Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An isocentered system for functional stereotactic procedures with the Cosman-Roberts-Wells frame and a CT localizer that allows extrapolation of target data directly from the CT slice is presented. Based on anatomical landmarks and on the scaled corresponding transverse plates of the Schaltenbrand and Wahren atlas, we delineate the thalamic and cerebellar nuclei. Twenty three image-directed functional procedures were performed in one year on 18 patients (7 with Parkinson's disease, 4 with dystonia, 3 persons with essential tremor, 2 patients with choreo-athetosis and 2 with de-afferentiation pain). The 23 procedures included 19 thalamotomies, two dentatotomies and two stereotactic implantations of deep seated brain electrodes. Successful targeting was verified by intra-operative electrical stimulation and postoperative CT scan. Complete reduction of symptoms was observed in 4 persons with Parkinson's disease and in 2 patients with essential tremor with significant improvement observed in the rest of the patients with the exception of the individual with choreo-athetosis. There were no operation-related complications. The reported technique is safer and less distressing for patients than previous radiological procedures and it makes image-directed stereotactic functional neurosurgery available to many units with the CRW frame.
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PMID:Image-directed functional neurosurgery with the Cosman-Roberts-Wells stereotactic instrument. 179 61

In later stages of the disease, patients with Parkinson's disease treated with levodopa may become severely disabled by pronounced and sudden motor fluctuations called "the on-off syndrome". In spite of optimal individual adjustment of doses and combinations, orally administered antiparkinson drugs are often not able to eliminate the off-conditions which may last from minutes to hours and sometimes are accompanied by dystonic pain. Apomorphine, a potent dopamine receptor agonist, administered subcutaneously as single injections or continuously by means of a pump, quickly passes on to striatal dopamine receptors. With suitable individually adjusted doses, a rapid, and in some cases, more stable anti-parkinson effect may be achieved. Peripheral side-effects can be avoided by concomitant treatment with domperidone. Nine levodopa treated patients with Parkinson's disease and severe on-off syndrome received apomorphine. Seven experienced considerable and long-term improvement of the disabling symptoms, and some patients reduction of levodopa and/or bromocriptine doses. Treatment with apomorphine should only be considered in patients whose on-conditions are not accompanied by pronounced dyskinesias and/or impairment of balance or to patients suffering from severe dystonic pain.
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PMID:[Apomorphine in the treatment of Parkinson disease]. 194 72

The authors established the appearance of pain in 54 (68.3%) patients suffering from Parkinson's disease (PD) with levodopa treatment, and in 16 (76.2%) PD patients without treatment. Pain preceded the motor disorders in 39% of PD patients. Pain involved most often the upper (72.2%) and the lower limbs (68.1%), as well as the paravertebral (45.8%) and the neck regions (15.2%). It was located more frequently in joints (54.0%) than in muscles (28.1%). The frequency of pain was higher in PD patients with depression (20.17%) than in those without depression (11%). At the same time, the pain was noted in 61.9% of depressive patients without treatment, as compared to 35.4% depressive PD patients following treatment. The authors discussed the potential pathophysiological mechanism of pain in PD patients.
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PMID:[Pain in patients with Parkinson disease]. 213 2

Despite astounding progress in the biochemical management of Parkinson's disease in particular and of other movement disorders, there are still patients disabled by severe tremor and not by bradykinesia in whom thalamotomy remains the treatment of choice. Though the irreducible complications of surgery must be taken into account, the problems of prolonged multiple drug therapy should not be ignored. The same rationale applies to selected patients with essential or familial tremor. For some patients with ataxic tremor caused by multiple sclerosis and other brain lesions, or with dystonia or, rarely, other movement disorders, thalamotomy may offer limited though significant relief from an otherwise intractable disability. Indications for the use of stereotactic destructive lesions in the treatment of nociceptive pain in those cases where cordotomy and intraspinal morphine infusion are unsuitable have contracted with the introduction of lower-risk alternatives such as intraventricular morphine instillation. When destructive lesions are indicated, the choice will lie between mesencephalic tractotomy, with its higher success rate but irreducible mortality and morbidity, and medial thalamotomy, which, though less risky, is also less effective. For central and deafferentation pain, the same two procedures may be considered. However, destructive lesions are seldom effective for the treatment of the most common element of these pain syndromes: steady burning or dysesthetic pain. They may be more promising, though, for the intermittent, often shooting pain and the evoked elements (hyperpathia and allodynia) of central and deafferentation pain. Even so, it is advisable first to carry out a trial of VC and PVG stimulation before considering a destructive lesion, which should be a last resort.
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PMID:Thalamotomy. 213 73

