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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vascular pseudoparkinsonism may be confused with idiopathic Parkinson's disease. Patients may be unnecessarily treated with anti-parkinsonian drugs while their underlying vascular disease is ignored. We investigated 250 parkinsonian patients seen in our Movement Disorders Clinic for a possible vascular etiology. After excluding those with a known secondary cause such as drug-induced parkinsonism, progressive supranuclear palsy, multiple system atrophy and hyperparathyroidism, brain computed tomography and/or magnetic resonance imaging were performed on those who showed poor or no response to levodopa. In those with an ischemic lesion demonstrated on neuroimaging, anti-parkinsonian drugs were stopped and the patients were reassessed. Eleven patients (4.4%) had ischemic brain lesions accounting for their parkinsonism. All were initially diagnosed as Parkinson's disease because of the prominence of bradykinesia and rigidity. Gait disturbance was also common, but resting tremor was distinctly absent. Three anatomical patterns with different prognosis were identified. Three patients with basal ganglia lacunar infarct recovered spontaneously, three with frontal lobe infarcts remained static and five with periventricular and deep subcortical white matter lesions had progressive deterioration. Autopsy in one patient confirmed bilateral frontal lobe watershed infarcts and the absence of brain stem Lewy bodies. Parkinsonian patients with poor or no response to levodopa therapy should be investigated for a vascular etiology.
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PMID:Vascular pseudoparkinsonism. 148 45

We report the clinical and neuropathological manifestations of Alzheimer's disease (AD) in nine kindreds of German ancestry all originating from the same two adjacent villages on the West bank of the Volga River. There have been 89 known demented persons (53 male, 36 female). Mean age of onset is 57.6 +/- 8.4 years with a range of 40 to 84. Mean age at death is 66.5 +/- 7.6 years with a range of 50 to 80. Mean disease duration is 10.3 +/- 4.8 years with a range of 3 to 23. Detailed medical records were available on 50 individuals. Of these, 24% had a seizure, 72% language disturbance, 36% rigidity, 16% tremor and 12% myoclonus. There were 15 autopsies on demented persons from 6 of the kindreds. One brain suggested Creutzfeldt-Jakob disease (CJD) in a woman with the typical clinical course. The remaining 14 brains showed typical neuropathological characteristics of AD including neuritic amyloid plaques, neurofibrillary tangles, amyloid angiopathy and granulovacuolar change. Amyloid plaques were also seen in the cerebellum in all but one brain in which this region was available for review. Autopsy material from five brains in four families has been stained with antibody directed against the amyloid peptide; in all cases, the neuritic plaques stained positively. Many of the families share common surnames. It is likely that these Volga German kindreds carry the same genetic mutation leading to Alzheimer's disease; and thus, they are a valuable resource for genetic investigations of AD. Thus far, the disease in these kindreds does not show close linkage to either the D21S1 or beta amyloid gene loci on chromosome 21.
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PMID:Characteristics of familial Alzheimer's disease in nine kindreds of Volga German ancestry. 260 19

The clinical manifestations of 24 cases and the autopsy findings of 6 cases of extremity myorhythmia are presented. Extremity myorhythmia is that form of myorhythmia in which rhythmic alternating movements predominantly involve the limbs. The main difference between the tremor of extremity myorhythmia and the tremor of parkinsonism is the slower tremor rate, 2 to 3 cycles/s in myorhythmia and 4 to 6 cycles/s in parkinsonism. The mechanograms, except for the slower frequencies in myorhythmia, can be very similar, including sinusoidal oscillation patterns in both conditions. Myorhythmia may be defined as a coarse, alternating tremor, present at rest and usually during movement, which occurs at rates varying from 50 to 240 oscillations/min but mostly at either 120 to 140 or 160 to 180 cycles/min. The alternating movements may be intermittent or continuous or both types may be present in different body parts. When multiple parts are involved, synchronous or asynchronous movements are about equally common. Movements are usually relatively rhythmic and regular but may vary over periods of time in rate, rhythm or amplitude and rarely so, even over the course of a few hours and are absent during sleep. Movements may involve single limbs, several limbs or a combination of limbs plus face, palate, head, jaw, neck, tongue, eyes or trunk. The frequency of the movements in the 24 cases varied from 120 to 180 oscillations/min with two exceptions the slowest being 60 and the fastest 240, with most tending to cluster near either 120 or 180 cycles/min. The most common aetiologies were brainstem vascular disease and cerebellar degeneration secondary to chronic alcoholism-nutritional deficiency. The best prognosis occurred in the latter group. Clinicopathological correlations in our autopsy series indicate that myorhythmia of the limbs may occur ipsilateral to the dentate nucleus or superior cerebellar peduncle lesions or contralateral to inferior olive involvement. Unilateral lesions of the dentate nucleus may result in bilateral limb movements and bilateral dentate lesions may be associated with unilateral limb movements. The frequent involvement of the cerebellum and the substantia nigra suggests possible roles for the cerebellum and substantia nigra in the myorhythmia process.
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PMID:Myorhythmia: a widespread movement disorder. Clinicopathological correlations. 669 62

