A modified compression model of spinal cord injury in rats: functional assessment and the expression of nitric oxide synthases.

STUDY DESIGN: Experimental study. OBJECTIVES: To investigate a modified compression model of spinal cord injury (SCI) in adult rats by using a room-air- inflated Fogarty balloon catheter. SETTING: Kaohsiung, Taiwan. METHODS: The rats were divided into injury, sham-operated and control groups. A 2-French Fogarty catheter was passed from the lumbar spine (L3-L4) epidurally, with a mini-laminectomy under the microscope, to the level of thoracic spine (T6-T7). The actual site of the catheter tip was confirmed with X-ray. The balloon of Fogarty catheter then was inflated with room air, 0.2 ml, for 10 min. Mini-laminectomy was performed without inserting the catheter in the sham-operated group. Quantitative neurological outcomes were evaluated with the Basso, Beattie and Bresnahan (BBB) locomotor rating scale daily. The gene expression of nitric oxide synthases (NOSs) of the spinal cord was investigated at the end of the functional assessment. RESULTS: The mean BBB locomotor scores were 10±1.85 and 10±1.85, respectively, on days 1 and 3 in the injury group, and 21 and 20.29±0.69, respectively, in the sham-operated group. There was a significantly increased gene expression of inducible NOS in the SCI group compared with the sham-operated group and control group. Endothelial NOS gene expression was not significantly different among the groups. CONCLUSION: The functional and molecular assessments show that this modified balloon-compression technique is a reproducible, simple and inexpensive model of SCI in rats.

Effect of silencing HIF-1α on proliferation, invasion and migration of glioblastoma U87 cells.

The objective of the study was to evaluate the effect of silencing hypoxia-inducible factor 1α (HIF-1α) on proliferation, invasion, and migration of glioblastoma U87 cells. HIF-1α-shRNA lentiviral vector was designed for liposome-mediated transfection into U87 cells. The efficiency of interference was assessed by RT-PCR and Western blot. Cell proliferation was measured by MTT assay. Cell migration was observed by the migration test. The capabilities of invasion and migration were detected using the Transwell model. The research involved experiments in the interference group (shRNA transfected), the control interference group (empty vector transfected), and the untreated (non-transfected) group. Compared with the control interference group and the untreated group, the expressions of HIF-1α mRNA and protein were significantly down-regulated, and the proliferation and invasion of U87 cells were significantly inhibited in the interference group. HIF-1α mRNA and protein are effectively suppressed by HIF-1α-shRNA in U87 cells, which appears to inhibit proliferation, invasion, and migration of U87 cells.

Epidermoid cysts associated with thoracic meningocele.

Intraspinal tumours of cutaneous origin associated with various spinal dysraphisms have been well documented in the literature. However, the metachronous development of intra- and extra-medullary tumours in conjunction with dorsal meningocele is rare. The authors report a patient with a thoracic dorsal meningocele and congenital intradural extramedullary epidermoid tumour. The patient developed an intramedullary epidermoid growth 12 years later. Subtotal resection of the tumour predisposed to a later recurrence. Meningocele is not always an isolated clinical entity but the concurrent occult lesions are usually veiled by the more conspicuous surface anomaly. Thorough magnetic resonance imaging of the whole neural axis helps to identify associated pathologies. Delicate intradural exploration by a microsurgical approach is necessary to achieve appropriate treatment.

Continuous intravenous infusion of CGS 26303, an endothelin-converting enzyme inhibitor, prevents and reverses cerebral vasospasm after experimental subarachnoid hemorrhage.

