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)

Dropped head syndrome is primarily based on weakness localized at neck extensors. It may result from motor neuron disease, myasthenia gravis, and chronic inflammatory demyelinating polyneuropathy and also from various neuromuscular diseases including inflammatory, dystrophic and metabolic myopathies. Camptocormia (CC) on the other hand is an unusual condition characterized by progressive weakness of the extensor vertebral muscles and results in involuntary trunk flexion. CC may emerge as a clinical feature of many different conditions such as several myopathies and Parkinson's disease. The association of dropped head syndrome with CC has been rarely published in the literature. However, this is the only case presenting with concomitant dropped head syndrome and CC as a clinical picture of myotonic dystrophy (MD). In this report we aimed to represent a female patient, who was diagnosed as having myotonic dystrophy, with concurrent dropped head syndrome and CC.
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PMID:Camptocormia and dropped head syndrome as a clinic picture of myotonic myopathy. 1863 87

In this study we investigate how the basal ganglia (BG) may process the behavioural relevance of environmental cues by recording local field potentials (LFPs) in the subthalamic nucleus of patients with Parkinson's disease who had undergone implantation of electrodes for deep brain stimulation. Fourteen patients were recorded as they performed a paradigm dissociating warning cue presentation from programming related to execution of specific tasks. Target and non-target warning cues of differing behavioural relevance were contrasted, and we evaluated if warning cue-evoked activities varied according to whether the eventual task to be performed was motor or cognitive and whether patients were receiving or withdrawn from dopaminergic therapy. Warning cues evoked a complex temporal sequence of activities with three epochs over the 760 ms following the onset of the warning cue. In contrast to the initial evoked LFP, evoked activities over two later periods were significantly influenced by behavioural relevance and by treatment state. The early activity was likely related to the initial orientating of attention induced by a novel target, while the delayed responses in our paradigm may reflect processing related to the non-motor resource implications of cues. The results suggest that the BG are intimately involved in the evaluation of changes in the environment and of their behavioural significance. The latter process is partly modulated by dopamine. Weakness in this function might contribute to the behavioural impairment that can follow BG lesions and surgery.
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PMID:Involvement of the subthalamic nucleus in engagement with behaviourally relevant stimuli. 1922 23

Muscle power (force x velocity) could clarify the relationship between weakness and bradykinesia in Parkinson's disease (PD). The aims of this study were to determine if patients with PD were weaker and/or less powerful in their leg extensor muscles than a neurologically normal control group and to determine the relative contributions of force and movement velocity/bradykinesia to muscle power in PD. Forty patients with PD and 40 controls were assessed. Strength in Newtons (N) was measured as the heaviest load the participant could lift. Power in Watts (W) was measured by having the participant perform lifts as fast as possible. The PD group were 172 N weaker (95% CI 28-315) and 124 W less powerful at peak power (95% CI 32-216) than controls. However, velocity at maximal power was only reduced compared with controls when lifting light to medium loads. When lifting heavy loads bradykinesia was no longer apparent in the PD group. These results suggest that reduced muscle power in PD at lighter loads arises from weakness and bradykinesia combined, but at heavier loads arises only from weakness. The absence of bradykinesia in the PD group when lifting heavy loads warrants further investigation.
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PMID:Bradykinesia, muscle weakness and reduced muscle power in Parkinson's disease. 1942 85

Controversy exists as to whether muscle weakness is present in Parkinson's disease (PD). Computerized literature searches identified clinical trials and reviews about muscular strength assessment in patients with Parkinson's disease, using the following databases: PubMed, Ovid MEDLINE, Ovid EMBASE, the Cochrane Database of Systematic Reviews, Cumulative Index to Nursing and Allied Health Literature, and Physiotherapy Evidence Database. Seventeen articles fulfilled all criteria for selection. These studies suggested that isokinetic muscle strength was decreased in patients with Parkinson's disease and that muscle weakness was not specifically related to tremor or rigidity. Bilateral asymmetrical muscle weakness was present in Parkinson's disease when presenting with clinical unilateral hemiparkinsonism. Recent studies using sensitive mechanical devices have provided evidence that muscle strength is reduced in patients with Parkinson's disease compared with age-matched controls. The specific cause of this weakness is not known. Questions under debate were whether this weakness was of central or peripheral origin and whether it was intrinsic to the disease or a secondary phenomenon.
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PMID:Is there muscular weakness in Parkinson's disease? 1948 24

This is a mini-review of vitamin D(3), its active metabolites and their functioning in the central nervous system (CNS), especially in relation to nervous system pathologies and aging. The vitamin D(3) endocrine system consists of 3 active calcipherol hormones: calcidiol (25OHD(3)), 1alpha-calcitriol (1alpha,25(OH)2D(3)) and 24-calcitriol (24,25(OH)2D(3)). The impact of the calcipherol hormone system on aging, health and disease is discussed. Low serum calcidiol concentrations are associated with an increased risk of several chronic diseases including osteoporosis, cancer, diabetes, autoimmune disorders, hypertension, atherosclerosis and muscle weakness all of which can be considered aging-related diseases. The relationship of many of these diseases and aging-related changes in physiology show a U-shaped response curve to serum calcidiol concentrations. Clinical data suggest that vitamin D(3) insufficiency is associated with an increased risk of several CNS diseases, including multiple sclerosis, Alzheimer's and Parkinson's disease, seasonal affective disorder and schizophrenia. In line with this, recent animal and human studies suggest that vitamin D insufficiency is associated with abnormal development and functioning of the CNS. Overall, imbalances in the calcipherol system appear to cause abnormal function, including premature aging, of the CNS.
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PMID:Vitamin D, nervous system and aging. 1966 Aug 71

