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)

In a series of 27 patients with proved pheochromocytoma, differential analysis of catecholamines in blood, urine, and tumor specimens of 19 patients enabled grouping of subjects into those whose tumors produced predominantly norepinephrine (NE) (11 patients), predominantly epinephrine (E [Two patients]) and approximately equal amounts of both (six patients). Sustained hypertension was more common in the first group and pallor and tremor in the latter two groups, but no distinctive syndrome could be recognized as signifying the secretion of NE or E. Headache was a symptom in 20 of 27 patients and was related to sudden, transient elevation of the blood pressure, rather than sustained hypertension. The variable duration and intensity of the headache in different patients can be explained by the pressor and cranial vasoconstrictor effects of the secreted amines, which respectively enhance and diminish vascular headache.
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PMID:Symptoms of pheochromocytoma, with particular reference to headache, correlated with catecholamine production. 125 42

The authors report 7 cases of infants presenting with an apparent life-threatening event associated with acute pericerebral haemorrhage (subarachnoid haemorrhage and/or subdural hematoma) without evidence of traumatism, abuse, or shaking. Clinical characteristics were the same in all cases, including limpness, severe dysautonomic disorders, and pallor; all infants had retinal and pre-retinal haemorrhages. Two infants died; the five survivors have severe neurologic sequelae. The symptoms revealing an infant's pericerebral haemorrhage are usually axial hypotonia and pallor. Traumatism remains the most common aetiology and must be searched for. Non-traumatic aetiologies are unusual and were excluded in these reported cases. The 'shaken baby' syndrome is not the sole aetiology of an apparent spontaneous pericerebral haemorrhage: a slight bump associated with predisposing vascular factors particular to infancy could be involved. When confronted with an apparent life-threatening event associating limpness and pallor, one must consider the diagnosis of pericerebral haemorrhage.
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PMID:[Is pericerebral hemorrhage a cause of severe malaise in infants?]. 133 65

The objective of this study was to determine which clinical features of typhoid and malaria are most helpful in distinguishing the two diseases among Papua New Guinean highlanders. In a study of 35 patients with culture-positive typhoid and 49 with blood-slide-positive malaria (Group 1), the odds of typhoid were increased most in patients with altered bowel habit, an illness of more than 2 week's duration, tremor or the presence of typhoid facies. The odds of typhoid were lowest in patients with pallor or jaundice. These findings were used to derive a clinical diagnostic algorithm, which was then evaluated in a further group of 34 typhoid patients and 41 malaria patients (Group 2). The sensitivity of the algorithm in diagnosing malaria was 91% in Group 1 and 71% in Group 2, with specificities of 85% and 79% respectively. For typhoid, the sensitivity of the algorithm was 85% and 79% for Groups 1 and 2, respectively, and the specificities were 91% and 71%. We conclude that the algorithm merits further evaluation in a primary health care setting and may prove useful in making an earlier diagnosis of typhoid.
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PMID:An algorithm for the clinical differentiation of malaria and typhoid: a preliminary communication. 134 Oct 91

An autopsy case of progressive supranuclear palsy (PSP) associated with central pontine myelinolysis (CPM) is reported. A 73-year-old male patient suffered from gait disturbance for about 5 years. The clinical features were characterized by gradual development of supranuclear ophthalmoplegia, tremor, bradykinesia, rigidity, neck dystonia, dementia and pseudobulbar palsy at the advanced stage of his illness. Treatment with levodopa did not improve his neurological signs and symptoms. PSP or multiple system atrophy was considered as a clinical diagnosis of the patient. He died of pneumonia, acute pancreatitis and liver dysfunction in November 1985. The main neuropathological findings were neuronal loss and gliosis with neurofibrillary tangles of globose type in the globus pallidus, subthalamic nucleus, substantia nigra and dentate nucleus, and at the base of the pons, bilateral and symmetrical demyelination was found. In addition, myelin staining revealed circumscribed pallor in the cerebral white matter. The histologic diagnosis was PSP associated with CPM. An association of PSP with CPM is rare in the elderly and possible etiologic factors of both diseases were discussed.
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PMID:[An autopsy case of progressive supranuclear palsy with central pontine myelinolysis]. 187 Feb 89

