Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 16-year-old female presented with clinical, morphologic and molecular features of mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS). Her early development was normal. Starting from the age of 14 years, she experienced recurrent episodes of headaches, with vomiting, seizures, transient right hemiparesis and decreased visual acuity. Computed tomographic brain scans revealed calcification in the bilateral basal ganglia. Biopsied specimens from her left biceps brachii and rectus femoris muscles revealed ragged-red fibers and strong succinate dehydrogenase-reactive blood vessels. Electron microscopy revealed paracrystalline inclusions in muscle mitochondria. Analysis of mitochondrial DNA (mtDNA) from blood, hair follicles and muscle specimens showed an A to G point mutation at nucleotide position 3,243 in the transfer RNA(Leu(UUR)). The proportion of mutant mtDNA in the patient's blood was 43%, in hair follicles 62% and in muscle 82%. The patient was followed up for 4 years and had progressive mental deterioration and died of an episode of status epilepticus. This patient and 5 other MELAS patients reported in Taiwan are compared.
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PMID:Heteroplasmic mitochondrial DNA mutation in a patient with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes. 761 32

A 4-year-old boy presented with developmental delay, aggressive behavior, and incoordination. His EEG showed a diffuse encephalopathy. At age 10 he developed convulsions and severe migraine-like headaches. Muscle wasting, arreflexia, and lactic acidemia following exercise were noted. Electromyography was myopathic and nerve conduction studies revealed a peripheral neuropathy. Muscle biopsy demonstrated variation in fiber size and an excess of lipid droplets. He than had several stroke-like episodes and periods of unconsciousness, associated with severe metabolic acidosis. Muscle cytochrome C oxidase was abnormally low. This boy displayed the classical clinical and biochemical features of MELAS syndrome, namely Mitochondrial myopathy, Encephalopathy, Lactic Acidosis, and Stroke-like episodes. Treatment included carnitine, vitamin C, vitamin K, riboflavin, coenzyme Q10, and corticosteroids. He died at the age of 14 years following an episode of seizures, coma, and gastrointestinal hemorrhage. This is the first reported case of MELAS syndrome in Israel.
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PMID:MELAS syndrome: peripheral neuropathy and cytochrome C-oxidase deficiency: a case report and review of the literature. 772 60

A 61-year-old woman was treated with cisplatin and etoposide for ovarian carcinoma. After the second course of chemotherapy she developed acute encephalopathy which manifested itself as headache, fever, a partial seizure, confusion, and mild right hemiparesis, although no evidence of a central nervous system infection was found. Ten days after the onset of neurological symptoms, she experienced a sudden loss of vision in both eyes. Neurological findings were compatible with cortical blindness. Neurological symptoms subsided and visual acuity completely returned over the next months. The total cumulative dose of cisplatin was 325 mg/m2. She died of aspiration pneumonia on the 43rd day. Postmortem examination revealed severe nerve cell loss, gliosis and spongy changes in the bilateral occipital cortex including visual field, and slight to moderate demyelination in the subcortical white matter of the occipital cortex, Goll's tract, and dorsal root ganglia. As far as we know this encephalopathy is the second report in which the neuropathological changes associated with cisplatin therapy have been demonstrated by autopsy findings. The first was a case report of leukoencephalopathy, which differed significantly from our case in the primary lesions of the brain. We measured the platinum level in several parts of the cerebrum and cerebellum, optic nerve, spinal cord, and cauda equina by using an atomic absorption spectrophotometric technique. Platinum was detected in the bilateral occipital cortex, spinal cord, and cauda equina. These results were consistent with the distribution of pathological lesions. The mechanism of cisplatin-induced focal encephalopathy remains speculative.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinicopathological report of cisplatin encephalopathy]. 778 Dec 18

Between 19 March 1990 and 24 December 1992, six persons in Nova Scotia presented with a unique neurological illness. A prodrome of fever and headache was followed by neurogenic bladder, transverse myelitis, and encephalopathy in association with mononuclear pleocytosis of the CSF and nerve-conduction study findings consistent with polyradiculopathy. The spinal cords of three of the patients appeared abnormal on myelograms or magnetic resonance imaging studies. No microbial agent was isolated or demonstrated serologically. All of the patients were treated with antimicrobial agents and corticosteroids. Three recovered completely, but neurogenic bladder persisted in the remaining three. We suggest that this group of patients manifested an encephalomyeloradiculopathy that is likely a new clinical entity of infectious or parainfectious etiology.
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PMID:Encephalomyeloradiculopathy of infectious or parainfectious etiology--a new entity? 779 99

