Development Of Central Post-stroke Pain Research Articles

The role of spinal neurons targeted by corticospinal neurons in central poststroke neuropathic pain.

Central poststroke pain (CPSP) is one of the primary sequelae following stroke, yet its underlying mechanisms are poorly understood. By lesioning the lateral thalamic nuclei, we first established a CPSP model that exhibits mechanical and thermal hypersensitivity. Innocuous mechanical stimuli following the thalamic lesion evoked robust neural activation in somatosensory corticospinal neurons (CSNs), as well as in the deep dorsal horn, where low threshold mechanosensory afferents terminate. In this study, we used viral-based mapping and intersectional functional manipulations to decipher the role of somatosensory CSNs and their spinal targets in the CPSP pathophysiology. We first mapped the post-synaptic spinal targets of lumbar innervating CSNs using an anterograde trans-synaptic AAV1-based strategy and showed these spinal interneurons were activated by innocuous tactile stimuli post-thalamic lesion. Functionally, tetanus toxin-based chronic inactivation of spinal neurons targeted by CSNs prevented the development of CPSP. Consistently, transient chemogenetic silencing of these neurons alleviated established mechanical pain hypersensitivity and innocuous tactile stimuli evoked aversion linked to the CPSP. In contrast, chemogenetic activation of these neurons was insufficient to induce robust mechanical allodynia typically observed in the CPSP. The CSNs and their spinal targets are required but insufficient for the establishment of CPSP hypersensitivity. Our study provided novel insights into the neural mechanisms underlying CPSP and potential therapeutic interventions to treat refractory central neuropathic pain conditions.

Spinal lipocalin 2 as a factor in the development of central post-stroke pain

Central poststroke pain (CPSP) is a type of central neuropathic pain whose mechanisms remain unknown. Recently, we showed that activated astrocytes and microglial cells are present in the spinal cord of CPSP model mice. Activated glial cells exacerbate cerebral ischemic pathology by increasing the expression of inflammatory factors. However, the involvement of spinal glial cells in CPSP remains unknown. We hypothesized that spinal glial cell-derived molecules cause hyperexcitability or promoted the development of CPSP. In this study, we identified glial cell-derived factors involved in the development of CPSP using a bilateral common carotid occlusion (BCAO)-induced CPSP mouse model. Male ddY mice were subjected to BCAO for 30 min. The von Frey test assessed mechanical hypersensitivity in the right hind paw of mice. BCAO mice showed hypersensitivity to mechanical stimuli and astrocyte activation in the spinal cord 3 days after treatment. DNA microarray analysis revealed a significant increase in lipocalin 2 (LCN2), is known as neutrophil gelatinase-associated lipocalin, in the superficial dorsal horns of BCAO-induced CPSP model mice. LCN2 colocalized with GFAP, an astrocyte marker. Spinal GFAP-positive cells in BCAO mice co-expressed signal transducer and activator of transcription 3 (STAT3). The increase in the fluorescence intensity of LCN2 and GFAP in BCAO mice was suppressed by intrathecal injection of AG490, an inhibitor of JAK2 and downstream STAT3 activation, or anti-LCN2 antibody. Our findings indicated that LCN2 in spinal astrocytes may be a key molecule and may be partly involved in the development of CPSP.

Repressing iron overload ameliorates central post-stroke pain via the Hdac2-Kv1.2 axis in a rat model of hemorrhagic stroke.

