PubMed · 14950106
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B BORNSTEIN. 1952. [Synkinesis].. https://pubmed.ncbi.nlm.nih.gov/14950106/
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The authors review relevant experimental studies on pain perception and processing in psychiatric disorders with traumatic stress as an etiological factor. In borderline personality disorder, post-traumatic stress disorder, and fibromyalgia neurophysiological and neuropsychological patterns of pain processing appear to be different. Experimental studies in borderline patients show a desensitization of pain thresholds whereas patients with fibromyalgia show an opposite pattern, which could be explained by a central augmentation of pain processing. Furthermore, the authors outline methods to assess pain perception (peripheral and central) and describe the neurobiological mechanisms of pain processing, particularly the distinction between the sensory-discriminative lateral system and the affective-motivational medial system. Finally, suggestions for further research and implications for therapy are proposed.
STUDY DESIGN: Clinical commentary. OBJECTIVE: To discuss the method of coordination training to enhance motor skills in persons after spinal cord injury (SCI). METHOD: From the literature and clinical experience, we learn that basic motor skills like walking are refined and maintained through the millions of repetitions that take place as part of normal development. These coordinated patterns function effectively as a form of training to the system because of the presence of neural pathways that mediate commands between higher and lower levels of the central nervous system (CNS). When these pathways are disrupted as a result of a lesion, the question that arises is whether retraining can be effective. RESULTS/DISCUSSION: The question is directed at the common practice among rehabilitation professionals to prescribe and carry out tireless repetitions of coordinated motor activities in people with SCI lesions. We discuss this fundamental question from the perspective of understanding differences in maturation and function of higher motor centres and lower motor centres.
Multiple sclerosis is a chronic neurologic disorder considered to result from relatively selective immune mediated injury of central nervous system (CNS) myelin and/or its cell of origin, the oligodendrocyte (OGC). Constituents of both the innate and adaptive immune systems are potential contributors to this process. Endogenous (microglia) and infiltrating (macrophages, dendritic cells) constituents of the innate immune system serve as sensors of events occurring within the CNS; their response to such events underlies the extent of their interaction (chemoattraction, antigen presentation) with the components of the adaptive immune system (alphabeta T cells, B cells) and ultimately the extent of the resultant inflammatory response. Constituents of both the innate and adaptive immune system can serve as effectors of tissue injury. The susceptibility of specific types of neural cells to injury further reflects the extent to which immune mediators modulate expression of crucial molecules (adhesion molecules, receptors) involved in effector-target interactions. Ongoing interactions between the constituents of the immune system themselves and between these constituents and neural cells are important determinants of disease recurrence and/or progression. Conversely, these interactions also impact on the mechanisms involved in target protection and repair.