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Object Microvascular decompression has become an accepted surgical technique for the treatment of trigeminal neuralgia, hemifacial spasm, glossopharyngeal neuralgia, and other cranial nerve rhizopathies. The senior author (P.J.J.) began performing this procedure in 1969 and has performed more than 4400 operations. The purpose of this article is to review some of the nuances of the technical aspects of this procedure. Methods A review of 4415 operations shows that numerous modifications to the technique of microvascular decompression have occurred during the last 29 years. Of the 2420 operations performed for trigeminal neuralgia, hemifacial spasm, and glossopharyngeal neuralgia before 1990, cerebellar injury occurred in 21 cases (0.87%), hearing loss in 48 (1.98%), and cerebrospinal fluid (CSF) leakage in 59 cases (2.44%). Of the 1995 operations performed since 1990, cerebellar injuries declined to nine cases (0.45%), hearing loss to 16 (0.8%), and CSF leakage to 37 (1.85%) (p < 0.01, test for equality of distributions). The authors describe slight variations made to maximize surgical exposure and minimize potential complications in each of the six principal steps of this operation. These modifications have led to decreasing complication rates in recent years. Conclusions Using the techniques described in this report, microvascular decompression is an extremely safe and effective treatment for many cranial nerve rhizopathies.

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Thiazolidinediones (TZDs) are potent synthetic agonists of the ligand-activated transcription factor peroxisome proliferatoractivated receptor-␥ (PPAR␥). TZDs were shown to induce neuroprotection after cerebral ischemia by blocking inflammation. As spinal cord injury (SCI) induces massive inflammation that precipitates secondary neuronal death, we currently analyzed the therapeutic efficacy of TZDs pioglitazone and rosiglitazone after SCI in adult rats. Both pioglitazone and rosiglitazone (1.5 mg/kg i.p.; four doses at 5 min and 12, 24, and 48 h) significantly decreased the lesion size (by 57 to 68%, p Ͻ 0.05), motor neuron loss (by 3-to 10-fold, p Ͻ 0.05), myelin loss (by 66 to 75%, p Ͻ 0.05), astrogliosis (by 46 to 61%, p Ͻ 0.05), and microglial activation (by 59 to 78%, p Ͻ 0.05) after SCI. TZDs significantly enhanced the motor function recovery (at 7 days after SCI, the motor scores were 37 to 45% higher in the TZD groups over the vehicle group; p Ͻ 0.05), but the treatment was effective only when the first injection was given by 2 h after SCI. At 28 days after SCI, chronic thermal hyperalgesia was decreased significantly (by 31 to 39%; p Ͻ 0.05) in the pioglitazone group compared with the vehicle group. At 6 h after SCI, the pioglitazone group showed significantly less induction of inflammatory genes [interleukin (IL)-6 by 83%, IL-1␤ by 87%, monocyte chemoattractant protein-1 by 75%, intracellular adhesion molecule-1 by 84%, and early growth response-1 by 67%] compared with the vehicle group (p Ͻ 0.05 in all cases). Pioglitazone also significantly enhanced the post-SCI induction of neuroprotective heat shock proteins and antioxidant enzymes. Pretreatment with a PPAR␥ antagonist, 2-chloro-5-nitro-N-phenyl-benzamide (GW9662), prevented the neuroprotection induced by pioglitazone.Peroxisome proliferator-activated receptor (PPAR) and retinoid X receptor are ligand-activated transcription factors of the nuclear hormone receptor superfamily. Upon ligand binding, PPAR forms a heterodimeric complex with retinoid X receptor that binds to the cis-acting sequences (peroxisome proliferator response element) on DNA to initiate or repress the transcription of target genes (Blanquart et al., 2003). PPAR exists as three isoforms (␣, ␥, and ␦/␤) that control many cellular functions including lipid metabolism, glucose absorption, and cell growth and differentiation (Escher and Wahli, 2000). 15-Deoxy-⌬-12,14-prostaglandin J 2 (15-d-PGJ 2 ) is the natural agonist and thiazolidinediones (TZDs) (troglitazone, ciglitazone, rosiglitazone, and pioglitazone) are potent synthetic agonists of PPAR␥. Of these, troglitazone was removed from the market because of hepatotoxicity, whereas rosiglitazone and pioglitazone are currently ap-

Using the techniques described in this report, microvascular decompression is an extremely safe and effective treatment for many cranial nerve rhizopathies.