Yutaka Taira

Localization of NADPHd-exhibiting neurons in the spinal cord of the rabbit

Segmental and laminar distributions of nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd)‐exhibiting neurons were examined in the rabbit spinal cord by using horizontal, sagittal, and transverse sections. A large number of NADPHd‐positive neurons in the spinal cord of rabbit appeared to fall into six categories (N1–N6), but others could not be classified. Major cell groups of NADPHd‐exhibiting neurons were identified in the superficial dorsal horn and around the central canal at all spinal levels and in the intermediolateral cell column at thoracic and upper lumbar levels. NADPHd‐exhibiting neurons of the pericentral region were divided into a thin subependymal cell column containing longitudinally arranged, small bipolar neurons with processes penetrating deeply into the intermediolateral cell column and/or running rostrocaudally in the subependymal layer. The second pericentral cell column located more laterally in lamina X contains large, intensely stained NADPHd‐exhibiting neurons with long dendrites radiating in the transverse plane. In the pericentral region (lamina X), close association of NADPHd‐exhibiting somata and fibers and mostly longitudinally oriented blood vessels were detected. Neurons of the sacral parasympathetic nucleus, seen in segments S1–S3, exhibited prominent NADPHd cellular staining accompanied by heavily stained fibers extending from Lissauers tract through lamina I along the lateral edge of the dorsal horn to lamina V. A massive dorsal gray commissure, highly positive in NADPHd staining, was found in segments S1–S3. Scattered positive cells were also found in the deeper dorsal horn, ventral horn, and white matter. Fiberlike NADPHd staining was found in the superficial dorsal horn and pericentral region in all the segments studied. Dense, punctate, nonsomatic NADPHd staining was detected in the superficial dorsal horn, in the pericentral region all along the rostrocaudal axis, and in the nucleus phrenicus (segments C4–C5), nucleus dorsalis (segments Th2–L2), Onufs nucleus (segments S1–S3), and the dorsal part of the dorsal gray commissure (S1–S3). J. Comp. Neurol. 406:263–284, 1999.

The Effect of Graded Postischemic Spinal Cord Hypothermia on Neurological Outcome and Histopathology after Transient Spinal Ischemia in Rat

BACKGROUND Previous data have shown that postischemic brain hypothermia is protective. The authors evaluated the effect of postischemic spinal hypothermia on neurologic function and spinal histopathologic indices after aortic occlusion in the rat. METHODS Spinal ischemia was induced by aortic occlusion lasting 10 min. After ischemia, spinal hypothermia was induced using a subcutaneous heat exchanger. Three studies were conducted. In the first study, the intrathecal temperature was decreased to 34, 30, or 27 degrees C for 2 h beginning with initial reperfusion. In the second study, hypothermia (target intrathecal temperature 27 degrees C) was initiated with reflow and maintained for 15 or 120 min. In the third study, the intrathecal temperature was decreased to 27 degrees C for 2 h starting 5, 60, or 120 min after normothermic reperfusion. Animals survived for 2 or 3 days, at which time they were examined and perfusion fixed with 4% paraformaldehyde. RESULTS Normothermic ischemia followed by normothermic reflow resulted in spastic paraplegia and spinal neuronal degeneration. Immediate postischemic hypothermia (27 degrees C for 2 h) resulted in decreasing motor dysfunction. Incomplete protection was noted at 34 degrees C. Fifteen minutes of immediate cooling (27 degrees C) also provided significant protection. Delay of onset of post-reflow hypothermia (27 degrees C) by 5 min or more failed to provide protection. Histopathologic analysis revealed temperature-dependent suppression of spinal neurodegeneration, with no effect of delayed cooling. CONCLUSIONS These findings indicate that the immediate period of reperfusion (0-15 min) represents a critical period that ultimately defines the degree of spinal neuronal degeneration. Hypothermia, when initiated during this period, showed significant protection, with the highest efficacy observed at 27 degrees C.

