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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a study of oesophageal motility in 20 patients with Parkinson's disease, intravenous atropine produced marked disruption of co-ordination in response to swallows, when compared with control subjects. This suggests that cholinergic rather than dopaminergic mechanisms are more important in the control of swallowing in patients with Parkinsonism. No conclusive evidence of peripheral dopamine depletion or autonomic neuropathy was found, although minor changes suggestive of the former were found in severely affected patients.
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PMID:Evidence for a change in neurotransmitter affecting oesophageal motility in Parkinson's disease. 2 87

Sixty-three male patients suffering from post-prostatectomy incontinence were studied by urodynamics and fluoroscopy. In almost half the patients (49%) the sole cause of incontinence was detrusor instability. Incontinence due to damage of the sphincter mechanism was present in less than half of the patients (47%). However, almost half of these patients (53%) had concomitant detrusor instability. Only a small number of patients (4%) had incontinence due to other causes. It appears that post-prostatectomy incontinence is not always due to a surgical misadventure. Many older patients may have preexisting neurologic disorders (e.g., Parkinson disease, diabetic autonomic neuropathy, alcoholic neuropathy, and various spinal cord disorders) which can profoundly affect the outcome of prostatic surgery. Detrusor instability should be considered when evaluating post-prostatectomy incontinence.
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PMID:Post-prostatectomy incontinence. A urodynamic and fluoroscopic point of view. 194 66

Autonomic neuropathy (AN) may occur in the elderly in connection with other common illnesses afflicting this age group, such as diabetes or Parkinson's disease, or even as the primary illness. Symptoms of AN are numerous, but syncope, with its risk for fractures and head trauma, is the most serious. The clinical presentation and differential diagnosis of AN are discussed, as are a group of diseases associated with AN. Treatment guidelines are outlined.
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PMID:Autonomic neuropathy: clinical presentation and differential diagnosis. 219 6

A series of 36 patients with specific neurological lesions affecting those parts of the nervous system thought to be involved in the control of bladder function have been studied by urodynamic, electromyographic and neurohistochemical means and the results compared with those obtained in 20 control subjects. In patients with pelvic nerve injury urethral sphincter electromyography (EMG) revealed abnormal motor units and the density of bladder innervation was significantly reduced (P less than 0.01). By contrast, in patients with distal autonomic neuropathy the innervation of the striated muscle of the urethra was unaffected and although there was an almost total loss of nerves from the bladder muscularis, the subepithelial plexus of nerves was preserved. In patients with progressive autonomic failure and multiple system atrophy, the bladder neck was incompetent in every case and the striated muscle of the urethra was affected by a process of denervation and re-innervation. These findings serve to distinguish patients with autonomic failure from those with idiopathic Parkinson's disease and influence the selection of patients for transurethral surgery.
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PMID:Studies of the neurogenic bladder. 319 Jan 28

Neurogenic orthostatic hypotension is a severely disabling condition due to deficient peripheral vasoconstrictor tone in response to the upright position and is characterized by a decrease in blood pressure upon standing associated with symptoms of lightheadedness, dizziness, visual "white-out", weakness, lack of energy, near syncope or even syncope. Previous pharmacologic treatment of neurogenic orthostatic hypotension has been problematic. Midodrine, a new specific alpha-1-agonist has been shown to produce arteriolar constriction and decrease in venous pooling via a constriction of venous capacitance vessels. Therefore, a recent multicenter study evaluated the safety and efficacy of midodrine therapy in 97 patients with neurogenic orthostatic hypotension due to various etiologies: Shy Drager syndrome (No. 18); Bradbury Eggleston syndrome (idiopathic orthostatic hypotension) (No. 20); diabetic autonomic neuropathy (No. 27); Parkinson's disease (No. 22); and miscellaneous (No. 10). Following one week of placebo therapy, the patients were randomized into 4 groups for a 4 week period of time; placebo, 2.5 mg, 5 mg, or 10 mg three times daily. The BE/SDS subgroup demonstrated a 27 +/- 8% (22 mmHg) increase in standing systolic blood pressure for the 10 mg dose. Diabetics achieved a significant increase at 5 mg. Similar increases were observed for the entire group on the 10 mg dose (p < 0.001). Symptoms or fainting, blurred vision, improved energy level, standing time, and depressed feelings were also significantly improved even at lower doses (p < 0.05 or less). Side effects were mild. Therefore, midodrine is an effective and safe agent for the treatment of neurogenic orthostatic hypotension.
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PMID:Midodrine in neurogenic orthostatic hypotension. A new treatment. 769 Mar 83

