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)

Camptocormia, also referred to as bent spine, is a gait disorder characterized by hyperflexion of the thoracolumbar spine that develops in recumbent position while walking and that disappears in supine position. Myopathy is one of the frequent causes of camptocormia. A 77-yr-old male patient who was followed up with the diagnosis of rheumatoid arthritis for 2 yrs was admitted with progressive gait deterioration. Hyperflexion of trunk, disappearing in supine position, was detected and diagnosed as camptocormia. He also exhibited the signs of parkinsonism. A paraspinal muscle biopsy showed myopathy with rods in many muscle fibers. Camptocormia in this patient may be attributable to the myopathic weakness of thoracolumbar paraspinal muscles. The normal biceps brachii muscle biopsy refers to the isolated affection of paraspinal muscles in this patient. A camptocormia (bent spine) case of myopathy with nemaline rods associated with Parkinson disease is presented.
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PMID:Camptocormia in a patient with Parkinson disease and a myopathy with nemaline rods. 1730 82

Fatigue or piercing feeling of weakness, lack of strength and energy or total exhaustion is a common complaint of patients with neurological disorders. From 40 to over 90 per cent of individuals with multiple sclerosis, Parkinson disease, amyotrophic lateral sclerosis, neuroboreliosis, post polio syndrome or stroke confirm its experience. It is not infrequently numbered among most disabling complaints. A separate entity, with fatigue as a cardinal sign, is a chronic fatigue syndrome, a disorder, though controversial, more and more frequently diagnosed. Fatigue ought to be discriminated from fatigability, paresis, somnolence and, first of all depression which commonly coexists in chronic disorders. The assessment is almost entirely based on self-estimate scales filled in by a patient. Attainable results of neuroimaging, electrophysiological, polisomnographic, vegetative, psychological and biochemical surveys have not allowed yet to define the pathogenesis of fatigue. The treatment basis consists of behavioral therapy, psychotherapy and a proper treatment of the basic disease.
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PMID:[The problem of fatigue in neurological disorders]. 1733 30

Head drop is characterized by marked anterior flexion of the cervical spine, caused by weakness of the neck extensors or by increased tone of the flexor muscles. We report a woman with Parkinson's disease and head drop not due to cervical dystonia (a common cause of antecollis in parkinsonisms). Clinical, radiological, and neurophysiological features together with responsiveness to anticholinesterases and plasma exchanges indicated the possibility of a concomitant myasthenia gravis.
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PMID:Myasthenia gravis: an unrecognized cause of head drop in Parkinson's disease. 1745 60

Seven children between 2 and 15 years of age with cerebral palsy and upper extremity dystonia were enrolled in an open-label, dose-escalation pilot clinical trial of botulinum toxin type B (Myobloc), injected into the biceps and brachioradialis muscles of I or both arms. The primary outcome measure was the change in maximum speed of hand movement during attempted forward reaching. Escalating doses of 12.5, 25, and 50 U/kg per muscle were injected at each of 3 visits. Reaching speed improved in response to injection, and dystonia scores on the Burke-Fahn-Marsden dystonia scale, the Unified Dystonia Rating Scale, and the Unified Parkinson's Disease Rating Scale improved. There was not a dose-related effect on efficacy. There were no serious adverse events. Two children reported transient weakness. These results support the use of botulinum toxin type B as a safe and effective treatment for upper extremity dystonia in children with cerebral palsy. Larger controlled trials are needed to confirm these results.
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PMID:Botulinum toxin type B improves the speed of reaching in children with cerebral palsy and arm dystonia: an open-label, dose-escalation pilot study. 1760 20

We report a man with Parkinson's disease who developed right spinal accessory neuropathy after right subthalamic nucleus deep brain stimulator and infraclavicular pulse generator implantation. He complained of right shoulder pain and weakness in the post-operative period. He was subsequently diagnosed with a right spinal accessory nerve injury, confirmed by neuromuscular electrodiagnostic studies - electromyography (EMG) and nerve conduction (NC) -, possibly caused by a stretch injury to the nerve at the time of creation of the subcutaneous tunnel for placement of the extension lead of the deep brain stimulator system. However, he had near complete clinical resolution of the spinal accessory neuropathy within nine months after surgery. As a result of this complication, we now map the spinal accessory nerve electrophysiologically during deep brain stimulation surgery.
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PMID:Spinal accessory neuropathy after deep brain stimulation for Parkinson's disease. 1770 83

Individuals with Parkinson's disease (PD) are not only burdened with disease-specific symptoms (i.e., bradykinesia, rigidity, and tremor), but are also confronted with age-associated progressive loss of physical function, perhaps to a greater extent than neurologically normal adults. Suggestions for the inclusion of resistive exercise into treatment to attenuate these symptoms were made over 10 years ago, yet very few well controlled investigations are available. The objective of this review is to establish a clear rationale for the efficacy of resistance training in individuals with PD. Specifically, we highlight musculoskeletal weakness and its relationship to function as well as potential training-induced adaptive alterations in the neuromuscular system. We also review the few resistance training interventions currently available, but limit this review to those investigations that provide a quantitative exercise prescription. Finally, we recommend future lines of inquiry warranting further attention and call to question the rationale behind current exercise prescriptions. The absence of reports contraindicating resistive exercise, the potential for positive adaptation, and the noted benefits of resistance training in other populations may provide support for its inclusion into a treatment approach to PD.
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PMID:Parkinson's disease and resistive exercise: rationale, review, and recommendations. 1789 27

