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 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cordotomy should be reserved for patients with intractable pain resistant to conservative treatment that is not of a dysaesthetic type. The high cervical percutaneous technique permits exploitation of the principles of stereotactic surgery, especially physiological localization of the lesion site. The induction by 100 Hz stimulation of a warm or cool tingling in some portion of the contralateral half of the body without muscle tetanization ensures location within the spinothalamic tract while attention to the somatotopographic organization of the responses permits a certain degree of tailoring of the extent of analgesia to the patient's needs. During 264 consecutive procedures the spinothalamic tract was successfully located in 99% with a 0.3% incidence of significant persistent paresis.
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PMID:Percutaneous cervical cordotomy. 14 48

Stimulation of human thalamus for pain relief: possible modulatory circuits revealed by positron emission tomography. J. Neurophysiol. 80: 3326-3330, 1998. Stimulation of the somatosensory thalamus was used for more than 2 decades to treat chronic pain in the human. However, despite clinical reports of successful results, little is known about the actual mechanisms mediating this form of stimulation-produced analgesia. To reveal possible neuronal pathways evoked by thalamic stimulation, we measured regional changes in cerebral blood flow (rCBF) in five patients who received successful long-term relief of chronic pain with somatosensory thalamic stimulation. Positron emission tomography during thalamic stimulation revealed significant activation of the thalamus in the region of the stimulating electrodes as well as activation of the insular cortex ipsilateral to the thalamic electrodes (contralateral to the patients' clinical pain). For these patients, thalamic stimulation also evoked paresthesiae that included thermal sensations in addition to tingling sensations. Results of this study indicate that in some cases somatosensory thalamic stimulation may activate a thalamocortical pain modulation circuit that involves thermal pathways. These results are consistent with other recent reports suggesting that activation of thermal pathways may contribute to modulation of nociceptive information.
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PMID:Stimulation of human thalamus for pain relief: possible modulatory circuits revealed by positron emission tomography. 986 26

We are proposing a unifying theory or law of pain, which states: the origin of all pain is inflammation and the inflammatory response. The biochemical mediators of inflammation include cytokines, neuropeptides, growth factors and neurotransmitters. Irrespective of the type of pain whether it is acute or chronic pain, peripheral or central pain, nociceptive or neuropathic pain, the underlying origin is inflammation and the inflammatory response. Activation of pain receptors, transmission and modulation of pain signals, neuro plasticity and central sensitization are all one continuum of inflammation and the inflammatory response. Irrespective of the characteristic of the pain, whether it is sharp, dull, aching, burning, stabbing, numbing or tingling, all pain arise from inflammation and the inflammatory response. We are proposing a re-classification and treatment of pain syndromes based upon their inflammatory profile. Treatment of pain syndromes should be based on these principles: 1. Determination of the inflammatory profile of the pain syndrome; 2. Inhibition or suppression of production of the appropriate inflammatory mediators, e.g. with inflammatory mediator blockers or surgical intervention where appropriate; 3. Inhibition or suppression of neuronal afferent and efferent (motor) transmission, e.g. with anti-seizure drugs or local anesthetic blocks; 4. Modulation of neuronal transmission, e.g. with opioid medication. At the L.A. Pain Clinic, we have successfully treated a variety of pain syndromes by utilizing these principles. This theory of the biochemical origin of pain is compatible with, inclusive of, and unifies existing theories and knowledge of the mechanism of pain including the gate control theory, and theories of pre-emptive analgesia, windup and central sensitization.
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PMID:The biochemical origin of pain--proposing a new law of pain: the origin of all pain is inflammation and the inflammatory response. Part 1 of 3--a unifying law of pain. 1724 81