OBJECTIVE: Endothelin-mediated vasoconstriction has been implicated in the pathophysiology of cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH). Endothelin-1, the most potent vasoconstrictor peptide of the endothelin family, is synthesized initially as a large prepropeptide that requires multiple steps of post-translational processing for activation. The final step of this processing involves the proteolytic cleavage of a relatively inactive precursor, big endothelin-1, by the metalloprotease endothelin-converting enzyme. Previous findings have demonstrated that intravenous bolus injections of an endothelin-converting enzyme inhibitor (CGS 26303) administered twice daily can prevent and reverse arterial narrowing in a rabbit model of SAH. However, attenuation of vasospastic response was incomplete and required relatively high doses to be effective in reversing vasospasm. Therefore, the present study evaluated an alternative protocol for administration of CGS 26303 to optimize the antispastic influence of this compound. METHODS: Continuous intravenous infusion of CGS 26303 at doses of 2.4, 8.0, or 24.0 mg/kg/d was initiated either 1 hour (prevention paradigm) or 24 hours (reversal paradigm) after experimental SAH in New Zealand White rabbits. All animals were killed by perfusion-fixation 48 hours after SAH. Basilar arteries were then removed and sectioned, and their cross-sectional areas were measured by use of computer-assisted video microscopy. RESULTS: Continuous intravenous infusion of CGS 26303 attenuated SAH-induced cerebral vasospasm in a dose-dependent manner in both the prevention and the reversal groups. These effects achieved statistical significance at all doses as compared with the SAH-only or SAH-plus-vehicle groups. Furthermore, the attenuation of vasospasm after continuous infusion of CGS 26303 was more efficacious than that obtained with bolus injections. CONCLUSION: These findings provide further support for the use of endothelin-converting enzyme inhibition as a therapeutic strategy for reduction of cerebral vasospasm, and they also support the effectiveness of this strategy even when initiated after arterial narrowing has been established. The findings also indicate that continuous intravenous infusion of CGS 26303 is a more effective approach for attenuation of vasospasm than bolus intravenous administration.

Systemic administration of the potassium channel activator cromakalim attenuates cerebral vasospasm after experimental subarachnoid hemorrhage.

OBJECTIVE: Cerebral vasospasm is a primary complication after aneurysmal subarachnoid hemorrhage (SAH). Recent evidence indicates that the activation of potassium (K+) channels may be of benefit in relieving spastic constriction. The present study examined the effects of systemic administration of a K+ channel activator, cromakalim, on cerebral vasospasm after experimental SAH. METHODS: Experimental SAH was performed in rabbits by injecting autologous blood into the cisterna magna. Intravenous injections of cromakalim or vehicle were administered twice daily with the first injection administered 1 hour after induction of SAH. Animals were killed by perfusion-fixation 48 hours after SAH. Basilar arteries were removed and sectioned, and the luminal cross-sectional areas were measured. RESULTS: Experimental SAH induced cerebral vasospasm in untreated and vehicle-treated animals. Cromakalim attenuated cerebral vasospasm in a dose-dependent manner. This effect achieved statistical significance at doses of 0.1 and 0.3 mg/kg. CONCLUSION: These results support the concept that targeting vascular K+ channels can be of benefit in preventing the development of cerebral vasospasm. The findings also indicate that cromakalim represents a potential therapeutic agent for the treatment of cerebrovascular pathophysiology after SAH.

Enhanced endogenous antioxidant activity and inhibition of cerebral vasospasm in rabbits by pretreatment with a nontoxic endotoxin analog, monophosphoryl lipid A.

OBJECT: Monophosphoryl lipid A (MPL) and diphosphoryl lipid (DPL) are derivatives of the lipopolysaccharide (endotoxin) of Salmonella minnesota strain R595. Monophosphoryl lipid A is relatively nontoxic and can stimulate the natural defense or immune system. Diphosphoryl lipid is relatively toxic; however, at higher concentrations, it can also stimulate an immune response. The purpose of the present study was to determine the effects of these endotoxin analogs on cerebral vasospasm after the onset of subarachnoid hemorrhage (SAH) in rabbits. METHODS: Intrathecal administration of MPL or DPL (5 microg/kg) was performed immediately before and 24 hours after induction of SAH in New Zealand White rabbits. Forty-eight hours after induction of SAH, the animals were killed by perfusion fixation for morphometric analyses of vessels or perfused with saline and assayed for superoxide dismutase (SOD) activity. Additional rabbits were administered MPL or DPL and killed 24 hours later for assessment of SOD activity; no SAH was induced in these animals. Experimental SAH elicited spasm of the basilar arteries in each group. Vasospasm was markedly attenuated in animals treated with MPL (p < 0.01 compared with vehicle-treated animals), but not in animals treated with DPL. A substantial reduction in SOD activity in the basilar artery accompanied the vasospasm; this loss of activity was significantly blocked by treatment with MPL, but not DPL. In animals that were not subjected to experimental SAH, MPL elicited a significant increase in SOD activity over basal levels, whereas DPL was ineffective. CONCLUSIONS: These data provide evidence of a marked protective effect of the endotoxin analog MPL against vasospasm. Although the mechanism(s) responsible for the protective effect of MPL remains to be verified, an enhancement of basal antioxidant activity and an inhibition of SAH-induced loss of this activity are attractive candidates. An MPL-based therapy could represent a useful addition to current therapies for SAH-induced cerebral injury.

