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)

The authors report the cases of three men who presented for evaluation of a rapidly progressing dementia. All were found to have a giant aneurysmal mass in the basifrontal region, and all were successfully treated by surgical excision of the mass. The presenting syndrome included rapidly progressive and severe loss of recent memory associated with confusion, chronic headache, wide-based staggering gait disturbance, urinary urgency, frequency, and incontinence, and a fine tremor of the hands exacerbated by purposeful movements. The clinical presentation, radiological assessment, and surgical treatment are discussed.
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PMID:Aneurysmal tumors of the basifrontal region. 84 29

We report an autopsy case of a 73 year-old female with idiopathic parkinsonism, characterized pathologically by the wide spread appearance of Lewy bodies (LBs) not only in the pigmented neurons in the midbrain and brainstem but also in the cerebral cortex. Initial symptoms at the age of 62 were finger tremor and gait disturbance, which were followed mainly by mental deterioration, such as regression, dependency, auditory hallucination, depression, emotional incontinence, and a personality change. In the terminal stage, nuchal stiffness in extension, one of the hallmarks of progressive supranuclear palsy, and slow and generalized tremor in all 4 extremities were noted. She died of aspiration pneumonia. The brain was somewhat small and weighed 1100 g after the fixation by formalin. Macroscopical findings included mild cerebral atrophy with mild pial thickening both in the frontal and temporal lobes and slight expansion of the ventricular system. Histopathologically, severe loss of neuronal cells in both the pallidum and Luy's body and moderate loss of large cells in the putamen were noted in addition to the typical findings of Parkinson's disease in the substantia nigra and locus caeruleus including neuronal cell loss, depigmentation, and gliosis. These findings in the basal ganglia were more conspicuous than the two controls of classical Parkinson's disease. The distribution, stainability in the routine methods of staining, and shape of Lewy bodies in the cerebral cortex conformed to those of previous reports. The similar case reports in the literatures do not seem to have paid much attention to the findings of the basal ganglia observed in our case.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[An autopsy case of idiopathic parkinsonism with numerous Lewy bodies in the cerebral cortex--diffuse Lewy body disease]. 165 48

The clinical effectiveness and safety of terodiline hydrochloride and clenbuterol hydrochloride were studied on 51 patients with neurogenic bladder, stress incontinence, unstable bladder and others, the chief complaints of which were urinary frequency or urinary incontinence. Overall improvement was graded as marked in 6 patients (11.8%), moderate in 20 patients (39.2%), slight in 11 patients (21.6%), unchanged in 13 patients (25.5%) and aggravated in one. The patients impression was "good" or better in 56.9%. There were a total of 13 cases (25.5%) of adverse reactions, namely, 7 cases of finger tremor, 3 cases of dry mouth and others. These reactions disappeared rapidly after the discontinuance of drug administration. The clinical efficacy in the treatment of subjective symptoms was 71.4% for urinary incontinence, 56.4% for diurnal pollakisuria. The examination of lower urethral functions demonstrated a significant (p less than 0.01) increase in bladder capacity at first desire and maximum desire to void. However, we found no significant increase in urethral clossure pressure. The findings of this study suggest that terodiline hydrochloride and clenbuterol hydrochloride are very useful for the treatment of urinary frequency and incontinence.
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PMID:[Clinical studies of terodiline hydrochloride and clenbuterol hydrochloride for urinary frequency and incontinence]. 176 84

