La neurologie centrale et les phénomènes posturaux douloureux

Pain, defined as an unpleasant or distressing sensory experience, has been recognized as feature of Parkinson's disease (PD) since the first descriptions of the disorder. Pain is estimated to occur in approximately 40% of patients with PD, and in a minority of individuals becomes severe enough to overshadow the motor symptoms of the disorder. Recent studies based on patients' descriptions of pain have enabled a classification of painful sensations into 1 or more of 5 categories: musculoskeletal pain, neuritic or radicular pain, dystonia-associated pain, primary or central pain, and akathitic discomfort. The existence of a central pain syndrome, intrinsic to PD, finds support in a collection of case reports, but the precise mechanism is unknown, and a correlation with pathology has not been made. This review describes the clinical features of the pain syndromes in PD, and provides a framework for evaluating, classifying, and treating painful symptoms in PD.

Pain in Parkinson's disease.

The motor score with and without levodopa was estimated in 193 parkinsonian patients with variable length of evolution. The effect of levodopa on akinesia, rigidity, and tremor remained quite stable during the course of the disease. In contrast, the aggravation of gait disorder, postural instability, and dysarthria was more severe, with decreased percentage of improvement on levodopa in patients with longer evolution. It is suggested that aggravation of Parkinson's disease mainly results from increasing severity of cerebral nondopaminergic lesions.

Does long‐term aggravation of Parkinson's disease result from nondopaminergic lesions?

Posture is often affected in Parkinson's disease. Postural abnormalities belong to the motor axial involvement. Generally, postural dysfunction induces clinical impairment at the latest stages of the disease, except in late-onset idiopathic Parkinson's disease and in atypical parkinsonian syndromes. Posture may be affected in its orientation component (stooped posture, camptocormia, Pisa syndrome) or in its balance component (loss of postural reflexes). Overall, postural impairment is poorly improved by levodopa, which implies that it is unlikely due to the nigrostriatal dopaminergic denervation. Several methods of investigation have been proposed but are generally not available in clinical practice. Medical treatment and deep brain stimulation (DBS) of the subthalamic nucleus or globus pallidus pars interna are less efficient on axial than on distal motor signs. The pedonculopontine nucleus seems promising as a new target for DBS in combination with the subthalamic nucleus. Physical therapy is, in most cases, the best way to improve postural dysfunction.

Postural disorders in Parkinson’s disease

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.

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La neurologie centrale et les phénomènes posturaux douloureux

References

Pain in Parkinson's disease.

Does long‐term aggravation of Parkinson's disease result from nondopaminergic lesions?

Postural disorders in Parkinson’s disease

Parkinson’s disease with camptocormia

Tête tombante fixée : efficacité d'une rééducation intensive