JOURNAL/nrgr/04.03/01300535-202412000-00027/figure1/v/2024-04-08T165401Z/r/image-tiff Thalamic hemorrhage can lead to the development of central post-stroke pain. Changes in histone acetylation levels, which are regulated by histone deacetylases, affect the excitability of neurons surrounding the hemorrhagic area. However, the regulatory mechanism of histone deacetylases in central post-stroke pain remains unclear. Here, we show that iron overload leads to an increase in histone deacetylase 2 expression in damaged ventral posterolateral nucleus neurons. Inhibiting this increase restored histone H3 acetylation in the Kcna2 promoter region of the voltage-dependent potassium (Kv) channel subunit gene in a rat model of central post-stroke pain, thereby increasing Kcna2 expression and relieving central pain. However, in the absence of nerve injury, increasing histone deacetylase 2 expression decreased Kcna2 expression, decreased Kv current, increased the excitability of neurons in the ventral posterolateral nucleus area, and led to neuropathic pain symptoms. Moreover, treatment with the iron chelator deferiprone effectively reduced iron overload in the ventral posterolateral nucleus after intracerebral hemorrhage, reversed histone deacetylase 2 upregulation and Kv1.2 downregulation, and alleviated mechanical hypersensitivity in central post-stroke pain rats. These results suggest that histone deacetylase 2 upregulation and Kv1.2 downregulation, mediated by iron overload, are important factors in central post-stroke pain pathogenesis and could serve as new targets for central post-stroke pain treatment.

Research Progress on the Mechanisms of Central Post-Stroke Pain: A Review.

Central Post-Stroke Pain (CPSP) is a primary sequelae of stroke that can develop in the body part corresponding to the cerebrovascular lesion after stroke, most typically after ischemic stroke but also after hemorrhagic stroke. The pathogenesis of CPSP is currently unknown, and research into its mechanism is ongoing. To summarize current research on the CPSP mechanism and provide guidance for future studies. Use "central post-stroke pain," "stroke AND thalamic pain," "stroke AND neuropathic pain," "post-stroke thalamic pain" as the search term. The search was conducted in the PubMed and China National Knowledge Infrastructuredatabases, summarizing and classifying the retrieved mechanism studies. The mechanistic studies on CPSP are extensive, and we categorized the included mechanistic studies and summarized them in terms of relevant pathway studies, relevant signals and receptors, relevant neural tissues, and described endoplasmic reticulum stress and other relevant studies, as well as summarized the mechanisms of acupuncture treatment. Studies have shown that the pathogenesis of CPSP involves the entire spinal-thalamo-cortical pathway and that multiple substances in the nervous system are involved in the formation and development of CPSP. Among them, the relevant receptors and signals are the hotspot of research, and the discovery and exploration of different receptors and signals have provided a wide range of therapeutic ideas for CPSP. As a very effective treatment, acupuncture is less studied regarding the analgesic mechanism of CPSP, and further experimental studies are still needed.

Role of Sensory Pathway Injury in Central Post-Stroke Pain: A Narrative Review of Its Pathogenetic Mechanism.

Central post-stroke pain (CPSP) is a severe chronic neuropathic pain syndrome that is a direct result of cerebrovascular lesions affecting the central somatosensory system. The pathogenesis of this condition remains unclear owing to its extensive clinical manifestations. Nevertheless, clinical and animal experiments have allowed a comprehensive understanding of the mechanisms underlying CPSP occurrence, based on which different theoretical hypotheses have been proposed. We reviewed and collected the literature and on the mechanisms of CPSP by searching the English literature in PubMed and EMBASE databases for the period 2002-2022. Recent studies have reported that CPSP occurrence is mainly due to post-stroke nerve injury and microglial activation, with an inflammatory response leading to central sensitization and de-inhibition. In addition to the primary injury at the stroke site, peripheral nerves, spinal cord, and brain regions outside the stroke site are involved in the occurrence and development of CPSP. In the present study, we reviewed the mechanism of action of CPSP from both clinical studies and basic research based on its sensory pathway. Through this review, we hope to increase the understanding of the mechanism of CPSP.

Spinal MCP-1 Contributes to Central Post-stroke Pain by Inducing Central Sensitization in Rats.

