Remote medulla ablongata ventral acute subarachnoid hemorrhage following cervical spinal surgery: A case report

IntroductionThe incidence of remote intracranial hemorrhage (RICH) in patients during spinal surgery is rare and the detailed mechanism remains unclear.Presentation of caseA 55-year-old man had undergone cervical discectomy and fusion at C5–6 and C6–7 due to herniated disc and secondary spinal canal stenosis. He had severe headache 20 h postoperatively and his drain output increased from 100 to 350 mL in the second 10 h after surgery. Computed tomography (CT) and magnetic resonance imaging (MRI) were performed and he was diagnosed with acute subarachnoid hemorrhage in the ventral medulla oblongata. The drainage tube was quickly removed. Infusion of hypertonic saline was used to reduce intracranial pressure and nimodipine prevented vasospasm around the brainstem. The patient made a gradual, satisfactory recovery with conservative treatment.DiscussionThe most likely pathomechanism leading to RICH is venous bleeding due to rapid leak of a large amount of cerebral spinal fluid (CSF) after spinal surgery. If the patient has a headache or neurological complaints after spinal surgery, immediate imaging is recommended to confirm the diagnosis. Treatment depends on the amount and location of intracranial hemorrhage.ConclusionRICH is a serious but rare complication of spinal surgery and cerebellar hemorrhage is the most common. The most important pathomechanism leading to RICH after spinal surgery is venous bleeding due to rapid leak of a large amount of CSF. Timely CT is necessary to exclude RICH. Treatment of RICH depends on the size of the intracranial hematoma and the patient’s symptoms.     

Effect of saline infusion on net reabsorption of endogenous sulfate relative to that of phosphate in intact and thyroparathyroidectomized rats

Clearance experiments have been performed to study the effects of saline infusion on the reabsorption of inorganic sulfate (SO₄) at endogenous levels. Adult female Sprague-Dawley rats on a standard diet were used. Both intact and thyroparathyroidectomized (TPTX) animals were infused with a 130 mmol/l sodium chloride solution at a low (0.15 ml/min) and a high (0.375 ml/min) rate. This increase of the infusion rate decreased the reabsorption of SO₄ in both groups of animals significantly. The fractional excretion of SO₄ in theintact rats increased from 9.9±5.6 to 18.4±3.6% (mean values±SD,p<0.001) and in theTPTX rats from 5.3±2.5 to 22.4±6.3% (p<0.001). It is concluded that endogenous parathyroid hormone has no major effect on the saline-induced inhibition of reabsorption of SO₄.This work was supported by a grant from the Deutsche Forschungsgemeinschaft (Fr 239/9-1)     

Parallel Detection of Bacterial Pathogens in Cerebrospinal Fluid with 16S rRNA Probe Microarray

The most commonly used method for detection ofpathogenic bacteria in cerebrospinal fluid (CSF) speci mens of clinical laboratories is isolation and identificationof the causative agents by cultural method, biochemicaland serological t…     

Mathematical study of the role of non-linear venous compliance in the cranial volume-pressure test

The role of the cerebral venous bed in the cranial volume-pressure test was examined by means of a mathematical model. The cerebral vascular bed was represented by a single arterial compartment and two venous compartments in series. The lumped-parameter formulation for the vascular compartments was derived from a one-dimensional theory of flow in collapsible tubes. It was assumed in the model that the cranial volume is constant. The results show that most of the additional volume of cerebrospinal fluid (ΔV_CSF) was accommodated by collapse of the cerebral venous bed. This profoundly altered the venous haemodynamics and was reflected in the cranial pressure P_CSF. The cranial volume-pressure curve obtained from the model was consistent with experimental data; the curve was flat for 0<-ΔV_CSF<-20 ml and 35<-ΔV_CSF<-40 ml, and steep for 20<-ΔV_CSF<-35 ml and ΔV_CSF>-40 ml. For ΔV_CSF>25 ml and P_CSF>5.3 kPa (40 mmHg), cerebral blood flow dropped. When P_CSF was greater than the mean arterial pressure, all the veins collapsed. The conclusion of the study was that the shape of the cranial volume-pressure curve can be explained by changes in the venous bed caused by various degrees of collapse and/or distension.     

