Arterial gas embolism as a pathophysiologic mechanism for spinal cord decompression sickness

A continuous infusion of air (1.0 ml.min-1) was delivered via a fine aortic cannula into the arterial circulation of 7 anesthetized dogs until no spinal cord function could be elicited by somatosensory evoked potentials. The animals were then rapidly perfusion-fixed and the spinal cords removed for histological examination. The appearance of the embolized cords differed substantially from eight spinal cords injured by fulminant decompression sickness (DCS). The embolized cords appeared essentially normal whereas the DCS cords featured extravascular, nonstaining, space-occupying lesions (SOLs) scattered throughout the cord, mainly in the white matter. Two spinal cords injured by DCS with a delayed onset (30 min from surfacing) appeared similar to the embolized cords. These findings are compatible with the hypothesis that two mechanisms are involved in the onset of spinal cord DCS. Fulminant disease is associated with SOLs, which are probably caused by the in situ evolution of a gas phase. Disease with a delayed onset is more likely to be caused by an ischemic mechanism, which in the acute phase is histologically indistinguishable from gas embolism.     

Experimental determination of latency, severity, and outcome in CNS decompression sickness

Twenty-eight dogs underwent a 300 fsw chamber dive designed to generate spinal cord decompression sickness (DCS), which was detected by observing a reduction in the amplitude of the spinal somatosensory evoked potential (SEP). After an interval of 15 min on the surface following diagnosis, the animals received a therapeutic recompression. The latency was defined as the time between surfacing from the dive and the diagnosis of DCS, the severity as the minimum SEP amplitude, and the outcome as the amplitude of the SEP after 2 h of treatment. Significant correlations between latency and severity (P less than 0.05), latency and outcome (P less than 0.01), and severity and outcome (P less than 0.05) were found. Canine spinal cord latency is shown to be very similar to that found in man up to a surface interval of 30 min. The association between latency, severity, and outcome of spinal cord DCS is discussed with reference to the possible mechanisms involved in this disease.     

Combined arterial gas embolism and decompression sickness following no-stop dives

Decompression sickness (DCS) has been clinically classified as Type I (predominantly joint pain) or Type II (predominantly spinal cord lesions). We present 3 cases that are all characterized by severe (Type II) DCS with signs and symptoms of spinal cord injury occurring in conjunction with arterial gas embolism (AGE). We consider the AGE "minor" because only 2 of the 3 subjects initially lost consciousness, and in all cases the signs and symptoms of the AGE had essentially resolved within 1 h or by the time recompression therapy began. DCS was resistant to recompression therapy, even though treatment began promptly after the accident in 2 of the 3 cases. None of the cases had a good neurologic outcome and there has been one death. None of the divers exceeded the U.S. Navy "no-stop" limits for the depths at which they were diving. We have observed a previously unreported clinical syndrome characterized by severe Type II DCS subsequent to AGE following pressure-time exposures that would normally not be expected to produce DCS. We postulate that AGE may have precipitated or predisposed to this form of DCS.     

Pressure in the treatment of spinal cord decompression sickness

Previous work had shown that a Po2 of about 2.0 bar was the optimal Po2 for the treatment of spinal cord decompression sickness (DCS). With 20 anesthetized dogs the hypothesis was tested that pressures in excess of a threshold, taken as 3 bar, did not enhance recovery of spinal cord DCS. Dogs were subjected to a 15-min air dive at 10 bar (300 ft) and decompressed over 5.5 min. At the surface, spinal cord evoked potentials (SEP) were observed for changes indicating DCS. Fifteen minutes after DCS was first detected the dogs were recompressed to 3, 5, 7, or 2.8 bar breathing 66, 40, 29, or 100% oxygen which gave a Po2 of 2.0 bar except in the 2.8 bar group. The recovery of the SEP over 2 h was observed. Group mean recoveries at 67, 62, 29, and 42% were not significantly different after 120 min. As the hypothesis was supported, a tentative proposal for changing current therapy was made.     

Oxygen in the treatment of spinal cord decompression sickness

Twenty-five anesthetized dogs were used to find the optimum Po2 for the delayed treatment of spinal cord decompression sickness (DCS). They were instrumented for the measurement of physiological variables and somatosensory spinal evoked potentials (SEP) given an air dive of 15 min at 10 bar (300 ft) and decompressed in under 6 min. At the surface SEP were observed for signs of DCS. Fifteen minutes after cord DCS was observed in the SEP, the dogs were compressed to 5.0 bar breathing one of 5 gas mixtures giving a Po2 of 1.0, 1.5, 2.0, 2.5, or 3.0 bar. At the start of therapy all groups were in a similar physiological state with a similar loss of SEP. Between 40 and 120 min, recovery was significantly different (P less than 0.05) between the groups, most SEP recovery having occurred within 15 min. The treatments ended with 22, 32, 70, 66, and 42% recovery, respectively. It would appear that the optimum Po2 is around 2.0 bar.     

