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 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuropathic pain, or pain after nervous system injury, can be very refractory to pharmacologic interventions. Through a better understanding of the pathophysiology of neuropathic pain, it has been suggested that nonopioid agents, such as antidepressants and anticonvulsants, may be more efficacious in the treatment of neuropathic pain than common analgesics, such as opioids or nonsteroidal anti-inflammatory drugs. However, this has not been consistently demonstrated in clinical studies. Conversely, many confounding factors of neuropathic pain make it difficult to interpret clinical studies. Therefore, we must develop a better understanding of the preclinical models of neuropathic pain to better understand the application of new and old drugs to the human neuropathic pain state. This article provides an overview of the commonly used preclinical neuropathic pain models, followed by a summary of the efficacy of currently available agents in preclinical pain models and human correlates.
Curr Pain Headache Rep 2001 Apr
PMID:Pharmacologic treatment of neuropathic pain. 1125 48

Retigabine [D23129; N-(2-amino-4-(4-fluorobenzylamino)-phenyl)carbamic acid ethyl ester] is an antiepileptic drug with a recently described novel mechanism of action that involves opening of neuronal K(V)7.2-7.5 (formerly KCNQ2-5) voltage-activated K(+) channels. These channels (primarily K(V)7.2/7.3) enable generation of the M-current, a subthreshold K(+) current that serves to stabilize the membrane potential and control neuronal excitability. In this regard, retigabine has been shown to have a broad-spectrum of activity in animal models of electrically-induced (amygdala-kindling, maximal electroshock) and chemically-induced (pentylenetetrazole, picrotoxin, NMDA) epileptic seizures. These encouraging results suggest that retigabine may also prove useful in the treatment of other diseases associated with neuronal hyperexcitability. Neuropathic pain conditions are characterized by pathological changes in sensory pathways, which favor action potential generation and enhanced pain transmission. Although sometimes difficult to treat with conventional analgesics, antiepileptics can relieve some symptoms of neuropathic pain. A number of recent studies have reported that retigabine can relieve pain-like behaviors (hyperalgesia and allodynia) in animal models of neuropathic pain. Neuronal activation within several key structures within the CNS can also be observed in various animal models of anxiety. Moreover, amygdala-kindled rats, which have a lowered threshold for neuronal activation, also display enhanced anxiety-like responses. Retigabine dose-dependently reduces unconditioned anxiety-like behaviors when assessed in the mouse marble burying test and zero maze. Early clinical studies have indicated that retigabine is rapidly absorbed and distributed, and is resistant to first pass metabolism. Tolerability is good in humans when titrated up to its therapeutic dose range (600-1200 mg/day). No tolerance, dependence or withdrawal potential has been reported, although adverse effects can include mild dizziness, headache, nausea and somnolence. Thus, retigabine may prove to be useful in the treatment of a diverse range of disease states in which neuronal hyperexcitability is a common underlying factor.
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PMID:Retigabine: chemical synthesis to clinical application. 1586 50

Orofacial pain is a common complaint, affecting the lives of millions of people around the world. Chronic orofacial pain often constitutes a challenging diagnostic problem that can be complicated by psychosocial factors and typically requires multidisciplinary treatment approaches. The fundamental prerequisite for successful management of orofacial pain is an accurate diagnosis. Generating a differential diagnosis, which will ultimately lead to a definite diagnosis, requires thorough knowledge of the diagnostic range of orofacial pain. There is a vast array of orofacial pain categories including: (1) musculoskeletal, (2) neuropathic, (3) vascular, (4) neurovascular, (5) idiopathic, (6) pain caused by local, distant, or systemic pathology, and (7) psychogenic. This article presents the salient clinical features and the therapeutic approaches for the various subtypes of musculoskeletal and neuropathic pain. Musculoskeletal pain is the most prevalent orofacial pain, with temporomandibular disorders and tension-type headache being the main examples. Neuropathic pain develops secondary to neural injury and/or irritation and can be distinguished into episodic, including trigeminal neuralgia and glossopharyngeal neuralgia, as well as continuous, such as herpetic and postherpetic neuralgia, traumatic neuralgia, and Eagle's syndrome.
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PMID:Orofacial pain--Part I: Assessment and management of musculoskeletal and neuropathic causes. 1608 36

Neuropathic pain encompasses a myriad of painful disease states that are often hard to treat, especially with one single medication. In the comprehensive treatment of neuropathic pain, the concept of complex polypharmacy is a rational approach, accompanied by physical and mental health therapies. Medications primarily used for neuropathic pain generally fall into the categories of anticonvulsants, antidepressants, opioids, and topical agents. Generally, most first-line medications used today show a response rate of approximately 30% to 50% reduction in pain in up to 50% of patients treated. There is no "gold standard" in regard to one medication for neuropathic pain. Some new medications have emerged during the past few years that help to augment the armamentarium of medications used in neuropathic pain. This paper reviews the definition of neuropathic pain and introduces the reader to the evidence-based literature on these new medications available for the treatment of neuropathic pain.
Curr Pain Headache Rep 2007 Jun
PMID:Update on pharmacotherapy guidelines for treatment of neuropathic pain. 1750 48

