Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present a clinicopathological report of a recent fatal case of a 27-year-old woman whom we consider to have had encephalitis lethargica. Clinical features of note were a presentation with vertigo, persistent vomiting and sleep disturbance including marked daytime somnolence and vivid nightmares. On examination, she had impaired slow pursuit vertical eye movements, dysarthria, an expressionless face and slow tongue movements. She went on to develop gross supranuclear gaze palsy, neck rigidity, bradykinesia, blepharospasm, profound somnolence and anarthria but no tremor, weakness or impairment of cognition. She died after an illness lasting 12 months. On investigation, the cerebrospinal fluid was found to contain a very high level of IgG with oligoclonal bands but no cells. Post-mortem examination revealed an active encephalitis, mainly centered on the upper brainstem and diencephalon with extensive Purkinje cell loss and marked plasma cell infiltrates and morula cells. No virus was recovered.
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PMID:A contemporary case of encephalitis lethargica. 1122 Jun 91

An epidemic of enterovirus 71 (EV71) infection compatible with hand, foot and mouth disease and associated with high morbidity and mortality occurred in Taiwan in 1998. We recruited 90 patients (50 males, 40 females) with definite EV71 infections for clinical and laboratory analysis. The neurological signs and symptoms, all of which occurred during the febrile period, in patients with central nervous system (CNS) involvement (aseptic meningitis, encephalitis or myelitis) were myoclonic jerks (23/33), vomiting (10/33), ataxia (7/33), lethargy (6/33), seizure (4/33) and tremor (2/33). Patients with CNS involvement had longer durations of fever (4.6+/-0.2 vs. 3.1+/-0.3 d; p <0.01) and a higher white blood cell count (12,512+/-658 vs. 10,607+/-409 cells/mm3; p = 0.01) than patients without CNS involvement. The case fatality rate in patients with CNS involvement was 4/33 (12%), whereas no fatalities (0/57) occurred in patients without CNS involvement. Six of 11 patients subjected to MRI showed a high intensity T2-weighted signal in the brainstem. A nested fluorescent RT-PCR for detection of virus in throat and stool specimens showed higher sensitivity than viral culture. Viremia was detectable using RT-PCR in 20% of cases (3/15), whereas no virus was isolated from culture or detected by RT-PCR in cerebrospinal fluid.
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PMID:Clinical manifestations and laboratory assessment in an enterovirus 71 outbreak in southern Taiwan. 1192 38

Among the enteroviruses, polioviruses and enterovirus 71 (EV71) are two major neurotropic viruses causing serious neurological manifestations. While polioviruses are being eradicated globally by vaccination, EV71 still has the potential to cause a large outbreak such as that in Taiwan in 1998, in which there were many fatalities. In this study, we determined the neurovirulence of EV71 by neuropathological analysis of cynomolgus monkeys after experimental infection with five EV71 strains, which were isolated from individual patients with fatal encephalitis; meningitis; and hand, foot, and mouth disease. After intraspinal inoculation, the monkeys developed neurological manifestations within 1-6 days post-inoculation, irrespective of the inoculated strains. These manifestations included not only pyramidal tract signs such as flaccid paralysis, but also extrapyramidal tract signs such as tremor and ataxia. Histological and viral examinations confirmed virus replication in the spinal cord, brainstem, cerebellar cortex, and dentate nuclei, and cerebrum. The strains isolated during the 1970s and 1990s showed no particular differences with respect to neurotropism. Thus, it is clear that EV71 has a wider neurotropism than that of polioviruses.
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PMID:Pyramidal and extrapyramidal involvement in experimental infection of cynomolgus monkeys with enterovirus 71. 1199 81

Human herpesvirus 6 (HHV-6) has recently been recognized as an important pathogen in immunocompromised hosts, such as patients who have undergone allogeneic bone marrow transplantation (allo-BMT). Here we report a case of HHV-6 meningoencephalitis in a patient who underwent allo-BMT from an HLA-identical sibling. The patient suffered from headache, high fever, tremor, and disorientation on day 35 after allo-BMT. Findings at magnetic resonance imaging, electroencephalography, and routine cerebrospinal fluid (CSF) examination suggested the presence of viral meningoencephalitis. We diagnosed HHV-6 meningoencephalitis by means of polymerase chain reaction (PCR) analysis of a CSF specimen. Successful treatment was achieved with ganciclovir. Because HHV-6 encephalitis has a potentially fatal and fulminant course, it is necessary that HHV-6 encephalitis be recognized as one of the central nervous system complications that can follow allo-BMT. PCR analysis for HHV-6 in the CSF specimen is necessary for appropriate diagnosis and treatment.
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PMID:Human herpesvirus 6 meningoencephalitis successfully treated with ganciclovir in a patient who underwent allogeneic bone marrow transplantation from an HLA-identical sibling. 1204 76