Central post-stroke pain (CPSP) is a highly refractory form of central neuropathic pain that has been poorly studied mechanistically. Recent observations have emphasized the critical role of the spinal dorsal horn in CPSP. However, the underlying mechanisms remain unclear. In this study, rats were subjected to thalamic hemorrhage to investigate the role of spinal monocyte chemoattractant protein-1 (MCP-1) and C-C motif chemokine receptor 2 (CCR2) in the development of CPSP. Immunohistochemical staining and ELISA were used to assess the expression changes of c-Fos, Iba-1, GFAP, MCP-1, and CCR2 in the dorsal horn of the lumbar spinal cord following thalamic hemorrhage, and the involvement of spinal MCP-1 in CPSP was examined by performing intrathecal anti-MCP-1 mAb injection to neutralize the spinal extracellular MCP-1. We demonstrated that intra-thalamic collagenase microinjection induced persistent bilateral mechanical pain hypersensitivity and facilitated the spontaneous pain behaviors evoked by intraplantar bee venom injection. Accompanying CPSP, the expression of c-Fos, Iba-1, and GFAP in the lumbar spinal dorsal horn was significantly increased up to 28 days post-intra-thalamic collagenase microinjection. Intrathecal injection of minocycline and fluorocitrate dramatically reverses the bilateral mechanical pain hypersensitivity. Moreover, intra-thalamic collagenase microinjection dramatically induced the up-regulation of MCP-1 but had no effect on the expression of CCR2 in the bilateral lumbar spinal dorsal horn, and MCP-1 was primarily localized in the neuron. Intrathecal injection of anti-MCP-1 mAb was also able to reverse CPSP and reduce the expression of c-Fos, Iba-1, and GFAP in the lumbar spinal dorsal horn. These findings indicated that spinal MCP-1 contributes to CPSP by mediating the activation of spinal neurons and glial cells following thalamic hemorrhage stroke, which may provide insights into pharmacologic treatment for CPSP.

The involvement of spinal glial cell-derived lipocalin2 in the development of central post-stroke pain

The involvement of spinal glial cell-derived lipocalin2 in the development of central post-stroke pain

Changes in the Brain Metabolism Associated with Central Post-Stroke Pain in Hemorrhagic Pontine Stroke: An 18F-FDG-PET Study of the Brain.

Central post-stroke pain (CPSP) is an intractable neuropathic pain that can occur following central nervous system injuries. Spino-thalamo-cortical pathway damage contributes to CPSP development. However, brain regions involved in CPSP are unknown and previous studies were limited to supratentorial strokes with cortical lesion involvement. We analyzed the brain metabolism changes associated with CPSP following pontine hemorrhage. Thirty-two patients with isolated pontine hemorrhage were examined; 14 had CPSP, while 18 did not. Brain glucose metabolism was evaluated using 18F-fluorodeoxyglucose-positron emission tomography images. Additionally, regions revealing metabolic correlation with CPSP severity were analyzed. Patients with CPSP showed changes in the brain metabolism in the cerebral cortices and cerebellum. Compared with the control group, the CPSP group showed significant hypometabolism in the contralesional rostral anterior cingulum and ipsilesional primary motor cortex (Puncorrected < 0.001). However, increased brain metabolism was observed in the ipsilesional cerebellum (VI) and contralesional cerebellum (lobule VIIB) (Puncorrected < 0.001). Moreover, increased pain intensity correlated with decreased metabolism in the ipsilesional supplementary motor area and contralesional angular gyrus. This study emphasizes the role of the many different areas of the cortex that are involved in affective and cognitive processing in the development of CPSP.

Pharmacotherapy to Manage Central Post-Stroke Pain.

Central post-stroke pain is a chronic neuropathic pain syndrome following a cerebrovascular accident. The development of central post-stroke pain is estimated to occur in 8 to 55% of stroke patients and is described as constant or intermittent neuropathic pain accompanied by dysesthesia of temperature and/or pressure sensations. These pain and sensory deficits are within the area of the body corresponding to the stroke lesion. The onset of pain is usually gradual, though it can develop either immediately after stroke or years after. Given the diversity in its clinical presentation, central post-stroke pain is a challenging diagnosis of exclusion. Furthermore, central post-stroke pain is often resistant to pharmacological treatment options and a clear therapeutic algorithm has not been established. Based on current evidence, amitriptyline, lamotrigine, and gabapentinoids should be used as first-line pharmacotherapy options when central post-stroke pain is suspected. Other drugs, such as fluvoxamine, steroids, and Intravenous infusions of lidocaine, ketamine, or even propofol, can be considered in intractable cases. In addition, interventional therapies such as motor cortex stimulation or transcranial magnetic stimulation have been shown to provide relief in difficult-to-treat patients.