A total of 49 patients complaining of pollakisuria and incontinence; 20 patients with overactive neurogenic bladder and 29 patients with stress incontinence, were treated with clenbuterol, and the effects of the drug were studied. Subjective symptoms were improved markedly in 8 patients (17%), moderately in 14 patients (29%), and slightly in 10 patients (21%). The symptoms were unchanged in 15 patients (31%) and aggravated in 1 patient (2%). In objective observation, the volume at first desire to void (P less than 0.01) and the maximum urethral closure pressure (P less than 0.05) significantly increased. The objective symptoms were improved markedly in 2 patients (5%), moderately in 12 patients (27%), and slightly in 11 patients (25%). The symptoms were unchanged in 15 patients (34%) and aggravated in 4 patients (9%). Overall improvement was graded as marked in 7 patients (15%), moderate in 17 patients (35%), slight in 11 patients (23%), unchanged in 13 patients (27%) and aggravated in none. In neurogenic bladder, the overall improvement was graded as marked in 2 patients (11%), moderate in 4 patients (21%), slight in 4 patients (21%), unchanged in 9 patients (47%) and aggravated in none. In stress incontinence, the overall improvement was graded as marked in 5 patients (17%), moderate in 13 patients (45%), slight in 7 patients (24%), unchanged in 4 patients (14%) and aggravated in none. Side effects were noted in 12 patients (25%) and they were all not serious. Finger tremor was the most common side effect (5 patients).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical effects of clenbuterol-HCL in urge incontinence and stress incontinence]. 234 15

Of 70 autopsied patients with the acquired immune deficiency syndrome (AIDS), 46 suffered progressive dementia that was frequently accompanied by motor and behavioral dysfunction. Impaired memory and concentration with psychomotor slowing represented the most common early presentation of this disorder, but in nearly one half of the patients either motor or behavioral changes predominated. Early motor deficits commonly included ataxia, leg weakness, tremor, and loss of fine-motor coordination, while behavioral disturbances were manifested most commonly as apathy or withdrawal, but occasionally as a frank organic psychosis. The course of the disease was steadily progressive in most patients, and at times was punctuated by an abrupt acceleration. However, in 20% of patients a more protracted indolent course was observed. In the most advanced stage of this disease, patients exhibited a stereotyped picture of severe dementia, mutism, incontinence, paraplegia, and in some cases, myoclonus. The high incidence and unique clinical presentation of this AIDS dementia complex is consistent with the emerging concept that this complication is due to direct brain infection by the retrovirus that causes AIDS.
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PMID:The AIDS dementia complex: I. Clinical features. 372 8

An autopsy case of a 52-year-old man suffering from chronic manganese poisoning (CMP) is reported with determination of the manganese distribution in the brain. The patient had been working in a manganese ore crushing plant since 1965. In 1967 he began to complain of difficulties in walking and diminished libido. Later, he developed various neuropsychiatric symptoms including euphoria, emotional incontinence, masked face, monotonous speech, "cock-walk", increased muscle tone, weakness of upper and lower extremities, tremor of the eye lids, and exaggeration of knee jerks. The major neuropathological change was degeneration of the basal ganglia, in which the pallidum was severely affected. The pallidum disclosed a loss and degeneration of nerve cells, which was especially marked in the medial segment, a prominent decrease of myelinated fibers, and moderate astrocytic proliferation. The substantia nigra was intact. Distribution of manganese in the brain of the present case of CMP was determined using flameless atomic absorption spectrometry and compared with control cases and also a case of Parkinson's disease (PD). There was no significant difference between the control cases and the case of PD in average concentration of manganese and its distribution in the brain. The present case of CMP showed no elevation in average concentration of manganese in the brain. However, there were some changes in its distribution. Thus, the continuance of neurological disorders in CMP is not linked to an elevated manganese concentration itself in the brain. CMP appears to be different from PD in neuropathology and manganese behavior in brain.
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PMID:Chronic manganese poisoning: a neuropathological study with determination of manganese distribution in the brain. 376 27

We studied a 68-year-old man who died after 13 years of progressive dementia, rigidity, bradykinesia, mild tremor, stooped posture, slow and shuffling gait, dystonia, blepharospasm, apraxia of eyelid opening, anarthria, aphonia, and incontinence. At autopsy, he had generalized brain atrophy with large deposits of iron pigment in the globus pallidus, caudate, and substantia nigra. Axonal spheroids were found in the globus pallidus, substantia nigra, medulla, and spinal cord. The neurochemical analysis of the brain revealed marked loss of dopamine in the nigral-striatal areas, with relative preservation of dopamine in the limbic areas. This is the oldest case of familial Hallervorden-Spatz disease reported and the first with neurochemical analysis of the brain.
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PMID:Late-onset Hallervorden-Spatz disease presenting as familial parkinsonism. 396 11