A description of the St. Louis encephalitis (SLE) outbreak in Northeast Louisiana is presented. In the fall of 2001 there were 63 cases of St. Louis encephalitis in Monroe and West Monroe and seven additional cases in the neighboring parishes of Richland, Morehouse and Franklin. All cases had a clinical presentation of encephalitis and were confirmed serologically. Clinically most cases presented with fever, meningitis syndrome with altered mental status. Tremors were common (56% of cases). There were three deaths. Age-group distribution showed a predominance among 45 and older. The epidemic curve based on diagnosis date showed an explosive outbreak starting August 8, 2001, reaching a peak by the second week, and progressively slowing down. The curve showed that by the time the first case was diagnosed, 60% or more of the cases were already infected. Most of the cases come from low socio-economic areas. Houses were often run down, many with screens in disrepair. Backyards were usually large, with heavy brush and many trees. There was an abundance of sources of mosquito larvae, particularly for Culex quinquefasciatus which is the main vector. Mosquito pools confirmed the presence of SLE virus. As soon as the first case was reported, a campaign of health education and increased mosquito adulticiding were implemented.
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PMID:St. Louis encephalitis outbreak in Louisiana in 2001. 1251 26

A previously neurodevelopmentally intact 5-year-old male was admitted to hospital with a right lower lobe pneumonia with pleural effusion, subsequently confirmed to be a Mycoplasma pneumoniae infection. On the seventh day of the illness he had a prolonged generalized tonic or tonic-clonic convulsion, requiring intubation and ventilation. He was slow to regain consciousness (Child's Glasgow Coma Score 7-10 over 6 days) and brain imaging with CT and then MRI demonstrated bilateral thalamic lesions with oedema and central haemorrhage suggestive of acute bilateral thalamic necrosis, without striatal or white-matter involvement. He was treated with a 2-week course of erythromycin, and as an autoimmune process was considered possible, 5 days of intravenous methylprednisolone (20 mg/kg/day) followed by a 4-week oral prednisolone taper. He made a slow recovery over the next few weeks with almost complete neurological recovery by 2 months but with significant dysarthria, drooling, and a mild left hemiparesis. At 9 months, significant dystonia continued to affect his speech and, together with tremor, his upper-limb fine motor function bilaterally. His gait, personality, and higher cognitive functions appeared to have recovered fully. Although acute striatal necrosis, acute disseminated encephalomyelitis, and encephalitis have been reported with Mycoplasma pneumoniae and a similar picture of acute bilateral thalamic necrosis with influenza-A ('acute necrotizing encephalopathy'), this is the first reported case of Mycoplasma pneumoniae-associated isolated acute bilateral thalamic necrosis.
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PMID:Acute bilateral thalamic necrosis in a child with Mycoplasma pneumoniae. 1499 91

Clinical data adequate for analysis were available in 386 laboratory-confirmed cases of arthropod-borne encephalitis - 38 St. Louis and 348 western equine. Consistently observed symptoms varied with the age of the patient. Symptoms that occurred in a high proportion of patients in each age group were:LESS THAN ONE YEAR OF AGE: Fever and convulsions. (None had the St. Louis disease.)ONE THROUGH FOUR YEARS: Fever, headache, vomiting, drowsiness, irritability, restlessness, nuchal rigidity, tremor, and sometimes convulsions. FIVE THROUGH FOURTEEN YEARS: Headache, fever, and drowsiness. Sometimes the disease progressed no further, but if it did, nausea, vomiting, muscular pain, photophobia and limitation of neck and back flexion often were noted; and sometimes convulsions and intention tremors. FIFTEEN YEARS AND OLDER: Drowsiness, lethargy, malaise, fever, stiffness at the back of the neck and, almost always, severe intractable occipital headache associated with nausea, disturbance of vision, photophobia and vertigo. The extreme difficulty of differential diagnosis on the basis of clinical observation was indicated by the wide range of diagnoses made in these cases before the invading organism was identified by laboratory studies.
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PMID:The 1952 outbreak of encephalitis in California; differential diagnosis. 1306 16