Thirty-six clinically diagnosed and pathologically confirmed Alzheimer's disease (AD) patients included 13 with cortical and subcortical Lewy bodies (LBs). The patients with LBs appeared to constitute a distinct neuropathologic and clinical subset of AD, the Lewy body variant (LBV). The LBV group showed gross pallor of the substantia nigra, greater neuron loss in the locus ceruleus, substantia nigra, and substantia innominata, lower neocortical ChAT levels, and fewer midfrontal tangles than did the pure AD group, along with a high incidence of medial temporal lobe spongiform vacuolization. Analysis of neuropsychological tests from 9 LBV subjects and 9 AD patients matched for age and degree of dementia revealed greater deficits in attention, fluency, and visuospatial processing in the LBV group. Similar comparisons of neurologic examinations showed a significant increase in masked facies; in addition there was an increase in essential tremor, bradykinesia, mild neck rigidity, and slowing of rapid alternating movements in the LBV group. Extremity rigidity, flexed posture, resting tremor, or other classic parkinsonian features were not characteristic of the LBV patient. In some cases, it may be possible to diagnose LBV premortem on the basis of the clinical and neuropsychological features.
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PMID:The Lewy body variant of Alzheimer's disease: a clinical and pathologic entity. 216 2

The occurrence of severe and mild hypoglycaemic attacks and their symptoms and signs were studied in 92 insulin-dependent diabetic children, 7-18 years old. A questionnaire was distributed to all families and they were interviewed by an experienced nurse. Severe attacks, for which the help of an adult was needed, were reported by 44% of the children during a 12-month period. Thirty-seven per cent of the attacks occurred in the mornings, most often attributed to extra physical exercise, but equally often without any obvious cause. They were more common in children with strict blood glucose control measured as HbA1c. Fast-acting carbohydrates, given by parents, relieved the attack in most children, but 15% needed a glucagon injection and 12% intravenous glucose. In all, 16% were admitted to hospital. Mild events occurred in 97% of the children, at least once per week in 53% of the children, and were not related to blood glucose control. They were often attributed to extra physical exercise and occurred mainly between breakfast and lunch. Initial symptoms were tremor and hunger; during the whole event tremor and sweating were most common. Parents noted pallor as the most common sign. The frequency of severe or mild attacks could not be correlated to the age of the child, duration of diabetes, daily dose or number of insulin injections.
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PMID:Symptomatic hypoglycaemia in childhood diabetes: a population-based questionnaire study. 252 88

A prospective study of symptomatic hypoglycaemia was conducted in 47 children over a 14-week period using a questionnaire completed at home for each episode of hypoglycaemia. Twenty-nine children (62%) experienced 150 episodes during the study. The average incidence was once every 33 days (range 0-5.2 mo-1). Hypoglycaemia occurred more frequently in children with lowest haemoglobin A1 levels. Episodes were not randomly distributed in time; hypoglycaemia occurred significantly more frequently in the evening, in the early morning and around midday. The majority of episodes were judged to be mild but 2 children had nocturnal convulsions and glucagon was used on three occasions. Symptomatic nocturnal hypoglycaemia occurred one or more times in 30% of the children. Daytime episodes were manifested by tremor, feeling weak, dizziness, pallor, and other symptoms and signs. In 46% of cases the cause was not evident to parents or children, but 25% were related to physical activity.
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PMID:A prospective study of symptomatic hypoglycaemia in childhood diabetes. 252 5