隐性神经管闭合不全的MRI诊断分析

目的 探讨隐性神经管闭合不全的临床表现及MRI征象，提高对该病的诊断水平。方法 搜集了39例经手术和病理证实的隐性神经管闭合不全的资料，对其临床表现、手术结果和MRI征象进行回顾性分析。结果 脑脊膜膨出4例，背侧皮窦7例，脊柱脂肪瘤19例，原发性脊髓栓系综合症5例，脊髓纵裂2例，骶尾部畸胎瘤2例。MRI术前诊断与手术结果符合37例，约94．9％，2例误诊，约占5．1％。结论 MRI能明确显示隐性神经管闭合不全的部位、范围、信号改变及其与邻近组织的关系，是目前诊断该病的最有效检查方法。     

Effect of maternal vitamin B-6 restriction on pyridoxal phosphate concentrations in developing regions of the central nervous system in rats

The effect of maternal vitamin B-6 deficiency on concentrations of pyridoxal phosphate (PLP) within four different regions of the central nervous system (CNS) of progeny, the corpus striatum (CS), hypothalamus (H), cerebellum (C), total brain and first cervical segment (C-1) of the spinal cord was determined at 7, 15, 21 and 50 days of age. PLP concentrations in each CNS region, as well as in total brain at 15, 21 and 50 days postnatally, paralleled the level of vitamin B-6 in the deficient (0.6, 0.8, 1.0 mg pyridoxine . HCl per kilogram diet) and control diets (7.0 mg pyridoxine . HCl per kilogram diet). By 21 days of age, PLP concentrations had essentially plateaued in CNS regions of controls, whereas in the vitamin B-6-restricted groups, a significant catch-up in concentration was observed between 21 and 50 days of age in all CNS regions except C-1 of the spinal cord. Throughout postnatal development, PLP concentrations in the C-1 region of spinal cord and in hypothalamus appeared least affected by vitamin B-6 restriction and levels in CS and C were most affected. These findings suggested that the mechanism for intracellular trapping of B-6 vitamers may develop in a caudal to rostral direction within the CNS.     

Pathogenesis of mouse scrapie: patterns of agent replication in different parts of the CNS following intraperitoneal infection

The dynamics of agent replication were studied at 8 levels of spinal cord and in 9 areas of brain of mice infected intraperitoneally with the 139A strain of scrapie agent. Replication in the CNS was first detectable at 2 levels of spinal cord between thoracic vertebrae 4 and 9. The onset of replication was progressively delayed by up to 4 weeks at increasingly lower levels of spinal cord. A similar trend was seen at higher levels of spinal cord and in brain. In brain, agent replication occurred first in medulla, then in the pons and midbrain, thalamus and hypothalamus and, finally, striatum, septum, hippocampus and cerebral cortex. These results are highly suggestive of spread of infection from peripheral sites of agent replication along autonomic fibres to midthoracic cord, followed by an ascending and descending spread of agent at an apparent rate of 0.5 to 1.0 mm/day until the whole CNS is infected. However, experiments involving sympathectomy gave inconclusive results and the evidence for neural spread of scrapie in the peripheral nervous system is circumstantial.     

Air and nitrox saturation decompression: a report of 4 schedules and 77 subjects

Seventy-seven subjects were decompressed from air or nitrogen-oxygen (nitrox) saturation exposures at 18.3 to 40.2 meters sea water (msw) [60 to 132 feet sea water (fsw)] using four different decompression schedules. A h schedule for decompression from an air saturation-excursion profile at 18.3 msw (60 fsw) resulted in pain-only decompression sickness (DCS) symptoms in 2 of 23 subjects. A 32 and 35 h schedule from a different air saturation profile at 19.8 and 22.9 msw (65 and 75 fsw), respectively, resulted in DCS symptoms in 1 of 24 subjects. A third and fourth schedule for air or nitrox saturation at 40.2 msw (132 fsw) resulted in DCS symptoms in 3 of 12 and 1 of 18, respectively. No serious (type II) symptoms were observed as a result of any of the decompressions. All DCS cases consisted of knee pain occurring either in the last 3 msw of the decompression or shortly after surfacing. Doppler ultrasound monitoring revealed venous gas emboli (VGE) in several subjects, but generally only shallow to 6.1 msw (20 fsw). Results demonstrate an overall DCS incidence of 9%, and all cases were pain-only and localized to the knee. The third schedule (U.S. Navy heliox saturation decompression schedule) seems to produce a higher incidence of DCS than the other schedules when used in air or nitrox exposures. Differentiation between the schedules designed for nitrox was impossible due to the limited number of subjects in each and the variable nature of the exposures.     

