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Titlebook: Mechanisms and Mediators of Neuropathic Pain; Annika B. Malmberg,Sandra R. Chaplan Book 2002 Birkhäuser Verlag 2002 Nervous System.adenosi

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Neuroinflammation, cytokines and neuropathic painhe nerve and importantly they reduce, but do not halt, blood flow through the epineurial vasculature. This model produces thermal hyperalgesia, mechanical allodynia and/or spontaneous pain of duration varying from one week to one month depending on the lab.
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Evaluation of neuropathic painitization that result in pain and tenderness in neighboring undamaged regions. Neuropathic pain is generally more difficult to treat than nociceptive pain. Clinicians typically treat all pains initially as nociceptive and only when these treatments fail do they ask the question, “Could the etiology be neuropathic?”
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Calcium channel antagonists for the treatment of painsible to use subtype-selective VDCC antagonists as antihypertensive and antiarrhythmic drugs, it may be possible to selectively modulate subytpes involved in painful sensations without unacceptable side effects.
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Glutamate receptor antagonists and neuropathic painvous system diseases, including acute excitotoxic neurodegeneration (e.g. cerebral ischaemia, stroke and brain injury), chronic excitotoxic neurodegeneration (e.g. dementia of the Alzheimer type, Parkinsonism and Huntington’s disease), epilepsy and psychiatric disorders (e.g. anxiety, depression and schizophrenia) [.].
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Antiepileptic drugs for treatment of neuropathic painry impairment and with the painful sensory phenomena of allodynia (pain from normally innocuous stimuli), hyperalgesia (exaggerated pain from normally painful stimuli) and hyperpathia (lack of sensation that can be accompanied by severe pain).
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Pre-clinical nerve ligation models: behavior and electrophysiologyat are likely associated with neuropathic pain. Determining the effect of various manipulations on behavioral endpoints provides a valuable tool to examine the potential mechanisms involved in neuropathic pain.
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