Chronic neurogenic quadriceps amyotrophies

Summary Two cases of quadriceps amyotrophy, probably of chronic neurogenic origin are reported. Only the knee jerks were diminished, the calves hypertrophic, and the serum creatine kinase level very high in one case, and there were neurogenic electromyographic abnormalities in the quadriceps. In the first case, biopsy of the quadriceps muscle revealed a neurogenic origin with hyalinized hypertrophic fibres. CT scan showed abnormalities not only in the quadriceps but also in the sartorius, gracilis and gastrocnemius muscles. A second biopsy specimen from the gastrocnemius muscle showed histological findings similar to those of the quadriceps. In the second case, the EMG and biopsy findings suggested a myogenic origin, but 6 years later they were compatible with neurogenic atrophy. Differentiation from Becker dystrophy is very difficult in the first case and the second case is more a focal spinal amyotrophy. Further, in spite of their localization, the extension of the affected muscles changes the diagnosis. The same applies to chronic quadriceps amyotrophy in general, which cannot be regarded as an entity, but which suggests muscular dystrophy, spinal atrophy, polymyositis or a metabolic disorder. These cases can be compared with the four cases reported in the literature, which were regarded as a forme fruste of chronic spinal amyotrophy.     

Effects of acute and chronic treatment with imipramine on 5-hydroxytryptamine nerve cell groups and on bulbospinal 5-hydroxytryptamine/substance P/thyrotropin releasing hormone immunoreactive neurons in the rat. A morphometric and microdensitometric analysis

Summary Groups of male rats were treated for a period of 14 days with imipramine (10mol/kg) given twice daily. Separate groups of rats received a single dose treatment using the same dose and experimental design as for the repeated treatment. Employing the avidin-biotin immunoperoxidase technique for immunohistochemistry 5-hydroxytryptamine (5-HT)-, substance P (SP)- and thyrotropin releasing hormone (TRH)-like immunoreactivities (IRs) were visualized in consecutive coronal sections of the brain stem and of the spinal cord. The IRs were studied by means of morphometric and microdensitometric procedures using automatic image analysis on profiles representing nerve terminal networks of the ventral horn of the cervical and lumbar enlargements of the spinal cord as well as their coexistence (5-HT/SP and 5-HT/TRH). With the same technique 5-HT IR was measured in the 5-HT nerve cell groups of the medulla oblongata (B 1, B 2, B 3) and of the nucleus raphe dorsalis (B 7) of the midbrain. In addition 5-HT and 5-hydroxyindolacetic acid (5-HIAA) levels were measured in the ventral and dorsal horns of the cervical and lumbar enlargements of the spinal cord using high performance liquid chromatography (HPLC). In the same parts of the spinal cord SP IR was studied by means of radioimmunoassay (RIA).The microdensitometric studies showed that chronic, but not acute, imipramine treatment selectively increased SP IR in the 5-HT/SP/TRH costoring nerve terminals of the medial part of the ventral horn in both the cervical and the lumbar enlargements. Furthermore, quantitative analysis of the entity of coexistence in the 5-HT nerve terminal networks of these areas showed that all the 5-HT nerve terminals contained SP and TRH IRs and that this phenomenon remained after acute and chronic imipramine treatment. The microdensitometric studies on the 5-HT nerve cell groups of the medulla oblongata and of the nucleus raphe dorsalis demonstrated that chronic, but not acute, imipramine treatment selectively increased 5-HT IR in the nerve cell bodies of the lateral part of group B 3 as evaluated from the median grey values. Acute, but not chronic, imipramine treatment significantly increased the field area of 5-HT IR of nerve cell bodies in group B 7, reflecting an increase in the mean profile area of the 5-HT IR nerve cell body profiles. Instead, the mean profile area of 5-HT IR cell bodies of group B 1 was acutely reduced by imipramine.The biochemical studies demonstrated that chronic imipramine treatment selectively reduced 5-HT utilization in the ventral horn of the spinal cord and selectively increased SP IR in the dorsal horn of the lumbar enlargement.In view of these observations it is suggested that chronic imipramine treatment specifically increases SP IR in the 5-HT/SP/TRH costoring nerve terminals of the ventral horn probably related to reduced SP release and reduced 5-HT utilization in these terminals. The results obtained in group B 7 may be explained by a regulation by the³H-imipramine raphe binding sites of fast axonal transport, an influence which may have therapeutic consequences. This mechanism may also be responsible for the increase in 5-HT IR seen upon chronic imipramine treatment in the lateral part of the 5-HT nerve cell body group B 3. Such an effect may lead to a metabolic down-regulation of group B 7, having a possible role for the antidepressant activity of imipramine. The reduction of the mean profile area of 5-HT IR cell bodies of group B 1 seen in the acute treatment can possibly be caused by, noradrenaline (NA) uptake inhibition in inhibitory NA terminals innervating the B 1 group. These results also illustrate the heterogeneities in the responses of the 5-HT nerve cell groups to antidepressant treatment. The ability of chronic imipramine treatment to increase SP IR in the dorsal horn of the lumbar enlargement may reflect the existence of a monoamine-SP interaction in the substantia gelatinosa due to the NA and/or 5-HT uptake blocking activity of imipramine. The existence of such an interaction may help to explain the antinociceptive effect of chronic imipramine treatment.Part of the paper was presented at the 17th International Congress of the International Society of Psychoneuroendocrinology, Bergen, June 29–July 4, 1986.     