Zero concordance for Parkinson disease was found in the first 12 monozygotic twin pairs examined in an ongoing twin study. One co-twin (subject without Parkinson disease) had essential tremor, another had cerebral vascular disease, and a third was an alcoholic. Cigarette smoking appeared to be less frequent in the probands than in the co-twins (11.9 versus 16.1 pack-years). There was also evidence of premorbid personality differences between probands and co-twins dating back to late adolescence or early adult years. These preliminary findings suggest that genetic factors do not play a major role in the etiology of Parkinson disease and point to a prodromal onset of the disease as early as late adolescence or early adult life.
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PMID:Twin study of Parkinson disease. 719 28

A study of 100 Day Hospital patients showed that 26 elderly patients with mild Senile Parkinsonism and varying degrees of dementia had subclinical tremor with the same frequency as Parkinson's Disease and distinguishable by amplified recordings from those of Parkinson's Disease and Senile Tremor. A significant history of cerebro-vascular disease was obtained in one-half of these patients. The recording of tremor is shown to be of value in diagnosing Parkinsonism and in assessing response to treatment.
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PMID:Tremor and senile parkinsonism. 720 98

Olivary pseudohypertrophy (OH) and its chronological change was examined by MR images in two patients with brainstem vascular disease. Patient 1 was a 63-year-old woman who developed an infarction in the red nuclei associated with "top of the basilar" syndrome. Two months later, she showed 2-4 c/s rhythmic myoclonus (rubral tremor) involving four extremities. Palatal myoclonus was absent. MR images of the inferior olives did not demonstrate a significant lesion in 10 days after the onset, but showed OH in 6 months, and then their size attained a maximum in 10 months after. On T2-weighted (T2) images and proton-density-weighted (PD) images obtained at 20 and 24 months, OH gradually became irregular but discrete in their intensity, and the intensity had also decreased to some extent. Rhythmic myoclonus had subsided to some extent after 20 to 24 months. Patient 2 was a 62-year-old woman who had a small hemorrhage in the pontine tegmentum. She developed 2.5 c/s vertical ocular myoclonus without palatal myoclonus two months after the onset. MR images showed OH in 6 and 8 months after the onset. On T2 and PD images obtained at 20 months, the image of OH gradually developed to become irregular in intensity and slightly atrophic in size. The ocular myoclonus somewhat reduced in their intensity 12 months after the onset. These serial changes in MR images were considered to correspond to the chronological changes of the pathology of OH. Appearance and subsidence of the myoclonic movement was also considered to correlate to the sequential changes of MR images of OH.
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PMID:[Chronological changes in MR imaging of inferior olivary pseudohypertrophy--report of two cases]. 789 37

Idiopathic Parkinson's disease (IPD) is a common and universal condition. Although its cause is still unknown, we now have some insights into pathogenetic mechanisms and genetic factors that may be important in causing the selective neuronal loss and presence of Lewy bodies that characterize its pathology. Clinically, as well as the classic features of akinesia, rigidity and often rest tremor, patients may present a wide range of other symptoms including pain, other sensory symptoms, impaired olfaction, personality change, mild executive cognitive deficits, dementia and depression, an extraordinary richness of symptoms and signs rendered even more extraordinary by the long-term effects of drug treatment. While there may be little difficulty recognizing typical cases of IPD, there has been, at least until recently, a considerable misdiagnosis rate in both atremulous (confusion with ageing, vascular disease, multiple system atrophy (MSA) or progressive supranuclear palsy (PSP)) and tremulous (confusion with essential tremor (ET), dystonic tremor, and MSA) forms. However, increasing awareness of the clinical features of all these conditions, together with adherence to exacting diagnostic criteria, is leading to improved diagnosis, which is crucial for patients (who want to know what the future holds for them), for their treatment (giving them the right drug and not the wrong one) and for research (since all the different diseases above have different aetiologies and pathology).
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PMID:Parkinson's disease: clinical features. 942 65