The present prospective study was carried out to observe the changing trends in the clinical pattern and multidrug resistance in typhoid fever. Fever was the main presenting feature. Other associated features were headache, vomiting, diarrhoea, altered sensorium and jaundice. Out of 78 patients, one patient died due to enteric encephalopathy and other due to septicaemia with peripheral circulatory failure. 12 patients responded to chloramphenicol and gentamycin. 51 patients responded to ciprofloxacin, while remaining 9 patients responded to combination of cefotaxime and amikacin. Three patients showed in vitro resistance to ciprofloxacin and two out of these also showed no response in vivo. This study re-emphasises the changing pattern, prolonged course and role of quinolones especially ciprofloxacin in the management of drug resistant typhoid fever, but at the same time indicates that ciprofloxacin is not the drug of choice in all cases of typhoid fever and resistance to it may be seen in some cases, where other drugs have to be used.
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PMID:A study of culture positive multidrug resistant enteric fever--changing pattern and emerging resistance to ciprofloxacin. 786 49

The clinical manifestations and mitochondrial DNA (mtDNA) mutations in a Taiwanese family with a female proband exhibiting mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes syndrome are reported. Clinically, the proband had a stroke-like episode with right hemiparesis, hemianopsia and mental dysfunction as well as short stature, hearing impairments, and elevated lactate levels. Brain magnetic resonance images showed multiple increased signal intensities over the left frontal, parietal and temporal areas. There were no ragged-red fibers, but paracrystalline inclusion bodies were shown in the muscle biopsies under electron microscopic examination. A deficiency of NADH-CoQ reductase was also found in biochemical studies of the muscles. The family survey revealed no abnormal findings except for headache and episodic vomiting in her mother. The molecular analysis of mtDNA disclosed a mutation from A to G at the nucleotide pair 3243 of the mitochondrial transfer RNA(Leu) gene in the blood, hair follicles and/or muscle of the maternal relatives. A characteristic finding of the MELAS family is variation of percentage of mutated mtDNA in various tissues and individuals. However, a higher proportion of mutated mtDNA was noted in the proband than that in the asymptomatic or oligosymptomatic family members. From the data, the variable clinical phenotypes in this MELAS family can be explained at least partly, by the different proportions of mutant mtDNA in the target tissues of the proband and maternal relatives.
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PMID:MELAS syndrome: correlation between clinical features and molecular genetic analysis. 788 36

A 19-year-old boy was admitted to our hospital because of impaired consciousness after experiencing fever and headaches for 7 days. The patient was in a deep coma or generalized convulsions, with retrocollis and decorticate posture. He never regained consciousness, remaining in an apallic state. The initial CSF pressure was 290 mm H2O, CSF cell count 18/3 mm3, protein 75 mg/100 ml, and sugar 74 mg/100 ml. There was no significant elevation in the viral titer in the serum or CSF. Plain CT on admission showed marked brain edema. MRI three months thereafter demonstrated symmetrical high intensity in the thalamus, the putamen and the cerebellum on both T1- and T2-weighted images, probably representing petechial bleeding. The lesions in the medial portion of the occipital lobes showed iso intensity on T1-weighted images and high intensity on T2-weighted images. These lesions were consistent with infarction of both posterior cerebral arteries, which may have been due to severe brain edema. The clinical and MRI findings were similar to those of patients with acute encephalopathy with low-density areas in the thalamus or bilateral striatal necrosis in childhood. To the best of our knowledge, there have been no reports of cases like ours in adults.
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PMID:[Acute encephalopathy with symmetrical lesions of the thalamus, the putamen and the cerebellum on magnetic resonance imaging]. 806 41