Reduced nicotinamide adenine dinucleotide phosphate diaphorase in the spinal cord of dogs

The distribution of somatic, fibre-like and punctate, non-somatic reduced nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase activity was examined in dog spinal cord using horizontal, sagittal and transverse sections. The morphological features of NADPH diaphorase exhibiting neurons divided into six different neuronal types (N1-N6) were described and their laminar distribution specified. Major cell groups were identified in the superficial dorsal horn and around the central canal at all spinal levels, and in the intermediolateral cell column at thoracic level. NADPH diaphorase exhibiting neurons of the pericentral region were distributed in a thin subependymal cell column containing longitudinally-arranged small bipolar neurons with processes penetrating deeply into the intermediolateral cell column and/or running rostrocaudally in the subependymal layer. The second pericentral cell column located more laterally in lamina X contains large, intensely-stained NADPH diaphorase exhibiting neurons with long dendrites radiating in the transverse plane. Neurons of the sacral parasympathetic nucleus seen in segments S1-S3 exhibited prominent NADPH diaphorase activity accompanied by heavily-stained fibres extending from Lissauers tract through lamina I along the lateral edge of the dorsal horn to lamina V. A massive dorsal gray commissure, with high NADPH diaphorase activity, was found in segments S1-S3. At the same segmental level a prominent group of moderately-stained motoneurons was detected in the dorsolateral portion of the anterior horn. Fibre-like NADPH diaphorase activity was found in the superficial dorsal horn and pericentral region in all segments studied. Punctate, non-somatic NADPH diaphorase activity was detected in the superficial dorsal horn, in the pericentral region all along the rostrocaudal axis and in the nucleus phrenicus (segments C4-C5), nucleus dorsalis (segments Th2-L2), nucleus Y (segments S1-S3), and the dorsal part of the dorsal gray commissure (S1-S3). A schematic diagram documenting the segmental and laminar distribution of NADPH diaphorase activity is given.

Incipient cauda equina syndrome as a model of somatovisceral pain in dogs: spinal cord structures involved as revealed by the expression of c-fos and NADPH diaphorase activity

Segmental and laminar distribution of Fos-like immunoreactive, reduced nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd)-exhibiting and double-labeled (Fos-like immunoreactive and NADPHd-exhibiting) neurons was examined in lower lumbar and sacral segments of the dog spinal cord using the model of multiple cauda equina constrictions. NADPHd histochemistry was used as marker of nitric oxide synthase-containing neurons. The appearance and the time-course of Fos-like immunoreactive, NADPHd and double-labeled neurons was studied at 2 h and 8 h postconstriction characterized as the incipient phase of cauda equina syndrome. The occurrence of Fos-like immunoreactive and NADPHd-exhibiting neurons in fully developed cauda equina syndrome was studied at five days postconstriction. An increase in Fos-like immunoreactivity in superficial laminae (I-II) and an enhanced NADPHd staining of lamina VIII neurons were found. A statistically significant increase in Fos-like immunoreactive neurons was found in laminae I-II and VIII-X 8 h postconstriction, and in contrast, a prominent decrease in Fos-like immunoreactive neurons was found in laminae I-II, accompanied by a statistically significant increase in Fos-like immunoreactive neurons in more ventrally located laminae VII-X at five days postconstriction. Quantitative analysis of laminar distribution of constriction-induced NADPHd-exhibiting neurons revealed a considerable increase in these neurons in laminae VIII-IX 8 h postconstriction and a statistically highly significant increase in NADPHd-exhibiting neurons in laminae VII-X five days postconstriction. Concurrently, the number of NADPHd-exhibiting neurons in laminae I-II was greatly reduced. While a low number of double-labeled neurons was found throughout the gray matter of lower lumbar and sacral segments at 2 h postconstriction, a statistically significant number of double-labeled neurons was found in lamina X 8 h and in laminae VII-X five days postconstriction. The course and distribution of anterograde degeneration resulting five days after multiple cauda equina constrictions are compared with segmental and laminar distribution of Fos-like immunoreactive and NADPHd-exhibiting neurons. Prominent involvement of the spinal cord neurons appearing in the lumbosacral segments at the early beginning and in fully developed cauda equina syndrome results in a Fos-like immunoreactivity and strongly enhanced NADPHd staining of some neuronal pools. Under such circumstances, an early cauda equina decompression surgery is advisable aimed at decreasing or preventing the derangement of the neural circuits in the lumbosacral segments.

