Camptocormia in Parkinson disease: an epidemiological and clinical study
01 Feb 2009-Journal of Neurology, Neurosurgery, and Psychiatry (BMJ Publishing Group)-Vol. 80, Iss: 2, pp 145-148
TL;DR: Camptocormia, a relatively common sign in Parkinson disease, seems to be related to the clinical severity of PD.
Abstract: Background: Camptocormia is an abnormal flexion of the thoracolumbar spine during standing and walking that abates in the recumbent position. Methods: In a single-centre epidemiological and clinical study, the prevalence of camptocormia in Parkinson disease (PD) and its relationship with the clinical features of PD were investigated. A total of 275 consecutive outpatients were systematically screened for camptocormia with a clinical evaluation. Patients who screened positive for camptocormia were subsequently reassessed by formal goniometric analysis. The demographic and clinical features of the patients with and without camptocormia were then compared. Results: A 6.9% (19/275, 95% CI, 4.2 to 10.6) prevalence of camptocormia was found. Camptocormia was found in patients with more severe PD, as clinically assessed by the Hoehn–Yahr (HY) staging and the motor Unified Parkinson Disease Rating Scale (UPDRS) part III, longer l-dopa treatment duration and greater l-dopa daily dose and presence of DSM-IV dementia. Camptocormia was reported to develop after the clinical onset of PD. No correlation was found between the degree of trunk flexion and age, duration of PD, UPDRS motor score, HY staging, and l-dopa treatment duration and dose. As a risk factor, the study identified previous vertebral surgery. Conclusions: Camptocormia, a relatively common sign in PD seems to be related to the clinical severity of PD.
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TL;DR: In this paper, the authors present a conciliatory explanation for the present publication, in which, it is acknowledged, that mere conjecture takes the place of experiment; and, that analogy is the substitute for anatomical examination, the only sure foundation for pathological knowledge.
Abstract: PREFACE The advantages which have been derived from the caution with which hypothetical statements are admitted, are in no instance more obvious than in those sciences which more particularly belong to the healing art. It therefore is necessary, that some conciliatory explanation should be offered for the present publication: in which, it is acknowledged, that mere conjecture takes the place of experiment; and, that analogy is the substitute for anatomical examination, the only sure foundation for pathological knowledge. When, however, the nature of the subject, and the circumstances under which it has been here taken up, are considered, it is hoped that the offering of the following pages to the attention of the medical public, will not be severely censured. The disease, respecting which the present inquiry is made, is of a nature highly afflictive. Notwithstanding which, it has not yet obtained a place in the classification of nosologists; some have regarded its characteristic symptoms as distinct and different diseases, and others have given its name to diseases differing essentially from it; whilst the unhappy sufferer has considered it as an evil, from the domination of which he had no prospect of escape. The disease is of long duration: to connect, therefore, the symptoms which occur in its later stages with those which mark its commencement, requires a continuance of observation of the same case, or at least a correct history of its symptoms, even for several years. Of both these advantages the writer has had the opportunities of availing himself, and has hence been led particularly to observe several other cases in which the disease existed in different stages of its progress. By these repeated observations, he hoped that he had been led to a probable conjecture as to the nature of the malady, and that analogy had suggested such means as might be productive of relief, and perhaps even of cure, if employed before the disease had been too long established. He therefore considered it to be a duty to submit his opinions to the examination of others, even in their present state of immaturity and imperfection. To delay their publication did not, indeed, appear to be warrantable. The disease had escaped particular notice; and the task of ascertaining its nature and cause by anatomical investigation, did not seem likely to be taken up by those who, from their abilities and opportunities, were most likely to accomplish it. That these friends to humanity and medical science, who have already unveiled to us many of the morbid processes by which health and life is abridged, might be excited to extend their researches to this malady, was much desired; and it was hoped, that this might be procured by the publication of these remarks. Should the necessary information be thus obtained, the writer will repine at no censurewhich the precipitate publication of mere conjectural suggestions may incur: but shall think himself fully rewarded by having excited the attention of those, who may point out the most appropriate means of relieving a tedious and most distressing malady.
869 citations
TL;DR: Improved understanding of the mechanisms underlying postural deformities in PD might ultimately lead to more effective management strategies for these disabling and drug-refractory complications.