Neurological complications are important contributors to morbidity and mortality after liver transplantation. We reviewed 391 patients who underwent 427 consecutive orthotopic liver transplantations to analyze the clinical features of patients who experienced one or more neurological complication (74 patients [19%]) and to compare postoperative neurological problems in adults versus children. Neurological complications were more frequent in adults (64 of 273 patients [23%]) than children (10 of 118 patients [8%]) (P < 0.01). The most common neurological complication was encephalopathy (59%), which ranged widely in severity and occurred with similar frequency in adults and children. Other common neurological complications were seizures (12 patients), brachial plexus and peripheral nerve injuries (16 patients, 15 of whom were adults), stroke (5 patients), and central nervous system infections (5 patients). In 27 patients, drug toxicity was the primary cause of neurological complications, all of which reversed with dosage reduction or discontinuation of drug. Cyclosporine and FK506, primarily during intravenous administration for induction of immunosuppression, accounted for 25 of 27 drug-induced neurological complications, which included encephalopathy, seizures, severe tremor, and severe headache. Despite a higher rate of neurological complications in adults, those in children were more severe and associated with a higher mortality rate. When compared with liver transplant recipients without neurological complications, patients with neurological complications had a higher posttransplant mortality rate (14% vs. 5% for adults, and 50% vs. 7% for children). In conclusion, neurological complications after liver transplantation are more common in adults, more severe and associated with a higher mortality rate in children, and associated with a higher mortality rate in both children and adults when compared with transplant recipients without neurological complications.
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PMID:Neurological complications of liver transplantation in adult versus pediatric patients. 807 14

Meningeal involvement occurred in eight (22%) of 36 adult patients with AIDS-related systemic non-Hodgkin's lymphoma, seen over a 10-year period. Clinical symptoms consisted of cranial nerve palsies, radicular involvement, headache or diffuse encephalopathy. CSF examination established the diagnosis in all cases. Systemic disease had been diagnosed seven to 33 weeks before lymphomatous meningitis in six patients, whereas in the remaining two patients diagnoses of systemic and meningeal disease were made simultaneously. All patients had intermediate or high grade lymphomas and widespread disease. In contrast to non-AIDS related lymphomas, bone marrow involvement at initial staging cannot be used to select patients for prophylactic treatment, as seven of our eight patients had no initial bone marrow involvement. In this retrospective review, prognosis of lymphomatous meningitis was extremely poor, with a mean survival of only five weeks. Survival of patients with systemic lymphoma who eventually developed lymphomatous meningitis was 4.0 months compared with 7.2 months for those who did not. Lymphomatous meningitis appears to have the worst outcome of all AIDS-related neurological complications, regardless of treatment.
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PMID:Lymphomatous meningitis in AIDS-related systemic non-Hodgkin's lymphoma: a report of eight cases. 812 96

BW12C79 stabilizes the oxyhemoglobin molecule resulting in a reversible left-shift of the oxygen saturation curve. The activity of a number of bioreductive anticancer drugs, such as mitomycin C, may be enhanced under hypoxic conditions. Twenty-four patients with various malignancies received BW12C79 and mitomycin C. BW12C79 was administered i.v. with a loading dose (20-50 mg/kg) over 1 h followed by a maintenance infusion of 4 mg/kg/h for 5 h. Percentage modification of the oxyhemoglobin (degree of left-shift) was dose related with maximum modification of 56% and was maintained for the duration of maintenance infusion of BW12C79. Hemoglobin electrophoresis showed a fast moving band consistent with the BW12C79-oxyhemoglobin complex. Side effects at the top dose level comprised headache, nausea/vomiting, vein irritation, and myocardial ischemia. One other patient suffered from an acute encephalopathy of unknown etiology a few days following BW12C79. 31P magnetic resonance spectroscopy of exercising calf muscles showed increased breakdown of high energy phosphate stores and a greater reduction in pH. Recovery of the high energy phosphate stores after exercise was slow. These results were consistent with reduced oxygen supply due to either a left shift of the oxygen saturation curve and/or reduced muscle blood flow. BW12C79 did not interfere with the pharmacokinetics of mitomycin C. In conclusion, this phase I study demonstrates the feasibility of achieving a significant left shift in the oxygen saturation curve in cancer patients which is maintained for at least 5 h with acceptable toxicity. The maximum tolerated dose of BW12C79 was 50 mg/kg loading infusion followed by a maintenance infusion of 4 mg/kg/h. Magnetic resonance spectroscopy results were consistent with reduced supply of oxygen to exercising skeletal muscle. BW12C79 may be of potential benefit as an adjunct to bioreductive drugs in the treatment of solid tumors.
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PMID:A phase I study of the left-shifting agent BW12C79 plus mitomycin C and the effect on the skeletal muscle metabolism using 31P magnetic resonance spectroscopy. 824 19


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