Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Among the white races, the prevalence rates of Parkinson's disease range from 66 to 187 per 100,000 population, through without any obvious geographical pattern. A similar variation is found in the annual incidence rates with estimates from 5 to 24 per 100,000 population. The black races may be partially protected against the disease. Both sexes are probably equally affected by the disease. Parkinson's disease usually begins after the age of 50 years, and the risk of the disease steeply rises with advancing age. Parkinson's disease is often omitted in death certificates; mortality rates with Parkinson's disease as an underlying cause of death vary from 0.5 to 3.8 per 100,000. Levodopa treatment, by reducing the excess mortality accompanying the natural course of Parkinson's disease, may increase the number of patients living with this disease in the near future. Postencephalitic Parkinson's disease, developing as a sequel to lethargic encephalitis and accounting for some two thirds of parkinsonian cases shortly after the epidemic, has probably been a transient phase in the epidemiology of Parkinson's disease and is now disappearing. Data from epidemiological investigations have advanced our understanding of the cause of Parkinson's disease only to a small extent. No other characteristic than race has been found to influence the susceptibility to the disease. The environmental risks for Parkinson's disease have not been unequivocally demonstrated. Highly conflicting information is available as to the contribution of hereditary to the pathogenesis of Parkinson's disease. Seroepidemiological investigations have shown an increased antibody response against herpes simplex virus in parkinsonian patients, but attempts to detect herpes virus specific products or DNA sequences in the brain material have been unsuccessful.
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PMID:Epidemiology of Parkinson's disease--an overview. 726 26

The intracerebral inoculation of hamster neurotropic measles virus produces a fatal acute encephalopathy in the majority of weanling BALB/c mice. The few survivors remain healthy indefinitely. In contrast, weanling SJL/J mice are relatively resistant to acute encephalopathy, and about one-third of the survivors predictably develop a chronic encephalitis many weeks after inoculation. This later illness is characterized clinically by wasting, lethargy, seizures, or focal paralysis, usually culminating in death. Pathologically, a considerable brain inflammatory response occurs in association with abundant measles viral antigen. Viral antigen and inflammation were demonstrable predominantly in the limbic system but was also present in the cerebellum and brain stem. Antibody to measles virus was readily demonstrated in all animals with chronic encephalitis. This report constitutes the first description of chronic measles encephalitis in an inbred host.
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PMID:Chronic measles encephalitis in mice. 744 Oct 20

A 2-phase study was conducted to evaluate the ability of the NEB-1 strain of porcine reproductive and respiratory syndrome virus (PRRSV) to potentiate common bacterial pathogens of swine. In phase I, 25 of 50 4-5-week-old specific-pathogen-free (SPF) pigs were exposed to NEB-1 PRRSV (day 0). Seven days after virus inoculation, 8 groups received 1 of 4 bacterial pathogens: Haemophilus parasuis, Streptococcus suis, Salmonella cholerasuis, and Pasteurella multocida. The ability of NEB-1 PRRSV to produce clinical disease, viremia, neutralizing antibody, gross and microscopic lesions and to potentiate bacterial pathogens was assessed. Response to NEB-1 PRRSV was similar among inoculated pigs; prolonged hyperthermia, lethargy, mild to moderate dyspnea, and cutaneous erythema were consistent clinical signs. No clinical differences were observed in groups after bacterial challenge. Virus was isolated from serum at weekly intervals through the end of the study, and all PRRSV-inoculated pigs had seroconverted by study termination. Two of 5 pigs died in non-PRRSV-inoculated groups challenged with H. parasuis and Streptococcus suis. Mortality in PRRSV-infected pigs was limited to 1 of 5 pigs from the Salmonella cholerasuis-challenged group. Gross lesions were seen in pigs dying after inoculation in H. parasuis- and Streptococcus suis-inoculated groups, in Salmonella cholerasuis- and P. multocida-challenged pigs, and in 1 non-PRRSV-inoculated control pig. Microscopic lesions consisted of mild to moderate proliferative interstitial pneumonia, nonsuppurative myocarditis, lymphoid hyperplasia, and nonsuppurative encephalitis in PRRSV-inoculated pigs. Findings in phase I indicated that NEB-1 PRRSV does not potentiate bacterial disease while inducing consistent clinical signs, viremia, seroconversion, and microscopic lesions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Porcine reproductive and respiratory syndrome: NEB-1 PRRSV infection did not potentiate bacterial pathogens. 757 44

