Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0423716 (Neuropathic pain)
 1,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This article has discussed the peripheral and central mechanisms of the various orofacial pain conditions, including musculoskeletal disorders, neurogenic inflammation, and neuropathic pain. To make an accurate diagnosis of orofacial pain and render treatment, all organ systems need to be considered and evaluated. Central sensitization was discussed as it relates to musculoskeletal disorders and neuropathic pain. It has been suggested that treatment of these disorders be problem oriented, addressing both peripheral and central mechanisms if present. Musculoskeletal disorders are characterized by pain that is provokable with function and manipulation. Neurovascular pain is episodic with pain-free periods between attacks. The pain is not related to or provoked by jaw function. Neuropathic pain is more continuous and may be aggravated by light touch. Neuropathy with peripheral involvement responds variably to local anesthetics but may need to be treated with topical or local agents as well as centrally acting agents. Neuropathic pain that does not respond to topical or local agents is more profoundly centralized. These conditions need to be treated with centrally acting agents. In addition, if there is no response to medications, sympathetic involvement needs to be ruled out with sympathetic ganglion blockade.
 ...
PMID:Orofacial pain mechanisms and their clinical application. 914 78

Orofacial pain, especially if the problem is chronic, presents a diagnostic and management challenge to all health practitioners. This paper suggests how clinicians might simplify the diagnosis of orofacial pain. First, the pain is classified into one of the three basic pain categories: somatic, neuropathic, or psychogenic pain. Somatic pain results from noxious stimulation of normal neural structures. Neuropathic pain is caused by a structural abnormality in the nervous system. Psychogenic pain arises from psychic causes; there is no apparent physiologic or organic basis for the pain. The next step is to determine the tissue system from which the pain arises: intracranial, extracranial, musculoskeletal, neurovascular, neurogenous, or psychological. Finally, some of the more common orofacial pain syndromes within each category are discussed.
 ...
PMID:Differential diagnosis of orofacial pain. 984 62

Neuropathic pain is defined as "pain initiated or caused by a primary lesion or dysfunction in the nervous system". Neuropathic orofacial pain has previously been known as "atypical odontalgia" (AO) and "phantom tooth pain". The patient afflicted with neuropathic oral/orofacial pain may present to the dentist with a persistent, severe pain, yet there are no clearly identifiable clinical or radiographic abnormalities. Accordingly, multiple endodontic procedures may be instigated to remove the likely anatomical source of the pain, yet the pain persists. There have been few studies and limited patient numbers investigating the condition. Two retrospective studies revealed the incidence of persistent pain following endodontic treatment to be 3-6% and 5% of patients; one author with wide experience in assessing the condition estimated its prevalence at 125,000 individuals in the USA alone. In one study, 50% of neuropathic orofacial pain patients reported persistent pain specifically following endodontic treatment. Patients predisposed to the condition may include those suffering from recurrent cluster or migraine headaches. Neuropathic pain states include postherpetic neuralgia (shingles) and phantom limb/stump pain. The aberrant developmental neurobiology leading to this pain state is complex. Neuropathic pain serves no protective function, in contrast to physiological pain that warns of noxious stimuli likely to result in tissue damage. The relevant clinical features of neuropathic pain include: (i) precipitating factors such as trauma or disease (infection), and often a delay in onset after initial injury (days-months), (ii) typical complaints such as dysaesthesias (abnormal unpleasant sensations), pain that may include burning, and paroxysmal, lancinating or sharp qualities, and pain in an area of sensory deficit, (iii) on physical examination there may be hyperalgesia, allodynia and sympathetic hyperfunction, and (iv) the pathophysiology includes deafferentation, nerve sprouting, neuroma formation and sympathetic efferent activity.
 ...
PMID:Neuropathic orofacial pain part 1--prevalence and pathophysiology. 1135 93

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.
 ...
PMID:Orofacial pain--Part I: Assessment and management of musculoskeletal and neuropathic causes. 1608 36

Neuropathic pain is still an under-diagnosed and undertreated problem in third world countries. This retrospective study was undertaken to detect the prevalence, etiology and treatment profile of neuropathic pain in cancer. During January-December 2007, 716 new cancer pain patients were examined in Tata Memorial Hospital Pain Clinic. A total of 180 patients with a mean age of 47.14 yrs were found to have neuropathic pain characteristics on the basis of clinical impression, site of pain and the underlying cause i.e. due to tumor itself or cancer therapy. Head and neck cancer (32.2%) was found to be the most common cause of neuropathic pain, followed by breast (20.6%), thoracic (14.4%), genitourinary or gynecology (10.0% each), GI (9.4%), and medical oncology (2.8%). About 56% patients were post surgery, 44.4% post chemotherapy and 51.1% patients were post radiotherapy. The most common site of pain was thoracic (36.7%) due to primary or secondary metastatic disease. Pricking type of pain was the most characteristic feature (47.8%) followed by shooting pain (38.3%). The mean pain score was 5.96 +/- 1.5 (SD) and mean duration (months) of pain was 2.8 +/- 2.5. Neuropathic pain was found commonly associated with somatic pain (59.4%). The most common pharmacological agents prescribed were: tricyclic antidepressants (93.9%), anticonvulsants (66%), Opioids (85%), and nonsteroidal anti-inflammatory drugs (NSAIDs) (97.2%). Only 35% patients followed up more than once at the pain clinic. The most common and challenging patients were of orofacial pain. Nerve blocks techniques have a limited role in neuropathic pain.
 ...
PMID:Prevalence, etiology, and management of neuropathic pain in an Indian cancer hospital. 1949 12

