Kazumasa Terada

Tortuosity of the vertebral artery in patients with cervical spondylotic myelopathy: Risk factor for the vertebral artery injury during anterior cervical decompression

Study Design The case report presented herein shows tortuosity of the vertebral artery in a patient with cervical myelopathy. This case led the authors to evaluate 22 other patients who also had undergone anterior cervical fusion. They were studied before operation by either magnetic resonance imaging angiography or selective vertebral angiography. Objectives To analyze the radiographs, computed tomography, magnetic resonance imaging, and angiography findings to detect any tortuosity of the vertebral artery in patients with cervical myelopathy to show the risk factors of vertebral artery injury during anterior decompression. Summary of Background Data Complications of vertebral artery laceration during cervical anterior decompression are rare, so this injury and abnormality in the course of vertebral artery in patients with cervical myelopathy receive little attention. Methods The tortuosity of the vertebral artery was assessed by angiography, magnetic resonance imaging, and computed tomography. Results Mild vertebral artery tortuosity was observed in 10 patients and loop formation in three associated with cervical spondylotic changes. Conclusions This study suggests that vertebral artery loop formation is developed associated with cervical spondylotic changes. During the anterior decompression of cervical spondylotic myelopathy or radiculopathy, the looped vertebral artery could be injured by an excessive wide rejection of the bone or disc material. In the case of vertebral artery migration, the looped vertebral artery can even be injured by routine procedures.

Blocking actions of Ca2+ antagonists on the Ca2+ channels in the smooth muscle cell membrane of rabbit small intestine

Actions of Ca2+ antagonists, verapamil, nicardipine and diltiazem, were investigated on the Ca2+ inward current in the fragmented smooth muscle cell membrane (smooth muscle ball; SMB) obtained from the longitudinal muscle layer of the rabbit ileum, by enzymatic dispersion. All Ca2+ antagonists inhibited the inward current, in a dose-dependent manner. The ID50 value on the maximum amplitude of the inward current of nicardipine was 24 nM, and this value was roughly 50 times lower than values obtained with verapamil and diltiazem, when the inward current was provoked by 0 mV command pulse from the holding potential of −60 mV. Lowering the holding potential to −80 mV shifted the dose-response curve to the right. When depolarizing pulses (100 ms, stepped up to 0 mV from −60 mV or −80 mV) were applied every 20 s, the peak amplitude of the inward current remained unchanged, but nicardipine immediately, and diltiazem and verapamil slowly reduced the peak amplitude. These slow inhibitions by the latter two drugs depended on the frequency or number of stimulations. Nicardipine but not diltiazem and verapamil shifted the voltage-dependent inactivation curve to the left (3 s duration of the conditioning pulse). However, with a longer conditioning pulse (10 s) verapamil and diltiazem shifted the voltage-dependent inactivation curves to the left. Therefore, the inhibitory actions of these Ca2+ antagonists differ. Namely, diltiazem and verapamil inhibit the Ca2+ channels, mainly in a frequency-or use-dependent manner while nicardipine does so in a voltage-dependent manner.

Ryanodine inhibits the Ca-dependent K current after depletion of Ca stored in smooth muscle cells of the rabbit ileal longitudinal muscle.

1 Effects of ryanodine on the membrane currents were investigated on dispersed smooth muscle cells of rabbit ileal longitudinal layer using voltage and patch clamp procedures. 2 With voltage clamp, membrane depolarization to 0mV from the holding potential of − 60 mV produced an inward Ca current (ICa) which was followed by transient and sustained outward currents (ITO and Iso, respectively). Prolonged depolarization of the membrane produced spontaneous oscillations of the outward current (oscillatory outward current; Ioo) on Iso. 3 Ryanodine (30 μm) modified neither the basal membrane current recorded at the holding potential (‐60 mV) nor Iso. Ryanodine inhibited both ITO and Ioo in a concentration‐dependent manner (IC50 = 5.5 and 4.5 μm, respectively, measured 12 min after application of ryanodine). These values were much higher than that observed in skeletal muscle for Ca release. 4 The time course of the ryanodine‐induced inhibition of Ioo was slow and the inhibition was irreversible. Caffeine (3mm) enhanced the amplitudes of ITO and Ioo in the presence of Ca, and only transiently enhanced Ioo in the absence of Ca. However, following application of 10 μm ryanodine, 3 mM caffeine did not increase Ioo. 5 Ryanodine (3–30 μm) slightly enhanced the amplitude of ICa evoked by depolarization pulses at potentials more negative than 0 mV but not that induced by larger depolarizations (positive potentials). 6 With patch clamp procedure, single Ca‐dependent K channel currents were recorded in cell free and cell attached configurations. Application of 30 μm ryanodine transiently enhanced the Ca‐dependent K current without any detectable changes in the amplitude of the single channel current recorded in the cell attached condition. In the inside‐out membrane patch, when the intracellular membrane side was superfused with 1 μm Ca buffered with 10 mM EGTA, bath application of 10 μm ryanodine had no effect on the Ca‐dependent K current. 7 It was concluded that both ITO and Ioo are generated by Ca released from intracellular stores, mainly sarcoplasmic reticulum. Ryanodine appears to open irreversibly the Ca channel in the store and to inhibit the Ca‐dependent K channel due to depletion of the stored Ca.

