CPSP remains to be an under-recognized sequel of stroke although it can lead to deterioration in quality of life and impairment in activities of daily living [8]. In this study, the CPSP prevalence rate was 35.4% that was subdivided as follows: 7.7% during the first week post-stroke, 9.2% during the first month, 7.7% during the third month, and 10.8% during the sixth month of follow-up. Prevalence of CPSP is reported between 8% and 35% [9] so our results are nearly within the rated prevalence of CPSP. Other studies reported that after stroke, time to CPSP onset varies considerably. Hansson, 2004 [10] and Leijon et al. 1989 [11] mentioned that CPSP onset was “immediate in 15% (4/27) of patients, occurred within the first month in 37%, and between 1 and 34 months in the remaining 48%; in 78% of cases, CPSP onset occurred within 3 months.” Andersen et al. 1995 [12] pointed that “CPSP onset occurred within 1 month in 63% (10/16) of patients, between 1 and 6 months in 19% (3/16), and at more than 6 months in 19% (3/16)”. Similarly, Nasreddine and Saver 1997 [13] reported that “CPSP initiated within the first week in 36%, at 1 week to 1 month in 20%, and at 1-6 months in 27%.” Although CPSP occurs predominantly in the first 6 months, it can occur up to 10 years after stroke [14]. Seifert et al. 2013 [15] mentioned that CPSP can persist for many years or even throughout life.
In our study, the mean age of the patients who developed CPSP was 53.6 + 9.6 compared to 62.8 + 9.4 on other group; some studies indicate that CPSP is more prevalent in younger patients [2, 3, 8, 11] and other studies considered that the prevalence of CPSP is not related to gender, age, or side of lesion [12].
The younger age of development of CPSP can be explained by that posterior territory infarcts, including brainstem and thalamic strokes, which are frequently associated with CPSP are relatively more common in the young age [3, 9]. Also, sensitivity to heat pain is higher in young age, whereas in the elderly, sensitivity to pressure pain was augmented [16]: finally, young age had lower pain threshold due to faster conduction so with increasing age, the thresholds of non-noxious stimuli increase [1, 17].
In this study, no gender difference in both groups was detected, same results reported by Andersen et al. 1995 [12], on the other hand, gender was identified as predictor in other studies [2, 8]. In this study, no significant association between depression and CPSP was detected; the same finding was reported by Andersen and colleague1995 [12], Mukherjee and colleague 1999 [18], and Naess and colleague 2010 [16]. While Heutink and colleague 2010 [19] reported that like pains and medical conditions, the CPSP experience may be affected by psychosocial factors.
In our study, smoking was a trigging factor, same results reported by Misra and colleague [17]. Deep sensory loss was the significant clinical predictor for the development of CPSP; the same finding was reported by Meschia and Bruno (1998) [20]. Although statistically non-significant the percentage of motor dysfunction was similar to that detected by previous studies [17, 21,22,23].
In this study, 47.8% of CPSP patients has thalamic location and 52.2% extrathalamic; the same finding was reported by Boivie et al. 1989 [24] who demonstrated that this type of pain has a complex pathophysiology. Thus, while the thalamus is still recognized as key pathophysiological component, radiological techniques have shown lesions which have led to CPSP may be located at any level along the neuraxis.
Central disinhibition, especially at the thalamic level, can cause CPSP. Activity of medial thalamus could be inhibited by lesions of lateral thalamus and cause pain via disturbance of inhibitory pathways between medial and lateral pathways. Inhibitory inter-neurons in thalamic reticular nuclei explain an indirect route of such disinhibition [25].
According to SSEP, our study demonstrates that the mean peak latency and IPL differences were prolonged in patients with CPSP with highly statistically significant difference between both groups. Other studies mentioned that SSEPs are unaffected in Wallenberg’s syndrome and in some of the hemispheric but are generally abnormal when medial lemniscus is involved [26]. On the other hand, Kumar et al. (2009) [9] demonstrated that SSEP shows complete loss of contralateral cortical response but maintenance of P9, P14, and N18 far-fields in one third of their CPSP patients. Also, Misra et al. 2008 [17] reported that SSEPs were abnormal in 68% of CPSP; higher rate of SSEP abnormality in their study may be explained by that they take both hemorrhagic and ischemic stroke.
Using regression analysis, predictors of CPSP were best fit to the presence of deep sensory dysfunction, smoking history, age < 50 years, thalamic stroke, prolonged tibial N21–P40 IPL, and prolonged median N9–N20 IPL. Similar results reported by Klit et al. 2014 [27] who find that early evoked pain (dysesthesia)—“an unpleasant abnormal sensation produced by normal stimuli”—is a predictor for CPSP. Misra and colleague [17] reported that smoking was a trigging factor for CPSP. Many studies indicate that CPSP is more prevalent in younger patients [2, 3, 8, 11]. Boivie et al. 1989 [24] reported that CPSP patients has been reported in thalamic location than in other locations. Misra et al. 2008 [17] reported that SSEPs were abnormal in 68% of CPSP.
Limitations of the study includes that large number of patients can be included, longer time of follow-up, management strategy and drugs used for every patient, and social factors for every patient.
