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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Central post-stroke pain (CPSP) is a neuropathic pain syndrome characterized by constant or intermittent pain in a body part occurring after stroke and associated with sensory abnormalities in the painful body part. This study describes CPSP prospectively during the first year after stroke and characterizes the cerebrovascular lesions and neurological signs associated with the CPSP syndrome. Two hundred and sixty-seven consecutively admitted patients younger than 81 years were examined in the first week, at 1, 6 and 12 months after stroke. Sensibility to touch (cotton wool), temperature (20 degrees C and 40 degrees C), and pinprick was studied using the contralateral face and extremity as control. A CT scan was done 8 (median) days (range: 1-34 days) after stroke. Two hundred and seven (78%) patients surviving at least 6 months who were able to communicate reliably formed the basis of the study. Abnormal sensory signs were found at least once in 87 (42%) patients. CPSP was found in 16 (8%) patients of whom all but 1 patient also had evoked dysesthesia or allodynia. Further 1 patient had persistent evoked dysesthesia but denied pain. CPSP was not related to sex or age. In patients with single acute cerebral lesions there were no relation between size or location of the lesions and the presence of CPSP. The pain was light in 6 (3%) patients and moderate to severe in 10 (5%) patients. The pain quality was usually lacerating or aching. Fifteen (94%) patients had decreased temperature, touch and pain sensibility and 9 (56%) reported allodynia to cold stimulation and another 9 (56%) patients reported this to touch.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Incidence of central post-stroke pain. 765 28

Central post-stroke pain (CPSP) used to be known as 'thalamic syndrome'. Early post-mortem studies showed that many cases had extrathalamic lesions, and modern imaging methods have confirmed and extended these findings. CPSP affects between 2 and 6% of stroke patients, ie, there is an annual incidence in the UK of between 2000 and 6000. Most patients with CPSP appear to be younger than the general stroke population, and usually to have relatively mild motor affliction; thus they may live for many years, giving a prevalence perhaps as high as 20,000. True CPSP, characterised by a partial or total deficit for thermal and/or sharpness sensations, is best treated initially with adrenergically active antidepressants. If these do not work, mexiletine may be added in suitable cases. Recent studies suggest that stimulation of the motor cortex or spinal cord by implanted electrodes may help patients resistant to medical treatment. Positive relaxation, as an adjuvant therapy, should be used in nearly all cases. Considerable or even total relief can be achieved in almost two thirds of patients. There is evidence that the sooner antidepressant treatment is begun, the more likely the patient is to respond; time should not be wasted trying conventional analgesics, which rarely have any significant effect.
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PMID:The management of central post-stroke pain. 854 88

Central post stroke pain is often difficult to manage satisfactorily with conventional treatment modalities for pain. In the last decade functional neurosurgery has offered hope with motor cortex stimulation achieving significant alleviation of pain in some patients. Unfortunately this has led to the neglect of chronic stimulation of deep grey matter as another modality of treating this condition. In this article we present our experience with motor cortex stimulation and that with deep grey matter stimulation in patients with post stroke pain. We argue that both modalities have a significant role and that what is required are better methods of identifying particular patients who are more likely to respond to one or the other.
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PMID:Peri-ventricular grey stimulation versus motor cortex stimulation for post stroke neuropathic pain. 1238 15

Central post-stroke pain (CPSP) is a syndrome characterized by sensory disturbances and neuropathic pain. In 40%-60% of CPSP patients, the onset of central pain following a stroke occurs more than 1 month after the stroke, creating a source of diagnostic uncertainty or significant delay in treatment since healthcare providers familiar with CPSP may no longer be caring for the patient when the symptoms occur. In addition to chronic pain, the presence of somatosensory abnormalities is the most important diagnostic corollary of CPSP. Neuropathic or central pain has been estimated to occur in up to 8% of patients after a stroke, and about 18% of stroke patients with a somatosensory disturbance will develop CPSP. Although largely a matter of conjecture, it is generally agreed that damage to spinothalamic sensory pathways plays a significant role in the pathogenesis of CPSP. A comprehensive examination of the patient for sensory deficits is essential before treatment can be initiated. Functional disturbances such as depression, anxiety and sleep disturbances are significant comorbid conditions associated with CPSP; the physician should incorporate an assessment of these potential comorbidities into the examination. Treatment options for CPSP are limited; at present, amitriptyline is the drug of first choice. Other drugs including antidepressants, anticonvulsants, antiarrhythmics, opioids and N-methyl-d-aspartate antagonists may provide relief for some patients who do not respond to amitriptyline. Included in this review is a case study outlining the challenges of managing the patient with CPSP.
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PMID:Post-stroke pain case study: clinical characteristics, therapeutic options and long-term follow-up. 1506 21

Central post-stroke pain syndrome develops in a minority of patients following a stroke. The most usual causative lesion involves the lateral thalamus. The classic presentation is of severe, unrelenting pain that involves the entire contralateral half of the body. It is largely refractory to current treatments. We found that in two patients with this condition their pain was substantially improved by vestibular caloric stimulation, whereas placebo procedures had no effect. We proposed that this is because vestibular stimulation activates the posterior insula, which in turn inhibits the generation of pain in the anterior cingulate.
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PMID:Rapid relief of thalamic pain syndrome induced by vestibular caloric stimulation. 1778 78

