Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vagus nerve stimulation (VNS) inhibits nociceptive behavior in animals. VNS might reduce pain in patients with VNS device implanted for intractable seizures. One case report described possible benefits on migraines. We contacted all patients who received VNS therapy for intractable epilepsy between 1993 and 1999 at Southern Illinois University, Springfield, Illinois. Patients who had concomitant chronic pain were subsequently interviewed. Pain intensity before and after VNS implantation was rated by the patient as average, worst, and least and on numeric rating scale from 1 to 10. Current pain measurements were compared to preimplantation by using Global Pain Relief Rating Scale. Of 62 patients who received VNS, 27 patients were interviewed; 4 patients had common migraine, and no other chronic pain syndromes were identified. All patients with migraine reported reductions in headache frequency and numeric rating scale score for average and least headache intensity. One patient reported complete relief of headaches. Improvement was reported to start 1 to 3 months after initiation of therapy. On Global Pain Relief Rating Scale, 1 patient reported complete pain relief, 2 reported a lot of pain relief, and 1 reported slight pain relief. Concomitant antiepileptic drugs were decreased in 3 patients and slightly increased in 1. VNS might be beneficial for prophylactic therapy of migraine.
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PMID:The effect of vagus nerve stimulation on migraines. 1504 23

A 47-year-old woman was diagnosed with secondary progressive multiple sclerosis, and was treated with intrathecal morphine for chronic pain via a slow-release subcutaneous pump. She accidentally received a 35-ml (510 mg) bolus injection of morphine by this route, which led to status epilepticus. She was treated with continuous intravenous naloxone infusion, and with medication to control hypertension and stop the seizure activity. The outcome was excellent, and the patient returned to her neurological baseline. This report describes the complications and the successful treatment of intrathecal morphine overdose. In order to prevent these serious errors, it is vital that only care providers who are proficient with these devices perform the refilling procedure.
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PMID:Successful treatment of intrathecal morphine overdose. 1465 57

Three cases are presented in which electroconvulsive therapy (ECT) for depression led to the relief of comorbid complex regional pain syndrome as well as depression. In one of the cases, concomitant fibromyalgia was not relieved during 2 separate series of ECT. The literature regarding the role of ECT in the management of chronic pain is reviewed and discussed in light of recent findings about ECT and changes in neurotransmission associated with seizures.
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PMID:Electroconvulsive therapy in complex regional pain syndromes. 1465 76

In contrast with acquired pain syndromes, molecular substrates for hereditary pain disorders have been poorly understood. Familial erythromelalgia (Weir Mitchell's disease), also known as primary erythermalgia, is an autosomal dominant disorder characterized by burning pain in the extremities in response to warm stimuli or moderate exercise. The cause of this disorder has been enigmatic, and treatment has been empirical and not very effective. Recent studies, however, have shown that familial erythromelalgia is a channelopathy caused by mutations in the gene encoding the Na(v)1.7 sodium channel which lead to altered channel function. Selective expression of Na(v)1.7 within dorsal root ganglion neurons including nociceptors (in which this channel is targeted to sensory terminals, close to impulse trigger zones) and within sympathetic ganglion neurons explains why patients experience pain but do not suffer from seizures or other manifestations of altered excitability within central nervous system neurons. Erythromelalgia is the first human disorder in which it has been possible to associate an ion channel mutation with chronic neuropathic pain. Identification of mutations within a peripheral neuron-specific sodium channel suggests the possibility of rational therapies that target the affected channel. Moreover, because some other pain syndromes, including acquired disorders, involve altered sodium channel function, erythromelalgia may emerge as a model disease that holds more general lessons about the molecular neurobiology of chronic pain.
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PMID:Erythromelalgia: a hereditary pain syndrome enters the molecular era. 1592 46

The use of functional stereotactic neurosurgery is increasing for treatment of patients with movement disorders and other chronic illnesses. The anesthetic considerations include the influence of the anesthetic agents on the microelectrode recordings and stimulation testing of an awake patient. The purpose of this study was to review the anesthetic management and incidences of intraoperative complications during functional neurosurgery in our institution. One hundred seventy-eight patients underwent an ablative procedure (n = 6) or the insertion of deep brain stimulator (n = 172) under monitored anesthesia care for movement disorders (n = 124), chronic pain (n = 20), and other procedures (n = 34). Local anesthetic was used for head frame pin sites and burr holes. No sedation/analgesia was administered to 57 (32%) patients. One patient required conscious sedation and another general anesthesia for the entire procedure. The remainder received small increments (mean +/- SD) of propofol (113 +/- 73 mg), midazolam (1.6 +/- 0.8 mg), and/or fentanyl (93 +/- 55 mug). Intraoperative complications that occurred in 16% of the patients included seizures (n = 8), change in neurologic status (n = 5), airway obstruction (n = 2), and hypertension (n = 7). Functional neurosurgery can be performed with minimal anesthesia in many patients. Awareness and vigilance can improve the identification and early treatment of intraoperative complications such as seizures, loss of airway, and changes in the neurologic status.
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PMID:Anesthesia for functional neurosurgery: review of complications. 1636 42