We report a sporadic case of unusual cerebral amyloid angiopathy (CAA) with prominent capillary involvement. A 67-year-old doctor developed gait disturbance, resting tremor and rigidity. He was diagnosed to have Parkinson's disease, for which the treatment with levodopa was effective. Four years later he began to exhibit progressive cognitive decline and behavioral abnormalities consisting of hallucination and agitation. Subsequently, his condition steadily worsened and became bedridden with severe dementia, and he died eight years after the disease onset. During the clinical course, there had been no episode of stroke. Postmortem examinations revealed the typical pathology of Parkinson's disease with frequent cortical Lewy bodies in the amygdala. The most striking pathological feature of this patient was widespread CAA where prominent beta-amyloid (A beta) deposition was observed in the capillaries of the neocortex, most pronouncedly in the occipital lobe, as well as leptomeningeal and cerebral medium-sized and small vessels. Further, perivascular plaques were found in half of the amyloid-laden capillaries. Tau-positive dystrophic neurites were only sparsely detectable within a few perivascular plaques. Despite the severe A beta pathology, there was no microaneurysmal dilatation, fibrinoid necrosis or vascular occlusion. There was only one small ischemic lesion in the brain. The cerebral white matter was unremarkable. Senile plaques of neuritic type and neurofibrillary tangles were mostly limited to the hippocampal regions and, to a lesser degree, in the amygdaloid nucleus, which did not meet the neuropathological criteria of Alzheimer's disease. On the gene analyses, his apolipoprotein E (ApoE) genotyping was verified to be heterozygous epsilon 3/epsilon 4, and no mutation was seen in exons 16 and 17 of the amyloid precursor protein gene. Severe A beta capillary angiopathy as seen in our patient is exceptional in sporadic CAA. Further, A beta angiopathy of this patient was notable in the absence of an associated cerebrovascular disease despite prominent A beta deposition in the vessel walls. Regarding the development of his severe dementia, the limbic pathology of Lewy body disease might be one of the potential causes, but A beta angiopathy appears more likely because of its severity. We speculate that widespread A beta deposition disregulates the blood-brain barrier of the capillaries leading to a disturbance of the microcirculation throughout the cerebral cortex without obvious ischemic disintegration of the neuropil. We should take into consideration that A beta angiopathy can present as progressive dementia without cerebrovascular disease.
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PMID:[Sporadic cerebral amyloid angiopathy presenting with dementia and prominent capillary beta-amyloid deposition: a case report]. 1260 81

The diagnosis of Parkinson's disease (PD) is clinical and is based on the identification of a combination of the cardinal motor signs of bradykinesia plus at least one of the following: rigidity, tremor or postural instability. There are many causes of parkinsonism such as drug induced parkinsonism, subcortical vascular disease, and multisystem atrophy. PD is a well characterised syndrome which represents only a part of the various causes of parkinsonism. A good response to dopaminergics is an important diagnostic criteria for PD. Pharmacotherapy for PD relies primarily on levodopa and dopamine agonists. Deep brain stimulation is increasingly used in the management of patients with severe dopa fluctuations and dyskinesias. Cholinesterase inhibitors are introduced for dementia in parkinsonism. Neuroprotective compounds, nerve growth factors such as GDNF and the implantation of dopaminergic cells are studied in clinical trials.
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PMID:[Diagnosis and treatment of Parkinson's syndrome. What is important for the general practitioner?]. 1457 97

Vascular parkinsonism has not been well defined and the clinical correlation of vascular parkinsonism is still not clear. The aim of the study was to estimate prevalence of occurrence of vascular parkinsonism, analysis of risk factors leading to its development and to identify clinical features that suggest a vascular origin. 214 patients with Parkinson's disease were examined. Their ages ranged from 37 to 88 years (median 66.4 years). Evidence of vascular parkinsonism was assessed using a vascular rating scale previously described by Winikates and Jankovic. Statistical analysis was performed with Mann-Whitney U test, chi 2 Pearson test, chi 2 Yates test, Spearman rank correlation and Student's t test. Out of 214 patients 8 were proved to have developed Parkinson's disease due to vascular disease, what gave 3.74%. Out of risk factors for stroke 5 patients had hypertension, 3 had diabetes mellitus, 2 suffered from heart disease, 2 had infarctus myocardii, 1 had hyperlipidemia, 1 had atrial fibrillation. Additionally, those patients had neuroimaging (CT or MRI) evidence of vascular disease in one or more vascular territories. Patients with vascular parkinsonism were older, had shorter duration of disease, were more likely to present rigidity rather than tremor. Dementia and incontinence were more common in vascular group than in Parkinson's disease group. Patients with vascular parkinsonism were also significantly more likely to have corticospinal findings. Proving that Parkinson's disease had vascular etiology is extremely difficult. The test results are inconclusive.
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PMID:[Clinical correlation of vascular parkinsonism]. 1509 42


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