北京地区病毒性脑炎患者病原体的分离和初步鉴定

１９９１年夏秋季，我们从４１例北京儿童医院临床诊断为病毒性脑炎（非乙脑）患者的７５份急性期血和／或脑脊液中分离到３３株病毒。对其中１２株进行电镜观察，电镜下均见大小相同的球形病毒颗粒，毒粒的直径约为４４．７８±１．３５ｕｍ，无囊膜，具双层蛋白外壳，视野内多见空心颗粒。超薄切片显示病毒在感染细胞的胞浆内发生，直径约为４７．６±２．３ｕｍ。正常细胞中未见病毒颗粒。对其中３株病毒进行理化性状分析，多次试验均显示该病毒抵抗５＇－碘脱氧尿苷，抵抗乙醚，耐酸，能在地鼠肾ＢＨＫ－２１和白纹伊蚊Ｃ６／３６细胞上增殖并出现细胞病变。该病毒与本室制备的披膜病毒科甲组、乙脑病毒和布尼亚病毒科的组特异性免疫腹水均不反应。脑内接种３日龄乳小白鼠可引起不规律的发病和死亡。上述结果表明，该病毒是一类４５ｕｍ左右、无囊膜、耐酸的ＲＮＡ病毒。     

Difenoxin and loperamide: studies on possible mechanisms of intestinal antisecretory action

Summary Experiments have been performed to determine whether the antisecretory (antidiarrhoeal) actions of difenoxin and loperamide are mediated by enteric neurones. An iso-osmotic perfusion solution was circulated around the lumen of the jejunum of anaesthetised rats. Vasoactive intestinal peptide was infused intra-arterially to induce net fluid secretion which was inhibited by difenoxin (ED₅₀, 0.23 mg/kg) and loperamide (ED₅₀, 0.5 mg/kg). However, neither were able to restore the fluid transport rate to the control level of absorption.The antisecretory effects of difenoxin (0.77 mg/kg) and loperamide (0.6 mg/kg) were blocked by the opiate receptor antagonist naloxone (2 mg/kg). Their effects were also abolished by pretreatment with the 5-HT synthesis inhibitor p-chlorophenylalanine (PCPA; 200 mg/kg; with desmethylimipramine given beforehand to protect noradrenergic nerves and enhance 5-HT depletion). The effect of difenoxin was blocked with methiothepin (1 mg/kg) and methysergide (30 g/kg) but not ketanserin (30 g/kg), ritanserin (30 mg/kg), ondansetron (10 g/kg) or ICS 205-930 (3 mg/kg). None of the above 5-HT receptor antagonists modified the antisecretory effect of loperamide. The antisecretory effect of difenoxin but not loperamide was prevented by phentolamine (2 mg/kg) and by pretreatment with 6-hydroxydopamine (150 mg/kg) total.It is concluded that both difenoxin and loperamide inhibit net fluid secretion by indirect mechanisms. It is proposed that the initial action is on enteric -opiate receptors and that this results in the release of 5-HT. In the case of difenoxin, the 5-HT may act on 5-HT₁-like receptors to release noradrenaline. However, the major difference in the mechanism of action of loperamide compared to difenoxin is that it does not utilize noradrenaline as the final mediator of its antisecretory action.Correspondence to A. De Luca at the above address     

Pharmacokinetics,cerebrospinal fluid penetration,and metabolism of piroxantrone in the Rhesus monkey

Summary Piroxantrone is an anthrapyrazole derivative with broad anti-tumor activityin vitro and less cardiac toxicity than the anthracyclines. The metabolic pathways and central nervous system penetration of piroxantrone have not been determined. In this study we examined the pharmacokinetic behavior of piroxantrone in plasma and cerebrospinal fluid in a non-human primate model. In addition, a urinary metabolite of piroxantrone was isolated and its cytotoxicity evaluatedin vitro. The disappearance of piroxantrone from plasma after an intravenous dose of 150 mg/m² given over 60 minutes was biexponential with mean t_1/2 alpha of 1.0 minutes and a mean t_1/2 beta of 180 minutes. The mean area under the curve was 220 M·min and the clearance was 1420 ml/min/m². Piroxantrone was not detectable in the cerebrospinal fluid.Piroxantrone and three other compounds not present in pre-treatment samples were detected in urine. The major urinary metabolite was isolated. Its cytotoxicity against MOLT-4 cellsin vitro was at least one log less than that of piroxantrone. In addition, one of the other compounds detected in urine was determined to be a glucuronide conjugation product of the major metabolite.The results of this study may be useful in the interpretation of the activity and toxicity of piroxantrone in clinical trials.