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 Table of Contents  
Year : 2016  |  Volume : 30  |  Issue : 1  |  Page : 34-37

Clinical features and imaging of central poststroke pain

1 Department of Neurology, Calcutta National Medical College and Hospital, Kolkata, West Bengal, India
2 Department of Pain, ESI Institute of Pain Management, Kolkata, West Bengal, India

Date of Web Publication7-Jan-2016

Correspondence Address:
Dr. Subrata Goswami
ESI Institute of Pain Management, 301/3A, A.P.C. Road, Kolkata - 700 069, West Bengal
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0970-5333.173462

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Introduction: Central post stroke pain is a variety of neuropathic pain that occurs after stroke as a result of dysfunction of either spino-thalamic tract or thalamo-cortical sensory pathway. Hyperirritability in surviving cells along the affected pain pathways found with changes in inhibitory pathways, spinal and cortical reorganization and central sensitization. Aim: Clinical features like character of pain and other sensory features with neuroimaging findings of central post stroke pain for a part of Indian population were analyzed in this study. Materials and Method including analysis: 120 numbers of patients, who developed new onset pain symptoms after stroke, attending outpatient and inpatient department of a neurology department during a whole year were examined with history including extensive sensory symptoms analysis; sensory examinations including assessment of pain score and other neurological examinations were done and rechecked by neurologists. All were investigated by neuroimaging with either MRI or CT scan or both. Neuro imaging was interpreted by experienced neuroradiologist and corroborated by neurologists and pain physician. Results: 45% of the lesions were in Thalamus when 75% of the lesions were detected as infarction. 57.5% symptoms started within 3 months. Ataxia found with 60%, increased threshold to warm and cold were seen in 40% of patients, burning sensation was seen in 40% followed by numbness with 20%, dysesthesia found with 60%, reduced sensation to temperature changes found with 40% patients. Conclusion: CPSP patients may presents with various sensory symptoms beside pain. Distribution of sensory symptoms may be with any part of the body as well as over one half of the body. Most common trigger factor was mechanical; while thalamic lesions found in 45%, extra thalamic lesions werefound with 55% of patients.

Keywords: Clinical features, imaging, central post stroke pain
Key message: Central Post Stroke Pain is associated with various sensory symptoms with pain, in majority of cases extra thalamic lesions in the sensory pathways were observed in a referral City Hospital in India.

How to cite this article:
Bhattacharyya R, Goswami S, Ghosh KC, Ghosh S, Mondal GP. Clinical features and imaging of central poststroke pain. Indian J Pain 2016;30:34-7

How to cite this URL:
Bhattacharyya R, Goswami S, Ghosh KC, Ghosh S, Mondal GP. Clinical features and imaging of central poststroke pain. Indian J Pain [serial online] 2016 [cited 2022 Dec 2];30:34-7. Available from: https://www.indianjpain.org/text.asp?2016/30/1/34/173462

  Introduction Top

Patients suffer from different types of pain after stroke. Central pain is a variety of neuropathic pain that occurs after stroke. Central pain occurs due to dysfunction of either spinothalamic tract or thalamocortical sensory fiber. Two French neurologists, Dejerine and Rousy, [1] first described poststroke pain in 1906 naming the condition "thalamic syndrome". It has been seen that the involvement of thalamus as well as other structures such as brainstem, subcortical white matter, and even cortex can produce central pain. The term "central poststrokepain" (CPSP) is preferred as the lesions in various areas of the brain may produce this syndrome. [2] Pathophysiological basis as proposed by Biovie, CPSP originates from hyperirritability in surviving cells along the affected pain pathways. [3] The rates of incidences of CPSP were estimated to be between 2% and 11%. [4]

Most common cause of CPSP is ischemic stroke (85%), almost 70% of the patients with CPSP symptoms develop this within 1 month. [5] Pain is described as numb, cold, burning, aching, swollen, achy, and in various combinations. [6]

Many of the CPSP patients may not have sensory deficit. [7]

The present study was undertaken to analyze clinical features and neuroimaging characteristics of CPSP, as there are very few study in our country although CPSP is very common.

  Materials and Methods Top

Patient attending the outdoor of the Department of Neurology and admitted in indoor on and from 1 November to 31 October 2014 who developed new onset pain symptoms after stroke are included in this study. Particular care was taken to exclude those patients who had past history of neck pain with or without upper limb pain, lower back pain with or without leg pain, symptoms and signs suggestive of pain of other peripheral origin, neurotrauma, or fibromyalgia. Those patients who are getting pharmacotherapy for CPSP with significant sensory symptoms are excluded from this study. History including extensive sensory symptom [5] analysis, detail sensory examinations, and other neurological examination were done and rechecked by other colleagues. All were investigated by neuroimaging either magnetic resonance imaging (MRI) or computed tomography (CT) scan or both.

  Results Top

The total number of patients were 120, out of which 66 (55.5%) were male. The age distribution of 45 (37.5%) patients was below 40 years, the onset of symptoms took place within 3 months in 69 (59.5%) patients [Table 1].
Table 1: Onset of symptoms

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Most commonly noted sensory symptoms are burning [48 (40%)] followed by numbness [24 (20%)] and heaviness [14 (11.6%)] [Table 2].
Table 2: Sensory symptoms

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The distribution of sensory symptoms most commonly over contralateral half of the body was 36 (30%). Still there are many who suffer from symptoms involving any contralateral part of the body or multiple areas [Table 3].
Table 3: Distribution

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Pain score was assessed by visual analogue scale (VAS) as mild (1-4), moderate (5-8), and severe (8-10). Sixty percent of the patients suffer from mild pain [Table 4].
Table 4: Score

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There are many triggering factors that can increase pain. In 40% of the patients mechanical stimuli increases pain [Table 5].
Table 5: Trigger factors