The Involvement of DDAH1 in the Activation of Spinal NOS Signaling in Early Stage of Mechanical Allodynia Induced by Exposure to Ischemic Stress in Mice.

The pathophysiological mechanism of central post-stroke pain (CPSP) is complicated and not well understood. Recently, it has been reported that an increase in the levels of spinal nitric oxide synthetase (NOS) occurs in cerebral ischemia, and spinal NOS is involved in the development of neuropathic pain. The aim of this study was to elucidate the mechanism of spinal NOS signaling in the development of CPSP. Male ddY mice were subjected to 30-min long bilateral carotid artery occlusion (BCAO). The withdrawal responses to mechanical stimuli were significantly increased as determined with von Frey test on days 1 and 3 after BCAO. Protein expression of spinal N(G),N(G)-dimethylarginine dimethylaminohydralase 1 (DDAH1), a key enzyme involved in the metabolism of the endogenous NOS, increased on day 1 after BCAO, but not on day 3. Intrathecal (i.t.) injection of PD404182, a DDAH1 inhibitor, significantly suppressed mechanical allodynia on day 1, but not on day 3 after BCAO. In addition, i.t. administration of NG-nitro-L-arginine methyl ester (L-NAME), a non-selective NOS inhibitor, significantly blocked mechanical allodynia on days 1 and 3 after BCAO. Furthermore, BCAO-induced increment of spinal NOS activity was inhibited by the pretreatment with PD404182. These results suggest that mechanical allodynia in the early stage of CPSP is caused by increment of NOS activity through upregulated DDAH1 in the spinal cord.

Metabolic Changes in Central Poststroke Pain Following Thalamic Intracerebral Hemorrhage: An 18F-FDG PET Study.

Central poststroke pain (CPSP) is one of the most refractory neuropathic pains following stroke. Injury in the spinothalamic pathway appears crucial for the development of CPSP, but changes in activity in multiple brain regions may also be related. We investigated brain metabolic changes in patients with CPSP following thalamic intracerebral hemorrhage (ICH). Forty-three patients with thalamic ICH were examined. Overall brain metabolism was measured with F-FDG PET. Images were analyzed with statistical parametric mapping (SPM12). Patients with CPSP (n = 20) were compared with patients without CPSP (n = 23). In addition, the association between regional brain metabolism and the severity of CPSP was investigated. In comparison to patients in the non-CPSP group, the CPSP group exhibited significant hypometabolism in the ipsilesional precentral, postcentral gyri, and the contralesional cuneus (Puncorrected < 0.001), whereas significant hypermetabolism was found in the medial dorsal nucleus of the contralesional thalamus (Puncorrected < 0.001). In addition, brain metabolism in the ipsilesional Crus I and Crus II of the cerebellum was positively correlated to pain intensity ratings (Puncorrected < 0.001). Our findings suggested that an altered state of resting brain metabolism in various brain regions related to sensory processing and cognitive functioning may be involved in the underlying mechanism of CPSP following thalamic ICH.

Central Poststroke Pain Can Occur With Normal Sensation.

In view of the paucity of studies on central poststroke pain (CPSP), in this hospital-based prospective study, we evaluated the frequency, the spectrum, imaging, and quantitative sensory testing in a cohort of stroke patients with CPSP. Stroke patients who developed CPSP at onset or during follow-up were included. Patients were subjected to clinical evaluation and sensory testing. The severity of stroke was defined by the Modified Rankin Scale and disability by the Barthel Index. Quantitative sensory testing included monofilament testing and evaluation for static and dynamic mechanical allodynia, punctuate hyperalgesia, temporal summation, cold allodynia, and cold hyperalgesia. Sleep, anxiety, and depression were also evaluated. Patients were treated with pregabalin 150 to 600 mg/d and good response was defined as >50% improvement in the VAS score. CPSP symptoms were correlated with demographic information, sensory findings, and imaging findings. A total of 319 patients with stroke were evaluated. CPSP occurred in 66 (20.7%) of them. The median age of the CPSP patients was 55 years (range, 25 to 80 y). About 31.8% patients were female. The onset, the duration, and the distribution of pain were variable. The severity of symptoms did not correlate with demographic variables and the site of lesion. Spinothalamic sensations were normal in 42.3% patients. On treatment with pregabalin (150 to 600 mg), half of the patients had a good response. CPSP was present in 20.7% of the stroke patients. Spinothalamic tract dysfunction may not be necessary for the development of CPSP, and it can also be seen with normal spinothalamic sensation. The location of the stroke, its type and quality, and the severity of CPSP were not related.

