川合 謙介

難治性局在関連癲癇15例に対して迷走神経刺激療法(VNS)を行った.全経過中全く無効であった1例を除くと治療開始前に対する発作頻度はVNSにより減少しその後は安定する傾向がみられた.又,全般発作や複雑部分発作は単純部分発住より早期に減少する傾向がみられた.両側前頭葉に癲癇性脳波異常を有し,atypical absenceやnonconvulsive status epilepticusを呈する患者にも有効であった.又,disablingな発作ほど早期に減少する傾向は難治性癲癇の患者にとって利点の一つに挙げられた.VNSでは根治的外科治療と異なり,発作を完全に消失させることは不可能であるが,根治的外科治療が不可能又は無効な例では,低侵襲な代替治療として大いに期待される

propentofylline(PPF)が,虚血耐性に及ぼす影響を検討した.2分虚血により虚血耐性を誘導し,その48時間後に5分虚血を行う砂ネズミ一過性前脳虚血モデルを用いた.薬剤は,2分虚血24時間後にvehicle,PPF10mg/kg,PPF20mg/kgを腹腔内投与し,更にnon-selective adenosine receptor antagonistであるtheophyllineを同時投与した.又,PPF20mg/kgを5分単独虚血24時間前に投与して,その影響を検討した.vehicle群では,preconditioning ischemiaによる海馬CA1錘体細胞死への保護効果が認められ,PPF10mg/kgでも同様であった.しかし,PPF20mg/kg投与群ではこれら2群に対し有意にCA1錐体細胞障害が軽く,虚血耐性増強効果が確認された.更に,この増強効果はtheophyllineの同時投与によって消失した

Levels of mRNAs encoding the microtubule-associated proteins MAP2b and MAP2c as well as the 70-kDa stress protein [72-kDa heat shock protein (hsp72)] were evaluated in postischemic rat brain by in situ hybridization with oligonucleotide probes corresponding to the known rat sequences. Rats were subjected to 10-min cardiac arrest, produced by compression of major thoracic vessels, followed by resuscitation. The normally expressed MAP2b mRNA showed transient twofold elevations in all hippocampal neuron populations at 6-h recirculation, followed by a return to control levels by 24 h. MAP2b hybridization was progressively lost thereafter from the vulnerable CA1 and outer cortical layers, preceding both the fall in immunoreactive MAP2b and the eventual cell loss in these regions, The depletion of MAP2b mRNA coincided with an increase in the alternatively spliced MAP2c in vulnerable regions during 12-48 h of recirculation, precisely overlapping the late component of hsp72 expression that persisted in these cell populations. Previous studies have suggested that the initial induction of hsp72 provides an index of potential postischemic injury in neuron populations that may or may not be injured, while lasting hsp72 mRNA expression is associated with cell damage. In contrast, the present results demonstrate that MAP2c expression under these conditions occurs uniquely in neuron populations subject to injury. Available evidence suggests that MAP2c expression represents a plastic response in subpopulations of neurons that will survive in these regions, although it remains to be explicitly determined whether it may also be transiently expressed in dying cells. In any case, these observations demonstrate that reexpression of developmentally regulated MAP2c mRNA is a relatively late postischemic response in vulnerable cell populations, indicating that pathways regulating MAP2 splicing may be closely associated with mechanisms of neuron injury and/or recovery.