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)

We represent a case of cystic dilatation of the fourth ventricle resulted from obstruction of the foramina of Luschka and Magendie and of the aqueduct of Sylvius which developed after a surgery of AVM. A 42-year-old woman was admitted to our clinic for the operation of AVM located at the trigone of lateral ventricle and the lateral wall of midbrain. VPS had been performed previously because of acute hydrocephalus resulted from several attacks of ventricular hemorrhage. Total removal of the AVM was performed. The patient was stuporous after the surgery, and CT scan showed marked distension of the fourth ventricle with shifted third ventricle and slightly dilated supra-tentorial ventricular system. Although a revision of the abdominal side of VPs performed and the lateral and the third ventricles were shunted effectively, the fourth ventricle continued to show remarkable distension. Since it was considered that the occlusion of the foramina of Luschka and magendie due to previous episodes of ventricular hemorrhage and the blockage of the aqueduct of Sylvius 'trapped' the fourth ventricle, suboccipital craniotomy and re-opening of the foramen of Magendie was performed. The arachnoid membrane around the cisterna magna was strongly adhered to the dura mater. When incision was made on the arachnoid membrane between the cerebellar tonsils, slightly turbid and xanthochromic CSF spurted out and some old clots were also aspirated from the opened fourth ventricle. The size of the fourth ventricle returned normal on CT scan ten days after the operation, and the patient recovered progressively afterwards.
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PMID:[A case of trapped fourth ventricle which developed after a surgery of AVM (author's transl)]. 727 34

The combination of mitozantrone, methotrexate and mitomycin (3M) gives a response rate of around 50% in patients with advanced breast cancer. The predominant toxicity is haematological. In this study, previously untreated patients were given 3M with increasing doses of mitozantrone (7-14 mg m-2) with recombinant human granulocyte colony-stimulating factor (metHuG-CSF) (filgrastim) to prevent marrow toxicity. Doses administered were 7 mg m-2 mitomycin i.v. 6 weekly, methotrexate i.v. 35 mg m-2 (maximum 50 mg) 3 weekly and mitozantrone i.v. 3 weekly as follows: 7 mg m-2, six patients (group 1); 10 mg m-2, six patients (group 2); 12 mg m-2, six patients (group 3); 14 mg m-2, six patients (group 4); all on day 1 for six cycles at the assigned dose. All patients received filgrastim (Amgen 0.3 mg ml-1) at a dose of 5 micrograms kg-1 subcutaneously daily on days 4-17 of each cycle. All treatment was given on an out-patient basis. A total of 24 patients were entered into the study. The median age was 63 years (range 48-75). ECOG performance status was 0 in ten, 1 in 11 patients and 2 in three patients. Locoregional disease alone was present in seven patients. The remainder had one or more sites of metastases. The actual dose administered to the 24 patients was as follows. The six patients in group 1 all completed six courses of treatment as per protocol. In group 2, three patients completed six courses, two stopped because of toxicity after one and four courses and one had progressive disease after one course. In group 3, three patients completed and three stopped early because of progressive disease. In group 4, two patients completed, one progressed after four courses and three responding patients stopped treatment because of toxicity. The maximum tolerated dose of mitozantrone in the 3M combination was 12 mg m-2. The use of filgrastim with increasing doses of chemotherapy prevents neutropenia, but other toxicities, namely thrombocytopenia and lethargy, then become dose limiting.
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PMID:Phase I study of mitozantrone, methotrexate and mitomycin with granulocyte colony-stimulating factor (filgrastim) in patients with advanced breast cancer. 752 7

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

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 patient with subacute sclerosing panencephalitis (SSPE) was treated with an intraventricular alpha interferon (IFN-alpha) through an Ommaya reservoir. A 17-year-old boy, who had a history of measles exposure at age 1, showed forgetfulness, difficulties in calculation, reading and writing. Two months later he developed generalized convulsions and myoclonic spasms. He was admitted to the National Saigata Hospital in May 20, 1992. On admission, anti-measles antibody titer in the CSF was 1:16 by complement-fixation method. His EEG revealed a periodic synchronous discharge. Therefore, the diagnosis of SSPE was confirmed. An Ommaya reservoir was implanted on July 7, 1992, and an intraventricular administration of INF-alpha was begun after two weeks. The dose of INF-alpha was gradually increased from 1.0 x 10(6) IU/m2 to 2.0 x 10(6) IU/m2 twice a week. Fever, vomiting and anorexia were developed when the INF-alpha injection was first started. When he received a total dose of 8.0 x 10(6) IU, he became bed ridden for remarkable lethargy. The lethargy was continued for about 10 days despite the therapy was interrupted, and then he gradually became alert. The frequency of myoclonus became more frequent and mentality got worse, so the treatment with INF-alpha was tried again in decreasing the dose to 1.0 x 10(6) IU/m2 twice a week. However, be became drowsy again after he received a total of 7.5 x 10(6) IU. With intramuscular or intravenous administrations of the high doses of INF-alpha (> or = 1.0 x 10(7) IU), significant neurological abnormalities were reported to occur.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of subacute sclerosing panencephalitis treated with intraventricular interferon--the side effects of interferon-alpha to the central nervous system]. 815 18