Divergent Astrovirus Associated with Neurologic Disease in Cattle

Using viral metagenomics of brain tissue from a young adult crossbreed steer with acute onset of neurologic disease, we sequenced the complete genome of a novel astrovirus (BoAstV-NeuroS1) that was phylogenetically related to an ovine astrovirus. In a retrospective analysis of 32 cases of bovine encephalitides of unknown etiology, 3 other infected animals were detected by using PCR and in situ hybridization for viral RNA. Viral RNA was restricted to the nervous system and detected in the cytoplasm of affected neurons within the spinal cord, brainstem, and cerebellum. Microscopically, the lesions were of widespread neuronal necrosis, microgliosis, and perivascular cuffing preferentially distributed in gray matter and most severe in the cerebellum and brainstem, with increasing intensity caudally down the spinal cord. These results suggest that infection with BoAstV-NeuroS1 is a potential cause of neurologic disease in cattle.     

Influence of occupational diving upon the nervous system: an epidemiological study

Neurological signs and symptoms were recorded from 156 air and saturation divers and 100 controls. Fifty one (33%) of the divers had had symptoms from the central nervous system during decompression. Also, 22 (14%) had been unconscious while diving. In total 79 (51%) had had decompression sickness (DCS). Twelve (8%) of the divers and no controls had had specific neurological symptoms (vision disturbances, vertigo, reduced skin sensitivity) in non-diving situations, and six (4%) of the divers (no controls) had had episodes of cerebral dysfunction (seizures, transient cerebral ischaemia, transient amnesia). The divers had significantly more general symptoms from the nervous system and more abnormal neurological findings than the controls. The most prominent symptoms were difficulties in concentration and problems with long and short term memory. The most prominent abnormal findings in the divers were compatible with dysfunction in the distal spinal cord or nerve roots, and polyneuropathy. The general neurological symptoms and findings were independently significantly correlated with diving exposure, prevalence of DCS, and age.     

Influence of occupational diving upon the nervous system: an epidemiological study.

Neurological signs and symptoms were recorded from 156 air and saturation divers and 100 controls. Fifty one (33%) of the divers had had symptoms from the central nervous system during decompression. Also, 22 (14%) had been unconscious while diving. In total 79 (51%) had had decompression sickness (DCS). Twelve (8%) of the divers and no controls had had specific neurological symptoms (vision disturbances, vertigo, reduced skin sensitivity) in non-diving situations, and six (4%) of the divers (no controls) had had episodes of cerebral dysfunction (seizures, transient cerebral ischaemia, transient amnesia). The divers had significantly more general symptoms from the nervous system and more abnormal neurological findings than the controls. The most prominent symptoms were difficulties in concentration and problems with long and short term memory. The most prominent abnormal findings in the divers were compatible with dysfunction in the distal spinal cord or nerve roots, and polyneuropathy. The general neurological symptoms and findings were independently significantly correlated with diving exposure, prevalence of DCS, and age.     

Light and electron microscopic alterations in spinal cord myelin sheaths after decompression sickness

Pathological examination of spinal cords from animals subjected to experimental decompression sickness (DCS) was undertaken in an attempt to explain the disparate response to treatment observed. Eight experimental animals, four undived control animals, and two dived but untreated animals were perfusion fixed, and the spinal cords were removed. Light microscopy of toluidine blue stained, ultrathin sections from dived animals demonstrated a distinctive widened myelin sheath showing a banded pattern of myelin disruption. This pattern was confirmed by electron microscopy and showed the separation to be between abutting double layers of myelin. Artifactual changes were also present in dived and undived animals. These previously unreported changes may be caused by DCS. They are compatible with the major mechanisms proposed in the pathophysiology of spinal cord DCS and may also account for the response to treatment seen in our experimental animals. It is suggested that these findings may also explain the response to treatment seen in patients, together with the formation of late lesions described in the spinal cords of long-term survivors of DCS.     