This was an open-label study in 19 children aged 9-13 years, weighing 27-44 kg, with bronchial asthma. Twenty-four-hour steady-state concentrations of theophylline and its metabolites 1,3-dimethyl uric acid, 3-methyl xanthine and 1-methyl uric acid were assessed after daily dosing of 600 mg (ca 18 mg/kg/day) of the sustained-release theophylline micro-pellet sprinkle system BY158K, for 4 days. The dosing regimen used was an unequal twice-daily dose of 200 mg in the morning after breakfast and 400 mg in the evening after dinner. Twenty-four-hour peak expiratory flow (PEF) profiles were compared before treatment and at steady-state, along with lung function parameters after bronchial provocation. Mean values +/- SD (n = 16) of the steady-state characteristics were Cmin 6.8 +/- 2.1 mg/l, Cmax 14.5 +/- 4.8 mg/l and Cav 10.5 +/- 2.9 mg/l, the plateau time was 11.7 +/- 4.8 hr and peak-trough fluctuation and swing were 72 +/- 21 and 118 +/- 52%, respectively. There was an excellent reproducibility of theophylline pre-dose levels at corresponding time points of the 24-hr sampling period [r = 0.864 (p less than 0.001)]. Mean values +/- SD of the 24 hr average serum metabolite levels were 0.9 +/- 0.2 mg/1 for 1,3-dimethyl uric acid, 0.6 +/- 0.1 mg/1 for 3-methyl xanthine and 0.4 +/- 0.1 mg/1 for l-methyl uric acid. Lung function (n = 17) following bronchial provocation, improved in 10 children after theophylline treatment of 4 days, remained stable in 2 patients and deteriorated in 5 patients. Serum theophylline profiles and PEF profiles ran largely in parallel over the 24-hr period. Six children exhibited typical theophylline induced side-effects, headache (n = 3), nausea (n = 4), dizziness (n = 1), vomiting (n = 4), sleep disturbances (n = 1), pallor (n = 1) and tremor (n = 1), necessitating in 3 children one dose omission/reduction (n = 2) or subsequent dose reduction (n = 1). It has been shown that a twice daily dosing regimen with unequal doses of anhydrous theophylline (BY158K) is well suited to this population of fast metabolisers. The patients were well protected throughout the day, including the critical early morning hours.
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PMID:Steady state pharmacokinetics, metabolism and pharmacodynamics of theophylline in children after unequal twice-daily dosing of a new sustained-release formulation. 367 17

Hypoglycaemia is the most frequent acute complication of insulin-dependent diabetes mellitus. The clinical symptoms of insulin-induced hypoglycaemia can be grouped into those attributable to the sympathetic and adrenergic responses, e.g. tremor, pallor, palpitation, sweating, mydriasis ('hypoglycaemia awareness'), and those attributable to brain dysfunction, ranging from headache to convulsions and coma. Hypoglycaemia in diabetic children can occur at any time of the day, but nocturnal hypoglycaemia is a particular fear and worry. The frequency of mild hypoglycaemia is almost impossible to ascertain and the incidence of severe hypoglycaemia varies between 0.07 and 3.6 episodes per patient-year, though most authors report a range of 0.1-0.2 episode per patient-year. The most frequent causes of hypoglycaemia in diabetic children are deviations from treatment routine such as strenuous exercise, omission of snacks or skipped meals, and gross deviations from the prescribed times of insulin injections and recommended doses of insulin. Other predisposing factors include intensified insulin treatment, improved glycaemic control, young age, longer duration of diabetes and defective counterregulation. The available paediatric studies do not seem to support the suggestion that human insulin impairs the perception of hypoglycaemic symptoms ('hypoglycaemia unawareness') and increases the frequency of hypoglycaemic episodes, but further conclusive studies are needed. Prolonged and recurrent severe hypoglycaemia, particularly in younger children, can cause permanent neuropsychological dysfunction (e.g. learning disabilities) and permanent electroencephalographic abnormalities. Mild hypoglycaemia has also been documented to affect cognitive function, and the performance of neuropsychological tasks can remain decreased for some time (up to several hours) after full clinical recovery from hypoglycaemia. An impending hypoglycaemic attack can usually be averted by the ingestion of 20 g of rapidly absorbed carbohydrate. A severe episode can be effectively treated outside hospital with subcutaneous or intramuscular glucagon (0.5-1.0 mg) or in the hospital by an intravenous bolus of 0.2-0.5 g/kg glucose followed by a continuous glucose infusion. Patient and parent education and vigilant application of diabetes self-care principles are perhaps the most effective means of prevention, but in very young children a less strict metabolic control (higher glycosylated haemoglobin levels) may be necessary.
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PMID:Hypoglycaemia in the diabetic child. 837 14

