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)

Irving S. Cooper was a pioneer in the field of functional neurosurgery. During his very productive and controversial career, he proposed the surgical treatment of Parkinson disease (PD) by ligating the anterior choroidal artery to control tremor and rigidity. Subsequently, he developed seminal techniques for chemopallidectomy and cryothalamectomy for PD. He also attempted to use electrical stimulation of the cerebellum or the thalamus to treat spasticity. Cooper continued his work on brain stimulation until his death in 1985. He made video recordings of nearly all of his patients during his tenure (1977-1985) at New York Medical College. Cooper's clinical video recordings were reviewed, and selected footage was compiled into a video history of Cooper's surgical management of various movement disorders. Included are pre-, post-, and some intraoperative recordings that Cooper made to document his treatment of patients with PD, tremor, Wilson disease, cerebral palsy, chorea, dystonia musculorum deformans, and some rarer entities.
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PMID:Irving S. Cooper and the early surgical management of movement disorders. Video history. 1660 79

1. Preparations from Cannabis sativa (marijuana) have been used for many centuries both medicinally and recreationally. 2. Recent advances in the knowledge of its pharmacological and chemical properties in the organism, mainly due to Delta(9)-tetrahydrocannabinol, and the physiological roles played by the endocannabinoids have opened up new strategies in the treatment of neurological and psychiatric diseases. 3. Potential therapeutic uses of cannabinoid receptor agonists include the management of spasticity and tremor in multiple sclerosis/spinal cord injury, pain, inflammatory disorders, glaucoma, bronchial asthma, cancer, and vasodilation that accompanies advanced cirrhosis. CB(1) receptor antagonists have therapeutic potential in Parkinson's disease. 4. Dr. Julius Axelrod also contributed in studies on the neuroprotective actions of cannabinoids.
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PMID:Implication of cannabinoids in neurological diseases. 1669 78

Continuous ambulatory monitoring is a promising technique for objective evaluation of movement disorders in man. Although technological progress make such devices currently available, no validated measurements exist. We propose an original approach to validate instrumental measurements in central neurological diseases, based upon the use of computer modeling of movement disorders. In such an approach, computer simulations of altered movement were used to validate accelerometric-derived measurements in spasticity and Parkinson's disease. We found that some measurements, derived from the frequency power spectrum of distal acceleration at the upper limb, may be suitable for evaluation of some motor disorders, as spasticity, parkinsonian rigidity and related motor disability. Direct applications are expected in ambulatory monitoring of neurological diseases.
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PMID:On the interest of computer modelling in the validation of ambulatory measurement of movement disorders in man. 1728 84

Spasticity is a complex disorder characterized by a velocity-dependent increase in muscle tone associated with exaggerated deep tendon reflexes. It can be caused by numerous diffuse or focal cerebral and spinal pathologic conditions. Spasticity indicates upper motor neuron dysfunction and if severe, can lead to considerable motion restriction and eventually to more serious disability. The therapeutic interventions available to treat spasticity are often of limited benefit. In the last decade, many open-label and several double-blind, placebo-controlled, studies have demonstrated the effectiveness of intramuscular botulinum toxin (BTX) injections for the management of spasticity caused by multiple sclerosis, brain / spinal cord injury, cerebral palsy, and stroke. BTX can also be beneficial in the treatment of spasticity, or a mixture of spasticity and rigidity, in many neurodegenerative conditions; including Parkinson disease, progressive supranuclear palsy, corticobasal degeneration, frontotemporal dementia and parkinsonism linked to chromosome 17, and in various sporadic and familial spinocerebellar ataxia syndromes. Currently, two BTX serotypes, which are serologically different but share a common subunit structure, are commercially available: type A (Botox(R), manufactured by Allergan, Inc, Irvine, California, USA; and Dysport(R), distributed by Beaufour-Ipsen Pharmaceuticals, Paris, France); and type B (manufactured by Elan Corporation, Dublin, Ireland, and available in the United States as MyoBloc(R) and in Europe as NeuroBloc(R)). BTX primarily affects the neuromuscular junction by inhibiting acetylcholine release. Dosages vary considerably depending on the particular preparation used, the muscle injected, the severity of the condition, and the duration of treatment.
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PMID:Treatment of spasticity with botulinum toxin. 1761 18

Hereditary movement disorders comprise a group of genetically defined diseases characterized by an impaired control of movements, ataxia and/or spasticity. Affected individuals are disabled, their quality of life significantly reduced and their life expectancy shortened. One or more genetic causes have been identified for many of these diseases, including Huntington's disease, Wilson's disease, spinocerebellar ataxias, recessive ataxias, hereditary spastic paraplegia and hereditary dystonias. Due to their characteristic molecular and biochemical pathogenesis, these rare diseases can often serve as models for more common disorders such as Alzheimer's disease or Parkinson's disease. The primary tasks of the German Network of Hereditary Movement Disorders (GeNeMove), funded by the German Ministry for Education and Research (BMBF), are to co-ordinate basic scientific research and clinical research into rare hereditary movement disorders and to improve the cooperation between the German centers specializing in hereditary movement disorders. For each of the diseases in its scope, GeNeMove works at creating standardized documentation of symptoms and the disease's progressive course over time; developing rating scales for clinical examinations and guidelines for therapy; improving genetic testing; fostering genetic research; and collecting samples of DNA, tissue, CSF and blood from sufferers of the disease for biobanks.
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PMID:[Hereditary movement disorders]. 1805 48

