• Physical Therapy Korea
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• v.5 no.2
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• pp.106-117
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• 1998

The pain is common among individuals with physical disabilities. It can interfere with therapy since patients with pain can become uncooperative and reluctant to move. This paper reviews the natural physiological mechanisms that can reduce pain perception, and considers physiological mechanisms which contribute to clinical pain by describing how the pain system changes its sensitivity depending upon the body's needs. The peripheral and central mechanisms contributing to sensitised nociceptive system are described with reference to the symptoms of clinical pain such as hyperalgesia, allodynia sopntaneous 'on-going'-projected and referred pain. It is suggested that in some chronic pain the nociceptive system maintains a state of sensitivity despite the absence of on-going tissue damage and under such circumstances the nociceptive system itself may have become dysfunctional. Such situations are often initiated by damage to nervous tissue which results in changes in the activity and organization of neuronal circuits within the central nervous system. The ability of the nociceptive system to operate in a suppressed state is also discussed with reference to pain modulation. The physical therapist can help facilitate the activation of these mechanisms through a combination of noninvasive modalities, functional activities, and the therapeutic use of self.

• Proceedings of the PSK Conference
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• 2003.10a
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• pp.106-107
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• 2003

tIn brain ischemic insult, inflammatory cells such as macrophages and lymphocytes are chemo-attracted into the brain lesion and release cytokines, resulting in an activation of microglia that are functionally equivalent to peripheral macrophages in the central nervous system. In cerebral ischemic insults, activated inflammatory cells such as microglia and macrophages may be implicated in the pattern and degree of ischemic injury by producing various bioactive mediators. (omitted)

• Annals of Clinical Neurophysiology
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• v.21 no.1
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• pp.66-69
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• 2019

Orthostatic hypotension (OH) is commonly associated with autonomic failure in the peripheral nervous system. Less often it is related to central lesions in brainstem and cerebellum. We describe a patient with OH associated with tuberculosis meningoencephalitis involving the brainstem including rostral ventrolateral medulla. This is the first case of OH resulting from focal lesions in the dorsal medulla in a patient with meningoencephalitis.

• Annals of Clinical Neurophysiology
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• v.23 no.2
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• pp.134-137
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• 2021

Primary hyperparathyroidism (PHP) is a disease in which excessive amounts of parathyroid hormone (PTH) are secreted and calcium levels in the blood increase. Hypercalcemia caused by PHP has a major influence on the peripheral nervous system and produces symptoms such as muscle cramps, paresthesia, and proximal muscle weakness. Here we report a rare case of sensory-dominant polyneuropathy caused by PHP, which improved after surgery.

• Journal of Korean Clinical Nursing Research
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• v.19 no.2
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• pp.298-308
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• 2013

Purpose: The purpose of this study was to identify factors influencing chemotherapy-induced peripheral neuropathy among colorectal cancer patients receiving oxaliplatin. Methods: A total of 132 patients hospitalized for chemotherapy were surveyed at K University Hospital in Seoul, Korea. This study was a descriptive causal relationship study using a self-report questionnaire survey method. Correlation and multiple regression analysis between the factors were performed using SPSS 18.0. Results: The regression model was significant (F=31.64, p<.001), which meaned that the experience of chemotherapy-induced peripheral neuropathy among the participants was statistically significant. The factors influencing the chemotherapy-induced peripheral neuropathy were depression (${\beta}=.34$, p<.001), followed by anxiety (${\beta}=.32$, p<.001), medical staff support (${\beta}=-.17$, p=.037) and the level of knowledge of anticancer drugs (${\beta}=-.16$, p=.045). The explanatory power of these factors on the chemotherapy-induced peripheral neuropathy of colorectal cancer patients was 69%. Conclusion: The factors influencing the chemotherapy-induced peripheral neuropathy of colorectal cancer patients receiving oxaliplatin were identified as depression, anxiety, level of knowledge of anticancer drugs and medical staff support.

• The Korean Journal of Physiology
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• v.17 no.2
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• pp.169-176
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• 1983

