Continuous Neuropathic Pain Research Articles

Altered Brainstem Pain-Modulation Circuitry Connectivity During Spontaneous Pain Intensity Fluctuations.

BackgroundChronic pain, particularly that following nerve injury, can occur in the absence of external stimuli. Although the ongoing pain is sometimes continuous, in many individuals the intensity of their pain fluctuates. Experimental animal studies have shown that the brainstem contains circuits that modulate nociceptive information at the primary afferent synapse and these circuits are involved in maintaining ongoing continuous neuropathic pain. However, it remains unknown if these circuits are involved in regulating fluctuations of ongoing neuropathic pain in humans.MethodsWe used functional magnetic resonance imaging to determine whether in 19 subjects with painful trigeminal neuropathy, brainstem pain-modulation circuitry function changes according to moment-to-moment fluctuations in spontaneous pain intensity as rated online over a 12-minute period.ResultsWe found that when pain intensity was spontaneously high, connectivity strengths between regions of the brainstem endogenous pain-modulating circuitry—the midbrain periaqueductal gray, rostral ventromedial medulla (RVM), and the spinal trigeminal nucleus (SpV)—were high, and vice-versa (when pain was low, connectivity was low). Additionally, sliding-window connectivity analysis using 50-second windows revealed a significant positive relationship between ongoing pain intensity and RVM-SpV connectivity over the duration of the 12-minute scan.ConclusionThese data reveal that moment-to-moment changes in brainstem pain-modulation circuitry functioning likely contribute to fluctuations in spontaneous pain intensity in individuals with chronic neuropathic pain.

The Neuralgias

Neuralgias are characterized by pain in the distribution of a cranial or cervical nerve. Typically, they are brief, paroxysmal, painful attacks, although continuous neuropathic pain may occur. The most commonly encountered conditions are trigeminal, postherpetic, and occipital neuralgia. Less common neuralgias include glossopharyngeal, superior laryngeal, auriculotemporal, and nervus intermedius neuralgia, among others. The approach to diagnosis and treatment of this group of disorders is reviewed. Recent guidelines of medication administration, the use of botulinum toxin, and more targeted procedures have improved treatment of neuralgias. Patients who present with neuralgias should have imaging studies to investigate for structural abnormalities unless the etiology is apparent. Management of both common and rare neuralgias can be challenging and is best guided by the most recent available evidence.

The neuralgias: diagnosis and management.

The neuralgias are characterized by pain in the distribution of a cranial or cervical nerve. While most often brief, severe, and paroxysmal, continuous neuropathic pain may occur. The most commonly encountered entities include trigeminal, postherpetic, glossopharyngeal, and occipital neuralgia. More unusual cranial neuralgias may occur in periorbital (eg, supraorbital neuralgia) and auricular (eg, nervus intermedius neuralgia) distributions. These disorders may be mimicked by structural and inflammatory/infectious neurologic disease, along with other primary headache disorders (eg, primary stabbing headache). The approach to diagnosis and treatment of this group of headache disorders is reviewed.

A Review of Burning Mouth Disorders

Burning mouth disorders (sometimes referred to as burning mouth syndrome) are characterized by a burning sensation in the tongue or other oral sites, usually in the absence of clinical and laboratory findings. Affected patients often present with multiple oral complaints, including burning, dryness and taste alterations. Burning mouth complaints are reported more often in women, especially after menopause. Typically, patients awaken without pain, but report increasing symptoms through the day and into the evening. Conditions that have been reported in association with burning mouth syndrome include chronic anxiety or depression, various nutritional deficiencies, diabetes and changes in salivary function. However, these conditions have not been consistently linked with the syndrome, and their treatment has had little impact on burning mouth symptoms. Recent studies have pointed to dysfunction of several cranial nerves associated with taste sensation as a possible cause of burning mouth disorders. The most common central mechanism that likely explains burning mouth disorders is a centrally mediated continuous neuropathic pain. Given in low dosages, benzodiazepine, tricyclic antidepressants or anticonvulsants may be effective in patients with burning mouth disorders.