Paraparesis after epidural catheterization is rare but may be multifactorial. We report a case of temporary paraparesis in a 32-year-old female patient after thoracic epidural catheterization performed analgesia. A 16 G epidural needle was introduced at the T(7)-T(8) interspace but as frank blood came through, it was withdrawn and was reinserted at the T(8)-T(9) interspace. An 18 G epidural catheter was introduced and 10 ml of 0.125% bupivacaine with buprenorphine 150 mcg was given. Further top-ups were given for 48 h on complain of pain. There was an episode of hypotension after giving the epidural drug but later on the patient remained haemodynamically stable. On the fourth post-operative day, the patient reported paraparesis with heaviness and tingling sensation in both lower extremities. MRI was normal with no evidence of spinal cord compression, oedema, haematoma or abscess. The patient improved gradually within a period of 3 days. The possible causes of delayed onset of neurological symptoms are discussed.
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PMID:Thoracic epidural catheterization leading to delayed transient neurological symptoms with normal imaging findings. 1912 26

LI.4 is a major acupoint but the method of locating it has not been standardized. In fact, description of method for locating this acupoint often varies in the classic and traditional texts. It might signify this point may be varied from one to another person. Our comparative study of locating and subsequent acupuncturing these locations revealed some interesting features of LI.4 from our collected clinical data in that location 1 had a better therapeutic effect for toothache relief and analgesia-anesthesia effect than for headache relief, location 2 was better for headache than toothache relief; locations 3 and 4 had a mixed effect whereas, location 5 seems to have a better chance to get bioenergy (De Qi) as manifested by tingling and numbing sensation at the acupunctured site. Our study also suggested that LI.4 location was about the size of 4 millimeters in diameter instead of a pin-point location, though needle inserted at correct point produced a better result.
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PMID:Comparing the clinical effect of five varying locations of LI.4 acupoint. 1930 24

The traumatic lesions during surgical interventions often turn into a persistent pain. Pain persists in the location of surgical intervention for a long time, beyond the usual course of natural healing of an acute pain and it is different from that suffered preoperatively. It is usually a chronic pain and it is associated to lesions of the central or peripheral nervous system. Pain is usually described as burning or tingling, or electric shock-like; it can be continuous or parossistic, often associated to paraesthesia, iperalgesia and allodinya. If circumstances preclude the surgical revision, the treatment of post-surgical neuropathic pain is based on drugs, according to the guidelines. The drugs of choice are the tricyclic antidepressants, the serotonin and adrenaline re-uptake selective inhibitors (SSRI), local antiepileptics of new generation (gabapentin, pregabalin) and topical anaesthetics. Drugs of second line are: opioid analgesics, tramadol; drugs of third line are: mexiletine, antagonist of NMDA receptor and capsaicine. The post-surgical neuropathic pain is often resistant to the pharmacologic treatment; for this reason the spinal cord neuromodulation can be applied only after careful selection of the patients according to the international guidelines. The incidence of post-surgical neuropathic pain in the Pain Units is approximately 20% of the patients admitted to hospital. Therefore it is necessary a greater attention for the post-surgical analgesia, adopting appropriate surgical techniques in order to avoid the onset of the post-surgical neuropathic pain.
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PMID:[Post-surgical neuropathic pain]. 1972 79

Significant fetal bradycardia occurred when a parturient receiving labor epidural analgesia experienced generalized numbness and tingling, a metallic taste and hot flushes. An emergent cesarean delivery under general anesthesia was performed with favorable outcomes for the mother and baby. The most likely source of the maternal symptoms was spiramycin, which was being administered for treatment of toxoplasmosis.
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PMID:Side effects of spiramycin masquerading as local anesthetic toxicity during labor epidural analgesia. 2062 89