Central post-stroke pain (CPSP) is one of the most common types of intractable pain. We reported that repetitive transcranial magnetic stimulation (rTMS) of primary motor cortex relieves pain for patients who were refractory to medical treatment. But the mechanism is unclear. In the present study, we investigated relations between the characteristics of CPSP and the results of fiber tracking, which is the only noninvasive method of evaluating the anatomical connectivity of white matter pathways. Fiber tracking of the corticospinal tract (CST) and thalamocortical tract (TCT) was investigated in 17 patients with CPSP. The stroke lesion was located in a supratentorial region in all cases (corona radiata, one case; thalamus, seven cases; putamen, nine cases). Relations between the delineation ratio (defined as the ratio of the cross section of the affected side to that of the unaffected side) of the CST and of the TCT, manual muscle test score, pain score, region of pain, and efficacy of rTMS were evaluated. Fiber tracking was successful in 13 patients with the stroke lesion involving the TCT. The rTMS-effective group had higher delineation ratio of the CST (p=0.02) and the TCT (p=0.005) than the rTMS-ineffective group. Previous studies suggested that an intact CST allows pain control but did not discuss the TCT. Our results suggest that the TCT also plays a role in pain reduction by rTMS of the primary motor cortex and that the efficacy of rTMS for patients with CPSP is predictable by fiber tracking.
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PMID:Diffusion tensor fiber tracking in patients with central post-stroke pain; correlation with efficacy of repetitive transcranial magnetic stimulation. 1900 54

Central post-stroke pain (CPSP) is a neuropathic pain syndrome that can occur after a cerebrovascular accident. This syndrome is characterised by pain and sensory abnormalities in the body parts that correspond to the brain territory that has been injured by the cerebrovascular lesion. The presence of sensory loss and signs of hypersensitivity in the painful area in patients with CPSP might indicate the dual combination of deafferentation and the subsequent development of neuronal hyperexcitability. The exact prevalence of CPSP is not known, partly owing to the difficulty in distinguishing this syndrome from other pain types that can occur after stroke (such as shoulder pain, painful spasticity, persistent headache, and other musculoskeletal pain conditions). Future prospective studies with clear diagnostic criteria are essential for the proper collection and processing of epidemiological data. Although treatment of CPSP is difficult, the most effective approaches are those that target the increased neuronal hyperexcitability.
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PMID:Central post-stroke pain: clinical characteristics, pathophysiology, and management. 2029 59

Antiepileptic drugs (AEDs) are commonly prescribed for a wide range of disorders other than epilepsy, including both neurological and psychiatric disorders. AEDs play also a role in pharmacological management of neuropathic pain. Central post-stroke pain (CPSP) is a disabling morbidity occurring in 35% of patients with stroke. The pathophysiology of CPSP is not well known but central disinhibition with increased neuronal excitability has been suggested. AEDs include many different drugs acting on pain through several mechanisms, such as reduction of neuronal hyperexcitability. To our knowledge conclusive evidence has not been published yet. The aim of this review is to delineate efficacy and safety of AEDs in CPSP.
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PMID:Antiepileptic drugs for central post-stroke pain management. 2192 2

Central post-stroke pain of thalamic origin is an extremely distressing and often refractory disorder. There are no well-established predictors for pain development after thalamic stroke, and the role of different thalamic nuclei is unclear. Here, we used structural magnetic resonance imaging to identify the thalamic nuclei, specifically implicated in the generation of central post-stroke pain of thalamic origin. Lesions of 10 patients with central post-stroke pain of thalamic origin and 10 control patients with thalamic strokes without pain were identified as volumes of interest on magnetic resonance imaging data. Non-linear deformations were estimated to match each image with a high-resolution template and were applied to each volume of interest. By using a digital atlas of the thalamus, we elucidated the involvement of different nuclei with respect to each lesion. Patient and control volumes of interest were summed separately to identify unique areas of involvement. Voxelwise odds ratio maps were calculated to localize the anatomical site where lesions put patients at risk of developing central post-stroke pain of thalamic origin. In the patients with pain, mainly lateral and posterior thalamic nuclei were affected, whereas a more anterior-medial lesion pattern was evident in the controls. The lesions of 9 of 10 pain patients overlapped at the border of the ventral posterior nucleus and the pulvinar, coinciding with the ventrocaudalis portae nucleus. The lesions of this area showed an odds ratio of 81 in favour of developing thalamic pain. The high odds ratio at the ventral posterior nucleus-pulvinar border zone indicates that this area is crucial in the pathogenesis of thalamic pain and demonstrates the feasibility of identifying patients at risk of developing central post-stroke pain of thalamic origin early after thalamic insults. This provides a basis for pre-emptive treatment studies.
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PMID:Assessing the risk of central post-stroke pain of thalamic origin by lesion mapping. 2280 75

Central post-stroke pain syndrome (CPSP) is a debilitating sequel that can follow thalamic sensory stroke. Less well recognized, CPSP follows lateral medullary stroke and parietal cortical stroke and may develop anywhere along the spinothalamic or trigemino-thalamic pathways. Patients describe sharp, stabbing, or burning pain and experience hyperpathia and especially allodynia. Although CPSP was first described over 100 years ago, CPSP is too frequently underrecognized. It is treatable disorder. Pharmacological therapy, magnetic stimulation, and invasive electrical stimulation are reviewed and recommendations made.
Top Stroke Rehabil
PMID:Central poststroke pain: current diagnosis and treatment. 2361 52


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