Functional characterization of a mouse model for central post-stroke pain

BackgroundStroke patients often suffer from a central neuropathic pain syndrome called central post-stroke pain. This syndrome is characterized by evoked pain hypersensitivity as well as spontaneous, on-going pain in the body area affected by the stroke. Clinical evidence strongly suggests a dysfunction in central pain pathways as an important pathophysiological factor in the development of central post-stroke pain, but the exact underlying mechanisms remain poorly understood. To elucidate the underlying pathophysiology of central post-stroke pain, we generated a mouse model that is based on a unilateral stereotactic lesion of the thalamic ventral posterolateral nucleus, which typically causes central post-stroke pain in humans.ResultsBehavioral analysis showed that the sensory changes in our model are comparable to the sensory abnormalities observed in patients suffering from central post-stroke pain. Surprisingly, pharmacological inhibition of spinal and peripheral key components of the pain system had no effect on the induction or maintenance of the evoked hypersensitivity observed in our model. In contrast, microinjection of lidocaine into the thalamic lesion completely reversed injury-induced hypersensitivity.ConclusionsThese results suggest that the evoked hypersensitivity observed in central post-stroke pain is causally linked to on-going neuronal activity in the lateral thalamus.

Early evoked pain or dysesthesia is a predictor of central poststroke pain

Central poststroke pain (CPSP) is a central neuropathic pain condition caused by a cerebrovascular lesion affecting the central somatosensory nervous system. Once developed, CPSP is difficult to treat, so there is an interest in identifying stroke patients at risk for the development of CPSP. This study examined if sensory abnormalities, including evoked dysesthesia, allodynia, or hyperalgesia to static and dynamic touch, cold, and pinprick, at stroke onset are a predictor for the development of CPSP. Consecutive stroke patients were recruited from a large prospective study of poststroke pain in Aarhus, Denmark, between 2007 and 2008. Patients underwent a structured pain interview and a standardized sensory examination within 4 days of admission, and a structured telephone interview was conducted after 3 and 6months. Patients who developed poststroke pain in the affected side without any other plausible cause were classified as having possible CPSP. A total of 275 stroke patients completed the study, and 29 patients (10.5%) were classified as having possible CPSP. The diagnosis was confirmed by a clinical examination in 15 of 17 patients, corresponding to a prevalence of 8.3%. The presence of allodynia, hyperalgesia, or dysesthesia in response to the sensory examination at stroke onset increased the odds for CPSP at 6months by 4.6 (odds ratio; 95% confidence interval 1.5–13.9). The combination of reduced or absent sensation to pinprick or cold and early evoked pain or dysesthesia at onset increased odds by 8.0 (odds ratio; 95% confidence interval 2.6–24.8). In conclusion, early evoked pain or dysesthesia is a predictor for CPSP.

The Prevalence of Central Poststroke Pain according to the Integrity of the Spino-Thalamo-Cortical Pathway

