针刺配合中药治疗24例小儿高热惊厥临床观察

针药并用，针刺人中、百合、涌泉、合谷，中药内服疏风情热，表里双解，止痉退烧，双管齐下治疗２４例小儿高热惊厥，经治疗均获痊愈。     

Effects of adrenalectomy and gonadectomy on sex and stress-induced differences in bicuculline-induced convulsions

The effects of adrenalectomy, gonadectomy and combined adrenalectomy plus gonadectomy on the previously described sex-dependent anticonvulsive effect of swim stress were studied in rats. The convulsive signs (myoclonic twitch, generalized convulsions, tonic hindlimb extension) were produced by constant i.v. infusion of γ-aminobutyric acid_A (GABA_A) antagonist bicuculline, which started 15 min after termination of swim stress (10-min swim at 18–19°C). Adrenalectomy decreased the threshold doses of bicuculline producing the first myoclonic twitch and the onset of generalized convulsions only in females. In adrenalectomized females, but not in males, swim stress enhanced the threshold dose of bicuculline producing generalized convulsions, but, unlike in adrenal-intact animals, it failed to enhance the dose of bicuculline producing tonic hindlimb extension. In gonadectomized stressed and unstressed animals all sex differences disappeared, and swim stress enhanced in both sexes only the threshold doses of bicuculline producing tonic hindlimb extension. Adrenalectomized plus gonadectomized animals displayed clear sex differences in doses of bicuculline necessary to produce all the convulsive signs. In the same animals swim stress postponed, especially in females, the onset of the first myoclonic twitch and generalized convulsions, but not the onset of tonic hindlimb extension. In summary, our results suggest that hormones of the adrenal and gonadal glands are only partly responsible for decreased susceptibility, especially of female rats, to the GABA_A antagonist bicuculline. Moreover, they have demonstrated that stress produces a gender-specific anticonvulsive effect even in the animals completely deprived of steroid hormones of peripheral origin. Received: 4 June 1998 / Accepted: 11 June 1999     

90例小儿发热惊厥脑电图与临床预后关系

本文报告了90例发热惊厥(FC)患儿的脑电图检查结果,认为对FC患儿的脑电图检查时间应在退热至少2周后进行;FC起病年龄低者再发率高,且脑发育成熟前起病的FC患儿脑损伤轻严重;对于某些患者,引起FC的体温逐渐降低,这些患儿转为无热惊厥(癫痫)的可能性明显增高;家族史不仅会影响FC的发病倾向而且会影响FC的复发及转归。     

Strain differences in mice in the development of tolerance to the anti-pentylenetetrazole effects of diazepam

The development of tolerance to the protective effects of diazepam (4 mg/kg) against seizures induced by pentylenetetrazole (PTZ) were studied in 3 strains of mice. Significant tolerance developed to protection against myoclonic jerks induced by PTZ (90-100 mg/kg) by day 5 in Tuck No. 1 and by day 10 in C3H/HE and CD-1 mice. Tolerance developed to protection against tonic-clonic convulsions by day 10 in Tuck No. 1 mice and by day 30 in the other strains. Diazepam remained protective against tonic-clonic convulsions (but not against myoclonus) induced by threshold doses of PTZ for 30 days in all 3 strains.     

“Dark” (compacted) neurons may not die through the necrotic pathway

Dark neurons were produced in the cortex of the rat brain by hypoglycemic convulsions. In the somatodendritic domain of each affected neuron, the ultrastructural elements, except for disturbed mitochondria, were remarkably preserved during the acute stage, but the distances between them were reduced dramatically (ultrastructural compaction). Following a 1-min convulsion period, only a few neurons were involved and their environment appeared undamaged. In contrast, 1-h convulsions affected many neurons and caused swelling of astrocytic processes and neuronal dendrites (excitotoxic neuropil). A proportion of dark neurons recovered the normal structure in 2 days. The non-recovering dark neurons were removed from the brain cortex through two entirely different pathways. In the case of 1-h convulsions, their organelles swelled, then disintegrated and finally dispersed into the neuropil through large gaps in the plasma membrane (necrotic-like removal). Following a 1-min convulsion period, the non-recovering dark neurons fell apart into membrane-bound fragments that retained the compacted interior even after being engulfed by astrocytes or microglial cells (apoptotic-like removal). Consequently, in contrast to what is generally accepted, the dark neurons produced by 1-min hypoglycemic convulsions do not die as a consequence of necrosis. As regards the case of 1-h convulsions, it is assumed that a necrotic-like removal process is imposed, by an excitotoxic environment, on dark neurons that previously died through a non-necrotic pathway. Apoptotic neurons were produced in the hippocampal dentate gyrus by intraventricularly administered colchicine. After the biochemical processes had been completed and the chromatin condensation in the nucleus had reached an advanced phase, the ultrastructural elements in the somatodendritic cytoplasm of the affected cells became compacted. If present in an apparently undamaged environment such apoptotic neurons were removed from the dentate gyrus through the apoptotic sequence of morphological changes, whereas those present in an impaired environment were removed through a necrotic-like sequence of morphological changes. This suggests that the removal pathway may depend on the environment and not on the death pathway, as also assumed in the case of the dark neurons produced by hypoglycemic convulsions.     

