Ganglionic local opioid analgesia for refractory trigeminal neuralgia

Ganglionic local opioid analgesia for refractory trigeminal neuralgia

THE LANCET At diagnosis Insulin requirements (IU/kg) Glycosylated haemoglobin (%) C-peptide (ng/mL) Number of patients in remission 3 mo 6 mo 9 m...

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THE LANCET

At diagnosis

Insulin requirements (IU/kg) Glycosylated haemoglobin (%) C-peptide (ng/mL) Number of patients in remission

3 mo

6 mo

9 mo

12 mo

BCG+NCT

NCT

BCG+NCT

NCT

BCG+NCT

NCT

BCG+NCT

NCT

BCG+NCT NCT

0·58 (0·35) 9·7 (2·1) 0·8 (0·5) . .

0·54 (0·36) 9·8 (2·5) 0·93 (0·6) . .

0·34 (0·22) 6·3 (1·7) 1·0 (0·6) 3

0·27 (0·1) 6·3 (1·7) 1·2 (0·5) 3

0·37 (0·26) 6·7 (2·0) 0·9 (0·6) 0

0·3 (0·2) 6·6 (1·6) 1·1 (0·75) 1

0·36 (0·27) 6·9 (2·2) 0·7 (0·6) 1

0·3 (0·2) 6·5 (1·3) 0·9 (0·5) 1

0·4 (0·3) 6·9 (2·2) 0·9 (0·7) 0

0·3 (0·1) 6·4 (1·1) 1·0 (0·7) 0

Mean (SD) measures of metabolic control in IDDM patients

might have been masked by nicotinamide; nevertheless, it is certain that BCG has no additional therapeutic value compared with nicotinamide. Today, intensive insulin therapy and the addition of nicotinamide, as recently shown in a meta-analysis,5 appears to be the only way to protect beta cells from end-stage destruction. 1

2 3

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Shehadeh N, Calcinaro F, Bradley BJ, et al. Effect of adjuvant therapy on development of diabetes in mouse and man. Lancet 1994; 343: 706–07. Williams G. IDDM: long honeymoon, sweet ending. Lancet 1994; 343: 684–85. Pozzilli P, Visalli N, Signore A, et al. Combination of nicotinamide and steroid versus nicotinamide in recent onset insulin-dependent diabetes (The IMDIAB II Study). Diabetes Care 1994; 17: 897–900. Pozzilli P, Visalli N, Signore A, et al. Double blind trial of nicotinamide in recent onset insulin dependent diabetes mellitus. Diabetologia 1995; 38: 848–52. Pozzilli P, Browne PD, Kolb H, and the Nicotinamide Trialists. Metaanalysis of nicotinamide treatment in patients with recent onset insulin dependent diabetes. Diabetes Care 1996; 19: 1357–63.

Instituto II Clinica Medica, University of Rome La Sapienza, 00161 Rome, Itally (P Pozzilli)

Ganglionic local opioid analgesia for refractory trigeminal neuralgia

the ganglion sphenopalatinum (GSP, n=11). Pain reduction was measured with a visual analogue scale (VAS, 0–10) before and after each GLOA injection during the treatment period. Statistical analysis was performed retrospectively with Student’s t-test and chi-square test with p<0·05 considered significant. The mean VAS values determined before the first GLOA treatment did not differ between the two groups and reflected the severity of pain (see table). After an average of nine or 12 consecutive local opioid injections, respectively, substantial and significant pain relief was observed in both groups, which lasted several months (range 1–18 months). In conclusion, our uncontrolled retrospective analysis suggests an adjunctive beneficial effect of GLOA in carbamazepine-treated patients with trigeminal neuralgia. The therapeutic effect was independent of the site of ganglionic opioid injection. Although GLOA was first described in 1981, its underlying mechanisms still wait to be elucidated. Since opioid peptide immunoreactivity has been shown in autonomic ganglia,5 it is tempting to speculate on a modulatory function of opioids on yet unknown neuronal pathways involved in the pathophysiology of trigeminal neuralgia. 1

2

Anna Spacek, Dagmar Böhm, Hans-Georg Kress

Neither the aetiology nor the underlying pathophysiological mechanism are understood in trigeminal neuralgia, and consequently various therapeutic approaches exist. Drug therapy with anticonvulsants, such as carbamazepine, is frequently limited by side-effects, and surgical procedures may be more hazardous. The injection of opioid drugs close to the sympathetic ganglia has been reported to provide good pain relief without side-effects in patients with postherpetic neuralgia, sympathetically maintained pain, and reflex sympathetic dystrophy.1–3 Since no controlled trials have been reported on the treatment of trigeminal neuralgia by ganglionic local opioid analgesia (GLOA), and only a few data are available on GLOA in patients with atypical facial pain,4 we retrospectively analysed the efficacy of this approach in our pain clinic patients. 32 patients (14 male; 18 female; median age 69·5 years) with chronic trigeminal neuralgia who were on continuous carbamazepine were recruited. Only those with a definite diagnosis and insufficient pain relief (table, visual analogue score before first GLOA) despite therapeutic carbamazepine plasma concentrations were included. After informed written consent, at least three ganglionic local opioid injections (once a day) with buprenorphine (0·045–0·06 mg) were given either to the ganglion cervicale superius (GCS, n=21) or to Patient group

VAS before first GLOA

VAS after last GLOA

Average number of injections

GCS, n=21 GSP, n=11

8·8 (1·6) 8·5 (2·1)

2·4 (2·9)* 3·2 (3·1)*

12 9

*p<0·05.

Mean (SD) VAS scores before and after GLOA

Vol 349 • May 24, 1997

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Fine PG, Ashburn MA. Effect of stellate ganglion block with fentanyl on postherpetic neuralgia with a sympathetic component. Anesth Analg 1988; 67: 897–99. Mays K, North WC, Schnapp M. Stellate ganglion “blocks” with morphine in sympathetic type pain. J Neurol Neurosurg Psychiatry 1981; 44: 189–90. Arias LM, Bartowski R, Grossman KL, Schwartzman RJ, Tom CMT. Sufentanil stellate ganglion injection in the treatment of refractory reflex sympathetic dystrophy. Reg Anesth 1989; 14: 90–92. Maier Ch, Hoffmeister B, Führung und Behandlung von Patienten mit atypischem Gesichtsschmerz. Dtsch Zahnärztl Z 1989; 44: 977–83. Schultzberg M, Hökfelt T, Terenius L, et al. Enkephalin immunoreactive nerve fibres and cell bodies in sympathetic ganglia of guinea-pig and rat. Neuroscience 1979; 4: 249–70.

Department of Anaesthesiology and General Intensive Care (B), University of Vienna, A-1090 Vienna, Austria (A Spacek)

Rifamycin-induced lupus syndrome Shaun E Berning, Michael D Iseman

Despite over 20 years of widespread use of rifamycin class antibiotics, which include rifampin and rifabutin, no cases of drug-induced lupus syndrome (DILS) have been reported in association with their use. We recently reported in abstract form five cases of DILS associated with rifamycin therapy1 and now report a total of seven cases in patients undergoing treatment for mycobacterial infections. Six of the seven patients were female; all were white; their mean age was 58·7 years (range 41–72). None were infected with HIV-1. Concomitant medications are listed in the table. Two had had Raynaud’s phenomenon; another reported a DILS reaction to izoniazid and thiacetazone 4 years before, but no manifestations of lupus in the interval. Four reactions were attributed to rifampin and three to rifabutin therapy. All were receiving standard doses (rifampin 450–600 mg daily, rifabutin 300 mg daily). Five reactions

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