Repetitive transcranial magnetic stimulation (rTMS) has been used as a potential therapeutic tool in various neurological and psychiatric diseases including depression, Parkinson disease, spinocerebellar degeneration, epilepsy, urinary incontinence, movement disorders, chronic pain, migraine and chronic tinnitus, etc. Several reports showed the therapeutic effects of rTMS as a treatment of depression and Parkinson disease (PD), whereas others found no significant effects. It is by now not yet fully understood whether rTMS has a therapeutic effect on those diseases. The controversy arises from the differences of the stimulation parameters and evaluation methods of the effects in those studies. The Japanese multi-center, double blinded, sham stimulation controlled trial in 85 patients with PD showed an efficacy in both the rTMS-treated and sham stimulated patients. This result does not prove the efficacy of the rTMS in PD; on the other hand, it does not rule out the efficacy. Possible mechanism of favorable effects of rTMS is related to increasing the release of dopamine in the mesolimbic and mesostriatal system. The other Japanese multi-center, double blinded, sham stimulation controlled trial in 99 patients with spinocerebellar degeneration revealed significant therapeutic effects of rTMS in 51 patients with SCA6. We studied the effects of rTMS on seizure susceptibility in rats which prevented the development of status epilepticus of pentylenetetrazol-induced convulsions. This finding suggests the possibility of therapeutic use of rTMS in epilepsy. Further studies should be performed aiming to reveal the optimal stimulation parameters, and are necessary to reveal the therapeutic role of the rTMS in neurological and psychiatric diseases.
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PMID:[Clinical applications of transcranial magnetic stimulation for the treatment of various neurological diseases]. 1644 38

In 1991 Tsubokawa and colleagues first published their landmark results from a series in which epidural motor cortex stimulation (MCS) was used in the treatment of eight patients with central and neuropathic pain. In ensuing studies authors have elaborated on the indications, technique, hypotheical mechanisms, and beneficial results of this treatment. Epidural MCS is effective for trigeminal neuropathy, lateral medullary and thalamic infarction, anesthesia dolorosa, postherpetic neuralgia, spinal cord injury, and limb stump pain. Postoperative outcomes are better when patients present with only mild or absent motor weakness in the region of pain and when there is pain in the trigeminal region. It is hypothesized that MCS is effective because it increases regional cerebral blood flow in the ipsilateral ventrolateral thalamus in which corticothalamic connections from the motor and premotor areas predominate. The extent of pain alleviation also correlates with the increase of blood flow in the cingulate gyrus. This suggests that stimulation reduces the suffering experienced by a patient with chronic pain. Procedure-related morbidity has included epidural hematoma, subdural effusion, gradual diminution of benefit, and painful stimulation. Although of concern, treatment-induced chronic seizure disorders have not occurred as a complication or in animal models of chronic cortical stimulation. Stimulation-induced pain relief occurs within minutes. There are no associated paresthesias or muscle contractions that confirm function. Pain relief may last for hours after electrical stimulation is discontinued. Motor cortex stimulation is an established therapy for the treatment of complex central and neuropathic pain syndromes that have proved refractory to medical treatment.
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PMID:Motor cortex stimulation. 1651 25

Accidental induction of convulsions by using repetitive transcranial magnetic stimulation (rTMS) has been reported to have occurred in 6 normal voluntary subjects, in 1 patient with depression and in 1 patient who had temporal lobe epilepsy, with secondary generalization. In addition, 3 other cases have been published relating its use with seizure induction and in 1 case, using 1-Hz stimulation. In this paper, we report a patient who was participating in a protocol for the use of rTMS in chronic pain, with stimulation in the motor cortex, who developed a generalized seizure in the fifth application. Intertrain interval was within safety guidelines, but the combination of 10 Hz for 10 seconds was excessive and must be considered the main cause for the episode. No further complication has been noted after she was withdrawn from the study protocol.
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PMID:Accidental seizure with repetitive transcranial magnetic stimulation. 1714 58

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

Chronic pain states and epilepsies are common therapeutic targets of voltage-gated sodium channel blockers. Inhibition of sodium channels results in central muscle relaxant activity as well. Selective serotonin reuptake inhibitors are also applied in the treatment of pain syndromes. Here, we investigate the pharmacodynamic interaction between these two types of drugs on spinal neurotransmission in vitro and in vivo. Furthermore, the ability of serotonin reuptake inhibitors to modulate the anticonvulsant and windup inhibitory actions and motor side effect of the sodium channel blocker lamotrigine was investigated. In the hemisected spinal cord model, we found that serotonin reuptake inhibitors increased the reflex inhibitory action of sodium channel blockers. The interaction was clearly more than additive. The potentiation was prevented by blocking 5-HT(2) receptors and PKC, and mimicked by activation of these targets by selective pharmacological tools, suggesting the involvement of 5-HT(2) receptors and PKC in the modulation of sodium channel function. The increase of sodium current blocking potency of lamotrigine by PKC activation was also demonstrated at cellular level, using the whole-cell patch clamp method. Similar synergism was found in vivo, in spinal reflex, windup, and maximal electroshock seizure models, but not in the rotarod test, which indicate enhanced muscle relaxant, anticonvulsant and analgesic activities with improved side effect profile. Our findings are in agreement with clinical observations suggesting that sodium channel blocking drugs, such as lamotrigine, can be advantageously combined with selective serotonin reuptake inhibitors in some therapeutic fields, and may help to understand the molecular mechanisms underlying the interaction.
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PMID:Concerted action of antiepileptic and antidepressant agents to depress spinal neurotransmission: Possible use in the therapy of spasticity and chronic pain. 1728 Jul 40


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