The value of the PCR for CMV in the CSF was evaluated. 23 samples from 20 patients were examined for CMV DNA, of which 11 were positive and 12 were negative for CMV. The clinical spectrum of the patients with positive samples included encephalitis, encephalitis, and polyradiculopathy, or isolated polyradiculopathy. The main symptoms were fever, confusion, lethargy, cognitive disturbance, cranial neuropathy, weakness of the legs, and incontinence. The laboratory evaluation showed a low CD4 lymphocyte count, a slightly increased blood sedimentation rate and a large variation of CSF patterns. The CMV early antigen tests were negative in all cases. In 4 cases the neuroradiological examination was compatible with CMV infection. 8 patients were treated with ganciclovir or foscarnet. Improvement of symptoms was observed in 2 cases and stabilization in 2 others. However, the CMV infection was rapidly progressive and 9 out of 10 patients died after a mean of 53 days after diagnosis.
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PMID:[Clinical value of a polymerase chain reaction on cytomegalovirus DNA in cerebrospinal fluid in HIV patients with neurological symptoms]. 774 Feb 95

In 1950, a 24-year-old man developed gait disturbance, incontinence of urine and increasing lethargy a week after a course of antirabies vaccination. He was diagnosed as having post-rabies vaccination encephalitis and had been in hospital for 37 years before he died in 1987. This is one of the rare cases in which the course of this disease was traced for an exceptionally long period. His personality began to deteriorate at an early stage of the illness, but his intellectual faculties seemed to be maintained rather well until a few years prior to his death. A neuropathological study revealed disseminated, patchy and somewhere perivascularly located demyelinated lesions in the cerebral white matter. Inflammatory lymphocytic infiltration was also remarkable in the CNS regions. But while the superimposed lesions due to convulsive attacks, traumatic contusion and terminal anoxia were remarkable, the whole aspect of neuropathological changes in rabies inoculation encephalitis cannot be observed.
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PMID:A case of antirabies inoculation encephalitis with a long clinical course. 790 39

This report concerns a 68-year-old male who was diagnosed as having purulent ventriculitis based on CT and MRI findings. He was first admitted to a nearby hospital with fever and impaired consciousness and thought to be suffering from herpes simplex encephalitis based on laboratory findings. In spite of treatment with acyclovir and antibiotics, his symptoms persisted for one and a half months. Because of gradual deterioration of his neurological status, he was transferred to our hospital. On admission he was stuporous with nuchal rigidity and a fever of 38.5 degrees C. The CSF leukocyte count was elevated (217/mm3) with predominantly polymorphonuclear cells (mononuclear 20, polymorphonuclear 197). Gd-DTPA MRI (T1-weighted) showed marked enhancement of the ependyma of the fourth ventricle and both lateral ventricles. A diagnosis of purulent ventriculitis was made and high-dose antibiotics (ABPC 12g, CTX 9g) were started intravenously. Gradual improvement in the clinical signs was observed with rapid normalization of the CSF cell-count. The patient had completely recovered one month after the start of treatment and this was associated with disappearance of abnormal enhancement on the MRI images. Although cerebral ventriculitis occasionally occurs as a complication of neonatal meningitis, it is rare in adult purulent meningitis. In our patient, persistent meningitis combined with impaired drainage of CSF from the ventricles are presumed to have caused ventriculitis. Serial enhanced MRI is particularly helpful in diagnosing ventriculitis, and can serve as a good index for monitoring the effects of treatment.
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PMID:[MRI imaging of purulent cerebral ventriculitis]. 806 40

A retrospective examination of lethargic encephalitis finds many parallels with neuroleptic effects. The encephalitis, like the neuroleptics, produced an acute continuum of cognitive disorders from emotional indifference through apathy and onto a rousable stupor. It also produced similar acute dyskinesias, including akinesia, akathisia, dystonia, oculogyric crises, and tremors. The encephalitis also caused similar chronic effects, including dementia and psychosis, and somewhat different persistent dyskinesias. The chronic motor and cognitive disorders, like those associated with the neuroleptics, were often delayed in onset. An acute, severe episode of lethargic encephalitis also finds a parallel in the neuroleptic malignant syndrome. These parallels are probably due to a common site of action in the basal ganglia. They provide a model for understanding many neuroleptic effects and alert us to the probability of persistent cognitive deficits, including dementia, from neuroleptic treatment.
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PMID:Parallels between neuroleptic effects and lethargic encephalitis: the production of dyskinesias and cognitive disorders. 810 24