It is well known that the acupuncture has been used effectively for the relief of certain types of pain. Although the precise mechanism of action of acupuncture analgesia is unknown, it is generally accepted that their analgesic properties are related to the activation of endogenous opiate system in central nervous system. And it is suggested that pain-relieving properties of acupunture may be related to a stimulation of peripheral nerve underlying the acupuncture point on the skin. However, the efficacy of acupuncture has no relationship between the site of pain and the acupuncture point. Consequently, the present study was undertaken to investigate electroacupuncture analgesia in relation to the site of peripheral nerve stimulation. Cats were decerebrated ischemically and the flexion reflex as an index of pain was elicited by stimulating the sural nerve (20V, 0.5 msec duration) and recored as a compound action potential from the nerve innervated to the posterior biceps femoris muscle in the ipsilateral hindlimb. Bilateral common peroneal nerve and contralateral superficial radial nerve were selected as the site of peripheral nerve stimulation. For the stimulation of peripheral nerve, a stimulus of 20 V intensity, 2 msec-duration and 2 Hz-frequency was applied for 60 min respectively. The results obtained are summarized as follows: 1) Both stimulation of contralateral common peronal nerve and contralateral superficial radial nerve did not change the flexion reflex and there were no significant differences between them. 2) Stimulation of ipsilateral common peroneal nerve markedly depress the flexion reflex, the effect being reversed by naloxone application. These results suggest that stimulation of ipsilateral common peroneal nerve has the analgesic effect but both stimulation of contralteral common peroneal nerve and contralateral superficial radial nerve to the pain site where flexion reflex was elicited have no analgesic effect.

• IMMUNE NETWORK
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• v.12 no.2
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• pp.41-47
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• 2012

Contemporary studies illustrate that peripheral injuries activate glial components of the peripheral and central cellular circuitry. The subsequent release of glial stressors or activating signals contributes to neuropathic pain and neuroinflammation. Recent studies document the importance of glia in the development and persistence of neuropathic pain and neuroinflammation as a connecting link, thereby focusing attention on the glial pathology as the general underlying factor in essentially all age-related neurodegenerative diseases. There is wide agreement that excessive glial activation is a key process in nervous system disorders involving the release of strong pro-inflammatory cytokines, which can trigger worsening of multiple disease states. This review will briefly discuss the recent findings that have shed light on the molecular and cellular mechanisms of glia as a connecting link between neuropathic pain and neuroinflammation.

• The Journal of the Korean dental association
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• v.49 no.6
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• pp.321-326
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• 2011

Neuropathic pain is caused by functional abnonnalities of structural lesions in the peripheral or central nervous system, and occurs without peripheral nociceptor stimulation. Trigeminal neuropathy always pose differential location difficulties as multiple diseases are capablc of producing them: they can be the result of traumatism, tumors, or diseases of the connective tissue, infectious or demyelinating diseases, or may be of idiopathic origin. There are a number of mechanisms described as causing neuropathy. They can be described as ectopic nerve activity, neuroma, ephatic trasmission, change of sodium channel expression, sympathetic activity, central sensitization, and alteration in central inhibition systems. More than I mechanism may be active to create individual clinical presentations. In order to provide better pain control, the mechanism-based approach in treating neuropathic pain should be familiar to physicians.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.34 no.2
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• pp.200-206
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• 2008

A variety of mechanisms may generate pain resulting from injury to the peripheral nervous system. None of these mechanisms is disease-specific, and several different pain mechanisms may be present simultaneously in any one patient. Diagnosis of neuropathic pain is often easily made from the information gathered on neurologic examination and from patient history. Evidence of sensory disturbances elicited by examination combined with laboratory tests confirming injury to peripheral nerve establishes the diagnosis of neuropathic pain. Although treatment of neuropathic pain may be difficult, optimum treatment can be achieved if dentist has a complete understanding of the therapeutic options. Pharmacologic therapy has been the mainstay of treatment. Selection of an appropriate pharmacologic agent is by trial and error since individual response to different agents, doses, and serum level are highly variable. An adequate trial for each agent tried is key to pharmacologic treatment of neuripathic pain. If pharmacologic treatment is not effective, nerve block using lidocaine, steroid and alcohol and neurectomy must be considered for treatment option.

• BMB Reports
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• v.42 no.8
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• pp.475-481
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• 2009

Emerging data demonstrate pivotal roles for brain insulin resistance and insulin deficiency as mediators of cognitive impairment and neurodegeneration, particularly Alzheimer's disease (AD). Insulin and insulin-like growth factors (IGFs) regulate neuronal survival, energy metabolism, and plasticity, which are required for learning and memory. Hence, endogenous brain-specific impairments in insulin and IGF signaling account for the majority of AD-associated abnormalities. However, a second major mechanism of cognitive impairment has been linked to obesity and Type 2 diabetes (T2DM). Human and experimental animal studies revealed that neurodegeneration associated with peripheral insulin resistance is likely effectuated via a liver-brain axis whereby toxic lipids, including ceramides, cross the blood brain barrier and cause brain insulin resistance, oxidative stress, neuro-inflammation, and cell death. In essence, there are dual mechanisms of brain insulin resistance leading to AD-type neurodegeneration: one mediated by endogenous, CNS factors; and the other, peripheral insulin resistance with excess cytotoxic ceramide production.