Objectives: Little is known about the prevalence of central poststroke pain (CPSP) according to the integrity of the spino-thalamo-cortical pathway (STP). Using diffusion tensor tractography, we investigated the prevalence of CPSP according to the integrity of the STP in patients with intracerebral hemorrhage. Methods: We recruited 52 consecutive chronic patients and 10 normal control subjects. Patients were classified into two groups according to preservation of the integrity of the STP. Each group was divided into two subgroups according to the presence of CPSP. Results: The preserved group included 34 patients [CPSP subgroup, 16 (47%) patients; non-CPSP subgroup, 18 (53%) patients], and 18 patients were enrolled into the disrupted group [CPSP subgroup, 3 (17%) patients; non-CPSP subgroup, 15 (83%) patients]. The fractional anisotropy and mean diffusivity values of the CPSP and non-CPSP subgroups of the preserved group were decreased and increased when compared with those of the control group, respectively (p < 0.05). Conclusions: We found that the prevalence of CPSP in patients with partial injury of the STP was higher than that of patients with complete injury of the STP. Partial injury of the STP appears to be more vulnerable to development of CPSP than complete injury of the STP in patients with intracerebral hemorrhage.

Injury of the Spino-Thalamo-Cortical Pathway Is Necessary for Central Post-Stroke Pain

Objectives: We investigated the relationship between injury of the spino-thalamo-cortical pathway (STP) and central post-stroke pain (CPSP) in patients with intracerebral hemorrhage, using diffusion tensor tractography (DTT). Methods: 30 consecutive chronic patients, in whom integrity of the STP and the medial lemnisco-thalamo-cortical pathway (MLP) were spared in both hemispheres, were recruited. We classified the patients into two groups according to the presence of the CPSP. DTTs were obtained using the FMRIB Software Library. Fractional anisotropy (FA), mean diffusivity (MD), and tract volume were measured. A laterality index (LI) was used to determine asymmetry of DTT parameters between the hemispheres. Results: The LI for tract volume of the STP in the CPSP group was lower than that of the non-CPSP group (p = 0.000). However, there were no differences between the CPSP group and non-CPSP group for the LIs of FA or MD of the STP or for the LIs of FA, MD, or tract volume of the MLP (p > 0.05). Conclusions: Decrease of tract volume without changes in the STP FA or MD values in the CPSP group indicates partial injury of STP. Therefore, injury of the STP seems to be a requirement for the development of CPSP in patients with intracerebral hemorrhage.

Patterns of sensory abnormality in cortical stroke

To characterize sensory symptoms in patients with stroke occurring in the cerebral cortex. We studied clinical and imaging findings of 24 patients who had prominent sensory symptoms without definitive motor dysfunction. According to the sensory manifestations, patients were divided into dominant impairment of primitive sensation (DIPS) group, dominant impairment of cortical sensation (DICS) group, and paresthesia-only group. DIPS was related to lesions involving the parietal operculum and the insular cortex, whereas DICS was related to the lesions affecting the postcentral gyrus. Patients with paresthesia only had smaller lesions located in the postcentral gyrus. DIPS group patients were more often women (p = 0.013), more often had dysarthria (n = 0.043), and more often developed central poststroke pain or paresthesia (n = 0.005) than the DICS group patients. Restricted sensory changes are common, predominantly involving the perioral or finger areas. Sensory patterns in these patients are generally consistent with the dichotomized (SI and SII) sensory system in the cerebral cortex. Involvement of insular and opercular areas is related to primitive sensory impairment and development of central poststroke pain, whereas postcentral gyrus involvement is related to cortical sensory loss without poststroke pain. The pattern of restricted sensory changes is generally consistent with the Penfield sensory topography.

Pharmacological classification of central post-stroke pain: comparison with the results of chronic motor cortex stimulation therapy

