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)

Seventy-four in- and out-patients (mean age 71.9 years) with Parkinsonian syndromes (summarized as "PS": idiopathic Parkinson's disease, vascular pseudo Parkinsonian syndrome (VPS), and Parkinson-dementia (PDK)) were prospectively evaluated as to present clinical state according to usual rating scales, as to clinical syndrome and physician's diagnosis and treatment at the start of the illness, and as to current medical and social care. 54% of the patients had history and findings of tremor, 14% had visual hallucinations, 19% had depression. Ratings on part II of the "Unified Parkinson's Disease Rating Scale" (UPDRS) describing "activities of daily living" correlated highly with the ratings of part III ("motor evaluation") and with another activity of daily living scale according to Schwab and England. The mean difference between time of diagnosis and start symptoms (the "diagnostic delay") was nearly 21 months. Initial symptoms did not show an impact on this difference. 68% of patients were presently treated by general physicians and were significantly older than those treated by neurologists. 59% were in-patients during the study and were more likely to carry a diagnosis of VPS or PDK. 75% of those patients who were ever in-patients during their illness had the disease for up to six years before they were first hospitalized. 77% of the patients had drug treatment; 88% of these took L-Dopa preparations. 23% of patients with drug treatment had L-Dopa-associated motor complications. 15% of patients lived alone, 66% with their family, and 19% in a nursing home. 24% of patients had assistance in their household by a professional caretaker. 16% of patients retired early from work. The long-term care of older Parkinsonian patients is a task for general medicine based on neurogeriatric expertise.
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PMID:[Medical management and social status of elderly Parkinson patients]. 797 17

Two cases of basal ganglia calcification involving the globus pallidus are presented. Both patients had cognitive dysfunction, temporal lobe-like symptoms (including amnestic state, perceptual distortions, or complex visual hallucinations), and myoclonus. Patient 1 manifested depression, auditory hallucinations, anxiety, paranoia, and postural tremor; patient 2 manifested multifocal dystonia with dystonic tremor. These cases supplement other reports of psychotic features and dementia associated with pallidal pathology. Additionally, the phenomena encountered in these cases are considered in light of recent advances in our understanding of basal ganglia functional pathways. These cases afford a potential pathophysiological window to the possible role of the globus pallidus in these neuropsychiatric conditions. In concert with other recent findings, these cases suggest specific pathway involvement in hallucinations, paranoia, depression, myoclonus, and dystonia. Further research will indicate if these pathways play a role in schizophrenia, mood disorders, and anxiety disorders.
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PMID:Neuropsychiatric disorders, myoclonus, and dystonia in calcification of basal ganglia pathways. 801 2

Thirty-seven male alcoholics admitted electively for detoxification were randomized to treatment with either diazepam or propranolol. Subjects were comparable both in age and in duration and quantity of alcohol consumed. Admission laboratory parameters did not distinguish between the groups. Eleven subjects required no medication to control withdrawal signs/symptoms. Both groups showed improvement in blood pressure, pulse, and withdrawal tremor. None of the subjects randomized to diazepam manifested withdrawal seizures or hallucinations. By contrast, one subject in the propranolol group had a single withdrawal seizure. Another subject manifested increasing withdrawal that required parenteral paraldehyde treatment. Thus, this study confirms that a significant number of subjects admitted electively for alcohol withdrawal can be managed without medication. Minor tranquilizers still remain the "gold standard" for management of the withdrawal syndrome.
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PMID:Propranolol versus diazepam in the management of the alcohol withdrawal syndrome: double-blind controlled trial. 819 30

We report a 75-year-old man with a ten-year history of parkinsonism, who developed acute delirium. He was well until 65 years of age, when there was an onset of tremor in his left hand. He had been treated with levodopa and trihexyphenidyl with marked improvement. He was doing well until July of 1991 at his age of 75-year-old, when he noted backache; he was found to have a compression fracture of the third lumbar spine. He had to use a wheel-chair most of the time since then. In December 1991, he started to have visual hallucinations and difficulty in swallowing. On December 25 of that year, he developed fever and delirium, and was admitted to our hospital on December 30. On admission, general physical examination was unremarkable except for low grade fever (37.3 degrees C). Neurologic examination revealed an alert but chronically ill patient. Apparently he had visual hallucinations. He was disoriented to all spheres; he could respond only to simple questions. Apparently he was demented. Cranial nerves were intact except for mumbling speech disturbance and masked face. He was unable to stand or walk. He had flexion contracture in his both knee joints. He had paratonic rigidity in all his limbs and marked bradykinesia. Once in a while, myoclonic jerks were seen in both upper and lower extremities. Deep reflexes were diminished bilaterally, and the plantar reflex was not elicited on either side. On laboratory examination, BUN was increased to 72 mg/dl, creatinine to 3.0 mg/dl, and WBC 16,000/microliter. Cranial CT scans were unremarkable.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A 75-year-old man with parkinsonism and delirium]. 819 65