Abstract: Postural deformities are frequent and disabling complications of Parkinson's disease (PD) and atypical parkinsonism. These deformities include camptocormia, antecollis, Pisa syndrome, and scoliosis. Recognition of specific postural syndromes might have differential diagnostic value in patients presenting with parkinsonism. The evidence to date suggests that postural deformities have a multifactorial pathophysiology. Contributing factors include muscular rigidity; axial dystonia; weakness caused by myopathy; body scheme defects due to centrally impaired proprioception; and structural changes in the spine. The relative contribution of these different factors varies between patients and across specific syndromes. Improved understanding of the mechanisms underlying postural deformities in PD might ultimately lead us to more effective management strategies for these disabling and drug-refractory complications.
402 citations
TL;DR: The major mechanisms leading to appearance and progression of NASH are reviewed, focusing on both extrahepatic signals and local inflammatory mechanisms, in an effort to identify the most promising molecular targets for the treatment of this condition.
Abstract: Non alcoholic steatohepatitis (NASH) is the more severe form of nonalcoholic fatty liver disease. In NASH, fatty liver, hepatic inflammation, hepatocyte injury and fibrogenesis are associated, and this condition may eventually lead to cirrhosis. Current treatment of NASH relies on the reduction of body weight and increase in physical activity, but there is no pharmacologic treatment approved as yet. Emerging data indicate that NASH progression results from parallel events originating from the liver as well as from the adipose tissue, the gut and the gastrointestinal tract. Thus, dysfunction of the adipose tissue through enhanced flow of free fatty acids and release of adipocytokines, and alterations in the gut microbiome generate proinflammatory signals that underlie NASH progression. Additional 'extrahepatic hits' include dietary factors and gastrointestinal hormones. Within the liver, hepatocyte apoptosis, ER stress and oxidative stress are key contributors to hepatocellular injury. In addition, lipotoxic mediators and danger signals activate Kupffer cells which initiate and perpetuate the inflammatory response by releasing inflammatory mediators that contribute to inflammatory cell recruitment and development of fibrosis. Inflammatory and fibrogenic mediators include chemokines, the cannabinoid system, the inflammasome and activation of pattern-recognition receptors. Here we review the major mechanisms leading to appearance and progression of NASH, focusing on both extrahepatic signals and local inflammatory mechanisms, in an effort to identify the most promising molecular targets for the treatment of this condition.
150 citations
Cites background from "Camptocormia in Parkinson disease: ..."
...possibility to translate these findings to the human setting [233]....
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TL;DR: It is indicated that camptocormia is a relatively common sign in PD and that patients with camptoormia scores on the PDQ-8 compared with PD patients without camptOCormia suggests that improvements in camptokormia of PD patients may improve their QOL.
Abstract: Objectives. Abnormalities of posture represent one of the main features of Parkinson's disease (PD). Among them, camptocormia has been considered as rare in PD. We investigated frequency and clinical features of camptocormia in PD patients. Methods. 153 PD patients (mean 68.5±10.7 years old, duration 5.9±2.4 years) outpatiently recruited. After neurologic examination, patients were rated on the Unified PD Rating Scale motor scale (UPDRS Part III), minimental state examination (MMSE). Also we evaluated patients with camptocormia by MRI. Of the 153 PD patients, 27 had camptocormia (mean age, 67.9±7.9 years old; disease duration, 6.1±3.9 years). For further evaluation, we recruited age- and sex-matched 27 PD patients without camptocormia (11 men and 16 women; mean age ±SD, 69.2±10.1 years, duration 6.0±2.7 years) These selected 54 patients completed several self-assessments. Lumbar and thoracic paraspinal muscles were studied by EMG. Results. There were no significant differences in age, duration, severity, and drug dose between patients with and without camptocormia. Analysis of NMSS subitems indicated that PD patients tended to show lower scores for sleep/fatigue, attention/memory, and miscellaneous items. Conclusions. We found significant differences concerning nonmotor signs and symptoms evaluated by FAB, PDQ-8, FSQ, VAS-F, and NMSS between patients with and without camptocormia. Our findings indicate that camptocormia is a relatively common sign in PD and that patients with camptocormia scores on the PDQ-8 compared with PD patients without camptocormia. This suggests that improvements in camptocormia of PD patients may improve their QOL.
95 citations
Cites result from "Camptocormia in Parkinson disease: ..."
...The 17% prevalence of camptocormia in our series is higher than that reported in previous studies [6, 14, 28], and is probably related to differences in the clinical features of the study population....
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TL;DR: Camptocormia (bent spine syndrome, cyphose hystérique) is an abnormality characterized by severe forward flexion of the thoracolumbar spine which typically increases during walking or standing and completely disappears in supine position.
Abstract: Camptocormia (bent spine syndrome, cyphose hysterique) is an abnormality characterized by severe forward flexion of the thoracolumbar spine which typically increases during walking or standing and com
91 citations
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