Surgical management of spinal epidural disease: an update

Management of spinal cord compression from metastatic malignant disease remains unsatisfactory. Results of surgical decompression are at best less than those of radiation therapy alone. However, new surgical approaches now focus on removing the anterior-situated tumor tissue which produces neural compression in about 85% of the cases. The results of these procedures that allow removal of the ventrally compressing tumor show significant improvement in the management of patients with spinal epidural disease. We review the surgical strategy of these new approaches and the attendant results.     

Exposure to methyl isobutyl ketone: toxicokinetics and occurrence of irritative and CNS symptoms in man

The toxicokinetics as well as irritative effects and CNS symptoms of methyl isobutyl ketone (MIBK) were studied in human volunteers during inhalation exposure. The volunteers were exposed (2h, 50 W) in an exposure chamber on four different occasions to about 10, 100 and 200 mg/m3 MIBK and to a combination of about 100 mg/m3 MIBK and 150 mg/m3 toluene. The relative pulmonary uptake of MIBK was about 60% and the total uptake increased linearly with increasing exposure concentration. The concentration of MIBK in blood rose rapidly after the onset of exposure and no plateau level was reached during exposure. No tendency for saturation kinetics could be observed within the dose interval and the apparent blood clearance was 1.61/h/kg at all exposure levels. The concentration of unchanged MIBK in the urine after exposure was proportional with the total uptake. Only 0.04% of the total MIBK dose was eliminated unchanged via the kidneys within 3 h post exposure. The concentrations of the metabolites 4-hydroxy-4-methyl-2-pentanone and 4-methyl-2-pentanol were below the detection limit (5 nmol/l). Irritative and CNS symptoms occurred during exposure. The degree of both irritative and CNS symptoms increased during exposure to 100 and 200 mg/m3 compared with 10 mg/m3, but combination exposure with toluene exhibited the most pronounced effect. There were no significant effects from exposure on the performance of a simple reaction time task or a test of mental arithmetic.     

62例肌萎缩侧索硬化的临床分析

目的探讨肌萎缩侧索硬化(Amyotrophic Lateral Sclerosis,ALS)的临床和电生理特征。方法收集2004年1月1日至2010年6月30日期间佛山市中医院神经内科收治的62例ALS患者,回顾性分析这些病人的资料并总结其临床特征。结果本组病人的主要临床特征为慢性隐袭起病,中老年发病(平均发病年龄为49.3岁),男性多发(男女比例为1.48∶1),首发症状多为单侧上肢肌无力(54.8%),可伴有肌肉萎缩,吞咽、言语困难等,电生理检查均表现为脑神经和多个脊髓节段广泛的神经源性损害。结论肌萎缩侧索硬化症是一种累及脊髓前角细胞、脑干运动神经核及锥体束,具有上下运动神经元损害并存的慢性进行性神经系统变性疾病。早期诊断是本病的难点,且容易出现误诊。肌电图对本病的诊断和鉴别诊断有重要意义。     

通过建立实验动物模型实现对伴有复杂脊髓损伤的先天性脊柱侧凸疾病的实验医学研究

目的通过建立大白鼠试验动物模型实现对伴有复杂脊髓损伤的先天性脊柱侧凸疾病的实验医学研究。方法采用经9．4％的氢氧化钠水溶液稀释后的6-巯基嘌呤液,按30ml／kg剂量行腹腔内注射造模,并对具有先天性脊柱侧弯临床和影像学诊断的20只仔鼠（其中5只仔鼠出生后立即出现脊髓瘫,临床症状）中剩余的15只无明显神经症状的仔鼠进行被动直立状态下的生活观察,6d～10d,13只仔鼠出现了典型的双侧后肢完全性瘫痪。对所有实验动物模型进行影像学和脊柱脊髓的组织学观察。结果脊柱影像学观察,所有实验动物模型都表现出典型的先天性脊柱侧弯畸形伴有楔形半椎体和附件的畸形;组织学观察,畸形半椎体发生了明显向椎管方向的移位,压迫相应节段的脊髓,在部分实验动物表现为侧弯顶点的楔形半椎体连同间盘一起向椎管方向移位;相应的骨性结构对脊髓节段形成压迫;骨与脊髓的滋养血管被破坏,楔形半椎体上部的椎管内软脊膜上瘀滞的静脉丛．下方无血管区和椎管狭窄区的血管分布缺失和侧弯顶点水平静脉丛的破败,血管的狭窄和动脉瘤样增宽的病灶区。结论模型大白鼠生长发育的脊柱在受到来自垂直方向上的动-静态负荷的作用,导致脊柱畸形的进一步加重,并通过影像学和组织学观察得到证实．其发病机制变化特点与临床资料相符合,为临床工作提供了实验医学基础,对临床治疗原则的制定起到指导作用。     