Alcohol withdrawal delirium (AWD) requires treatment with an adequate sedative, anticonvulsant, and antipsychotic agent next to general intensive care measures. Optimal medication should have a rapid onset of action and the possibility of parenteral application. A specific antagonist should be available. Flunitrazepam is a benzodiazepine that fulfills all these criteria. Twenty five patients suffering from AWD (mean age 45 years) took part in an open trial and underwent treatment with infusions of flunitrazepam (concentration: 8 mg/250 ml NaCl; speed, 250 ml/hr). Psychopathological, vegetative, and vital parameters were assessed every hour. All patients survived. They were treated with a mean total dose (SD) of 83.9 (45.4) mg of flunitrazepam (1.3 mg/kg body weight), which induced sedation 13.2 (5.3) min after the initiation of intravenous treatment. The mean duration of AWD (85.1 +/- 39.4 hr) corresponded to other studies, whereas the frequency of preexisting and concomitant diseases was higher (92%) in our patients. A patient who suffered from bronchitis and had a nasopharyngeal tamponade showed severe respiratory depression after having received 4 mg of flunitrazepam. This complication remitted immediately when 0.5 mg of flumazenil was given intravenously. No epileptic manifestation was observed during the treatment or after discontinuation of flunitrazepam. Vegetative and psychopathological symptoms (tremor, sweating, hallucinations, confusion, and restlessness) remitted rapidly. Our data suggest that intravenous flunitrazepam can be an efficacious and safe alternative to traditional treatment strategies of AWD.
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PMID:Intravenous flunitrazepam in the treatment of alcohol withdrawal delirium. 821 8

The indole alkaloids ibogaine and harmaline are beta-carboline derivatives that cause both hallucinations and tremor. Reports that ibogaine may have potent anti-addictive properties have led to initiatives that it be tested for the treatment of opiate and cocaine addiction. In this study, ibogaine-treated rats were analysed for evidence of neurotoxic effects because human clinical trials of ibogaine have been proposed. We recently found that ibogaine induces a marked glial reaction in the cerebellum with activated astrocytes and microglia aligned in parasagittal stripes within the vermis. Based on those findings, the present study was conducted to investigate whether ibogaine may cause neuronal injury or degeneration. The results demonstrate that, after treatment with ibogaine or harmaline, a subset of Purkinje cells in the vermis degenerates. We observed a loss of the neuronal proteins microtubule-associated protein 2 and calbindin co-extensive with loss of Nissl-stained Purkinje cell bodies. Argyrophilic staining of Purkinje cell bodies, dendrites and axons was obtained with the Gallyas reduced silver method for degenerating neurons. Degenerating neurons were confined to narrow parasagittal stripes within the vermis. We conclude that both ibogaine and harmaline have selective neurotoxic effects which lead to degeneration of Purkinje cells in the cerebellar vermis. The longitudinal stripes of neuronal damage may be related to the parasagittal organization of the olivocerebellar climbing fiber projection. Since these drugs produce sustained activation of inferior olivary neurons, we hypothesize that release of an excitatory amino acid from climbing fiber synaptic terminals may lead to excitotoxic degeneration of Purkinje cells.
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PMID:Degeneration of Purkinje cells in parasagittal zones of the cerebellar vermis after treatment with ibogaine or harmaline. 837 27