Interadductor approach to obturator nerve block for transurethral resection procedure: comparison with traditional approach

AbstractPurpose. We compared the interadductor approach of obturator nerve block with the traditional approach in terms of the insertion-adductor contraction interval (ICI), success rate, completion of the block, and plasma lidocaine concentration. Methods. An obturator nerve block by the interadductor approach was performed by needle insertion 1 cm behind the adductor longus tendon and 2 cm lateral to the pubic arch in 12 patients, and by the traditional approach in 12 patients. Results. The ICI with the interadductor approach was significantly shorter than that with the traditional approach. The success rate, completion of the block, and plasma lidocaine concentrations were similar with both approaches. Conclusion. The interadductor approach can provide faster identification of the obturator nerve than the traditional approach.

Epidural injection with saline for treatment of postspinal headache: comparison with epidural blood patch.

to receive either EBP therapy or ESI. The cause of the headache was spinal anesthesia in all patients. Spinal anesthesia using 0.24% dibucaine dissolved by p-butylaminobenzoyl diethylaminoethyl hydrochloride (Neo-percamin S) had been performed, at the L3–4 interspace, with the patient in a left decubitus position with the use of a 23 or 25 G spinal needle. More than one puncture attempt was required to perform spinal anesthesia in one patient. The surgical procedures of the patients were ceasarean section (two patients in EBP and two patients in ESI), appendectomy operation (four patients in EBP and five patients in ESI), and stripping of varix (two patients in EBP and one patient in ESI). All procedures were done in the operating room under the monitoring of electrocardiography, noninvasive blood pressure, and pulse oxymetry. The patients in both groups were placed in the left lateral decubitus position, an 18G Tuohy needle was inserted at the L4–L5 interspace, and the loss of resistance technique with 0.9% saline solution was applied to confirm that the needle tip had reached the epidural space. Then, in the EBP group, 10 to 15 ml of blood was withdrawn in an aseptic manner from veins on the dorsal and lateral aspect of the right foot and was slowly injected into the epidural space. In the ESI group, after 15 to 20 ml of 0.9% saline had been injected aseptically through the needle into the epidural space, an epidural catheter was inserted 3cm cephalad for 3 h of continuous infusion of saline at 20ml·h 1. Subsequently, the patients remained at least 3h in the supine position. If the patient complained of any symptoms during the epidural injection of saline or blood, this injection was ceased immediately. Headache intensity was assessed by the patients using a Visual Analogue Scale (VAS), with 0 cm none to 10 cm worst pain imaginable, and was recorded by nurses 5 min after the patient assumed a sitting position at pretreatment, 15min, 3 h, and 24 h after the epidural

The effect of gamma-aminobutyric acid (GABA) receptor drugs on morphine-induced spastic paraparesis after a noninjurious interval of spinal cord ischemia in rats.

We have previously demonstrated that intrathecal morphine given after a noninjurious interval of spinal cord ischemia induced transient spastic paraparesis in a rodent model. However, the mechanism of this paraparesis is unknown. We hypothesized that morphine inhibits &ggr;-aminobutyric acid (GABA)ergic interneurons that control the tonus of spinal cord &agr;-motoneurons and that inhibition of spinal cord interneurons may cause spastic paraparesis. In this study, we investigate interactions between morphine and GABAergic agonists or antagonists on motor function after spinal cord ischemia and then clarified the mechanism of the spastic paraparesis induced by intrathecal morphine. Spinal cord ischemia was induced by aortic occlusion lasting 6 min. We first determined whether intrathecally administered GABA agonists (muscimol or baclofen) improve the spastic paraparesis in this model. GABA agonists did not improve the paraparesis. Next, we examined the effect of GABA antagonists (bicuculline or 5-aminovaleric acid) and determined the interaction between morphine and GABA antagonists. In an isobolographic analysis, the 50% effective dose decreased below the theoretical additive line, indicating a synergistic interaction between morphine and GABA antagonists. These results indicate that the spastic paraparesis induced by intrathecal morphine may be mediated in part by GABA receptors.

Propofol suppressed electromyographic fibrillation potentials in a patient with amyotrophic lateral sclerosis.

