Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0233565 (bradykinesia)
 2,352 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report an autopsied case of Parkinson's disease manifesting Shy-Drager syndrome. At the age of 63 years, the patient noticed an onset of progressive orthostatic dizziness, which was followed by constipation, dysuria, and sexual impotence. When he was 66 years old, syncopal attack for a few minutes, tremor in the bilateral hands, and memory disturbance developed. On admission, his blood pressure was 142/72 mmHg in supine position, which fell to 58/42 mmHg on standing with appropriate increase of heart rate. Neurological examination revealed hallucination, memory disturbance, masked face, muscular rigidity, bradykinesia, mild postural tremor, and autonomic dysfunction including severe orthostatic hypotension, hypohydrosis, constipation, dysuria, and sexual impotence. Electroencephalogram showed diffuse slowing. Brain CT demonstrated absence of severe atrophy of the cerebellum, and brain stem. Pharmacological study revealed denervation hypersensitivity to the intravenously administrated noradrenaline. A diagnosis of Shy-Drager syndrome was made, and he was treated with anti parkinsonian drugs. However, no improvement was observed in his clinical symptoms. Seven months later, he died of pneumonia. Neuropathological examination revealed marked neuronal cell loss and gliosis in the substantia nigra and locus ceruleus. Lewy bodies were seen in those pigmented nuclei, dorsal vagal nucleus, hypothalamus and nucleus basalis of Meynert. No abnormality was found in the intermediolateral nucleus of the spinal cord. This is the first report on a Japanese patient who presented clinically Shy-Drager syndrome and pathologically typical Parkinson's disease. In this patient, from the pharmacological and pathological findings, sympathetic ganglia were supposed to be the responsible lesion for orthostatic hypotension.
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PMID:[An autopsied case of Parkinson's disease manifesting Shy-Drager syndrome]. 130 25

Nursing interventions for each of the symptoms of Parkinson's disease, muscle rigidity, bradykinesia, tremors at rest and postural reflex abnormalities, are designed to increase the patient's quality of life by minimizing symptoms. Nurses are responsible for planning patient medication schedules to maximize drug effectiveness. Dietary implications include a low-protein regimen for the patient during the day, eliminating foods high in Vitamin B6, high caloric foods, and soft-solid foods offered at frequent feedings. Constipation is addressed by increasing the patient's fiber and fluid intake and by increasing the patient's mobility. Patient mobility is increased when the patient is taught purposeful activities and to concentrate on the way he walks. Communication is facilitated if the patient takes deep breaths before speaking and uses diaphragmatic speech. A telephone receiver which amplifies the patient's voice is also available. Interventions are good only if the patient chooses to implement them; he is the head of the health team planning his care.
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PMID:Nursing care of patients with Parkinson's disease. 322 57

A case of familial juvenile parkinsonism with dementia, orthostatic hypotension, neurogenic bladder and constipation was reported. He had been in a good health until the age of 28 when a finger tremor occurred on effort to hold hands in a definite position, and disturbances in gait and speech were noted. These symptoms were relieved by levodopa treatment followed by dyskinesia and motor fluctuations. Three years later, he complained of faintness, constipation and urinary frequency. The neurological examination revealed mentally sound male with masked face, tremor and rigidity in his extremities, and short step gait with lateropulsion. Urodynamic study showed uninhibited bladder. In the following years, orthostatic hypotension, dysuria and urinary retention developed gradually. He became mentally loose and was unable to take medicines appropriately. When in the Nishiojiya Byoin National Sanatorium, he tried to snake out the hospital many times. His parents and a brother suffered from Parkinson's disease and juvenile parkinsonism, respectively, suggesting an autosomal dominant inheritance. On admission to our hospital, he was apathetic. He had masked face, bilateral postural tremor, frozen gait and dyskinesia in the right lower extremity. Little bradykinesia or rigidity was noted. His muscle tone and deep tendon reflexes were decreased but neither muscular wasting, weakness, ataxia nor sensory disturbance was observed. Laboratory data including ceruloplasmin, copper, dopamine-beta-hydroxylase and lysosomal enzyme activities were normal except for mild anemia. A cranial CT scan revealed mild cortical atrophy in the frontal and temporal lobes, but nerve conduction study and cortical evoked potentials showed no abnormality. While in the hospital, his mental functions deteriorated to the state of dementia and orthostatic hypotension became apparent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Familial juvenile parkinsonism with dementia and autonomic failure--a case report]. 833 79

Shy Drager Syndrome (SDS) is a movement disorder which is often referred to as a parkinson plus syndrome or Multiple System Atrophy (MSA). For patients afflicted with this condition, rigidity and bradykinesia are the primary extrapyramidal symptoms which are present. The "plus" refers to autonomic nervous system dysfunction which leads to much of the disability seen in this disorder. Syncope, urinary incontinence, impotence, constipation, fecal incontinence, cardiac arrythmias as well as other symptoms occur as a result of widespread pathological changes in multiple areas of the central and autonomic nervous system. The goal of this paper is to provide an overview of the pathophysiology, signs and symptoms of and treatment for SDS. Nursing Care of the patient and family coping with Shy Drager Syndrome and the challenges it presents to the Movement Disorder Nurse are discussed. A coordinate, multidisciplinary team approach is suggested.
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PMID:Shy Drager syndrome. 929 81