To observe the incidence of complications in severely hyponatraemic hospitalized patients and relate outcome to rate of correction, all patients admitted to a tertiary referral hospital in New York City, USA or a group of hospitals in Oxford, UK with a sodium < or = 120 mmol/l were studied. Review of the notes and prospective evaluation were used to ascertain cause of hyponatraemia, method of management and outcome. There were 84 episodes in New York and 100 in Oxford, over 9.5 months and one year, respectively; 79% had chronic hyponatraemia ( > 3 days duration). During hyponatraemia, 76% of patients had clouding of consciousness with 11% in coma. Other hyponatraemic complications included long track signs (including hemiparesis) (6.0%), seizures (3.3%), hallucinations (0.5%), tremor (1.0%), intellectual impairment without clouding of consciousness (0.5%), and acute psychosis (0.5%). 4.3% died as a direct result of their electrolyte disturbance. After correction, central pontine myelinolysis (0.5%), post-correction seizures (1.0%), intellectual impairment (2.2%), tremor (0.5%), paraesthesiae (0.5%), and striatal syndrome (0.5%) were observed. Correction of hyponatraemia was started in 158 patients, and the mean maximum rate of correction in 24 h was 8.4 mmol/l (SD 5.6, range 2-42). The maximum rate of correction was higher in those who developed neurological sequelae (12.1 mmol/l/24 h vs. 8.2 mmol/l/24 h; p = 0.0125, t-test, separate variance, two-tail). Neurological sequelae were associated with faster rates of correction, and correction of chronic severe hyponatraemia should be < 10 mmol/l in 24 h.
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PMID:Severe hyponatraemia: complications and treatment. 859 51

Alzheimer's disease (AD) is a heterogeneous entity presenting as sporadic and familial disease. In familial AD, there is evidence for genetic linkage to a yet undefined gene on chromosome 14 in early-onset pedigrees and on chromosome 19 in late-onset pedigrees. In a few early-onset kindreds, there were mutations in the amyloid precursor gene on chromosome 21. There is an increased frequency of apolipoprotein E (ApoE) epsilon4 allele in patients with late-onset AD. We studied the clinical presentation and profile of cognitive deficits in 58 AD patients at the early stage of the disease. We divided the AD patients into subgroups of sporadic late-onset (SLO) (> or = 65 years), familial late-onset (FLO) (> or = 65 years), sporadic early-onset (SEO) (<65 years), and familial early-onset (FEO) (<65 years) patients and into three subgroups according to their ApoE genotype zero epsilon4, one epsilon4, and two epsilon4 alleles. The AD subgroups did not differ in the global clinical severity of dementia or the duration of the disease. SLO, FLO, SEO, and FEO subgroups did not differ in clinical characteristics such as occurrence of rigidity, hypokinesia, tremor, myoclonus, hallucinations, delusions, or epileptic seizures nor in the profile of deficits on tests assessing memory, language, visuospatial, executive, and praxic functions. The epsilon4++ allele frequency was 0.43 for all AD patients and did not differ across subgroups divided according to the familial aggregation and age of onset. Patients with two epsilon4 alleles had earlier age at onset of dementia than those with no epsilon4 allele (63 +/- 9 versus 68 +/- 9 years), but otherwise the clinical symptoms and signs were not related to the ApoE genotype. However, the AD patients with two epsilon 4 alleles had lowest scores on memory tests and differed significantly from those with one or zero epsilon4 allele in the delayed list learning (p<0.05) and from those with zero epsilon4 allele in the immediate and delayed story recall. In contrast, verbal functions were better preserved in two epsilon4 patients than in those with other ApoE genotypes. This study failed to confirm the earlier reports of severe aphasia, agnosia, and apraxia in familial AD patients, but the clinical phenotype was similar irrespective to the familial aggregation. However, AD patients with two epsilon4 alleles are characterized by more severe memory loss and earlier age of onset than those without the epsilon4 allele.
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PMID:Clinical and neuropsychological characteristics in familial and sporadic Alzheimer's disease: relation to apolipoprotein E polymorphism. 861 4

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

We compared clinical features in three groups of pathologically defined patients evaluated for dementia during life: (i) Alzheimer's disease (AD); (ii) Lewy body variant of Alzheimer's Disease (LBV), with Lewy bodies (LB) and AD; (iii) diffuse Lewy body disease (DLBD), with LB alone. All three groups had similar initial cognitive symptoms. LBV and DLBD had Parkinsonian signs, though resting tremor was extremely rare. Delusions and hallucinations were relatively more frequent in LBV and DLBD than in AD. On neuropsychological testing, the LBV group had relatively greater impairment than AD on visuospatial and executive tests. LB therefore contribute to the clinical picture of dementia.
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PMID:Clinical and neuropathological findings in Lewy body dementias. 881 93


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