A 68-year-old man who ingested an improperly prepared extract of pokeweed had sweating, confusion, tremor, weakness, incontinence, and syncope. Analysis of the symptoms from this and similar patients previously reported suggests that the pokeweed plant contains an agent that produces peripheral and central cholinergic stimulation.
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PMID:Pokeweed poisoning. 724 29

We report a 20-year-old female with Hallervorden-Spatz syndrome (HSS). This patient is the product of consanguineous parents. She developed genu valgum, tendency to fall and mental deterioration at the age of 6, decrease of the number of spoken words at the age of 14, dysarthria, unsteady gait, postural tremor of the upper extremities, dystonic posture of hands and double incontinence at the age of 16. Her disease progressed slowly. Neurological examination on admission revealed severe mental retardation, optic atrophy, forced grasping, hyperactive tendon reflexes in the upper extremities and bilateral Babinski sign. An extensive laboratory investigation including the leukocyte lysosomal enzymes, serum amino acid analyses, copper studies and ceruloplasmin were almost within normal limits. MRI, T2 weighted images, showed markedly decreased signal intensity in the globus pallidus but substantia nigra and increased signal intensity in diffuse cerebral white matter. T1 weighted images showed marked atrophy of the brainstem and cerebellum. She met the diagnostic criteria for HSS by Swaiman; we diagnosed her as HSS group II. HSS is characterized by the presence of many spheroids in the central nervous system which is similar to neuroaxonal dystrophy (ND). However, clinical and pathological differences exist between HSS and ND, the precise classification of the two conditions has remained controversial. Although there are many reported cases in which both conditions overlap, this is the first reported case that simultaneously demonstrates increased iron deposition in the globus pallidus, marked atrophy of the brainstem and cerebellum and typical clinical course compatible with HSS.
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PMID:[A case of Hallervorden-Spatz syndrome with marked atrophy of the brainstem and cerebellum]. 836 59

We report a 46-year-old man with right side dominant parkinsonism who died suddenly two years after the onset. The patient was well until the age of 42 years in January of 1993, when he noted an onset of difficulty in using his right hand and then the right leg. Soon after he noted nocturnal urinary incontinence. In January of 1994, a local doctor prescribed 200 mg of levodopa with benserazide and 5 mg of bromocriptine. The patient noted some improvement. Cystometry revealed 300 ml of residual urine. He visited our clinic on 24th of December, 1996. He was alert and oriented. BP was 106/60. He showed masked face and small voice. He walked in stopped posture dragging his feet; retropulsion was noted. He showed moderate bradykinesia and rigidity more on the right side. No resting tremor or cerebellar ataxia was noted. Ankle jerks were somewhat exaggerated but no Babinski sign was noted. He continued to show residual urine, but orthostatic hypotension was absent. Routine laboratory examination was unremarkable, however, his cranial MRI showed atrophy of the left putamen and a T2-linear high signal intensity lesion along the lateral border of the left putamen. On January 15, 1997, he ate certain amount of rice cake and drank alcohol. After coming back home and while changing his clothes, he suddenly complained of chest discomfort and lost consciousness. He was pronounced dead in the afternoon. The patient was discussed in a neurological CPC. Opinions were divided between Parkinson's disease and striatonigral degeneration. The chief discussed arrived at a conclusion that the patient had Parkinson's disease, because he responded to levodopa to some extent and except for nocturnal incontinence he did not have wide spread autonomic failure. Postmortem examination revealed marked loss of neurons and extensive gliosis in the left putamen. The right putamen did not show such changes. The substantia nigra showed gliosis in the lateral part on both side, however, neuronal loss was not apparent. The locus coeruleus was well retained. No Lewy bodies were found. The pontine nucleus and the cerebellum were intact. However, glial cytoplasmic inclusions were seen in oligodendrocytes of the cerebral white matter and the pontine base. The heart and lungs were intact and the cause of the sudden death could not be determined. The pathologic diagnosis is striatonigral degeneration. Such a marked asymmetry of the pathologic change is quite unusual. Probably, the death in the early stage of the disease is the reason for this asymmetry.
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PMID:[A 46-year-old man with right-side dominant parkinsonism, who suffered a sudden death]. 895


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