Systemic administration of an inhibitor of endothelin-converting enzyme for attenuation of cerebral vasospasm following experimental subarachnoid hemorrhage.

The potent vasoconstrictor peptide, endothelin-1 (ET-1), has been implicated in the pathophysiology of cerebral vasospasm that occurs after subarachnoid hemorrhage (SAH). This peptide is synthesized as a large prepropeptide that requires a series of modifying steps for its activation. The last of these steps involves the proteolytic conversion of a relatively inactive propeptide, Big ET-1, to its active, 21-amino acid peptide form. The enzyme responsible for converting Big ET-1 to ET-1 is a metalloprotease called endothelin-converting enzyme (ECE). In the present study the authors examined the effects of a newly developed inhibitor of ECE on responses to ET peptides in the normal basilar artery and on pathophysiological constriction in the spastic basilar artery after SAH. In the first series of experiments the authors examined normal basilar arteries in the rabbit, which were exposed transclivally and measured on-line using videomicroscopy. Intravenous administration or topical application of an active inhibitor of ECE, CGS 26303, blocked vasoconstrictor responses to topically applied Big ET-1 but not to ET-1. In contrast, topical application of a structurally related compound that does not inhibit ECE, CGS 24592, was ineffective in blocking vasoconstriction that was elicited by a topical application of Big ET-1. These findings indicate that CGS 26303 when administered systemically is capable of blocking the conversion of Big ET-1 to ET-1 in the basilar artery without affecting the ability of the vessel to respond to ET-1. In the second series of experiments the authors examined the effects of the ECE inhibitor on cerebral vasospasm after experimental SAH. Intraperitoneal administration of CGS 26303 via osmotic minipumps significantly attenuated the delayed spastic response of the basilar artery to an intracisternal injection of autologous blood. This study provides the first evidence that systemic administration of an inhibitor of ECE is capable of preventing cerebral vasospasm after SAH. The results reinforce a growing body of evidence that ETs play a critical role in the development of spastic constriction after SAH. Moreover, the findings indicate that blocking the conversion of Big ET-1 to its active ET-1 form using CGS 26303 may represent a feasible strategy for ameliorating cerebral vasospasm.

Prevention and reversal of cerebral vasospasm by an endothelin-converting enzyme inhibitor, CGS 26303, in an experimental model of subarachnoid hemorrhage.

Delayed cerebral ischemia due to cerebral vasospasm is a major cause of morbidity and mortality in patients with aneurysmal subarachnoid hemorrhage (SAH). Increasing evidence implicates the potent vasoconstrictor peptide endothelin (ET) in the pathophysiology of cerebral vasospasm. In the present study the authors examined the therapeutic value of blocking the production of ET-1 by inhibiting the conversion of its relatively inactive precursor, Big ET-1, to a physiologically active form. An inhibitor of ET-converting enzyme (ECE), CGS 26303, was injected intravenously after inducing SAH in New Zealand white rabbits. Injections of CGS 26303 were initiated either 1 hour after SAH (prevention protocol) or 24 hours after SAH (reversal protocol). One of three concentrations (3, 10, or 30 mg/kg) of CGS 26303 was injected twice daily, and all animals were killed by perfusion fixation 48 hours after SAH occurred. Basilar arteries were removed and sectioned, and their cross-sectional areas were measured in a blind manner by using computer-assisted videomicroscopy. Treatment with CGS 26303 attenuated arterial narrowing after SAH in both the prevention and reversal protocols. The protective effect of CGS 26303 achieved statistical significance at all dosages in the prevention protocol and at 30 mg/kg in the reversal protocol. These findings demonstrate that inhibiting the conversion of Big ET-1 to ET-1 via intravenous administration of an ECE inhibitor can be an effective strategy for limiting angiographic vasospasm after SAH. Moreover, the results demonstrate that treatment with the ECE inhibitor is capable of reducing vasospasm even when initiated after the process of arterial narrowing has begun. Finally, the results provide further support for the role of ET in the establishment of cerebral vasospasm. The ECE inhibitor CGS 26303 thus represents a promising therapeutic agent for the treatment of cerebral vasospasm following aneurysmal SAH.