Effects of inositol phosphates on the membrane activity of smooth muscle cells of the rabbit portal vein

The effects of intracellular perfusion of inositol 1,4,5-trisphosphate (InsP3) or inositol 1,3,4,5-tetrakisphosphate (InsP4) on electrical responses of smooth muscle cell membranes of the rabbit portal vein were studied using the whole cell voltage clamp technique. Depolarisation to 0 mV from a holding potential of −60 mV, evoked inward Ca (ICa), transient outward (ITO), oscillatory outward (IOO) and sustained outward (ISO) currents. Generation ofIOO was dependent on the [Ca]o, but it was also generated in 0 mM Ca solution for over 10 min. Form amplitude histograms,IOO was divided into two components. Reduction in [Ca]o inhibited the appearance of but not the amplitudes of bothIOO components. However, the larger component ofIOO was more resistant to a reduction in [Ca]o than the smaller one. InsP3 (10 μM) increased the frequency of bothIOO components to a greater extent than their amplitude, but the larger component was more sensitive to InsP3 than the smaller one. The increase in the occurrence ofIOO induced by InsP3 did not occur following pretreatment with 3 mM caffeine or 1 nM A23187. In normal PSS, InsP3 was evoked by a depolarising pulse positive to −40 mV, whereas following perfusion with InsP3 (10 μM),IOO was evoked at −60 mV. In normal PSS, intracellular perfusion with 10 μM InsP4 changed neither the frequency nor the amplitude ofIOO, and the amplitudes ofICa,ITO andISO were also unchanged. However, in 10 mM Ca solution, 10 μM InsP4 generatedIOO at a membrane potential of −60 mV. It is concluded that InsP3 activatesIOO in smooth muscle cell membranes of the rabbit portal vein by causing an increase in intracellular Ca by facilitating Ca release from the storage sites. In 10 mM Ca solution, InsP4 also accelerates the generation ofIOO, and it is possible that this effect is mediated by inositol 1,3,4-trisphosphate, a metabolite of InsP4 rather than by InsP4 itself.

Different inhibitions of the voltage-dependent K+ current by Ca2+ antagonists in the smooth muscle cell membrane of rabbit small intestine

Actions of Ca2+ antagonists (verapamil, nicardipine and diltiazem) on the voltage-dependent K+ current, obtained from the fragmented smooth muscle cell membrane (smooth muscle ball; SMB) of the rabbit small intestine, were investigated using voltage clamp techniques. To eliminate the influence of the Ca2+-dependent K+ current, the voltage-dependent K+ current was recorded in 2.5 mM Mn2+ (Ca2+ omitted) solution. These three Ca2+ antagonists inhibited the peak amplitude of the K+ current, in a dose-dependent manner. During application of a long command pulse (duration, 3 s), the amplitude of the voltage-dependent K+ current decreased slowly with time. Diltiazem inhibited the K+ current with a slight prolongation of the 20% decay time, while TEA (tetraethyl-ammonium), a K+ channel blocker, inhibited the current, without affecting the decay. By contrast, verapamil and nicardipine accelerated inactivation. In the control, the voltage-dependent inactivation was also seen in the K+ current. This inactivation curve below 0 mV was not modified by 10 μM diltiazem, 5 μM verapamil nor 3 μM nicardipine. These results indicate that inhibition of the voltage-dependent K+ current by verapamil or nicardipine differed from that by diltiazem.

Herniation of calcified cervical intervertebral disc causes dissociated motor loss in a child.

Herniation of the calcified nucleus pulposus is a rare complication of intervertebral disc calcification in children. Surgical intervention is rarely indicated in the majority of such cases. This paper reports a 12-year-old boy with a calcified nucleus pulposus at C7-T1 which had ruptured into the spinal canal, causing dissociated motor loss. Anterior discectomy and fusion were performed and the patients muscle weakness markedly improved after surgery.