Subthalamic (STN) deep brain stimulation (DBS) is an effective treatment for advanced Parkinson's disease. We present a patient with significant gait problems due to Parkinson's disease (PD) who underwent STN DBS. Gait worsened after surgery despite significant improvement in parkinsonian signs, due to underlying spasticity previously overshadowed by his parkinsonian motor symptoms. This case illustrates an emergence of dysfunction in gait in a patient with otherwise improved function and reinforces the need for an interdisciplinary approach to care of these patients.
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PMID:Gait changes after deep brain stimulation for Parkinson's disease in a patient with cervical myelopathy. 1856 Jan 43

Adenosine is an endogenous neuromodulator which alters neuronal excitability and firing rate. In recent years there has been growing interest in the manipulation of adenosine levels to understand the pathophysiology of various diseases. Dipyridamole (DPM) is a potent adenosine transport inhibitor that causes a several-fold increase in brain adenosine concentration. The present study was undertaken to investigate the effect of DPM on MPTP-induced neurotoxicity. Mice weighing 30 +/- 3 g were administered with MPTP (30 mg/kg, i.p.) daily for 5 days. DPM was given daily 1 h before MPTP in doses of 250, 500 and 1000 mg/kg body weight, (P.O.) respectively, in three different groups of mice for 7 days. Twenty four hours after the last dose of DPM, the animals were observed for neurobehavioral changes including locomotor activity and pole descending time. Immediately after behavioral studies, all the animals were sacrificed and brains were isolated for biochemical studies. The treatment of mice with MPTP or DPM individually produced no significant change in mobility or spasticity; however, the combination of these drugs produced significant bradykinesia. There was no incidence of mortality when the mice were treated with MPTP or DPM individually, though the combination of MPTP and DPM produced significant mortality which was proportional to the doses of the later drug. The treatment of mice with MPTP produced significant depletion of striatal dopamine and glutathione. Concomitant treatment of DPM with MPTP further reduced the striatal glutathione level without affecting dopamine. The result of this study shows the ability of DPM to potentiate MPTP-induced neurobehavioral toxicity and mortality in mice. Further studies are warranted to determine the role of adenosine in experimental and clinical Parkinson's disease.
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PMID:Dipyridamole potentiates 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced experimental Parkinsonism in mice. 1859 Oct 87

The protein botulinum neurotoxin A (BoNT/A) is one of seven distinct neurotoxins produced by Clostridium botulinum. BoNT/A blocks cholinergic synapses with an extremely high specificity and potency. Appropriately purified and diluted, BoNT/A serves as a reliable and well tolerated drug that is applied by local injection.The efficacy of BoNT/A is evident in the symptomatic therapy of disorders in which muscular hyperactivity plays a prominent role, such as focal dystonias and hemifacial spasm; in these disorders, BoNT/A is considered first-line therapy. BoNT/A is also beneficial in the treatment of both adults and children with spasticity of various causes. The pain that frequently accompanies these conditions is effectively reduced by BoNT/A. A genuine analgesic effect for BoNT/A unrelated to skeletal muscle spasmolysis has been suggested on the basis of in vitro and in vivo (animal) data. However, studies in humans designed to detect such an effect were negative, as were controlled studies of BoNT/A in patients with primary headache disorders.BoNT/A also acts on cholinergic synapses of the autonomic nervous system, and injection of BoNT/A into salivary glands significantly decreases the production of saliva. This may be beneficial for patients with Parkinson's disease, in whom the excessive production of saliva may be problematic.Overall, BoNT/A has been confirmed as an efficacious, predictable and well tolerated drug in an ever-increasing number of neurological disorders.
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PMID:Use of botulinum toxin A in adult neurological disorders: efficacy, tolerability and safety. 1869 73

In this paper we report a patient with Parkinson's disease (PD) presenting with subacute motor symptoms, especially rigidity. The 75-year-old man had relatively moderate PD for 12 years, which was treated with levodopa until he developed marked rigidity. The rigidity became worse, with prolonged off-periods, despite treatment with increased doses of levodopa. At the time of hospitalization he was unable to walk independently, but the clinical neurological examination only revealed aggravation of parkinsonian signs. MRI of the brain showed an intracerebral lesion, which was later confirmed as glioblastoma multiforme. The main feature was onset of marked rigidity a few weeks before severe tumour-specific symptoms developed, but spasticity or hyperreflexia were neither reported at the time of symptom exacerbation nor during hospitalization. This case demonstrates the importance of considering other underlying neurological disease in parkinsonian patients presenting with rapid progression of parkinsonian symptoms.
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PMID:[Subacute worsening of rigidity in a patient with Parkinson disease]. 1885 23

To develop an objective and scientific method to evaluate the brain injured and brain diseased persons with motor dysfunction, American Medical Association's Guides to the Evaluation of Permanent Impairment was used as an exemplar. After the motor dysfunction due to brain injury or brain disease was confirmed, active range of motion and muscle strength of affected extremities were measured. Also, the total function of extremities was evaluated through the assessment of activities of daily living, fine coordination of hand, balance and gait. Then, the total score of manual muscle test and functional assessment of impaired upper and lower extremity were added, respectively. Spasticity of upper and lower extremity was used as minus factors. Patients with movement disorder such as Parkinson's disease were assessed based on the degree of dysfunction in response to medication. We develop a new rating system based on the concept of total score.
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PMID:Development of the Korean Academy of Medical Sciences Guideline for rating the impairment in the brain injured and brain diseased persons with motor dysfunction. 1950 80


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