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On careful examination, weakness, ataxia, sensory abnormality, apraxia, hemianopia, and agnosia are found in significant number of patient [Table 6].
Table 6: Examination findings

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Detailed sensory examination showed increase threshold for heat and cold although many of these patients also suffer from dysesthesia [60 (50%)] and allodynia [48 (40%)] [Table 7].
Table 7: Reduced sensation

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Neuroimaging in the form of CT scan of brain was done on 20 (16.6%) patients. MRI brain was done on 90 (75%) patients, and both CT scan and MRI brain were done on 10 (8.3%) patients. CT scan of brain was done for those patients who could not afford the cost of MRI. Neuroimaging was interpreted by an experienced neuroradiologist and corroborated by us. Ischemic stroke and extrathalamic involvement was most common [Table 8] and [Table 9].
Table 8: Nature of the lesion

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Table 9: Site of the lesion

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  Discussion Top

CPSP is a specific type of central pain that occurs due to stroke-related dysfunction of sensory pathway in brain stem and cerebral hemisphere. Pathophysiologically mechanisms involved are changes in inhibitory pathway, spinal and cortical reorganization, and central sensitization. Pain and sensory symptoms develop in 20% of the case within 7 days, in 50% of the cases within 7-30 days, and in the rest 30% of the cases within 1 month to 3 years. [5] In our study, 95% of patients came within 1 year of stroke onset because as they were not getting any specific treatment for their discomfort. Although burning sensation was probably the most common type of pain it is rare in cortical lesions. [8] This study shows various types of symptoms including those vague discomforts which could not be elaborated.

Affected areas were found to vary from entire half of the body to small portion of limb in the latter case it is very difficult to mark it as symptoms of post stroke. Neuropathic characters of the symptoms are of much help.

Pain score by VAS are unable to assess the degree of discomfort produced by sensory symptoms. One of the most important triggering factors for pain is movement that produces movement allodynia. Movement allodynia restricts ambulation and aggravates contracture. [6] Movement and other mechanical stimuli can stimulate (33%) pain sensation. Associated neurological signs include hemiparesis, ataxia, and choreoathetosis on the affected side. [9] In this study, 70% of patient had either no weakness or mild weakness. Ataxia was present in 60% of the subjects. Sensory abnormality was found in 50% of patients although sensory complaints are present in 100% of the patients. In a study by Bovie [3] et al. (1989) it was found that hypoesthesia to temperature is most common followed by touch, vibration, and kinesthesia. In this study, dysesthesia (50%), allodynia (40%), increased threshold to warm and cold (40%) position (7.5%), and vibration (5.8%) were noted.

There appears to be no difference between hemorrhage and infarcts as regards the tendency to induce central pain. [10]

In a study by Leijon et al. (1989), [5] cerebrovascular lesion (CVL) by neuroimaging were detected in thalamus (33.3%), brain stem (29.62%), supratentorial extrathalamic (22.2%), unidentified location (14.8%). In this study, 75% of the patients suffered from infarction, 20% from hemorrhage, 45% have thalamic lesion, 14.1% have internal capsular lesion, and 55% of the CPSP patients had CVL of extrathalamic origin.

  Conclusion Top

CPSP patients may present with various sensory symptoms apart from pain. Distribution of sensory symptoms may be any part of the body as well as one half of the body. A significant number of patients suffer from mild pain that is not less bothering than severe pain. The most common triggering factor was mechanical so wearing loose clothes can be of help. If motor weakness is subtle ataxia, hemianopia and agnosia can help to detect CPSP. Increased threshold to warm and cold were seen in 40% of the patients. Extrathalamic CVLs were seen in 55% of the CPSP patients.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Djerine J, Roussy G. Le syndrome thalamique. Revue Neurologique (Paris) 1906;14:521-3.  Back to cited text no. 1
Jensen TS, Lenz FA. Central post-stroke pain: A challenge for the scientist and the clinicians. Pain 1995;61:161-4.  Back to cited text no. 2
Bowsher D. Some population data about central post stroke pain. Proc 9 th World Congress Pain 1999;435, Abstract.  Back to cited text no. 3
Boivie J. Central pain. In: Wall PD, Melzak R, editors. Textbook of Pain 3 rd ed. London: Churchill Livingstone; 1994. p. 871-48.  Back to cited text no. 4
Leijon G, Boivie J, Johansson I. Central post-stroke pain-neurological symptoms and pain characteristics. Pain 1989;36:13-25.  Back to cited text no. 5
Bowsher D. Central pain: Clinical and physiological characteristics. J Neurol Neurosurg Psychiatry 1966;61:62-9.   Back to cited text no. 6
Wessel K, Vieregge P, Kessler C, Konf D. Thalamic stroke. Thalamic stroke: Correlation of clinical symptoms, somatosensory evoked potentials, and CT findings. Acta Neurol Scand 1994;90:167-73.  Back to cited text no. 7
Kimyai-Asadi A, Nousari HC, Kimyai-Asadi T, Milani F. Poststroke pruritus. Stroke 1999;30:692-3.  Back to cited text no. 8
Kumar B, Kalita J, Kumar G, Misra UK. Central poststroke pain: A review of pathophysiology and treatment. Anesth Analg 2009;108:1645-57.  Back to cited text no. 9
Bowsher D, Leijon G, Thoumas KA. Central poststroke pain: Correlation of MRI with clinical pain characteristics and sensory abnormalities. Neurology 1998;51:1352-8.  Back to cited text no. 10


  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8], [Table 9]

This article has been cited by
1 Pain after stroke: A review
B. Delpont,C. Blanc,G.V. Osseby,M. Hervieu-Bgue,M. Giroud,Y. Bjot
Revue Neurologique. 2018;
[Pubmed] | [DOI]


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