GI motility changes little--if at all--with age in healthy patients. However, a variety of diseases, including diabetes and Parkinson's disease, may cause autonomic neuropathy that is manifest as a motility disorder in the GI tract. Autonomic neuropathy can cause dysmotility in the esophagus, stomach, and gut. Symptoms are often nonspecific, including difficulty in swallowing, nausea, vomiting, heartburn, indigestion, diarrhea, and constipation. Nonpharmacologic treatment includes management of underlying diseases, avoidance of anticholinergic medications, and dietary changes. Agents with prokinetic action are the therapy of choice when drug treatment is indicated.
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PMID:GI motility disorders: diagnostic workup and use of prokinetic therapy. 790 Nov 29

An autonomic reflex screen, which consisted of a quantitative sudomotor axon reflex test, orthostatic blood pressure and heart rate response to tilt, heart rate response to deep breathing, the Valsalva ratio, and beat-to-beat blood pressure measurements during phases II and IV of the Valsalva maneuver, tilt, and deep breathing, was used to develop a 10-point composite autonomic scoring scale of autonomic function. The scheme allots 4 points for adrenergic and 3 points each for sudomotor and cardiovagal failure. Each score is normalized for the compounding effects of age and sex. Patients with a score of 3 or less on the composite autonomic scoring scale have only mild autonomic failure, those with scores of 7 to 10 have severe failure, and those with scores between these two ranges have moderate autonomic failure. The sensitivity and specificity of the method were assessed by evaluating the composite autonomic scoring scale in four groups of patients with known degrees of autonomic failure: 18 with multisystem atrophy, 20 with autonomic neuropathy, 20 with Parkinson's disease, and 20 with peripheral neuropathy but no autonomic symptoms. The composite scores (means +/- SD) for these four groups, respectively, were as follows: 8.5 +/- 1.3, 8.6 +/- 1.2, 1.5 +/- 1.1, and 1.7 +/- 1.3. Patients with symptomatic autonomic failure had scores of 5 or more, those without symptomatic autonomic failure had scores of 4 or less, and no overlap existed in these groups. Thus, autonomic laboratory tests should be useful in grading the degree of autonomic failure.
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PMID:Composite autonomic scoring scale for laboratory quantification of generalized autonomic failure. 839 53