A 26-year-old man, who had received a ventriculo-peritoneal shunt for obstructive hydrocephalus after possible encephalitis, complained of disturbance of upward gaze and difficulty in movement seven months after the shunt implantation. One month later, neurological examination revealed upward gaze paresis and rigidity of all four limbs, but the neuroimaging studies revealed no ventricular dilatation. His symptoms deteriorated, and tremor of the extremities appeared. He was admitted to our hospital 10 months after the shunt implantation. He developed akinetic mutism soon after admission. Cerebrospinal fluid protein was elevated (62 mg/dl). At that time, the shunt reservoir was found to be insufficiently filled, and neuroimaging showed dilatation of the lateral and third ventricles with no dilatation of the fourth ventricle. A neuroendoscopic third ventriculostomy with removal of the previous shunt system gradually resolved the parkinsonism within two months, and the patient became capable of walking. The dilatation of the ventricles improved on neuroimaging. The present report suggests that shunt malfunction should be suspected when parkinsonism occurs in patients who have undergone a shunt placement, even though hydrocephalus on neuroimaging is not observed.
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PMID:[A case of severe parkinsonism induced by failure of ventriculo-peritoneal shunt for aqueductal stenosis]. 1458 70

An apparently novel neurological disease clinically characterized by shaking, tremors, seizures, staggering gait, and ataxia was first observed in farmed mink kits in Denmark in 2000 and subsequently in Sweden, Denmark, and Finland in 2001, and again in Denmark in 2002. Lymphoplasmacytic encephalomyelitis was found in the affected kits. The lesions were most severe in the brainstem and cerebellum and consisted of neuronal degeneration and necrosis, neuronophagia, focal and diffuse gliosis, perivascular cuffs formed by lymphocytes, plasma cells and macrophages, and segmental loss of Purkinje cells. Testing was conducted to determine the cause of the disease, including general virological investigations (virus culture, negative-staining electron microscopy, immunoelectron microscopy, polymerase chain reaction for herpesviruses, adenoviruses, pestiviruses, and coronaviruses), tests for specific viral diseases (canine distemper, Borna disease, Louping ill, West Nile virus infection, tick-borne encephalitis, Aleutian disease), tests for protozoa (Toxoplasma gondii, Neospora caninum, Encephalitozoon cuniculi), bacteria (general culture, listeria, Clamydophila psittaci), and intracerebral inoculation of neonatal mice. The results of all these investigations were negative. One group of 3 mink kits inoculated intracerebrally with brain homogenate of affected mink developed clinical signs and histological lesions similar to those observed in naturally infected mink. Based on the histopathological features, it is postulated that the disease is caused by a yet unidentified virus.
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PMID:Investigations into shaking mink syndrome: an encephalomyelitis of unknown cause in farmed mink (Mustela vison) kits in Scandinavia. 1530 41

Poliovirus and enterovirus 71 (EV71) are both neurotropic enteroviruses that cause serious neurological diseases, such as poliomyelitis and encephalitis. The neurovirulence of EV71 in cynomolgus monkeys was demonstrated previously by intraspinal inoculation. In this study, an improved simian model of EV71 infection was established by using intravenous inoculation, which revealed clinical and neuropathological similarities between this model and human cases of encephalitis. Experimental EV71 infection induced direct neurological manifestations, such as tremor, ataxia and brain oedema, but not non-neurological complications, such as pulmonary oedema and cardiac failure. Using this model of EV71 infection, the neurotropic characteristics of the prototype strains of EV71 and poliovirus type 1 (PV1) were compared. Three monkeys were inoculated intravenously with 10(5.5) TCID50 EV71 and all developed neurological disease signs within 4-6 days of inoculation. However, after inoculation with 10(5.5) TCID50 PV1 strain OM1 (PV1-OM1), the major manifestation was flaccid paralysis, starting from the lower limbs 6-9 days post-inoculation. Histopathological and virological analyses of moribund monkeys revealed that disseminated EV71 infection was characterized by severe panencephalitis involving both the pyramidal and extrapyramidal systems. In contrast, the lesions induced by PV1-OM1 were mainly restricted to the pyramidal tract, particularly the spinal motor neurons, thalamus and motor cortex. In conclusion, neuropathological involvement in this model correlated well with the apparent differences in neurological disease induced by EV71 and PV1-OM1. Thus, intravenous inoculation with EV71 is an excellent model to study the neuropathology of EV71 and to evaluate candidate vaccines and potential antiviral agents.
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PMID:Differential localization of neurons susceptible to enterovirus 71 and poliovirus type 1 in the central nervous system of cynomolgus monkeys after intravenous inoculation. 1544 61


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