic emergency. Therapy should be initiated immediately with high-dose intravenous methylprednisolone sodium succinate and followed by high-dose oral prednisone. Treatment may begin with high-dose oral prednisone in patients without visual or neurologic symptoms. Calcium, vitamin D, and peptic ulcer prophylaxis should accompany steroid therapy, as indicated. The following treatments should be considered for patients with suspected GCA and acute visual or neurologic signs or symptoms: intravenous methylprednisolone sodium succinate (250 mg intravenously every 6 hours) should be given for 3 days, followed by oral prednisone (80 mg per day or 1 mg/kg) for 4 to 6 weeks. Prednisone should then be tapered by 10 mg per day every month. Most patients require 1 year of therapy to avoid relapse. Taper and duration should be modified according to erythrocyte sedimentation rate, C-reactive protein, and signs and symptoms of GCA. Rheumatologic consultation and follow-up is often helpful for these patients. For patients with suspected GCA and no acute visual or neurologic signs or symptoms, therapy may begin directly with oral prednisone (80 mg per day or 1 mg/kg) with same taper and duration based on laboratory values and clinical signs and symptoms.

Cerebral Metastases of a Choriocarcinoma During Pregnancy

In Brief BACKGROUND Cerebral metastasis of choriocarcinoma during pregnancy is rare. Described is the fourth case in the literature. CASE A pregnant women at 28 weeks' gestation sought care for headaches followed by loss of consciousness. The diagnosis of choriocarcinoma metastases was made on the basis of the combination of cerebral and pulmonary lesions, all suspected to be metastatic, and a high β human chorionic gonadotropin level. A premature cesarean delivery was performed to improve the mother's prognosis; the responsiveness of choriocarcinoma to chemotherapy made it important for treatment to begin as rapidly as possible. The outcome has been on balance favorable, even though her sequelae include paraplegia. The child has no apparent sequelae. CONCLUSION The diagnosis of choriocarcinoma must be considered when acute neurological signs appear in a pregnant patient. Acute neurological signs in pregnant women require consideration of a diagnosis of choriocarcinoma and of emergency cesarean delivery to allow rapid treatment and improve maternal prognosis.

Cerebral metastases of a choriocarcinoma during pregnancy

Background Cerebral metastasis of choriocarcinoma during pregnancy is rare. Described is the fourth case in the literature. Case A pregnant women at 28 weeks' gestation sought care for headaches followed by loss of consciousness. The diagnosis of choriocarcinoma metastases was made on the basis of the combination of cerebral and pulmonary lesions, all suspected to be metastatic, and a high β human chorionic gonadotropin level. A premature cesarean delivery was performed to improve the mother's prognosis; the responsiveness of choriocarcinoma to chemotherapy made it important for treatment to begin as rapidly as possible. The outcome has been on balance favorable, even though her sequelae include paraplegia. The child has no apparent sequelae. Conclusion The diagnosis of choriocarcinoma must be considered when acute neurological signs appear in a pregnant patient.

Findings in cerebrospinal fluids of horses infected with West Nile virus: 30 cases (2001).

To evaluate CSF in horses with confirmed West Nile virus encephalomyelitis. Retrospective study. 30 horses. Results of CSF analyses from horses with acute neurologic signs attributed to West Nile virus infection that was confirmed by immunoglobulin M antibody capture ELISA were reviewed and analyzed. Among 30 CSF samples, findings in 8 (27%) were within reference ranges and in 22 (73%) were abnormal. Among the 22 abnormal samples, mononuclear pleocytosis was found in 16 (73%) and high protein concentration with nucleated cell count within reference range was found in 6 (27%) samples. A predominance of lymphocytes was found in 11 of 16 samples with mononuclear pleocytosis, and a predominance of large mononuclear cells was found in 5 of 16 samples. Sensitivities of analyses of CSF obtained from the lumbosacral and atlanto-occipital regions of the spinal cord were 89 and 50%, respectively. Results suggest that in horses with acute onset of neurologic signs caused by West Nile virus encephalomyelitis, findings in the CSF are likely to be abnormal, mononuclear pleocytosis with lymphocytic predominance may be most commonly observed, and CSF collected from the lumbosacral region may be abnormal more commonly than CSF collected from the atlanto-occipital region.

Atlantoaxial Instability in a White-tailed Deer Fawn (Odocoileus virginianus)

On 14 March 2001, an 8 mo old, male white-tailed deer (Odocoileus virginianus) was found in lateral recumbency exhibiting neurologic signs including inability to rise, opisthotonus, paddling, and respiratory distress. There was evidence of minor cranial trauma. Postmortem examination revealed atlantoaxial instability with ventral deviation of the axis due to malformation of the caudal atlas and cranial axis. Given the age of the fawn, the instability was assumed to be congenital with minor trauma inducing severe, acute neurologic signs.

Reexamination of Amphotropic Murine Leukemia Virus Neurovirulence: Neural Stem Cell-Mediated Microglial Infection Fails to Induce Acute Neurodegeneration

The 4070A amphotropic murine leukemia virus (A-MuLV) has been variably reported to harbor neurovirulence determinants within its env gene. In this report we reexamined this issue by applying two approaches previously demonstrated to amplify murine leukemia virus neurovirulence. The first approach involved introducing the 4070A env gene into the background of Friend virus clone FB29 to enhance peripheral virus replication kinetics and central nervous system entry. The resulting chimeric virus, FrAmE, exhibited widespread vascular infection throughout the central nervous system (CNS); however, parenchymal infection was quite limited. Neither clinical neurological signs nor spongiform neurological changes accompanied FrAmE CNS infection. To overcome this CNS entry limitation, 4070A and FrAmE were delivered directly into the CNS via transplantation of infected C17.2 neural stem cells (NSCs). Significantly, NSC dissemination of either 4070A or FrAmE resulted in widespread, high-level amphotropic virus expression within the CNS parenchyma, including the infection of microglia, the critical target required for inducing neurodegeneration. Despite the extensive CNS infection, no associated clinical neurological signs or acute neuropathological changes were observed. Interestingly, we observed the frequent appearance of circulating polytropic (MCF) virus in the serum of amphotropic virus-infected animals. However, neither peripheral inoculation of an amphotropic/MCF virus mixture nor transplantation of NSCs expressing both amphotropic and MCF viruses induced acute clinical neurological signs or spongiform neuropathology. Thus, the results generated in this study suggest that the 4070A env gene is not inherently neurovirulent. However, the frequent appearance of endogenous MCF viruses suggests the possibility that the interactions of amphotropic viruses with endogenous retroviral elements could contribute to the development of retrovirus-induced neurodegenerative disease.