Chronic neuropathic pain, resulting from damage to the central or peripheral nervous system, is a prevalent and debilitating condition, affecting 7-18% of the population(1,2). Symptoms include spontaneous (tingling, burning, electric-shock like) pain, dysaesthesia, paraesthesia, allodynia (pain resulting from normally non-painful stimuli) and hyperalgesia (an increased response to painful stimuli). The sensory symptoms are co-morbid with behavioural disabilities, such as insomnia and depression. To study chronic neuropathic pain several animal models mimicking peripheral nerve injury have been developed, one of the most widely used is Bennett and Xie's (1988) unilateral sciatic nerve chronic constriction injury (CCI)(3) (Figure 1). Here we present a method for performing CCI and testing pain hypersensitivity. CCI is performed under anaesthesia, with the sciatic nerve on one side exposed by making a skin incision, and cutting through the connective tissue between the gluteus superficialis and biceps femoris muscles. Four chromic gut ligatures are tied loosely around the sciatic nerve at 1 mm intervals, to just occlude but not arrest epineural blood flow. The wound is closed with sutures in the muscle and staples in the skin. The animal is then allowed to recover from surgery for 24 hrs before pain hypersensitivity testing begins. For behavioural testing, rats are placed into the testing apparatus and are allowed to habituate to the testing procedure. The area tested is the mid-plantar surface of the hindpaw (Figure 2), which falls within the sciatic nerve distribution. Mechanical withdrawal threshold is assessed by mechanically stimulating both injured and uninjured hindpaws using an electronic dynamic plantar von Frey aesthesiometer or manual von Frey hairs(4). The mechanical withdrawal threshold is the maximum pressure exerted (in grams) that triggers paw withdrawal. For measurement of thermal withdrawal latency, first described by Hargreaves et al (1988), the hindpaw is exposed to a beam of radiant heat through a transparent glass surface using a plantar analgesia meter(5,6). The withdrawal latency to the heat stimulus is recorded as the time for paw withdrawal in both injured and uninjured hindpaws. Following CCI, mechanical withdrawal threshold, as well as thermal withdrawal latency in the injured paw are both significantly reduced, compared to baseline measurements and the uninjured paw (Figure 3). The CCI model of peripheral nerve injury combined with pain hypersensitivity testing provides a model system to investigate the effectiveness of potential therapeutic agents to modify chronic neuropathic pain. In our laboratory, we utilise CCI alongside thermal and mechanical sensitivity of the hindpaws to investigate the role of neuro-immune interactions in the pathogenesis and treatment of neuropathic pain.
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PMID:Chronic constriction of the sciatic nerve and pain hypersensitivity testing in rats. 2243 11

Capsaicin 8% patch (Qutenza) is mainly used to treat postherpetic neuralgia and human immunodeficiency virus-associated neuropathy. However, evidence of the efficacy of Qutenza in other forms of neuropathic pain is lacking. A 24-year old Libyan man, with no previous medical history, sustained multiple wounds in the right side of the chest and back after a bomb explosion. The patient experienced pain, which persisted in a wide location around the surgical intervention for a long time, beyond the usual course of natural healing of an acute pain and was different from that suffered preoperatively. The characteristics of the pain included burning, electric shock-like sensation, tingling, and numbness, and it was paroxysmal. The pain was associated with hyperalgesia and intense allodynia in a wide area, approximately of 1,100 cm2. Our initial treatment strategy included pregabalin, tramadol, and duloxetine. However, our patient's pain responded to treatment with capsaicin 8% patch when the initial treatments showed only minimal effectiveness regarding the intensity of pain. Interestingly, the most important finding was that capsaicin 8% patch showed a more than 80% reduction of the area of allodynia associated with the pain, when other treatments failed. Moreover, although recent data showed that in patients who respond to Qutenza, analgesia starts within a few days of treatment and lasts on average 5 months, our patient showed an initial response within 7 days of treatment but a longer duration of more than 18 months. Although further controlled studies are needed to explore the efficacy of the capsaicin 8% patch in patients who experience posttraumatic neuropathic pain, we encourage clinicians to try the capsaicin 8% patch when alternative treatments fail.
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PMID:Posttraumatic and postsurgical neuropathic pain responsive to treatment with capsaicin 8% topical patch. 2465 88

Subarachnoid block with local anaesthetic agent and opiod as an adjuvant is a well-known technique with a good record of safety. However, some rare neurological complications like aphonia, dysphagia and tingling sensation have been reported following their administration in pregnant females posted for labour analgesia or caesarean section. We report a case of transient aphonia, aphagia and facial tingling following intrathecal administration of bupivacaine along with fentanyl for lower limb wound debridement in a male patient.
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PMID:Transient aphonia, aphagia and facial tingling following intrathecal administration of fentanyl. 2588 13


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