Parkinson’s disease with camptocormia
01 Nov 2006-Journal of Neurology, Neurosurgery, and Psychiatry (J Neurol Neurosurg Psychiatry)-Vol. 77, Iss: 11, pp 1223-1228
TL;DR: Patients with camptocormia were characterised by prominent levodopa-unresponsive axial symptoms (ie, axial rigidity, gait disorder and postural instability), along with a tendency for greater error in the antisaccade paradigm, and it is suggested that the salient features of parkinsonism observed in patients with camps are likely to represent a specific form of Parkinson’s disease.
Abstract: Background: Camptocormia is defined as an abnormal flexion of the trunk that appears when standing or walking and disappears in the supine position. The origin of the disorder is unknown, but it is usually attributed either to a primary or a secondary paravertebral muscle myopathy or a motor neurone disorder. Camptocormia is also observed in a minority of patients with parkinsonism. Objective: To characterise the clinical and electrophysiological features of camptocormia and parkinsonian symptoms in patients with Parkinson’s disease and camptocormia compared with patients with Parkinson’s disease without camptocormia. Methods: Patients with parkinsonism and camptocormia (excluding patients with multiple system atrophy) prospectively underwent a multidisciplinary clinical (neurological, neuropsychological, psychological, rheumatological) and neurophysiological (electromyogram, ocular movement recording) examination and were compared with age-matched patients with Parkinson’s disease without camptocormia. Results: The camptocormia developed after 8.5 (SD 5.3) years of parkinsonism, responded poorly to levodopa treatment (20%) and displayed features consistent with axial dystonia. Patients with camptocormia were characterised by prominent levodopa-unresponsive axial symptoms (ie, axial rigidity, gait disorder and postural instability), along with a tendency for greater error in the antisaccade paradigm. Conclusion: We suggest that (1) the salient features of parkinsonism observed in patients with camptocormia are likely to represent a specific form of Parkinson’s disease and camptocormia is an axial dystonia and (2) both camptocormia and parkinsonism in these patients might result from additional, non-dopaminergic neuronal dysfunction in the basal ganglia.
Citations
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TL;DR: A phased and integrated approach was shown to be required for managing patients with camptocormia caused by dystonic hyperkinesis, and local botulinum toxin injections and deep brain stimulation are the most effective treatments.
Abstract: This study was aimed at assessing clinical features of camptocormia as one of the dystonia symptoms and evaluating the efficacy of various treatments for this condition. The study involved 39 patients with dystonia and camptocormia symptoms. We analyzed the clinical features of dystonic camptocormia and evaluated the results of pharmacotherapy and botulinum therapy as well as neuromodulation methods, namely transcranial magnetic stimulation and deep brain stimulation. A phased and integrated approach was shown to be required for managing patients with camptocormia caused by dystonic hyperkinesis. Local botulinum toxin injections and deep brain stimulation are the most effective treatments. More extensive use of low-frequency transcranial magnetic stimulation may be advisable for everyday practical use in patients with dystonic camptocormia.
Additional excerpts
...“kamptos”—to bend and “kormos”—trunk [7]....
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06 Aug 2020
TL;DR: Clinical findings available, without attempting invasive diagnostic procedures, point to a citalopram induced camptocormia, or "bent-spine", in a patient who suffered mixed dementia with depression.
Abstract: This case report reviews a patient who suffered mixed dementia with depression. The addition of citalopram to the medication regimen was shortly followed by the manifestation of camptocormia, or “bent-spine.” Clinical findings available, without attempting invasive diagnostic procedures, point to a citalopram induced camptocormia. The frequent use of SSRI medications in the geriatric population call for an increased awareness of the possibility of SSRI induced postural side effects.
Cites background from "Parkinson’s disease with camptocorm..."
...Today, camptocormia is mainly regarded as a symptom of Parkinson’s disease, described as a forward bended prominent posture while standing or walking [4]....
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TL;DR: In this article , the authors used muscle ultrasonography (mUSG) to detect changes in paraspinal lumbar musculature in Parkinson's disease (PD) patients.
Abstract: Background: Camptocormia (CC) is the forward-bending of the spine of more than 30 degrees that can be found in Parkinson’s disease (PD) as a disabling complication. Detection of changes in paraspinal lumbar musculature in CC is of value for choosing treatment strategies. Objective: To investigate whether these changes can be detected using muscle ultrasonography (mUSG). Methods: Age and sex-matched groups comprised 17 PD patients with CC (seven acute, PD-aCC; 10 chronic PD-cCC), 19 PD patients with no CC, and 18 healthy controls (HC). Lumbar paravertebral muscles (LPM) on both sides were assessed using mUSG by two different raters blinded to the group assignment. Groups were compared with regard to the linear measurements of the muscle thickness as well as semi-quantitative and quantitative (grayscale) analyses of muscle echogenicity using a univariate general linear model. Results: All assessments showed substantial interrater reliability. The PD-cCC group had significantly thinner LPM compared to groups with no CC (PD and HC). Groups of PD-aCC and PD-cCC differed from the groups of no CC in quantitative and semi-quantitative analyses of LPM echogenicity, respectively. Conclusion: Assessment of LPM in PD patients with CC can be reliably performed using mUSG. Also, mUSG may be used as a screening tool to detect CC-related changes in thickness and echogenicity of the LPM in patients with PD.
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TL;DR: This investigation has found that it is crucial to follow up with patients who present with bradykinesia for the development of postural disorder, and axial posture disorders were observed in nearly half of PD patients and were more frequently observed in patients with an advanced condition.
Abstract: BACKGROUND
Postural disorders are frequently observed in Parkinson's disease (PD). The underlying mechanisms that cause postural disorders are not fully understood and the majority of these disorders have no response to antiparkinsonian treatments. These disabling conditions require further investigation to better understand the underlying mechanisms in order to develop effective treatments.
OBJECTIVE
The aim of this study was to investigate the frequency of axial postural disorders in PD and to determine the associated clinical risk factors.
METHODS
In this single-center clinical trial, the data of PD patients were reviewed retrospectively. The frequencies of postural disorders were determined, and the demographic clinical characteristics of the patients were compared.
RESULTS
The records of 127 patients with idiopathic PD were analyzed. Axial posture disorders were found in 42.6% of patients. Patients with axial posture disorders were older when the disease onset was detected, amongst these patients the condition was also longer lasting. The mean levodopa dose was higher in the patients with posture disorders. The initial symptom was bradykinesia and the Hoehn and Yahr's score was ⩾ 3 in the majority of the patients with posture disorder. Additionally, constipation, hallucinations, postural instability, and falls were significantly more common in patients with posture disorders.
CONCLUSION
Posture disorders were observed in nearly half of PD patients and were more frequently observed in patients with an advanced condition. In addition, our investigation has found that it is crucial to follow up with patients who present with bradykinesia for the development of postural disorder.
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TL;DR: The Mini-Mental State (MMS) as mentioned in this paper is a simplified version of the standard WAIS with eleven questions and requires only 5-10 min to administer, and is therefore practical to use serially and routinely.
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