Neuropathic pain is a common problem in our society affecting nearly 1.5% of the US population. There currently are five medications approved by the US Food and Drug Administration (FDA) for the treatment of neuropathic pain, which include gabapentin, pregabalin, duloxetine, 5% lidocaine patch, and carbamazepine. Other agents with proven efficacy in multiple randomized, placebo-controlled trials include opioids, tricyclic antidepressants, venlafaxine, and tramadol. All of these agents, both FDA-approved and off-label, have been recommended as first-line treatments for neuropathic pain. This article discusses these agents in detail as they relate to the treatment of neuropathic pain.
Curr Pain Headache Rep 2006 Jun
PMID:Update on pharmacotherapy guidelines for the treatment of neuropathic pain. 1877 72

Neuropathic pain syndromes (ie, pain after a lesion or disease of the peripheral or central nervous system) are clinically characterized by spontaneous pain (ongoing, paroxysms) and evoked types of pain (hyperalgesia, allodynia). Different pathophysiologic mechanisms occur solitarily or combined at peripheral nociceptors, spinal cord, or in the brain, which cause a broad variety of signs and symptoms. Currently, the medical management is still arduous. Therefore, a new concept was proposed in which pain is analyzed on the basis of underlying mechanisms. The increased knowledge of pain-generating mechanisms and their translation into signs and symptoms may allow for a dissection of the individual mechanisms, and it ultimately should be possible to design optimal treatments for each patient.
Curr Pain Headache Rep 2006 Jun
PMID:Neuropathic pain: translational research and impact for patient care. 1877 73

Chronic low back pain is highly prevalent in Western societies. Large epidemiological studies show that 20% to 35% of patients with back pain suffer from a neuropathic pain component. Presently, chronic lumbar radicular pain is the most common neuropathic pain syndrome. The pathophysiology of back pain is complex and nociceptive, and neuropathic pain-generating mechanisms are thought to be involved, which established the term mixed pain syndrome. Neuropathic pain may be caused by lesions of nociceptive sprouts within the degenerated disc (local neuropathic), mechanical compression of the nerve root (mechanical neuropathic root pain), or by action of inflammatory mediators (inflammatory neuropathic root pain) originating from the degenerative disc even without any mechanical compression. Its diagnosis and management remain an enigma, mainly because there is no gold standard for either. Accuracy of diagnostic tests used to identify the source of back pain and their usefulness in clinical practice, particularly for guiding treatment selection, is unclear. In connection with the specific instance of back pain (one of the single most costly disorders in many industrialized nations), neuropathic pain components are a significant cost factor.
Curr Pain Headache Rep 2009 Jun
PMID:The evaluation of neuropathic components in low back pain. 1945 78

Neuropathic pain remains a serious medical problem because of patient morbidity and the absence of effective therapeutic interventions. Recent evidence suggests that this type of pain may be particularly difficult to manage because underlying mechanisms are influenced by a variety of factors, including type of injury, site of injury, and time after injury. This situation is exacerbated by the fact that different mechanisms may contribute to unique aspects of neuropathic pain, including ongoing pain as well as mechanical and thermal hypersensitivity. The different ion channels present in primary afferent neurons implicated in each of these aspects of neuropathic pain are reviewed.
Curr Pain Headache Rep 2009 Jun
PMID:Contribution of primary afferent channels to neuropathic pain. 1945 80

Neuropathic pain is an increasingly common problem facing the cancer patient. Painful neuropathy can come from various sources and significantly impact quality of life. The most commonly observed scenario is paraesthesia and dysesthesia as a result of toxic effects of chemotherapies on the distal peripheral nerves. Neuropathic pain should be addressed ideally with the help of a neuro-oncologist, and it usually can be successfully treated with a variety of agents, including atypical analgesics such as antidepressants, newer drugs with analgesic benefit, and opioids for more refractory cases. Direct and indirect effects of the primary neoplasm need to be considered in the etiology of specific syndromes of mononeuropathies and plexopathies.
Curr Pain Headache Rep 2009 Aug
PMID:Assessment of neuropathic pain in cancer patients. 1958 91

Neuropathic pain is a debilitating chronic pain condition, which remains difficult to treat. The current mainstays of treatment include physical therapy, interventional procedures and medications. Among medications, ion channel blockers and gabapentinoids are the 2 classes of drugs commonly used to treat neuropathic pain. It has been suggested that these medications may be useful to treat a variety of neuropathic pain conditions. This article provides several updates on the utility of both ion channel blockers and gabapentinoids for the treatment of neuropathic pain.
Curr Pain Headache Rep 2013 Sep
PMID:Update on neuropathic pain treatment: ion channel blockers and gabapentinoids. 2388 70


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