In an attempt to clarify the neurochemical background of central post-stroke pain and to undertake a pharmacological analysis, the basic pharmacological characteristics of this intractable pain syndrome were investigated by the morphine, thiamylal and ketamine tests. In addition, the correlation between the pharmacological characteristics and the effects of chronic motor cortex stimulation therapy was examined. The study employed 39 central post-stroke pain patients who had intractable hemibody pain associated with dysesthesias, and radiologically demonstrated lesions in the thalamic area (thalamic pain, n=25) or suprathalamic area (suprathalamic pain, n=14). The pharmacological evaluations showed that definite pain reduction occurred in eight of the 39 cases (20.5%) by the morphine test, in 22 of the 39 cases (56.4%) by the thiamylal test, and in 11 of 23 cases (47.8%) by the ketamine test. Based on these pharmacological assessments, there was no obvious difference between thalamic and suprathalamic pain. A comparison of the long-term follow-up results of chronic motor cortex stimulation therapy revealed that thiamylal and ketamine-sensitive and morphine-resistant cases displayed long-lasting pain reduction with chronic motor cortex stimulation therapy, whereas the remaining cases did not show good results. We conclude that pharmacological classification of central post-stroke pain by the morphine, thiamylal and ketamine tests could be useful for predicting the effects of chronic motor cortex stimulation therapy. It has recently been suggested that excitatory amino acids may be involved in the development of central post-stroke pain. However, the fact that only 23 of the present 39 cases (59.0%) of thalamic and suprathalamic pain were sensitive to the thiamylal or ketamine test reflects the complex pharmacological background and the difficulties associated with treating central post-stroke pain.

Thalamic or Central Pain States Poststroke

Thalamic or central pain states are generally regarded as rare in stroke, occurring in fewer than 2% of patients. However, a recent study suggests that they may be more common, occurring in up to 8% of unselected stroke patients. Cerebrovascular lesions leading to central pain states do not necessarily involve the thalamus, but can occur following lower brainstem and suprathalamic lesions. Damage to the spinothalamocortical tract appears to be a prerequisite to the development of central poststroke pain (CPSP). Development of CPSP is likely related to denervation hyperexcitability of third or fourth order, thalamic or cortical neurons. Central pain is often described as a ′burning′ sensation in association with an unpleasant association of tingling, pins and needles, or numbness. Spontaneous or evoked dysesthesia and allodynia/hyperalgesia are common. Central or thalamic pain is generally intractable to most therapeutic interventions. One case is presented to illustrate the typical clinical presentation of thalamic pain states and the difficulties in treating this pain.

Central post-stroke pain - relation of sep to location of cvl and sensory signs

The intention of the present study was to characterize patients with central post-stroke pain (CPSP) with regard to type and location of the cerebrovascular lesion (CVL), the characteristics of the pain and the neurological symptoms and signs in addition to the pain.Twenty men and 7 women with a mean age of 67 years and a mean pain duration of 44 months were examined 9–188 (mean 53) months after their stroke. The clinical symptoms and signs and the CT scans indicated that the CVL were located in the lower brain-stem in 8 patients, involved the thalamus in 9 patients and were located lateral and superior to the thalamus in 6 patients. In the remaining 4 patients the location of the CVL could not be determined with certainty. The 3 identified hematomata were all located in the thalamus.The onset of the pain was immediate in 4 patients, within the first post-stroke months in 10 patients and delayed by 1–34 months in the rest.The pain was on the left side in 18 patients. Twenty patients had hemipain. Most patients experienced more than one type of pain. The most common qualities were burning, aching, pricking and lacerating, with some differences in the frequencies according to the location of the CVL. Burning pain was most common, except among the patients with thalamic CVL, in whom lacerating pain was more common. Aching and pricking pain were also frequent.All patients considered the pain to be a great burden and most rated the pain intensity as high on a visual analogue scale. The intensity was increased by external stimuli, the most common being joint movements, cold and light touch. Five patients reported aggravation by emotional stimuli.Besides pain, the only neurological symptom common to all patients was decreased temperature sensibility, as shown by quantitative methods. It is possible that pain sensibility was also abnormal in all. Hypersensitivities to cutaneous stimuli, including evoked dysesthesias were found in 88% of the patients, while the detection thresholds for touch and vibration were abnormal in only 52% and 41%, respectively. Similarly, low figures were found for paresis and ataxia, which were present in 48% and 62%, respectively.It is concluded that only a minority of patients with central pain after stroke have thalamic lesions. The term thalamic pain is therefore inaccurate in most cases of CPSP. The symptoms and signs indicate that the crucial factor for the development of CPSP is a lesion affecting the spino-thalamo-cortical pathway important for temperature and pain sensibility. The level of the lesion along the neuroaxis is not critical for occurrence of the pain, but decides the nature of the associated neurological symptoms and appears to affect the features of the pain.