A 74-year-old man became unable to walk two days following the initiation of administration of oral distigmine bromide, 10 mg per day, for his constipation. Neurological examination revealed bradykinesia, rigidity and fine postural tremor without laterality. T2 weighted MRI showed mild front-temporal atrophy and multiple hyperintensities in both deep white matters. His symptoms fully improved one week after discontinuance of distigmine bromide. This is the first case report of distigmine bromide induced Parkinsonism.
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PMID:[Distigmine bromide induced Parkinsonism. A case report]. 1618 Jul 10

Headache makes one of the most common side effects of frequently pesticide application. This is to be taken care of in rural areas. Headaches have been reported with the use of ivermectin, ivermectin-diethylcarbamazine, organophosphates, and also with the fungicide maneb and copper sulfate, carbofuran, hexonal, dioxin, methomyl and its salts, as well as rare cases of poisoning with the fungicide combination of propineb and cymoxanil. Headache often occurs after long term work with pesticides and/or in laboratories. There are numerous symptoms accompanying headache in pesticide poisoning the most common being elevated body temperature, lassitude, dizziness, irritability, nausea, vomiting, epigastric pain, diarrhea, myalgia, pains in the arms and legs, sleepiness, pains in joints, irritation of eyes/face/skin, sweating. Much less common are respiratory disturbances, tachycardia, tachypnea and other cardiac distur bances, fall of blood pressure, gastrointestinal discomforts, constipation, poor appetite, significant decrease in leukocyte count, anemia, albuminuria, azotemia, fasciculations, miosis, blurred vision, memory disturbances and other neurologic disturbances, postural tremor, signs of cerebral function damage, bradykinesia, etc.
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PMID:[Headache caused by pesticides--a review of the literature]. 1871 90

Parkinson's disease (PD) is the second most common neurodegenerative disease and primarily considered as a movement disorder defined by the presence of motor symptoms, such as bradykinesia, tremor and rigidity. However, it is nowadays widely recognized that in addition there is impairment of cognitive function, mood and the autonomic nervous system in a high percentage of PD patients, which is sometimes even more harming quality of life. These symptoms not only occur during the course of the disease but may even precede the onset of motor symptoms. Typical examples of non-motor features of PD are depression, constipation, REM sleep behaviour disorder, and hyposmia.
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PMID:Non-motor features of Parkinson's disease: depression and dementia. 2008 17

So far, the diagnosis of an idiopathic Parkinson-syndrome was based on the British Brain Bank Criteria, that is the occurrence of bradykinesia together with at least one more of the cardinal symptoms, i. e. resting tremor, rigidity or postural instability. The latter symptom is not useful, since it occurs only in the Hoehn and Yahr stage III which is seen in advanced PD patients. Thus, this symptom is certainly not useful for EARLY diagnosis. Early signs for PD are hyposmia, constipation, REM sleep behaviour disorder and depression. Early diagnosis is still a clinical one, which can be supported by a levodopa test. It can be expected that in the near future gene chips will be available for patients with a positive family history for PD or with an early onset. As long as a blood test for PD is not available, methods such as SPECT and PET are extremely useful in patients with an unclear clinical symptomatology. In my own view, each PD patient should receive once in his career a cranial CT or MRI.
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PMID:[Future standards in diagnosing Parkinson syndrome]. 2019 42

Parkinson's disease (PD) occurs with an annual incidence of 13/100.000, is slightly more frequent in men and is characterized by the motor symptoms tremor, rigidity, bradykinesia and postural instability. In addition, non-motor symptoms have been increasingly connected to the disease although already described in James Parkinson's 'Essay on the shaking palsy' from 1817. The motor symptoms in PD are related to the degeneration of dopaminergic cells in the substantia nigra (SN). These symptoms respond well to dopaminergic substitution. It is much more unclear whether non-motor symptoms like dysautonomia, insomnia, day-time sleepiness, fatigue, pain and neuropsychiatric symptoms respond to levodopa. Autonomic symptoms include dizziness because of orthostatic hypotension, constipation, nausea, voiding symptoms and increased sweating. Such symptoms as well as sensory symptoms like hyposmia and pain are very frequently reported in PD and seem to occur early in the disease process. Braak proposed a sequential model of neuropathology in PD starting with affection of the olfactory bulb and the autonomic innervation of the heart and gut. Affection of SN is seen from Braak stage 3, and limbic and cortical structures are affected in the later stages of the disease. Currently, the evidence for sensory and autonomic involvement in PD is reviewed with special focus on the early phase of the disease.
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PMID:Are dysautonomic and sensory symptoms present in early Parkinson's disease? 2058 40

The diagnosis of Parkinson's disease (PD) follows the UK Brain Bank Criteria, which demands bradykinesia and one additional symptom, i.e. rigidity, resting tremor or postural instability. The latter is not a useful sign for the early diagnosis of PD, because it does not appear before Hoehn and Yahr stage 3. Early symptoms of PD which precede the onset of motor symptoms are hyposmia, REM sleep behavioral disorder, constipation, and depression. In addition, an increasing number of patients whose PD is related to a genetic defect are being described. Thus, genetic testing may eventually develop into a tool to identify at-risk patients. The clinical diagnosis of PD can be supported by levodopa or apomorphine tests. Imaging studies such as cranial CT or MRI are helpful to distinguish idiopathic PD from atypical or secondary PD. SPECT and PET methods are valuable to distinguish PD tremor from essential tremor if this is clinically not possible. Using all of these methods, we may soon be able to make a premotor diagnosis of PD, which will raise the question whether early treatment is possible and ethically and clinically advisable.
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PMID:Clinical criteria for the diagnosis of Parkinson's disease. 2061 63


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