Symptomatic hyponatraemia due to inappropriate antidiuretic hormone secretion following minor surgery

A rare case of the syndrome of inappropriate antidiuretic hormone secretion occurring after minor surgery is presented. A ten-year-old, previously healthy boy underwent general anaesthesia for detorsion and right orchiopexy. Throughout the operations, which lasted for one hour, he received 120 ml Ringer's lactate solution. The immediate postoperative period was uneventful. Twenty-two hours postoperatively he was found unconscious with generalized tonic-clonic seizures. Simultaneously obtained serum sodium concentration (121 mEq.L-1) serum osmolarity (265 mEq.L-1), urine sodium concentration (87 mEq.L-1) and urine osmolarity (525 mEq.L-1) suggested inappropriate antidiuretic hormone secretion which was confirmed by an elevated serum arginine-vasopressin (AVP) level of 14.5 pcg.ml-1 (normal 1-5 pcg.ml-1) measured by radioimmune assay. He was treated with a single iv dose of 30 mg furosemide and fluid restriction, which produced a gradual increase of his serum sodium concentration to normal within two days. He was well during the remainder of his hospitalization.     

掌叶半夏超临界CO_2乙醇萃取物的抗惊厥作用(英文)

目的研究掌叶半夏超临界CO2乙醇萃取物(SEE-CO2 PP)对青霉素诱发惊厥的对抗作用。方法采用大鼠皮质局部定位注射青霉素诱发惊厥模型,研究SEE-CO2 PP对惊厥发作的潜伏期以及惊厥行为变化的影响,并用RM6240C型多道生理信号采集处理仪记录皮质和海马痫性放电的潜伏期、频率和痫波最高发放波幅,同时应用高效液相色谱法测定海马谷氨酸(Glu)、天冬氨酸(Asp)、甘氨酸(Gly)和γ-氨基丁酸(GABA)递质的含量。结果 SEE-CO2 PP 15和30 g·kg-1(ig)可延长青霉素诱发惊厥的潜伏期,并减弱发作强度。SEE-CO2PP能够延长痫性放电的潜伏期,减少痫性放电的频率,减小皮质和海马发放痫波的最高波幅,同时,SEE-CO2PP可以增加海马GABA的水平,对Gly,Asp和Glu水平无明显影响。结论 SEE-CO2PP可对抗青霉素诱发的惊厥行为和痫样放电,具有抗惊厥作用。     

PRRT2 mutations and paroxysmal disorders

In the past year, mutations in the PRRT2 gene have been identified in patients with paroxysmal kinesigenic dyskinesia and other paroxysmal disorders. We conducted a review of the literature on PRRT2 mutation‐associated disorders. Our objectives were to describe the wide clinical spectrum associated with PRRT2 mutations, and to present the current hypotheses on the underlying pathophysiology. PRRT2 mutations are associated with a wide range of clinical syndromes: the various paroxysmal dyskinesias, infantile seizures, paroxysmal torticollis, migraine, hemiplegic migraine, episodic ataxia and even intellectual disability in the homozygous state. The PRRT2 protein, through its interaction with SNAP‐25, could play a role in synaptic regulation in the cortex and the basal ganglia. The pathogenesis may be caused by PRRT2 loss of function, which may induce synaptic deregulation and neuronal hyperexcitability. However, this does not explain the phenotypic variability, which is likely modulated by environmental factors, modifier genes or age‐dependent expression. The clinical spectrum of PRRT2 mutations has expanded among paroxysmal disorders and beyond. Unraveling the molecular pathways linking the genetic defect to its clinical expression will be crucial for the diagnosis and treatment of these disorders.