A study of literature concerning Lyme borreliosis related to animals was done. In the research work the epidemiology, pathogenesis, diagnosis and treatment of horses, cattle and dogs affected with Lyme borreliosis have been discussed. The clinical signs of Lyme borreliosis in horses are: chronic weight loss, sporadic lameness, laminitis, low grade fever, swollen joints, muscle tenderness and anterior uvetitis. In addition to these clinical sings, neurological sings such as depression, behavioral changes, dysphagia and encephalitis can be seen in chronic cases. Cattle affected with acute Lyme borreliosis often show fever, stiffness, swollen joints and decreased milk production. Chronic weight loss, laminitis and abortion are also a possible outcome of borreliosis in cattle. An early infection of Lyme borreliosis in dogs may give evidence of inapetenca, lethargy, lyphadenopathy, and an acute onset of stiffness or pain while a recurrent intermittent nonerosive arthritis is a more advanced manifestation of canine Lyme borreliosis. Glomerulonephritis and tubular damage secondary to Borrelia burgdorferi infection have been reported to occur in normally infected dogs. In an endemic area atrioventricular heart block has also been reported. The underlying pathogenesis of Lyme disease is still unknown. The diagnosis of clinical Lyme borreliosis is difficult and it depends on a successful recognition of clinical signs, a history of possible exposures to the infection and on serologic testings. The therapy of Lyme borreliosis in animals is based upon the principal therapy of this disease in human medicine.
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PMID:[The importance of Lyme borreliosis in veterinary medicine]. 826 22

We describe a fatal case of adenovirus pneumonia accompanied by encephalitis in a neonate who showed lethargy on the 6th day and died on the 12th day. Adenoviral particles as well as viral intranuclear inclusions were noted in pulmonary alveolar epithelium cells. Neuropathological examination revealed diffuse oedema, perivascular cuffing and gliosis in the white matter. Adenovirus type 11 was isolated from lung, hilar lymph node, and brain tissue. This is the first instance of adenovirus isolation from brain tissue in a newborn infant. The virological and neuropathological findings suggest the invasion of neural tissue by adenovirus and substantiate the significance of neurological symptoms observed in neonatal adenovirus infection.
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PMID:Isolation of adenovirus type 11 from the brain of a neonate with pneumonia and encephalitis. 833 17

Clinicopathological and immunohistochemical studies were performed in a patient with paraneoplastic limbic encephalitis, myelitis, sensory neuropathy and cerebellar degeneration secondary to small cell lung cancer. A 67-year-old male smoker developed orthostatic dizziness 6 months prior to admission. Over the following months, his wife noticed that he became forgetful and confused. Over the next three weeks, he became unable to sit or stand unaided and admitted to our service. On admission, he was lethargic and disoriented in time and place. Neurological examination revealed marked limb weakness with distal dominant muscle atrophy. A chest radiograph demonstrated a mass in the right middle lobe and a bronchial biopsy revealed a small cell carcinoma. CT scan and MRI of the brain revealed abnormalities in the bilateral medial temporal lobes and putamen. He was treated with anti-cancer chemotherapy, but died of respiratory failure after 13 months illness. Postmortem examination showed a mass in the right middle lobe of the lung. No tumor metastases were noted in the nervous tissue. Microscopical examinations of the nervous system revealed neuronal loss, astrogliosis and perivascular and parenchymatous lymphocytic infiltration in the hippocampus, subiculum, amygdala, putamen, medulla oblongata, spinal cord and dorsal root ganglia. Loss of Purkinje cells was also seen in the cerebellum without lymphocytic infiltration. Immunohistochemical analysis of the patient's serum and CSF by the use of adult rat brain revealed immunoreactivity at the hippocampal pyramidal neurons CA3 and CA4. At the higher dilution, neuronal nuclei were specifically stained.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A clinicopathological study of a patient with paraneoplastic limbic encephalitis, myelitis, sensory neuropathy and cerebellar degeneration, associated with a unique antineuronal antibody]. 839 16


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