It has been believed that patients with neurogenic orthostatic hypotension (NOH) usually develop denervation supersensitivity of cardiovascular alpha-, beta 1- and beta 2-adrenoceptors, because the majority studies have shown augmented cardiovascular responses to intravenously given noradrenaline (NA) or isoprenaline (IP) in these patients. This view, however, leaves room for discussion. First, drugs were administered by means of drip infusion method in most of the previous studies. Since this method necessarily provokes baroreflex, which is buffering fluctuations in blood pressure and heart rate, the results may reflect diminished baroreflex rather than denervation supersensitivity. Second, adrenoceptor functions are modulated by multiple factors, such as ageing, thyroid hormone and chronic inflammation. It is, thus, inappropriate to explain the whole picture of functional change in adrenoceptors by the denervation mechanism only. In order to look over the cardiovascular adrenoceptor functions in NOH, we performed bolus infusion tests of NA and IP on the patients. The subjects comprised 7 cases of NOH with pre-ganglionic sympathetic deficit (NOH-I), 6 cases with post-ganglionic deficit (NOH-II) and 15 healthy controls. NOH-I group included 6 patients with multiple system atrophy and one with Parkinson disease, while NOH-II group consisted of 3 patients with idiopathic orthostatic hypotension (pure autonomic failure) and 3 with diabetic autonomic neuropathy. Both NA and IP infusion tests were carried out under the continuous measurement of blood pressure and heart rate. In NA test, different bolus doses (0.01, 0.02, 0.05 and 0.1 microgram/kg) of NA were intravenously administered, and a degree of subsequent rise in mean blood pressure was used as an index for alpha-adrenoceptor function. IP test was performed in the same manner, and an increase in heart rate and a fall in mean blood pressure in response to the drug (0.001, 0.002 and 0.005 microgram/kg) were measured as indices for beta 1- and beta 2-functions, respectively. A rise in blood pressure following the administration of any dose of NA did not statistically differ among three groups. An increase in heart rate in IP test was generally lower in both NOH groups, and a significant difference was obtained between NOH-I and control when a given dose was 0.005 microgram/kg) (p < 0.02). A fall in blood pressure in IP test was significantly greater in NOH-I compared to control when doses were 0.002 and 0.005 microgram/kg (p < 0.02 and 0.01, respectively). It was also greater in NOH-II than in control when a dose was 0.002 microgram/kg (p < 0.01). In disagreement with most of the previous studies, the present results suggest that alpha-adrenoceptor function is hardly altered, beta 1-function is suppressed, and beta 2-function is augmented in NOH.
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PMID:[Cardiovascular alpha-, beta 1- and beta 2-adrenoceptor functions in neurogenic orthostatic hypotension]. 882 96

Parkinson's disease (PD) and Alzheimer's dementia (AD) are often associated with an autonomic neuropathy. The extent of autonomic involvement, however is poorly defined and unpredictable. In order to assess the autonomic cardiovascular regulation baroreflex sensitivity (BRS) was determined non-invasively in 23 patients (age: 65 +/- 9.3 years) with PD and 24 patients with AD (age: 72.3 +/- 7.2 years). The results were compared with those on 22 healthy age- and sex-matched volunteers. Patients with PD and AD exhibited marked abnormalities in cardiovascular autonomic reflex regulation showed by markedly depressed BRS. The possible predictive value of centrally based depression of baroreflex sensitivity necessitates further studies.
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PMID:Depressed baroreflex sensitivity in patients with Alzheimer's and Parkinson's disease. 1137 50

On the basis of current literature, clinical and neuropathologic features of idiopathic autonomic neuropathy is presented. Idiopathic autonomic neuropathy is a disease characterized by acute or subacute onset, monophasic course over a period of several years, it is often preceded by an infection. The spectrum of autonomic changes ranges from cholinergic or adrenergic dysfunction to pandysautonomia, leading to heterogeneity of its clinical features. Possible sympathetic system abnormalities found in autonomic neuropathy are: poor pupillary response to light in darkness, orthostatic hypotension leading to syncope, hypotension without compensatory tachycardia, ejaculation disturbances and vasomotor instability. Possible parasympathetic dysfunctions are: salivation and lacrimation disturbances, absent pupillary constriction to light and near gaze, gastrointestinal tract immobility and impairment of gastrointestinal function, atonic bladder with large residual volume, erectile impotence. Pandysautonomia is thought to result from an immune mediated mechanism and responds well to plasmaferesis and intravenous immunoglobin therapy leading to gradual, sometimes not full, recovery. Moreover in this article we pay attention to the clinical value of many tests like cardiovascular or pharmacological studies in the diagnosis of pandysautonomia and in differentiation of pre- and postganglionic changes. In order to diagnose idiopathic autonomic neuropathy one has to rule out a large number of diseases with autonomic dysfunction e.g.: diabetes, malignant neoplasms, acute intermittent porphyria, Shy-Drager syndrome, Riley-Day's dysautonomia, Parkinson's disease, amyloidosis and others.
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PMID:[Idiopathic autonomic neuropathy (pandysautonomia)]. 1173 67


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