“High spinal” dysrhaphism

Summary High spinal (cervical and upper thoracic) dysrhaphism usually involves either a meningocele or a dermal sinus tract. These high spinal lesions can have a complex intradural anatomy at the level of the lesion (as this case reports) and are associated with an increased incidence of lower spinal occult dysrhaphic anomalies. It is therefore recommended that patients with high spinal dysrhaphism undergo radiological evaluation of the entire spine to identify those patients with intradural anomalies, define the anatomy for surgery, and investigate the lower spine for associated occult anomalies.     

脑血管性痴呆的辨证治疗经验

大脑动脉粥样硬化引起的脑血管性痴呆,以神智痴呆、记忆力减退、表情淡漠、呆滞或欣快感、头晕肢麻、手足瞤动等为特点,属于祖国医学的“文痴”、“语言颠倒”、“癫狂”、“善忘”等病症。中老年以后,肝血衰少,肾精亏损,脑失所养,大病久病,热灼真阴,心肝肾阴阳失调,肝阳化风,挟火挟痰,冲犯脑髓,元神失聪。因此,本病是本虚标实之证。虚者,治以培补真阴,补髓填精;实者,则平肝泻火,涤痰醒神,调气化瘀。文中附病案两例,经两个多月治疗,智力提高、记忆增强、精神活动基本恢复正常、生活自理,好转出院。     

Isolation and characterization of a cDNA coding for a novel human 17.3K myelin basic protein (MBP) variant

Human fetal spinal cord poly A (+) mRNA was found to direct the synthesis of three major myelin basic protein (MBP) variants with molecular weights of 17K, 18.5K, and 21.5K when translated in reticulocyte lysates. In order to investigate the structural relationships between these MBP variants and their corresponding mouse variants, human fetal spinal cord and mouse brain cDNA libraries were constructed and screened for MBP cDNAs. A number of MBP cDNA clones were isolated and characterized. One of these, PP535 contained the entire coding region of the mouse 14K MBP; and another mouse cDNA clone, PP1.85, was almost full-length and coded for either the 21.5K MBP or the 18.5K MBP. A human clone (KK36), 1,173 nucleotides in length, contained the entire coding region of an MBP variant with a molecular weight of 17,342. The structure of this clone within its coding region is significantly different from the corresponding mouse 17K MBP cDNA. It is missing two sequences found in the mouse 17K MBP cDNA (exons 2 and 5); and it contains a sequence (exon 6) that is missing from the mouse 17K MBP cDNA. Thus, this human 17.3K cDNA codes for a "17K" human MBP variant that is quite different from the corresponding mouse variant and is identical to the human 18.5K MBP except for a deletion of a peptide consisting of 11 amino acids that includes the single tryptophan residue of the 18.5K MBP. An analysis of the structure of this 17.3K human MBP cDNA suggests that the major pathway for splicing the primary human MBP gene product may be different from that in the mouse.     

神经生长因子对脊髓损伤后脊髓组织一氧化氮生成的影响

目的 :探讨神经生长因子 ( NGF)对脊髓损伤保护作用的机制 ,为临床应用提供理论依据。方法 :采用 Allen法以 2 5 g/cm3力致伤大鼠 T8脊髓 ,插蛛网膜下隙导管于术后即刻、2、4、8、12、2 4 h各注入神经生长因子 ( NGF)溶液 ,并与生理盐水组和正常对照组作对照。采用免疫组化法 ( ABC法 )和原位杂交法检测神经元型固有型一氧化氮合成酶 ( nc NOS)在脊髓中的表达。结果 :大鼠伤后脊髓前角运动神经元出现 nc NOS蛋白和 nc NOS m RNA异常表达 ,NGF组与生理盐水组相比较 ,nc NOS蛋白和nc NOS m RNA异常表达明显减少 ( P<0 .0 1或 P<0 .0 5 )。结论 :NGF能通过抑制脊髓损伤 nc NOS的异常表达 ,抑制一氧化氮( NO)过多释放所致的神经毒性作用 ,从而保护了损伤的神经组织。     

恩丹西酮预防椎管内阻滞后寒战的效果

①目的观察麻醉前静脉注射恩丹西酮预防椎管内阻滞后寒战的效果和对腋温的影响.②方法选择腰麻-硬膜外联合麻醉下行经腹全子宫切除术病人160例,随机分为两组,实验组(n=80)麻醉前静脉注射恩丹西酮8mg;对照组(n=80)麻醉前静脉注射生理盐水4mL,观察两组术中平均动脉压、心率、腋温变化和寒战发生情况.③结果实验组8例出现寒战(10.0%),对照组26例出现寒战(32.5%),两组比较差异有显著性(x2=7.05,P＜0.01).两组平均动脉压、心率、腋温变化差异无显著性(t=0.14～1.71,P均＞0.05).④结论恩丹西酮可预防椎管内阻滞后寒战的发生,但对腋温无影响.     