Exposure to methyl isobutyl ketone: toxicokinetics and occurrence of irritative and CNS symptoms in man

Summary The toxicokinetics as well as irritative effects and CNS symptoms of methyl isobutyl ketone (MIBK) were studied in human volunteers during inhalation exposure. The volunteers were exposed (2 h, 50 W) in an exposure chamber on four different occasions to about 10,100 and 200 mg/m³ MIBK and to a combination of about 100 mg/m³ MIBK and 150 mg/m³ toluene. The relative pulmonary uptake of MIBK was about 60% and the total uptake increased linearly with increasing exposure concentration. The concentration of MIBK in blood rose rapidly after the onset of exposure and no plateau level was reached during exposure. No tendency for saturation kinetics could be observed within the dose interval and the apparent blood clearance was 1.6 l/h/kg at all exposure levels. The concentration of unchanged MIBK in the urine after exposure was proportional with the total uptake. Only 0.04% of the total MIBK dose was eliminated unchanged via the kidneys within 3 h post exposure. The concentrations of the metabolites 4-hydroxy-4-methyl-2-pentanone and 4-methyl-2-pentanol were below the detection limit (5 nmol/l). Irritative and CNS symptoms occurred during exposure. The degree of both irritative and CNS symptoms increased during exposure to 100 and 200 mg/m³ compared with 10 mg/m³, but combination exposure with toluene exhibited the most pronounced effect. There were no significant effects from exposure on the performance of a simple reaction time task or a test of mental arithmetic.     

通过建立实验动物模型实现对伴有复杂脊髓损伤的先天性脊柱侧凸疾病的实验医学研究

目的通过建立大白鼠试验动物模型实现对伴有复杂脊髓损伤的先天性脊柱侧凸疾病的实验医学研究。方法采用经9.4%的氢氧化钠水溶液稀释后的6-巯基嘌呤液,按30ml/kg剂量行腹腔内注射造模,并对具有先天性脊柱侧弯临床和影像学诊断的20只仔鼠(其中5只仔鼠出生后立即出现脊髓瘫临床症状)中剩余的15只无明显神经症状的仔鼠进行被动直立状态下的生活观察,6d～10d,13只仔鼠出现了典型的双侧后肢完全性瘫痪。对所有实验动物模型进行影像学和脊柱脊髓的组织学观察。结果脊柱影像学观察,所有实验动物模型都表现出典型的先天性脊柱侧弯畸形伴有楔形半椎体和附件的畸形;组织学观察,畸形半椎体发生了明显向椎管方向的移位,压迫相应节段的脊髓,在部分实验动物表现为侧弯顶点的楔形半椎体连同间盘一起向椎管方向移位;相应的骨性结构对脊髓节段形成压迫;骨与脊髓的滋养血管被破坏,楔形半椎体上部的椎管内软脊膜上瘀滞的静脉丛,下方无血管区和椎管狭窄区的血管分布缺失和侧弯顶点水平静脉丛的破败,血管的狭窄和动脉瘤样增宽的病灶区。结论模型大白鼠生长发育的脊柱在受到来自垂直方向上的动-静态负荷的作用,导致脊柱畸形的进一步加重,并通过影像学和组织学观察得到证实。其发病机制变化特点与临床资料相符合,为临床工作提供了实验医学基础,对临床治疗原则的制定起到指导作用。     

后路减压及内固定手术治疗合并脊髓损伤的多节段脊柱不稳的疗效观察

目的探讨和学习脊柱各节段后路手术的内固定装置技术治疗因多种原因所致的伴不同部位脊髓损伤的多节段脊柱不稳，并观察其疗效。方法特性化各个不同节段脊柱后路的开窗减压、内固定和融合技术治疗69例此类病例，包括暴力性急性多节段脊柱骨折、慢性多节段椎管狭窄和外伤后的先天性颈椎和颅底凹陷畸形等三种情况。术后随访1-3年，术前和术后随访的脊髓损伤情况按ASIA的标准作分级和疗效分析。结果52例病人完全恢复。9例绝大部分恢复。4例需扶杖行走。2例全瘫病人恢复不理想。1例仍全瘫。1例半年死亡。其治愈率和基本治愈率分别是75％和13％，总有效率88％。结论该技术对多节段脊柱不稳治疗有效，特别对伴有不完全性脊髓损伤病例。