• The Korean Journal of Pain
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• v.14 no.2
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• pp.193-198
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• 2001

Background: Anterior atlantoaxial subluxation (AAS) is a frequent phenomenon in rheumatoid arthritis (RA). AAS compresses the C2 ganglion or nerve and is a cause of posterior neck pain or occipital headache. Methods: We selected RA patients that had developed posterior neck pain or occipital headache caused by AAS. AAS was diagnosed by an increase of ADI (atlantodental interval). A distance of 3 mm or more was considered significant. Patients with vertical subluxation or symptoms suggestive of myelopathy were excluded. Before C2 RF ganglionotomy, we proceeded with a C2 ganglion block or greater occipital nerve block used by local anesthetics. For C2 RF ganglionotomy, the patient was placed in the supine position on a fluoroscopic table. A 100 mm, 4 mm active tip electrode was chosen. Following sensory stimulation at 0.2 to 0.6 V, the lesion was performed at a temperature of $60^{\circ}C$ to $65^{\circ}C$ for 60 sec. We followed up the patient after 6 months later. Results: All cases were female and the average duration of RA was 8.5 years. The duration of posterior neck pain or occipital headache was 1-8 months. The average ADI was 4.2 mm and the McGregor index was 3.3 mm on the average. In all cases, the score on the 4 point Likert scale was 4 (pain free) during the follow-up period. Conclusions: We found that the occipital headache or posterior neck pain caused by AAS in rheumatoid arthritis patients was alleviated over a short term follow up. C2 RF ganglionotomy is suggested as an effective palliative treatment for AAS in RA patients.

• The Korean Journal of Pain
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• v.10 no.1
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• pp.121-123
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• 1997

Stellate ganglion block(SGB) is frequently performed to relieve a patient from headache of various. We experienced a rare case of subarachnoid hemorrhage by aneurysmal rupture after SGB. A 46-year-old female patient diagnosed with tension headache, and normal MRI finding consulted our pain clinic. We performed right SGB in combination with greater occipital nerve block. The next day, we performed left SGB with 6 ml of 0.25% bupivacaine. She had no evidence of subarachnoid block or intravascular injection. 15 minutes after injection, she abruptly developed convulsion and loss of consciousness. She was given artificial respiration with oxygen. The diagnosis of ruptured left posterior communicating aneurysm was confirmed by 4-vessels angiography.

• International Journal of Oral Biology
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• v.42 no.3
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• pp.129-135
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• 2017

The present study investigated the role of spinal glutamate recycling in the development of orofacial inflammatory pain or trigeminal neuropathic pain. Experiments were carried out on male Sprague-Dawley rats weighing between 230 and 280 g. Under anesthesia, a polyethylene tube was implanted in the atlanto-occipital membrane for intracisternal administration. IL-$1{\beta}$-induced inflammation was employed as an orofacial acute inflammatory pain model. IL-$1{\beta}$ (10 ng) was injected subcutaneously into one vibrissal pad. We used the trigeminal neuropathic pain animal model produced by chronic constriction injury of the infraorbital nerve. DL-threo-${\beta}$-benzyloxyaspartate (TBOA) or methionine sulfoximine (MSO) was administered intracisternally to block the spinal glutamate transporter and the glutamine synthetase activity in astroglia. Intracisternal administration of TBOA produced mechanical allodynia in naïve rats, but it significantly attenuated mechanical allodynia in rats with interleukin (IL)-$1{\beta}$-induced inflammatory pain or trigeminal neuropathic pain. In contrast, intracisternal injection of MSO produced anti-allodynic effects in rats treated with IL-$1{\beta}$ or with infraorbital nerve injury. Intracisternal administration of MSO did not produce mechanical allodynia in naive rats. These results suggest that blockade of glutamate recycling induced pro-nociception in na?ve rats, but it paradoxically resulted in anti-nociception in rats experiencing inflammatory or neuropathic pain. Moreover, blockade of glutamate reuptake could represent a new therapeutic target for the treatment of chronic pain conditions.