Prevention of cerebral vasospasm by a capsaicin derivative, glyceryl nonivamide, in an experimental model of subarachnoid hemorrhage.

BACKGROUND: Cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH) remains a major complication in patients suffering from SAH. In our previous study, we reported that stimulating vascular K(+) channel activity prevented the development of cerebral vasospasm. Recent evidence indicates that glyceryl nonivamide (GLNVA), a capsaicin derivative, has a vasorelaxant effect on the aortic vascular smooth muscle due to the release of coronary calcitonin gene-related peptide, which in turn stimulates K(+) channel opening. The purpose of the present study was to examine the preventive effects of GLNVA on vasospasm. METHODS: New Zealand white rabbits were subjected to experimental SAH by injecting autologous blood into the cisterna magna. GLNVA or vehicle was injected intrathecally immediately after the induction of SAH. All animals were killed by perfusion-fixation at 48 hours after SAH. The basilar arteries were removed and sectioned, and their cross-sectional areas were measured. RESULTS: The average cross-sectional areas of basilar arteries were reduced by 69% and 71% in the SAH only and SAH plus vehicle groups, respectively, when compared with the healthy controls. After treatment with 0.35, 1.75, and 3.5 mg/kg GLNVA in rabbits subjected to SAH the average cross-sectional area was decreased by 46%, 12% and 2%, respectively, when compared with the healthy controls. The protective effect of GLNVA achieved statistical significance at all dosages. Morphologically, corrugation of the internal elastic lamina of vessels was often observed in the vehicle-treated group, but was not prominent in the GLNVA-treated groups or healthy controls. CONCLUSION: The findings showed that GLNVA dose-dependently attenuated cerebral vasospasm after SAH in the rabbit. These results suggest that intrathecal administration of GLNVA could be an effective strategy for preventing cerebral vasospasm after SAH.

Attenuation of vasospasm and hemoglobin-induced constriction in the rabbit basilar artery by a novel protease inhibitor.

Calcium-activated proteolysis mediated by the protease inhibitor, calpain, has recently been implicated in the pathogenesis of cerebral vasospasm. The effect of one inhibitor of calcium-activated proteolysis, z-Leu-Phe-CONH-morpholene (zLF), on cerebrovascular constriction was examined in two experimental paradigms. In the first paradigm, the rabbit basilar artery (BA) was visualized via a transclival exposure, and its diameter was monitored using videomicroscopy. In the second experimental paradigm two intracisternal injections of autologous blood were administered to mimic a subarachnoid hemorrhage (SAH). The BA was visualized via the transclival exposure, and its luminal diameter was measured. Topical application of oxyhemoglobin (OxyHb), a known pathogenic agent in cerebral vasospasm, elicited vasoconstriction in normal animals, reducing arterial diameter to approximately 75% of resting levels. Pretreatment with zLF (100, 200, or 300 microM) attenuated vasoconstriction induced by OxyHb. In an experimental model of SAH, the diameter of the BA was reduced after the first injection of blood to approximately 67% of normal resting levels when measured 3 to 4 days later. This vasospastic response was reversed significantly by topical application of zLF (100 microM); vascular diameter was increased to approximately 84% of normal resting levels. These findings demonstrate that both acute OxyHb-induced constriction and blood-induced vasospasm are sensitive to an inhibitor of the proteolytic enzyme, calpain. Together, these observations indicate an important role for calcium-activated proteolysis in the development and maintenance of vasospasm after SAH. In addition, it may be inferred from the data that inhibitors of calcium-activated proteolysis may be useful therapeutic agents for treating this form of cerebrovascular disease.

Brain metastasis from pericardial angiosarcoma.