D600 blocks the Ca2+ channel from the outer surface of smooth muscle cell membrane of the rabbit intestine and portal vein

The voltage dependent Ca2+ inward current in single smooth muscle cells dispersed from the longitudinal muscle layer of the rabbit ileum and rabbit portal vein was recorded using the whole-cell voltage clamp technique. D600 added to the bathing solution inhibited the Ca2+ current, while the intracellular perfusion of this agent did not reduce the amplitude of this current. Thus, D600 probably acts from the outer surface of the membrane. The nature of the Ca2+ channel in smooth muscle cells seems to differ from that in cardiac muscle cells.

A novel technique for surgical resection of spinal meningioma.

Study Design. A technical note. Objectives. To describe and discuss a novel technique for surgical resection of spinal meningioma. Summary of Background Data. With conventional methods for surgical resection of isolated intradural spinal meningioma, there are two ways of dealing with the dural attachment of the tumor. One is complete resection of the involved dura together with the tumor, and the other is coagulation only of the tumor base of the dura. In the case of the novel technique herein described, the dura mater is preserved in a new manner. Methods. In the surgical procedure a small incision is made in the surface of the dura mater after the conventional laminectomy. The spinal dura can be easily divided into two layers, comprising inner and outer layers. The outer layer is stripped away from the inner layer surrounding the tumor base. The tumor is then resected together with the inner layer alone outside the arachnoid membrane, and finally the outer layer is simply closed. Results. This method has been applied to three cases. The preserved outer layer of the dura mater did not demonstrate the existence of tumor cells histologically. Neither complications nor tumor recurrence have been experienced. Conclusion. The authors introduced a novel technique for surgical resection of isolated intradural spinal meningioma. Using this simple procedure the outer part of the dura mater, which is not involved by the tumor, can be preserved and complicated dural reconstruction is not necessary. Furthermore, there is less risk of postoperative cerebrospinal fluid fistulas than when the dura is completely resected together with the tumor. However, long-term observation as a result of the possibility of local recurrence is strongly recommended.

The effect of nerve root lesioning on various somatosensory evoked potentials in the hog

Somatosensory evoked potentials (SEPs) were recorded at the lumbar spine following stimulation of the tibial nerve (mixed-nerve SEP; MSEP), the sural nerve (specific nerve SEP; SSEP), and the skin corresponding to the L6 and S1 dermatomes (dermatomal field SEP; DSEP-L and DSEP-S) in the hog. To determine the sensitivity of these three SEPs to the single nerve root (S1 root) function, the effects of nerve roots lesioning were investigated. Cutting S1 nerve root reduced the peak-to-peak amplitude of MSEP by only 28% in comparison with baseline values. The relative amplitudes of SSEP, DSEP-L, and DSEP-S were decreased by 46%, 11% and 51%, respectively. When S1 nerve root was left intact and L5, L6, and S2 nerve roots were cut, the relative amplitudes of MSEP, SSEP, DSEP-L, and DSEP-S were decreased to 68%, 73%, 31%, and 74%, respectively. These results indicate that DSEP-S is as sensitive to the function of S1 nerve root as SSEP but the sensitivities of DSEP-S and SSEP are low in the hog. MSEP is shown unsuitable to monitor the single nerve root dysfunction.

Characteristics of lumbar scoliosis in patients with rheumatoid arthritis

BackgroundAlthough a substantial percentage of patients with rheumatoid arthritis (RA) experience low back pain, the characteristics of lumbar spine pathology in RA patients has been poorly investigated. In our institutions, lumbar spine radiographs indicated scoliosis in 26 patients. The present study aimed to clarify the characteristics of lumbar scoliosis in RA patients.MethodsThis is a retrospective study of 26 RA patients with lumbar scoliosis. Patient characteristics such as disease duration, disease stage and class according to Steinbrockers classification, and medication for RA and osteoporosis were reviewed. Radiologic evaluation of scoliosis was performed at two different time points by measuring Cobb angles. The progression of scoliosis per year was calculated by dividing the change in Cobb angles by the number of years. Apical vertebral rotation, lateral listhesis, and the level of the intercrestal line at the first observation were also measured. The correlation between different factors and changes in the Cobb angles per year was analyzed.ResultsMajority of the patients had a long disease duration and were classified as stage 3 or 4 according to Steinbrockers classification. During the observation period, most patients were treated with glucocorticoids. Unlike the previous studies on degenerative scoliosis, apical vertebral rotation, lateral listhesis, and the level of the intercrestal line at initial observation were not significantly related to the progression of scoliosis. Initial Cobb angles were inversely related to the progression of scoliosis. Patients who were treated with bisphosphonates showed slower progression of scoliosis.ConclusionsOur results indicate that the characteristics of lumbar scoliosis in RA patients differ from those of degenerative lumbar scoliosis. Bone fragility due to the long disease duration, poor control of disease activity, and osteoporosis is possibly related to its progression.