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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cannabis sativa L. is possibly one of the oldest plants cultivated by man, but has remained a source of controversy throughout its history. Whether pariah or panacea, this most versatile botanical has provided a mirror to medicine and has pointed the way in the last two decades toward a host of medical challenges from analgesia to weight loss through the discovery of its myriad biochemical attributes and the endocannabinoid system wherein many of its components operate. This study surveys the history of cannabis, its genetics and preparations. A review of cannabis usage in Ancient Egypt will serve as an archetype, while examining first mentions from various Old World cultures and their pertinence for contemporary scientific investigation. Cannabis historians of the past have provided promising clues to potential treatments for a wide array of currently puzzling medical syndromes including chronic pain, spasticity, cancer, seizure disorders, nausea, anorexia, and infectious disease that remain challenges for 21st century medicine. Information gleaned from the history of cannabis administration in its various forms may provide useful points of departure for research into novel delivery techniques and standardization of cannabis-based medicines that will allow their prescription for treatment of these intractable medical conditions.
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PMID:History of cannabis and its preparations in saga, science, and sobriquet. 1771 11

Nociceptive pain and its emotional component can result in the development of a "chronic pain memory". This report describes two patients who had long histories of chronic pain and opioid dependence. Both patients experienced sudden memory loss that was followed by significant pain reduction and an eradication of their need for opioid management. Neural centers involved in sensory pain, its affective component, opioid dependence, and memory overlap in the brain and share common pathways. The anterior cingulate cortex, the insular cortex, and the amygdala are examples of regions implicated in both pain and memory. One of the patients in the report experienced multiple seizure episodes, which may have contributed to memory loss and pain relief. The role of electroconvulsive therapy as it relates to amnesia and pain is reviewed. Questions are raised regarding whether therapies that address the memory component of pain may have a role in the treatment of long-term chronic pain patients.
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PMID:Sudden amnesia resulting in pain relief: the relationship between memory and pain. 1782 47

Adenosine is a modulator of brain function uniquely positioned to integrate excitatory and inhibitory neurotransmission. The past few years brought a wealth of new data fostering our understanding of how the adenosine system is involved in the pathogenesis of neurological diseases. Thus, dysregulation of the adenosine system is implicated in epileptogenesis and cell therapies have been developed to locally augment adenosine in an approach to prevent seizures. While activation of inhibitory adenosine A(1) receptors is beneficial in epilepsy, chronic pain and cerebral ischemia, inhibition of facilitatory A(2A) receptors has profound neuroprotective effects, which are currently exploited in clinical trials in Parkinson's disease. A new era of adenosine-based therapies has begun, with the prospect to cover a wide range of neurological diseases.
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PMID:Adenosine as a neuromodulator in neurological diseases. 1794 68

Etoricoxib is presently the most commonly prescribed cyclooxygenase-2 (Cox-2) inhibitor for chronic pain and inflammatory conditions. In clinical practice, phenytoin and etoricoxib are used in chronic conditions of generalized seizure with concomitant chronic pain. Hence, there are chances of drug-drug interaction because modulations of isoenzymes involved in metabolism CYP2C9/10 and CYP2C19 which partially inhibited by etoricoxib. It is important to maintain the therapeutic level of phenytoin in plasma for effective control of seizure. So, the aim of the study was to determine the effect of etoricoxib on the pharmacokinetics of phenytoin in rabbits. In a parallel design study, phenytoin (30 mg/kg/day) was given daily for seven days. On day 7, blood samples were taken at various time intervals between 0-24 h. In etoricoxib group, phenytoin was administered for seven days as above. On day 8, etoricoxib (5.6 mg/kg) along with phenytoin (30 mg/kg/day) was administered and blood samples were drawn as above. Plasma phenytoin levels were assayed by HPLC and pharmacokinetic parameters were calculated. In etoricoxib group, there was a decrease in t(1/2)a phenytoin and t(1/2)el decreased significantly as compared to phenytoin group. Significant changes were observed in the pharmacokinetic parameters in etoricoxib-treated group. These results suggest that etoricoxib alters the pharmacokinetics of phenytoin. Confirmation of these results in human studies will warrant changes in phenytoin dose or frequency when etoricoxib is co-administered with it.
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PMID:Effects of etoricoxib on the pharmacokinetics of phenytoin. 1844 85

Myoclonus is a well-known side effect of anticonvulsant drugs. Pregabalin is one of the newer drugs approved for the treatment of focal epilepsies. Frequently it is also used to treat chronic pain syndromes. We describe a patient who, after receiving his first dose of pregabalin to relieve neuropathic pain, presented with a negative myoclonus. Clinical aspects and electrophysiological data such as polygraphic studies, electroencephalography, and measurement of somatosensory evoked potentials support the cortical origin of negative myoclonus. Our findings reveal that even in patients without a history of seizures, pregabalin can cause a cortical negative myoclonus.
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PMID:Pregabalin-induced cortical negative myoclonus in a patient with neuropathic pain. 1849 17

Over the past decade, the importance of acceptance of chronic pain has been demonstrated. Acceptance has often been assessed using the 20-item, two-factor Chronic Pain Acceptance Questionnaire (CPAQ; McCracken, Vowles, Eccleston, Pain 2004;107:159-66). This two-factor model has been supported but awaits further confirmation. The present investigation sought to address this issue in two large samples of pain suffers. Exploratory factor analyses (N=333) examined a number of solutions, ranging from two to five factors. Evaluation indices provided clear support for a 20-item, two-factor solution. Confirmatory factor analyses, using the second sample (N=308), examined a number of models. Fit indices demonstrated that the model identified in the exploratory analyses had the best fit. Finally, a series of cluster analyses were performed using a combined sample (N=641). Results indicated three clusters: one with high scores on both subscales (n=146), one with low scores on both subscales (n=239), and one with discrepant scores that were high on the Activity Engagement subscale and low on the Pain Willingness subscale (n=286). Follow-up analyses indicated significant differences among the clusters across multiple measures of functioning. The cluster with low CPAQ scores reported more difficulties in comparison to the group with high scores, while the group with discrepant CPAQ scores generally reported difficulties that fell in between. These results provide further support for the 20-item, two-factor CPAQ and indicate that it is both theoretically and practically useful.
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PMID:The Chronic Pain Acceptance Questionnaire: confirmatory factor analysis and identification of patient subgroups. 1882 1