Different spinal effects of opioid agonists on spinal and spino-bulbo-spinal reflexes in rats

Summary The effects of morphine-HCl (MOR), methionine-enkephalin (ME) and dynorphin_1–13 (DYN) on spinal and spino-bulbo-spinal (SBS) reflexes were studied. Although spinal intrathecal administration of MOR (15g) did not produce any apparent effect on these reflexes, systemically administered MOR (3mg/kg i.v.) reduced the electrical toe stimulation-induced SBS reflex. Furthermore, MOR (3mg/kg i.v.) increased the polysynaptic reflex induced by electrical stimulation of low-threshold dorsal root afferents in intact (non-spinal) rats, but not in spinal rats. Intrathecally administred DYN (0.5 and 5 g) reduced both the electrical toe stimulation-induced spinal and SBS reflexes, while ME (15g) only reduced the SBS reflex. These results indicate the physiological multiplicity of spinal opioid receptors. MOR may affect supraspinal nuclei but not the spinal pathway which possesses MOR-sensitive opioid receptors, whereas ME and DYN affect spinal opioid peptide receptors and modulate the reflex activities in which they participate.     

Characterization and Function of Spinal Excitatory Interneurons with Commissural Projections in Xenopus laevis embryos

The multipolar somata of dorsolateral commissural (dlc) interneurons (Roberts and Clarke, 1982) lie in a superficial dorsolateral position in the spinal cord of Xenopus laevis embryos. By applying horseradish peroxidase to one-half of the 100 microm diameter spinal cord, these neurons have been backfilled. Their dendritic branching pattern, commissural axonal projection and distribution near the time of hatching is described. Using Lucifer yellow-filled microelectrodes a population of sensory interneurons with dlc morphology has been identified. They have multipolar somata in a dorsolateral superficial position, obliquely projecting dendrites and a ventral commissural axon. They receive presumed monosynaptic excitation in response to electrical stimulation of sensory neurites in the skin on the same side as the soma. During fictive swimming activity in curarized embryos the dlc interneurons are rhythmically inhibited in time with ventral root discharge on the same side. Dlc interneurons can fire multiple impulses and can turn on fictive swimming when stimulated by intracellular current injection. Skin stimulation is followed by excitatory postsynaptic potentials (EPSPs) in contralateral ventral rhythmic neurons. These EPSPs are reduced by the application of NMDA receptor antagonist. We conclude that dlc interneurons are excited by primary skin afferent Rohon - Beard neurons, carry sensory information across the spinal cord to excite neurons on the opposite side by release of an excitatory amino acid transmitter and participate in reflexes and in the initiation of swimming.     

Comparison of Effects of Various Types of NA and 5-HT Agonists on Transmission from Group II Muscle Afferents in the Cat

A number of noradrenaline and serotonin agonists were tested to investigate which of them replicate the depressive actions of monoamines on transmission from group II muscle afferents in the cat spinal cord. The agonists were applied ionophoretically at the two sites at which maximal monosynaptic focal field potentials are evoked from group II afferents-in the intermediate zone and the dorsal horn of the 4th and 5th lumbar segments. Their effects were estimated from changes in the amplitude of the field potentials. The compounds tested fell into three categories according to the site at which they depressed transmission from group II afferents: one category with highly selective actions in the intermediate zone, a second category with similarly selective actions in the dorsal horn, and a third category with non-selective actions. Drugs in the first category included three noradrenaline agonists (tizanidine, B-HT 933 and clonidine), included in the second were five serotonin agonists (8-OH-DPAT, 5-methoxytryptamine, alpha-methyl serotonin, DOI and 2-methyl-serotonin), and in the third two noradrenaline agonists (phenylephrine and isoproterenol) and two serotonin agonists (RU 24969 and 5-carboxamidotryptamine). Field potentials evoked by group I afferents remained unaffected by all but one compound (8-OH-DPAT). Effects of one noradrenaline agonist and one serotonin agonist (tizanidine and 5-methoxytryptamine) were also tested on responses of single extracellularly recorded neurons. Tizanidine depressed responses induced by stimulation of group II afferents in intermediate zone interneurons, but not in dorsal horn neurons, while 5-methoxytryptamine depressed activation of the latter. Tizanidine had no effect on responses evoked by group I afferents, either in intermediate zone interneurons or in the dorsal spino-cerebellar tract neurons of Clarke's column. It is hypothesized that noradrenaline and serotonin released by descending monoaminergic neurons differ in the potency with which they depress transmission from group II afferents to different functional types of neuron. The results suggest that this depression may involve different membrane receptors at different locations, primarily alpha2 adrenoceptors in the intermediate zone/ventral horn and 5-HT1A serotonin receptors in the dorsal horn.