We report on two children who presented acute, severe, neurological dysfunction with bilateral, reversible, selective thalamic lesions demonstrated by brain MRI. In both children neurological symptoms appeared two weeks after a febrile respiratory illness. Clinical conditions worsened in a few days to a stuporous state and tetraplegia in one and to coma with decerebrate posturing in the other. Three weeks after the onset, both children improved and recovered within one month. During the acute phase, brain MRI showed in both children bilateral hyperintense areas on T2-weighted sequences limited to both thalamic regions. During the follow-up, repeated brain MRI showed complete disappearance of abnormalities in one patient and a small residual left thalamic lesion in the other. In both patients hematological routine exams were normal. Bacterial and viral studies of serum and CSF were negative. CSF findings showed elevated white blood cell count and protein levels, with no oligoclonal IgG bands. Urine and CSF organic acids by GC/MS and plasma as well as CSF amino acids were normal. We believe that the benign evolution of this disorder and CSF findings strongly suggest a postinfectious process of the central nervous system.
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PMID:Bilateral, reversible, selective thalamic involvement demonstrated by brain MR and acute severe neurological dysfunction with favorable outcome. 820 52

Ornithine transcarbamylase deficiency (OTCD) is caused by an alteration of urea synthesis, linked with partial modification of the X-chromosome, whose clinical manifestations are: lethargy, nausea, vomiting and cerebral edema. While in newborn males OTCD presents with hyperammoniemia leading to cerebral palsy with profound neurological impairment and eventually death, in women who are healthy carriers, it is possible to detect the disorder only through specific tests, since heterozygote women are rarely symptomatic. We describe the case of a young woman admitted to the hospital after an episode of mental confusion with vomiting and psychomotor restlessness, which had previously occurred several times during the premenstruum and lasted a few hours. A 2 day history of stupor made admission mandatory. Tests carried out during the hospital stay showed marked hyperammoniemia and unconjugated hyperbilirubinemia, marked cerebral edema documented by a CT scan. Liver biopsy and CSF test were normal. Screening of plasma and urinary aminoacids, level of orotic acid in the urine and OTC activity in the liver, confirmed the diagnosis of OTCD. The possibility of early diagnosis and therapy of a disease which otherwise leads to death, emphasizes the importance of precise evaluation of a possible organic cause of anorexia and behaviour disorders in young women.
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PMID:Hyperammoniemic coma in an adolescent girl: an unusual case of ornithine transcarbamylase deficiency. 828 23

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

This community-based study analyzed 54 patients with definite or probable tuberculous meningitis (TBM) in New Mexico from 1970 through 1990. Patients ranged in age from 4 months to 86 years. The highest age-specific incidence occurred in the elderly, but 22% of patients were less than 10 years old. Native American patients were overrepresented. Patients were as likely to live in small towns as in large urban cities. Symptoms were present for a median of 13 days before admission. The majority of patients had fevers, headache, stiff neck, and mental changes, such as confusion or lethargy. No patient was admitted comatose. Focal neurologic signs were present in 33%. Laboratory testing found hyponatremia in 79%, pulmonary infiltrates on chest x-ray in 40%, ventricular dilatation on CT or MRI in 52%, and tuberculomas in 16%. PPD skin tests were positive in 64%. CSF cultures grew Mycobacterium tuberculosis in 50%, but colony counts were always lower than 10(2)/ml. As a consequence, acid-fast stains of CSF sediment were reported as positive in only 4%. Six patients were not diagnosed during the hospitalization and died of complications. Twenty-three percent of patients who were appropriately treated also died of complications during the initial hospitalization. Tuberculous meningitis continues to be an important disease in small communities, and affects all ages and ethnic and socioeconomic backgrounds.
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PMID:Tuberculous meningitis in the southwest United States: a community-based study. 841 30

A 2-day-old infant with lethargy and hypoventilation had pachygyria and agenesis of the corpus callosum on CT scan. Increased concentrations of glycine in plasma and CSF, together with an increased CSF/plasma ratio, confirmed a clinical diagnosis of non-ketotic hyperglycinaemia. This is the first report of pachygyria in this disorder, although agenesis of the corpus callosum is well recognized, and non-specific gyral malformations have been described previously. The specific diagnosis of an inborn error of metabolism in infants with structural brain malformations is of critical importance for accurate genetic counseling.
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PMID:Non-ketotic hyperglycinaemia presenting as pachygyria. 875 Jun 2


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