We report the case of a patient with Parkinson's disease who developed rapidly progressive weakness of the four limbs due to an acute motor axonal neuropathy (AMAN). This occurred days after a neuroleptic malignant syndrome (NMS). Serologic evidence of a preceding Campylobacter jejuni infection was detected and treatment with intravenous immunoglobulins proved effective. This case suggests that the rarely described neuropathies occurring with NMS may have a postinfectious immune basis and respond to immunomodulatory therapy.
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PMID:Neuroleptic malignant syndrome and acute motor axonal neuropathy after Campylobacter jejuni infection. 1971 63

Symptoms of cardiovascular dysautonomia are a common occurrence in Parkinson's disease (PD). In addition to this dysautonomia as part of PD itself, dysfunction of the autonomic nervous system (ANS) can be triggered as a side-effect of drug treatment interacting with the ANS or - if prominent and early - an indication of a different disease such as multiple system atrophy (MSA). Various diagnostic tests are available to demonstrate autonomic failure. While autonomic function tests can differentiate parasympathetic from sympathetic dysfunction, cardiac imaging can define the pathophysiologically involved site of a lesion. Standard tests such as 24-h ambulatory blood pressure measurements can identify significant autonomic failure which needs treatment. The most frequent and disturbing symptom of cardiovascular autonomic dysfunction is orthostatic hypotension. Symptoms include generalized weakness, light-headiness, mental "clouding" up to syncope. Factors like heat, food, alcohol, exercise, activities which increase intrathoraric pressure (e.g. defecation, coughing) and certain drugs (e.g. vasodilators) can worsen a probably asymptomatic orthostatic hypotension. Non-medical and medical therapies can help the patient to cope with a disabling symptomatic orthostatic hypotension. Supine hypertension is often associated with orthostatic hypotension. The prognostic role of cardiovagal and baroreflex dysfunction is still not yet known.
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PMID:Cardiovascular autonomic dysfunction in Parkinson's disease. 1974 Apr 84

Camptocormia is an abnormal truncal flexion posture that occurs while walking or standing. It is usually caused by various hypokinetic movement disorders such as Parkinson disease and multiple system atrophy. Myopathy or motor neuron disease can also be infrequent causes of camptocormia. Paraspinous muscle biopsy usually reveals focal myositis, regardless of the etiology of camptocormia. We describe the first case of generalized inflammatory myopathy with prominent camptocormia and proximal muscle weakness. Muscle biopsy of the quadriceps confirmed the diagnosis of polymyositis, and the posture showed modest improvement in response to steroid treatment.
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PMID:Camptocormia as a presentation of generalized inflammatory myopathy. 1975 May 41

Some studies have demonstrated altered circulating levels of cytokines, including IL-6, in Parkinson's disease (PD), implying a possible involvement of inflammatory and immune-mediated mechanisms in its pathogenesis. Moreover, the increased production of inflammatory cytokines has been associated with cognitive impairment and poor physical performance in the elderly. We compared serum levels of IL-6 in 44 PD patients and 22 healthy subjects, and correlated them with PD specific instruments and functional tests. Serum levels of IL-6 were significantly increased in PD (p=0.015). There was no correlation between serum levels of IL-6 and instruments traditionally used to assess PD severity. However, we found that PD patients with higher serum levels of IL-6 spent more time at functional mobility tests and had lower gait speed. Also, these patients had major problems to keep balance during functional tasks that required postural changes and that had a reduced base support. These results showed that high levels of IL-6 can be involved with an acceleration of muscle catabolism leading to sarcopenia, therefore contributing to weakness and fatigue, and may also be associated with functional disability in PD.
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PMID:Serum levels of interleukin-6 are elevated in patients with Parkinson's disease and correlate with physical performance. 1985 51

Camptocormia, also referred to as bent spine syndrome (BSS) is defined as an abnormal flexion of the trunk, appearing in standing position, increasing during walking and abating in supine position. BSS was initially considered, especially in wartime, as a psychogenic disorder. It is now recognized that in addition to psychiatric syndromes, many cases of reducible BSS have a somatic origin related to a number of musculo-skeletal or neurological disorders. The majority of BSS of muscular origin is related to a primary idiopathic axial myopathy of late onset, appearing progressively in elderly patients. Diagnosis of axial myopathy first described by Laroche et al. is based upon CT/MRI examination demonstrating massive fatty infiltration of paravertebral muscles. The non-specific histological aspect includes an extensive endomysial fibrosis and fat tissue with irregular degenerated fibers. Weakness of the paravertebral muscles can be secondary to a wide variety of diseases generating diffuse pathologic changes in the muscular tissue. BSS can be the predominant and sometimes revealing symptom of a more generalized muscular disorder. Causes of secondary BSS are numerous. They must be carefully assessed and ruled out before considering the diagnosis of primary axial myopathy. The principal etiologies include on the one hand inflammatory myopathies, muscular dystrophies of late onset, myotonic myopathies, endocrine and metabolic myopathies, and on the other hand neurological disorders, principally Parkinson's disease. Camptocormia in Parkinsonism is caused by axial dystonia, which is the hallmark of Parkinson's disease. There is no specific pharmacologic treatment for primary axial myopathy. General activity, walking with a cane, physiotherapy, and exercises should be encouraged. Treatment of secondary forms of BSS is dependent upon the variety of the disorder generating the muscular pathology. Pharmacologic and general management of camptocormia in Parkinson's disease merge with that of Parkinsonism. Levodopa treatment, usually active on tumor rigidity and akinesia, has poor or negative effect on BSS.
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PMID:Camptocormia: the bent spine syndrome, an update. 2030 Jul 81


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