We report a right-handed 78-year-old man with early onset parkinsonism. The patient had an onset of micrographia at 23 years of the age in 1939. Seven years later he started to drag his right foot, and at 38 years of age, he walked with small steps with festination. Tremor was also present in his right hand. His daily life was independent as a otorhinolaryngologist. He visited our clinic on March 24, 1977 when he was mentally sound and showed mild parkinsonism consisting of masked face, stooped posture, small step gait, bradykinesia, and right side dominant rigidity and tremor. He showed good response to trihexyphenidyl and amantadine HCl. Two month later, he developed dyskinesia and some worsening of parkinsonism, and was admitted to our hospital for the first time. He was treated with 400 to 600 mg/day of levodopa/ carbidopa. He showed marked improvement, however, dyskinesia remained in his mouth. He was doing well until 77 years of age (June of 1993) when he developed hallucination and motor fluctuations. He was admitted again to our hospital on June 22, 1993. On admission, he was alert and appeared mentally sound. However, Hasegawa dementia scale was 18/30. Upward gaze was slightly restricted (3/5). Voice was somewhat small but no masking was noted. His posture was stooped and the gait was of small step. Dyskinesia was noted during walk. No rigidity nor tremor was noted. Deep tendon reflexes were lost but no sensory loss or motor weakness was noted. Routine laboratory studies were unremarkable. A cranial CT scan revealed only mild to moderate cortical atrophy. Motor and sensory conduction velocities were within normal limits, however, motor action potentials could not be obtained with stimulation to the right common peroneal nerve. He was treated with 600 mg/day of levodopa with carbidopa, 100 mg of amantadine HCl, 300 mg of Dops, and 25 mg of tiapride. He continued to show motor fluctuations, and was discharged on July 23, 1993. Since then his motor functions had become progressively worse with frequent falls, but he was still able to walk without support. On October 3 of 1994, he went to bed as usual. On the next morning, he was found dead in his bed at 9: 30. The patient was discussed in neurological CPC, and the chief discussant arrived at the conclusion that the patient had young-onset Parkinson's disease with Lewy bodies in the substantia nigra. Opinions were divided between Parkinson's disease and Lewy body negative young onset parkinsonism. Postmortem examination revealed obstruction of the trachea by aspirated foods, and the cause of death appeared to have been suffocation by the foods. Macroscopically, the external appearance of the brain was unremarkable except for slight frontal atrophy. The substantia nigra showed depigmentation in the lateral part, but the pigmentation of the medial part was well preserved. Upon histologic examination, the number of pigmented neurons in the dorsomedial part was well preserved. In the lateral part, pigmented neurons were well preserved in the dorsal area, however, in the ventral area, only non-pigmented neurons were seen; they appeared to be neurons in the pars reticulata. No gliosis was seen in any of the nigral areas. No Lewy bodies were seen in the remaining neurons. So-called immature neurons with rounded shape without neuromelanin could not be detected. The locus coeruleus neurons were well preserved. The putamen and the other basal ganglia structures were also intact. Slight myelin pallor was noted in the subcortical white matter, however, otherwise cerebral cortices were normal. The histology of this patient is unique in that only the ventrolateral part of the substantia nigra showed abnormal finding consisting of lack of pigmented neurons without gliosis. It is not clear whether the nigral change represents degeneration or a congenital "hypoplasia'. To our knowledge, such a unique pathology of the substantia nigra has not been reported in the literature. Our patient ma
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PMID:[A 78-year-old man with young onset parkinsonism and sudden death]. 867 9


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