Central post-stroke pain due to injury of the spinothalamic tract in patients with cerebral infarction： a diffusion tensor tractography imaging study

Many studies using diffusion tensor tractography（DTT） have demonstrated that injury of the spinothalamic tract（STT） is the pathogenetic mechanism of central post-stroke pain（CPSP） in intracerebral hemorrhage; however, there is no DTT study reporting the pathogenetic mechanism of CPSP in cerebral infarction. In this study, we investigated injury of the STT in patients with CPSP following cerebral infarction, using DTT. Five patients with CPSP following cerebral infarction and eight age-and sex-matched healthy control subjects were recruited for this study. STT was examined using DTT. Among DTT parameters of the affected STT, fractional anisotropy and tract volume were decreased by more than two standard deviations in two patients（patients 1 and 2） and three patients（patients 3, 4, and 5）, respectively, compared with those of the control subjects, while mean diffusivity value was increased by more than two standard deviations in one patient（patient 2）. Regarding DTT configuration, all affected STTs passed through adjacent part of the infarct and three STTs showed narrowing. These findings suggest that injury of the STT might be a pathogenetic etiology of CPSP in patients with cerebral infarction.

Delayed degeneration of an injured spinothalamic tract in a patient with diffuse axonal injury

Diffuse axonal injury （DAI） is one of the devastating mechanisms of traumatic brain injury （TBI） and shows extensive sub- cortical lesions due to shearing forces induced by rapid acceleration-deceleration and rotation of the brain （Adams et al., 1982; Meythaler et al., 2001）. As a result, conventional brain imaging techniques including brain MRI have been limited in demon- strating neuronal degeneration in patients with DAI. However, diffusion tensor tractography （DTT）, which is derived from diffusion tensor imaging （DTI） has enabled three-dimensional reconstruction of the neural tracts （Jang and Seo, 2014）. Since the introduction of DTI, several studies have demonstrated neuronal degeneration after TBI （Tomaiuolo et al., 2005; Hong and lang, 2010; Kwon and Jang, 2014）. However, little is known about delayed neuronal degeneration in patients with TBI.

Central Pain Syndrome: Etiological Perspectives from the 3D Default Space Model of Consciousness

In this article, the mechanisms of central pain syndrome (CPS) are examined for the purpose of gaining insight into how a unified conscious experience arises from brain and body interaction. We provide a novel etiology for CPS via implementation of the previously proposed 3D Default Space (3DDS) consciousness model in which consciousness and body schema arise when afferent information is processed by corticothalamic feedback loops and integrated via the thalamus. Further, we propose the mechanisms by which CPS represents deficits in dynamic interactions between afferent and efferent signaling. Modern hypotheses of CPS suggest roles for maladaptive neuroplasticity, a deafferentated somatosensory cortex and/or thalamus, and reorganization along the sensory pathways of the spinothalamic tract in the pathogenesis of the painful sensations. We propose that CPS arises when painful sensory signals originating along the maladapted and/or dysfunctional spinothalamic tract become accentuated by the dominant top down mechanisms of the brain.

New Insights on Stimulating the Lung Meridian Based on Modern Neurophysiology

Chronic obstructive pulmonary diseases (COPD) caused 3.2 million deaths worldwide in 2015 [1]. Therapeutic treatments, including acupuncture & herbal medicine have been applied to handle this disease with certain efficacies in the domain of traditional Chinese Medicine. However, very few analyses on the mechanisms behind the efficacies can be found in literature. Without understanding the basic mechanisms behind any medical treatment is the bottle-neck to advancement of possibly effective therapy of any kind. Based on this argument, we start off a series of studies on the neurophysiological consequence of acupuncture/acupressure applied to the Lung Meridian. We explain how the sensory signals (by sympathetic nerves) follow the spinothalamic tracts to the thalamus and then to the primary sensory cortex. The neurons of these ascending tracts synapse the motor neurons which activate some of the different organs of the respiratory system—diaphragm, nose, larynx, scalene muscles, trachea, lungs, intercostal and supporting abdominal muscles. The sensory signals at the neo-cortex are then passed on to the motor neurons in the primary motor cortex. The activated neurons project mainly along two descending tracts: anterior and lateral corticospinal tracts. Neurons of these tracts project to activate again some of the respiratory organs, plus the motors neurons related to the digestive system, including the large intestine. On the other hand, an intrinsic, automatic breathing system in the brainstem sends rhythmic signals through the bulbospinal tract system, which contains a special type of neurons—the pre-sympathetic neurons. These neurons, via interneuron relay, synapse motor neurons which mobilize the organs of the respiratory organs to function. Since the “Lung Meridian induced” signals and the intrinsic signals are sent by different types of neurons, we propose that stimulating the Lung Meridian might activate/supplement the action of the intrinsic system during some pathological states. Though the initial suggestion is supported by in vitro/(in vivo) experiments in detailed steps, clinical trials await future development.