Human brain imaging investigations have revealed that acute pain is associated with coactivation of numerous brain regions, including the thalamus, somatosensory, insular, and cingulate cortices. Surprisingly, a similar set of brain structures is not activated in all chronic pain conditions, particularly chronic neuropathic pain, which is associated with almost exclusively decreased thalamic activity. These inconsistencies may reflect technical issues or fundamental differences in the processing of acute compared with chronic pain. The appreciation of any differences is important because better treatment development will depend on understanding the underlying mechanisms of different forms of pain. In this investigation, we used quantitative arterial spin labeling to compare and contrast regional cerebral blood flow (CBF) patterns in individuals with chronic neuropathic orofacial pain (painful trigeminal neuropathy) and chronic nonneuropathic orofacial pain (painful temporomandibular disorder). Neuropathic pain was associated with CBF decreases in a number of regions, including the thalamus and primary somatosensory and cerebellar cortices. In contrast, chronic nonneuropathic pain was associated with significant CBF increases in regions commonly associated with higher-order cognitive and emotional functions, such as the anterior cingulate and dorsolateral prefrontal cortices and the precuneus. Furthermore, in subjects with nonneuropathic pain, blood flow increased in motor-related regions as well as within the spinal trigeminal nucleus.
...
PMID:Differential brain activity in subjects with painful trigeminal neuropathy and painful temporomandibular disorder. 2426 92

Neuropathic pain is a significant social and economic burden. Back pain, joint pain and headaches affect over 30% of the population. Chronic orofacial pain is a common condition and is difficult to diagnose and manage. This two-part paper aims to provide an overview of novel understanding of neuropathic pain, and furnish clinical teams with an update on the less common and less well-recognized chronic orofacial conditions. Headaches and temporomandibular disorders are the most common conditions and are covered in separate papers (6 and 10). Trigeminal neuralgia, burning mouth, and trigeminal autonomic cephalgias are also covered in separate papers (7, 8 and 9). The remaining conditions: post-traumatic neuropathy (nerve injury); and persistent idiopathic facial pain and atypical odontalgia are discussed in this and the following paper. Clinical Relevance: Neuropathic pain, though rare, is a consequence of dental treatment. Nerve injury in relation to M3M surgery, dental implants, endodontics and local anaesthesia result in 70% of affected patients experiencing chronic neuropathic pain.
 ...
PMID:Pain Part 5a: Chronic (Neuropathic) Orofacial Pain. 2668 73

Neuropathic pain of the orofacial region can cause much distress in individuals presenting with this condition. It may be easily mistaken for dental pain, and hence many individuals may undergo unnecessary dental work. Knowledge of the types of neuropathic orofacial pain may assist in timely diagnosis and improvement of a patient's quality of life.
 ...
PMID:Neuropathic Orofacial Pain. 3018 83

Neuropathic pain conditions including neuropathic orofacial pain (NOP) are difficult to treat. Contemporary therapeutic agents for neuropathic pain are often ineffective in relieving pain and are associated with various adverse effects. Finding new options for treating neuropathic pain is a major priority in pain-related research. Cannabinoid-based therapeutic strategies have emerged as promising new options. Cannabinoids mainly act on cannabinoid 1 (CB1) and 2 (CB2) receptors, and the former is widely distributed in the brain. The therapeutic significance of cannabinoids is masked by their adverse effects including sedation, motor impairment, addiction and cognitive impairment, which are thought to be mediated by CB1 receptors in the brain. Alternative approaches have been developed to overcome this problem by selectively targeting CB2 receptors, peripherally restricted CB1 receptors and endocannabinoids that may be locally synthesized on demand at sites where their actions are pertinent. Many preclinical studies have reported that these strategies are effective for treating neuropathic pain and produce no or minimal side effects. Recently, we observed that inhibition of degradation of a major endocannabinoid, 2-arachydonoylglycerol, can attenuate NOP following trigeminal nerve injury in mice. This review will discuss the above-mentioned alternative approaches that show potential for treating neuropathic pain including NOP.
 ...
PMID:Targeting Peripherally Restricted Cannabinoid Receptor 1, Cannabinoid Receptor 2, and Endocannabinoid-Degrading Enzymes for the Treatment of Neuropathic Pain Including Neuropathic Orofacial Pain. 3209 66