Studies of genetic forms of epilepsy, chronic pain, and migraine caused by mutations in ion channels have given crucial insights into molecular mechanisms, pathogenesis, and therapeutic approaches to complex neurological disorders. Gain-of-function missense mutations in the brain type-I sodium channel Na(V)1.1 are a primary cause of generalized epilepsy with febrile seizures plus. Loss-of-function mutations in Na(V)1.1 channels cause severe myoclonic epilepsy of infancy, an intractable childhood epilepsy. Studies of a mouse model show that this disease is caused by selective loss of sodium current and excitability of GABAergic inhibitory interneurons, which leads to hyperexcitability, epilepsy, and ataxia. Mutations in the peripheral sodium channel Na(V)1.7 cause familial pain syndromes. Gain-of-function mutations cause erythromelalgia and paroxysmal extreme pain disorder as a result of hyperexcitability of sensory neurons, whereas loss-of-function mutations cause congenital indifference to pain because of attenuation of action potential firing. These experiments have defined correlations between genotype and phenotype in chronic pain diseases and focused attention on Na(V)1.7 as a therapeutic target. Familial hemiplegic migraine is caused by mutations in the calcium channel, Ca(V)2.1, which conducts P/Q-type calcium currents that initiate neurotransmitter release. These mutations increase activation at negative membrane potentials and increase evoked neurotransmitter release at cortical glutamatergic synapses. Studies of a mouse genetic model show that these gain-of-function effects lead to cortical spreading depression, aura, and potentially migraine. Overall, these experiments indicate that imbalance in the activity of excitatory and inhibitory neurons is an important underlying cause of these diseases.
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PMID:Inherited neuronal ion channelopathies: new windows on complex neurological diseases. 1900 38

Fibromyalgia (FM) is a common, chronic pain disorder with unknown etiology, characterized by widespread musculoskeletal pain and tenderness, and accompanied by several other symptoms such as sleep disturbance, fatigue, and mood disorders. Pregabalin is the first drug approved for the treatment of FM. Pregabalin has analgesic, anticonvulsant, and anxiolytic activity and has earlier demonstrated efficacy in the management of neuropathic pain associated with diabetic peripheral neuropathy, postherpetic neuralgia, and as adjuvant therapy for adult patients with partial onset seizures. Pregabalin, a lipophilic gamma-aminobutyric acid (GABA) analog, is alpha(2)delta-1 ligand that binds to, and modulates, voltage-gated calcium channels. This modulation is characterized by a reduction of the excessive neurotransmitter release that is observed in certain neurological and psychotic disorders. Several randomized, double-blind, placebo-controlled studies have demonstrated that pregabalin has been effective in pain management, improving sleep quality and fatigue, as well as in several domains of health related quality of life. Because of mild to moderate adverse effects it can be considered a well-tolerated therapy for FM.
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PMID:New treatment options in the management of fibromyalgia: role of pregabalin. 1933 59

The measurement of pain behavior is a key component of the assessment of persons with chronic pain; however, few self-reported pain behavior instruments have been developed. We developed a pain behavior item bank as part of the Patient-Reported Outcome Measurement Information System (PROMIS). For the Wave I testing, because of the large number of PROMIS items, a complex sampling approach was used where participants were randomly assigned to either respond to two full-item banks or to multiple 7-item blocks of items. A web-based survey was designed and completed by 15,528 members of the general population and 967 individuals with different types of chronic pain. Item response theory (IRT) analysis models were used to evaluate item characteristics and to scale both items and individuals on the pain behavior domain. The pain behavior item bank demonstrated good fit to a unidimensional model (Comparative Fit Index = 0.94). Several iterations of IRT analyses resulted in a final 39-item pain behavior bank, and different IRT models were fit to the total sample and to those participants who experienced some pain. The results indicated that these items demonstrated good coverage of the pain behavior construct. Pain behavior scores were strongly related to pain intensity and moderately related to self-reported general health status. Mean pain behavior scores varied significantly by groups based on pain severity and general health status. The PROMIS pain behavior item bank can be used to develop static short-form and dynamic measures of pain behavior for clinical studies.
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PMID:Development and psychometric analysis of the PROMIS pain behavior item bank. 1968 73

Vagus nerve stimulation (VNS) for medically refractory seizures has been an approved therapy by the Food and Drug Administration since 1997, with additional approval as an adjunct therapy for major depression granted in 2005. Potential applications for VNS therapy in obesity, neuropsychiatric disorders, and chronic pain syndromes are under investigation. Bradyarrhythmias, including asystole, may occur during VNS device placement or as a delayed complication. A peritracheal hematoma may develop following VNS device placement, necessitating emergent management. Other respiratory complications may include vocal cord movement abnormalities with potential for aspiration. Vagus nerve stimulation results in sleep-related breathing pattern changes, with an associated increase in the number of obstructive apneas and hypopneas in both children and adults, which may impact perioperative care.
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PMID:Intraoperative and perioperative complications with a vagus nerve stimulation device. 2040 10


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