We sought to explore the phenomenon of disproportionate antecollis in multiple system atrophy (MSA) and Parkinson's disease (PD). The etiology is much debated and the main issue is whether it represents a primary myopathy or is secondary to the underlying motor disorder. The clinical, electrophysiological, and biopsy data of MSA or PD patients with antecollis were reviewed. We reviewed 16 patients (7 MSA and 9 PD) who developed antecollis during the course of their disease. The interval between onset of motor symptoms and of antecollis was shorter in the MSA group (4.6 +/- 1.7 years vs. 10.5 +/- 7.0 years). In 6 patients, the antecollis developed subacutely, and in 2 the abnormal neck flexion was initially an off-period phenomenon. Two additional patients also showed some dopa-responsiveness. Clinically, the antecollis was characterized by a forward flexion and anterior shift of the neck, with prominent cervical paraspinal and levator scapulae muscles, usually without weakness of residual neck extension. Electromyography of cervical paraspinal muscles showed mixed myopathic, normal, and neurogenic units, without early recruitment. Cervical paraspinal muscle biopsy in 2 patients disclosed fibrosis and nonspecific myopathic changes. We suggest that, in the context of MSA or PD, the initiating event in antecollis could be a disproportionately increased tone in anterior neck muscles that leads to secondary fibrotic and myopathic changes. However, a primary but yet unexplained neck extensor myopathy still remains the alternative possibility and longitudinal studies are necessary to settle this issue.
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PMID:The phenomenon of disproportionate antecollis in Parkinson's disease and multiple system atrophy. 1796 Aug 14

Isolated severe weakness of the paraspinal musculature, either at the cervical level leading to a "dropped head syndrome" or at the thoracic level leading to a "bent-spine syndrome", is a rare disorder. Etiologically it may be present in a variety of neurological diseases including Parkinson's disease, multiple system atrophy, neuromuscular or motor neuron diseases, as well as non-inflammatory, inflammatory, dystrophic or metabolic myopathies. We present a previously healthy 74-year-old man with a 2-month history of progressive difficulty in lifting his chin off his chest. Magnetic resonance imaging and skeletal muscle biopsy revealed an isolated myositis of the neck extensor and trapezius muscles, which responded well to steroid therapy. This case and other rare reports obtained from a systematic review of the literature indicate that in a subgroup of patients "dropped head syndrome" or "bent spine syndrome" is caused by a myositis, which emphasizes the necessity to obtain a MRI examination, as well as a muscle biopsy to diagnose this potentially treatable disease.
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PMID:Dropped-head syndrome due to steroid responsive focal myositis: a case report and review of the literature. 1796 3

Ten years after the therapeutic revolution that emerged from the discovery of l-dopa, some pioneer teams led the rebirth of a new nonablative stereotaxical surgical treatment, which came from the interest of high frequency stimulation. Three targets were retained as the main location of a reversible functional inhibition: Vim, GPI and STN. The unilateral or bilateral stimulation, adjustable and possibly reversible, led to an exceptional medicosurgical collaboration, within expert dedicated places, based on the control of the Parkinson's disease's (PD) triad. The stimulation was initially applied to the most advanced forms of PD, after the medical control period of the motor performance, when the pejorative effects of the evolution settled and/or when side effects of the treatment appeared. Subsequently, the research of selection criterions and the strict control of the stereotaxical procedure during the per- and postoperatory period, with the collaboration of the patient and his family, progressively brought different teams to an earlier indication of this new treatment option, up to now reserved for fully medicosurgical concerted cases. Apparition of cognitive and postural decline as well as the known resistance stage to l-dopa tend to become a real contra-indication. Despite the initial relative weakness of controlled studies with limited number of patients, the multiplication of follow-up studies among high quality multicentric cohorts enabled the validation of practices respecting the differences related to the initial background of each different team. In Europe first, the prevalence of the subthalamic target is now to be generally admitted. A new objective is now imposing itself: trying to maintain the patient's quality of life, beyond the only motor benefit. The social adaptation of a young patient is now also taken into account. If this exemplary clinical research approach, efficient for a few highly selected patients, has not transformed the long-term prognostic of the PD, it will continue to improve the comprehension of this degenerative pathology and its extension. It still remains hopeful for the future in the actual constant technological progress, and that probably beyond the only PD.
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PMID:[Deep brain stimulation and Parkinson's disease]. 1855 Jan 97

Parkinson's disease (PD), Alzheimer's disease (AD), and motor neuron disease (MND) share epidemiological, clinical, and pathological features. Few studies have reported comprehensively on individuals who demonstrate a neurodegenerative 'overlap' syndrome, comprising idiopathic parkinsonism, dementia, and motor neuron dysfunction. We describe clinical, electrophysiological, and pathological features in six patients with neurodegenerative 'overlap' syndrome. All had cardinal features of PD (duration 6-26 years), and any mixture of dementia (slowly advancing), fasciculations, hyperreflexia, Babinski signs and mild atrophy and weakness of distal muscles (slowly progressive). EMG often demonstrated a lack of denervation in conjunction with abnormal MEPs (high thresholds). Patients had either 6FD-PET or pathological studies consistent with PD. Pathological studies also demonstrated moderate numbers of neurofibrillary tangles and plaque formation, typically with sparing of motor neurons in the spinal cord. We conclude that neurodegenerative 'overlap' syndrome may represent forme frustes of traditionally accepted diagnostic categories. Patients with parkinsonism, fasciculations, hyperreflexia and mild atrophy are unlikely to demonstrate active denervation on EMG; their prognosis is better than for classical MND. Neurodegenerative overlap syndrome (clinicopathological mixtures of PD, AD, and MND) may develop in some individuals as a reflection of common etiology, pathogenesis or susceptibility.
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PMID:Neurodegenerative 'overlap' syndrome: Clinical and pathological features of Parkinson's disease, motor neuron disease, and Alzheimer's disease. 1859 Sep 98


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