Abnormal Neural Circuits Model in Central Post-stroke Pain

Yufen Zhang1,2, Sehui Ma1,2, Yao Yi1,2 and Lei Pei1,2

1Department of Neurobiology, Huahzong University of Science and Technology, Wuhan, 430030, China

2The Institute for Brain Research (IBR), Huazhong University of Science and Technology, Wuhan, 430030, China

Corresponding Author:
Lei Pei
Lecturer and Researcher
Department of Neurobiology, Tongji Medical College, The Institute for Brain Research (IBR)
Collaborative Innovation Center for Brain Science
Huazhong University of Science and Technology, Wuhan, China
Tel: +86-27-83692630
Fax: +86-27-83692625
E-mail: [email protected]

Received date: June 25, 2016; Accepted date: June 26, 2016; Published date: June 30, 2016

Citation:Yufen Zhang, Sehui Ma, Yao Yi, et al. Abnormal Neural Circuits Model in Central Post-stroke Pain. Acta Psychopathol. 2016, 2:31.doi: 10.4172/2469-6676.100057

 
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Keywords

Central post-stroke pain; Neural circuits

Editorial

Central post-stroke pain (CPSP) was first described by Dejerine and Roussy as a consequence of stroke-related lesions in the thalamus [1]. CPSP can develops after both haemorrhagic and ischemic lesions occurring at any level of somato-sensory pathway of the brain, including medulla, thalamus, and cerebral cortex. CPSP is characterized by either spontaneous or evoked unpleasant sensory described as allodynia, hyperalgesia, and dysesthesia, which severely affect the quality of life. The prevalence of CPSP has been reported to be 8–55%, which is due to different locations of the lesion in the brain. Evidences suggest that the occurrence of CPSP is particularly high after lateral medullary infarction or lesions in the ventroposterior thalamus [2]. In addition, lesions in other brain areas in the somatosensory pathway also result in CPSP [3-5].

Even though the mechanisms of CPSP remain elusive, CPSP has been considered to be maladapted reorganization of neural network after stroke [6]. Based on basic and clinical studies, the following various neural circuit models have been proposed to illustrate the abnormal network of CPSP in the brain [4, 6].

First, Spino-Thalamo-Cortical (STC) circuit model. Studies show hyperactivities of neurons in STC circuit after cerebral ischemic stroke. Spontaneous pain has been found to be due to hyper excitability in STC circuit [7], and neurophysiological examinations on CPSP patients showed abnormally increasing bursting activities in the thalamus [8]. Medications suppressing neuronal activities or inhibiting neural projecting fibers between Spino-Thalamo area or Thalamo-Cortical area were effective for CPSP alleviation [9].

Second, Cortical-Thalamic (CT) circuit model. Like STC circuit, hyperactivity in the CT circuit is one of the mechanisms of CPSP. This abnormal neural activity in the CT circuit is due to the disinhibition from the cortex, which called the “disinhibition theory” [10]. The sensory in central nervous system is modulated by a tonic balance between excitation and inhibition [11]. Stroke induced lesion in the CT circuit could interrupt this balance, thus cause abnormal sensations like pain in CPSP.

Third, Limbic-Amygdala-Insular cortex (LAIc) circuit model. Recently, using functional magnetic resonance imaging (fMRI) technique, clinical scientists have shown changes of activities in the LAIc neural network in chronic pain states of CPSP patients [12]. LAIc circuit is composed by amygdale and insular cortex in the limbic structures [13]. Damages in the LAIc circuit after stroke could produce both structural and functional abnormalities of the sensory neural network, which causes generation and development of CPSP.

Last but not least, Inter-hemispheric circuit model. The malfunctioning in inter-hemispheric circuit after stroke may be another pathogenesis of CPSP. Recent studies have shown that electrical stimulation of the contralesional hemisphere could suppress the activities in the epilesional hemisphere, which indicates that inter-hemispheric inhibition might be contributed to the pain suppression mechanisms in CPSP patients treated with electric stimulation [14, 15]. Therefore, electric brain stimulation could be choosed as an alternative treatment for CPSP patients.

In this editorial, we briefly summarized a few proposed CPSP neural circuit models contributing to the mechanisms of CPSP.

We conclude that abnormal structure (damage in the inhibitory neurons or neural fibers) and dysfunctions (hyper excitability) in these neural circuits play important roles in the generation of hyperalgesia and allodynia in CPSP patients. Applying newly developed single synaptic tracing technique with optogenetics on CPSP animal models, new specific neural circuits will be revealed, interventions or treatments targeting these abnormal circuits may be more effective for CPSP patients than traditional antipsychotic medicine. In spite of this, further investigation of network abnormalities in CPSP may shed light on the mechanisms and treatment of CPSP.

Acknowledgement

This work was supported by National Natural Science Foundation of China (81200863, 81571078).

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