服薬状況を用いて評価した持続性神経障害性とう痛患者の長期治療経過

The patient was a 56-year-old female, suffering from severe burning pain in the left maxillary alveolar area. The pain was initiated by periodontal curettage under no local anesthesia. No abnormal local findings in dental X-ray images and no abnormal central nervous system findings in brain magnetic resonance images were observed. Extraction of the tooth temporarily abated her pain, however the pain recurred gradually. Since the observed signs and symptoms of the patient agreed well with the diagnostic standard for continuous neuropathic pain (atypical alveolar pain) of Graff-Radford & Solberg (1992), medications (tricyclic antidepressant, non-steroidal anti-inflammatory drug (NSAID), anxiolytics, topical application of capsacin cream) and supportive psychological therapy have been administered continuously. To measure symptom severity over a long term, daily amounts of taken NSAID and anxiolytics were recorded continuously by the patient in a simple table diary for 7 years. As a result, the total amount of the drugs per month gradually decreased with the passage of time. Clinical evidence regarding the prognosis of continuous neuropathic pain in the orofacial region is obviously insufficient, making it difficult to inform such patients of their prognosis of the disorder on the basis of clinical evidence. In this report, we have plotted the total amount of drugs taken per month by the patient as a good reference for the pain severity and the results clearly suggest that pain severity decreased with time. This kind of information may help both clinicians and patients for case-based explanation of the disorder.

歯科治療に関連して発症した持続性神経障害性とう痛 非定型性歯痛

歯科治療に関連して発症した持続性神経障害性とう痛 非定型性歯痛

顎関節症類似の症状を呈した間代性神経障害性とう痛 血中カルバマゼピン濃度測定

Recently, it has been recognized that temporomandibular disorders may include not only jawrelated musculoskeletal disorders but also orofacial pain. Further, the signs and symptoms of orofacial pain closely resemble those of the temporomandibular musculoskeletal disorders, which leads to much confusion and misdiagnosis. Therefore, it is necessary to expand the scope from temporomandibular joint disorders to orofacial pain, including neurovascular pain and neuropathic pain. In this article, a case of continuous neuropathic pain exhibiting temporomandibular joint pain is described.The case was a 53-year-old male whose right side temporomandibular joint pain was initially diagnosed as a temporomandibular joint disorder by a general dentist and was not ameliorated by common occlusal treatment and anti-inflammatory drug therapy.Since his pain was characterized by sudden bursts of electric-like pain, episodic neuropathic pain was doubted, carbamazepine (initially 100 mg/day, up to 800 mg/day) and bacrofen (15 mg/day) were administered, and serological monitoring of carbamazepine was performed. These medications worked very well, ameliorating his pain.

Die Klassifikation der Trigeminusneuralgie und ihr Einfluß auf die Ergebnisse der operativen Behandlung*

The trigeminal neuralgia has to be differentiated from the trigeminal neuropathy in respect of pain character and etiology. The neuralgia is characterized by paroxysmal pain evoked by trigger stimuli. The most frequent cause of this type of pain is a parapontine vascular compression of the trigeminal root without neurological deficits. The symptoms of neuropathy are some sensory loss associated with continuous pain resulting from peripheral damage of the trigeminal nerve. This distinction alleviates the indication for specific operative procedures and is more precise than the subdivision in typical and atypical neuralgia. The results of neurovascular decompression and thermorhizotomy can be much improved if neuropathic pain syndromes are excluded from operation. Out of 180 patients suffering from trigeminal neuralgia 94% were pain-free after neurovascular decompression and 96% of 144 patients following thermorhizotomy. For the treatment of continuous neuropathic pain augmentative electrostimulation of the Gasserian Ganglion via implanted electrodes is recommended.