Central pain

Association of Pain, neuropathic pain is defined as pain initiated or caused by a primary lesion, dysfunction in the nervous system". Neuropathy can be divided broadly into peripheral and central neuropathic pain, depending on whether the primary lesion or dysfunction is situated in the peripheral or central nervous system. In the periphery, neuropathic pain can result from disease or inflammatory states that affect peripheral nerves (e.g. diabetes mellitus, herpes zoster, HIV) or alternatively due to neuroma formation (amputation, nerve transection), nerve compression (e.g. tumours, entrapment) or other injuries (e.g. nerve crush, trauma). Central pain syndromes, on the other hand, result from alterations in different regions of the brain or the spinal cord. Examples include tumour or trauma affecting particular CNS structures (e.g. brainstem and thalamus) or spinal cord injury. Both the symptoms and origins of neuropathic pain are extremely diverse. Due to this variability, neuropathic pain syndromes are often difficult to treat. Some of the clinical symptoms associated with this condition include spontaneous pain, tactile allodynia (touch-evoked pain), hyperalgesia (enhanced responses to a painful stimulus) and sensory deficits. 

Central pain Pain that results from a lesion or dysfunction in the central nervous system. 

None. I got used to it, in a way. But even though the giddiness subsided, the misery at my core—the central, painful joy—didn t... 

Pharmacology Although the mechanism of the antidepressant and central pain inhibitory action of duloxetine in humans is unknown, it is believed to be related to its potentiation of serotonergic and noradrenergic activity in the CNS. Preclinical studies have shown that duloxetine is a potent inhibitor of neuronal serotonin and norepinephrine reuptake and a less potent inhibitor of dopamine reuptake. 

In 1974, Liebeskind showed the existence of a central pain-suppressive system, and was able to produce analgesia by electrical stimulation of the periventricular gray matter within the brain. This electroanalgesia could be reversed by opiate antagonists, and showed a cross-tolerance with morphine-induced analgesia. These results indicated the existence of a neuronal system that uses an endogenous neuromodulator or neurotransmitter with opiate-like properties. 

In fact, carbamazepine is recommended as the drug of first choice in the treatment of trigeminal neuralgia. Results from clinical trials have been positive in the treatment of painful diabetic neuropathy (Rull et al., 1969 Wilton, 1974 Gomez-Perez et al., 1996). After 4 weeks treatment with carbamazepine, central pain after stroke was improved only in five out of 14 patients (Leijon and Boivie, 1989). Carbamazepine was found to be effective for migraine prophylaxis (Rompel and Bauermeister,... 

Yezierski, R.P., Liu, S., Ruenes, G.L., Kajander, K.J., Brewer, K.L. Excitotoxic spinal cord injury behavioral and morphological characteristics of a central pain model, Pain 1998, 75, 141-155. 

Bennett, A.D., Chastain, K.M., Hulsebosch, C.E. Alleviation of mechanical and thermal allodynia by CGRP(8-37) in a rodent model of chronic central pain, Pain 2000, 86, 163-175. 

Cellular assay Central pain Assay run on whole living cells. Pain associated with a lesion of the central nervous system. 

Max M. B. and Flagen N. A. (2000). Do changes in brain sodium channels cause central pain Neurology 54 544-545. 

Although angina pectoris is believed to be caused by the buildup of lactic acid and other metabolites, the exact mechanisms responsible for mediating anginal pain remain unknown. Also, the emotional state of the patient and other factors that influence central pain perception play an obvious role in angina pectoris.20,34 In fact, the majority of anginal attacks may be silent in many patients, and myocardial ischemia may ffe-... 

Sensory descending roof of trigeminal Extramedullary tumor (Central pain)... 

Peyron, R., Garcia-Larrea, L., Gregoire, M. C., Convers, P., Richard, A., Lavenne, F., Barral, F. G., Mauguiere, F., Michel, D., and Laurent, B. (2000). Parietal and cingulate processes in central pain. A combined positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) study of an unusual case. Pain 84, 77—87. 

A physiological role of Bv8-Prokineticins as peripheral and central pain modulators is supported by the observation that mice lacking the PKRs or PK2 are less sensitive to noxious stimuli than wild-type (WT) mice and exhibit impaired development of hyperalgesia after tissue injury (Hu et at, 2006 Negri et at, 2006a). 

In a randomized, double-blind, placebo-controlled, crossover trial the effect of the synthetic delta-9-tetrahy-drocannabinol dronabinol on central neuropathic pain was evaluated in 24 patients with multiple sclerosis (58). Oral dronabinol reduced central pain. Adverse events were reported by 96% of the patients compared with 46% during placebo treatment. They were more common during the first week of treatment. The most common adverse events during dronabinol treatment were dizziness (58%), tiredness (42%), headache (25%), myalgia (25%), and muscle weakness (13%). There was increased tolerance to the adverse effects over the course of treatment and with dosage adjustments. 

Svendsen KB, Jensen TS, Bach FW. Does the cannabinoid dronabinol reduce central pain in multiple sclerosis Randomised double blind placebo controlled crossover trial. BMJ 2004 329(7460) 253. 

These include postherpetic neuralgia, phantom limb pain, peripheral neuropathies of various causes, central pain, e.g. following a stroke, compression neuropathies, and the complex regional pain syndromes (comprising causalgia, when there is nerve damage, and reflex sympathetic dystrophy, when there is tissue but no nerve injury) they present the most challenging problems. 

Attal N, Gaude V, Brasseur L, Dupuy M, Guirimand F, Parker F, Bouhassira D. Intravenous lidocaine in central pain a double-bhnd, placebo-controUed, psychophysical study. Neurology 2000 54(3) 564-74. 

Mills CD, Johnson KM, Hulsebosch CE (2002) Group I metabotropic glutamate receptors in spinal cord injury roles in neuroprotection and the development of chronic central pain. J Neurotrauma 19 23-42... 

---