Madopar Hydrodynamically Balanced System (HBS), a new sustained-release levodopa preparation, was used to control severe nightly disabilities in 15 outpatients suffering from Parkinson's disease in an advanced state and with long-term levodopa therapy. This medication was given ante noctem in addition to an otherwise unchanged daily regimen of levodopa administration. In 13 patients a considerable diminution in nocturnal akinesia and in the frequency of waking up was reached with a mean dosage of 308 mg of Madopar HBS. Early morning akinesia was only slightly alleviated in four patients. The nocturnal off-period pain disappeared in one patient. Adverse effects consisted of nocturnal dyskinesia in two patients and early morning dystonia in another two patients. The regular use of sleeping pills was clearly reduced after Madopar HBS therapy.
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PMID:Madopar HBS in nocturnal symptoms of Parkinson's disease. 223 93

1. Cysteamine is formed by degradation of coenzyme A (CoA) and causes somatostatin (SS), prolactin and noradrenaline depletion in the brain and peripheral tissues. 2. Cysteamine influences several behavioral processes, like active and passive avoidance behavior, open-field activity, kindled seizures, pain perception and SS-induced barrel rotation. 3. Cysteamine has several established (cystinosis, radioprotection, acetaminophen poisoning) and theoretical (Huntington's disease, prolactin-secreting adenomas) indications in clinical practice. 4. Pantethine is a naturally occurring compound which is metabolized to cysteamine. 5. Pantethine depletes SS, prolactin and noradrenaline with lower efficacy compared to that of cysteamine. 6. Pantethine is well tolerated by patients and has been suggested to treatment of atherosclerosis. The other possible clinical indications (alcoholism, Parkinson's disease, instead of cysteamine) are discussed.
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PMID:Preclinical and clinical studies with cysteamine and pantethine related to the central nervous system. 227 50

A patient with Parkinson's disease had severe levodopa-associated leg pain in a beginning-of-dose and peak-dose pattern. Local anesthetic block of the lumbar sympathetic chain or differential epidural block did not alter the pain. Spinal anesthesia abolished the pain. We postulate that levodopa-associated pain in Parkinson's disease either originates in or is mediated by spinal cord dopaminergic systems.
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PMID:Evidence for the role of spinal cord systems in Parkinson's disease-associated pain. 232 8

Sensory symptoms related to pain perception have been reported to occur in 30-50% of parkinsonian patients. Two patients with Parkinson's disease are reported, in whom painful sensory phenomena preceded or accompanied the disease process. In both patients the sensory phenomena were unresponsive to therapy with oral narcotics, anti-inflammatory drugs or administration of levodopa/carbidopa. Benzhexol (4-6 mg/day) produced dramatic amelioration of symptoms, indicating a role for the cholinergic system in the pathophysiology of abnormal sensory symptoms in Parkinson's disease and possibly in human analgesia in general.
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PMID:Anticholinergic-induced analgesia: possible role for the cholinergic system in abnormal sensory symptoms in Parkinson's disease. 243 Feb 73

Intravenous administration of methylphenidate hydrochloride, a central stimulant, was unexpectedly found to exert a potent analgesic effect on primary sensory symptoms in a group of patients with Parkinson's disease. This effect, which has now been studied in a short-term, double-blind, placebo-controlled experiment, subsequently disappeared if patients were pretreated with a beta-blocker or with a serotonin antagonist. Cerebrospinal fluid monoamine metabolites were determined in some of these patients, and the 5-hydroxyindoleacetic acid level was found to be significantly lower than in parkinsonian patients without pain and in normal volunteers. Given the mechanism of action of methylphenidate on the central nervous system, the adrenergic and serotoninergic mediation of its analgesic effect, and the demonstration of impaired central serotonin metabolism in the patient group, it is concluded that not only central dopaminergic deficiency but also altered noradrenergic and serotoninergic transmission in the spinal cord are quite likely to play a role in the pathophysiology of pain in Parkinson's disease.
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PMID:Analgesic action of methylphenidate on parkinsonian sensory symptoms. Mechanisms and pathophysiological implications. 245 94

Sensory symptoms have been reported in 40-60% of patients with Parkinson's disease, and in at least 10% of patients these symptoms precede the onset of the motor disorder. The pathophysiology of these symptoms remains unknown. Diminished brain serotonin concentration has been reported to be associated with sensory symptoms. Serotonin metabolism is regulated by pineal melatonin. The secretory activity of the pineal gland may be diminished in Parkinson's disease. In experimental animals pineal melatonin has been shown to exert analgesic effects by interacting with opiate receptors. In addition, since opioid peptides mediate the analgesic effects of melatonin, decreased opioid peptide functions in Parkinson's disease may be associated with disruption of the "fine-tuning" pain modulatory functions of melatonin and possibly indirectly facilitate the emergence of sensory symptoms.
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PMID:Pineal melatonin and sensory symptoms in Parkinson disease. 267 5


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