Address correspondence to: M. Kakinohana Received for publication on September 1, 1998; accepted on January 12, 1999 (EMG) of the lower extremities confirmed the advanced stage of ALS (Fig. 1). The only lesion in which significant waves could be detected by EMG was the sublingual muscles, and spontaneous potentials were demonstrated reproductively. She was not able to move her legs or arms by herself and had needed respiratory care for 6 years. The patient and her family had been informed of the aim of the study, and their consents were obtained before the operation. She was not premedicated for the surgery, and controlled mechanical ventilation was started in the operating room. After placement of a peripheral intravenous catheter, electrocardiography (ECG), pulse oximetry, capnometry, and noninvasive blood pressure monitoring were performed. A coaxial needle electrode continuous electromyographic for monitoring was inserted percutaneously into the sublingual muscles deeply enough that motor unit potentials were displayed on the oscilloscope. Before induction of anesthetia, spontaneous potentials, referred to as “fibrillation potentials,” were detected on the oscilloscope (Fig. 2a). Two hundred micrograms of fentanyl was injected intravenously, and then 50mg of propofol was administered, followed by intravenous infusion of propofol 2mg·kg21·h21. After the intravenous injection of 200μg of fentanyl, the amplitude of the fibrillation potentials decreased by half (Fig. 2b) as preinduction but did not vanish completely. On the other hand, fibrillation potentials on the oscilloscope disappeared completely following administration of 50mg of propofol (Fig. 2c). All operative procedures were accomplished uneventfully, and emergence from anesthesia was prompt after the infusion of propofol ceased. In this patient with ALS, we were able to demonstrate that fibrillation potentials in the EMG recorded from sublingual muscles were suppressed completely after administration of propofol, but

A method of radiographic guiding for maxillary nerve block (pterygopalatine fossa oblique view)

Maxillary nerve block is considered the most difficult among the techniques of trigeminal nerve block. The difficulty may be associated with the following factors: (1) Insertion of a block needle into the pterygopalatine fossa is sometimes troublesome due to anatomical variations in the shape of the anterior edge of the lateral pterygoid palate of the sphenoid, which is the first target of this block. (2) The occurrence of vascular puncture or ocular complications may be more frequent due to repeated insertion [1-3]. (3) Although trigeminal neuralgia occurs most frequently in the second division, 80% of the cases may be treated by infraorbital nerve block. Therefore, physicians have less access to the cases that call for maxillary nerve block, the technique which takes time to master. (4) The diameter of the maxillary nerve is small compared to that of the mandibular nerve. (5) The fact that the occipito-mental projection, known as the only established radiographic method to confirm needle direction, is incapable of indicating the direction to the pterygopalatine fossa may be the major reason making maxillary nerve block even more difficult, associated with a low rate of success. To solve this problem, we devised the pterygopalatine fossa oblique view for clinical application during the procedure of maxillary nerve block. Before clinical trials of the new fluoroscopic method of maxillary nerve block, the angles formed between the tangential direction of the pterygopatatine fossa and the sagittal plane (angle A) and between the tangent of

Effect of intrathecal pretreatment with taurine on neurological outcome after transient spinal cord ischemia in the rat

Spinal cord ischemia and the resulting irreversible loss of neurological function is a devastating complication associated with transient aortic occlusion [1,2]. Several experimental studies indicate involvement of multifactorial changes comparable to those in supraspinal structures. This may involve excessive release of excitatory amino acids such as glutamate from spinal parenchyma and resulting activation of N-methyl-D-aspartate (NMDA) and non-NMDA receptors [3-5]. Increased intracellular Ca 2+ influx resulting from the activation of the NMDA receptor calcium ionophore is then believed to activate several classes of intracellular enzyme systems (lipases, endonucleases, and proteases) leading subsequently to irreversible neuronal degeneration [6,71. We have observed a comparably significant increase in taurine in the spinal dorsal horn after transient aortic occlusion in the rat [3], and an effect of transient brain ischemia on secondary extracellular taurine release has been also reported [8,9]. Although the precise role of taurine in the modulation of neuronal transmission is not known, it has been reported that taurine has the ability to inhibit NMDA receptor-induced calcium influx [10]. The above data would jointly predict that the exogenous activation of these neuromodulatory systems should provide protection under pathological conditions associated with excessive and/or prolonged activation of NMDA receptors. Accordingly, it has been