A case of metastatic intracranial angiosarcoma in a 17-year-old female is presented. The patient underwent a sternotomy for treatment of a primary angiosarcoma arising from the pericardium. The postoperative course was uneventful but the patient died as a result of multiple metastases. The metastatic intracranial tumor had features characteristic of angiosarcoma as revealed by light microscopy with positive immunohistochemical staining of factor VIII-related antigen. Only a few cases of intracranial metastasis from cardiac angiosarcoma have been reported in the literature.

[Intracranial aneurysm in Taiwan].

We reviewed the epidemiologic and clinical features of ruptured intracranial aneurysms based on the available data in the literature reported in Taiwan. Among 28,763 stroke patients registered by members of the Neurological Society of Taiwan, 600 patients had verified intracranial aneurysms (2.1%), constituting only 34.7% of 1,730 patients with subarachnoid hemorrhage. The male to female ratio was 0.68.1. The mean age was 54.6 +/ 14.3 years in men, and 56.5 +/ 13.8 years in women. Among the 409 patients whose aneurysmal sites were recorded, the aneurysm occurred at the anterior communicating artery in 109 (26.7%), at the posterior communicating artery in 90 (22.0%), at the internal carotid artery in 82 (20.1%), at the middle cerebral artery in 80 (19.6%), at the anterior cerebral artery in 50 (12.2%), at the vertebral-basilar system in 13 (3.2%), and multiple sites in 33 (8.1%). Cerebral angiography was performed in 72.2% of patients and operation was undergone in 57.7%. A randomized follow-up study in 59 patients showed survival rates of 63% for 1 month, 53.3% for 6 months and 43.6% for 1 year. The reported surgical mortality rates ranged from 7.7% to 12.5%. Prognosis was related to the score on the World Federation of Neurological Societies Subarachnoid Hemorrhage Scale. In Taiwan, the number of patients with intracranial aneurysm has been underestimated among who have presented with subarachnoid hemorrhage. The high mortality and morbidity of aneurysm rupture justify an aggressive attempt to establish a prompt and accurate diagnosis.

Surgical outcome of anterior communicating artery aneurysms.

During a 6-year period, 65 consecutive patients who had undergone anterior communicating artery aneurysmal surgery were reviewed at a follow-up examination from 6 to 78 months (mean 35 months) after operation. On admission 69% of cases had a good Hunt and Hess scale (grades I to II) and 31% a poor grade (grades III to V). The degree of subarachnoid hemorrhage (SAH) was determined by Fisher's grade. Sixteen (25%) patients were classified in grades I and II. Forty-six percent of cases had pre-existing hypertension. Early surgery (within the first three days after the bleeding) was performed in 17% of cases. Intraoperative rupture of aneurysm occurred in six (9.2%) patients. Symptomatic cerebral vasospasm was diagnosed in 14 (22%) cases, but only 8 (12%) had evidence of low density on the computerized tomographic scan. Hydrocephalus developed in 16 (25%) cases and 10 needed ventriculoperitoneal shunting. The outcome was determined using the activity of daily life. Sixty-five percent of the patients made a good recovery and 13.8% died. The significant poor prognostic factors included a poor pre-operative grade of the Hunt and Hess scale, the presence of symptomatic cerebral vasospasm, and the Fisher's SAH grade of greater than II. Other factors which apparently were not related to the outcome included age, sex, timing of surgery, history of hypertension, intraoperative rupture, and the development of hydrocephalus.

Acute hydrocephalus and chronic hydrocephalus with the need of postoperative shunting after aneurysmal subarachnoid hemorrhage.

During a 6-year period, 168 consecutive patients who presented with subarachnoid hemorrhage (SAH) and underwent surgical clipping of aneurysms were reviewed at a follow-up examination from 6 to 77 months (mean 38 months) after the ictus. Acute hydrocephalus was defined when the bicaudate index was greater than the 95th percentile for age on a computed tomographic scan within 72 hours of the hemorrhage. Forty (24%) patients developed acute hydrocephalus. The Hunt and Hess grades and Fisher's SAH grades at the time of admission, the presence of intraventricular hemorrhage and symptomatic cerebral vasospasm, and cerebrospinal fluid (CSF) diversion were found to be significantly associated with acute hydrocephalus. The overall mortality in this study was 16%. Of the 141 surviving patients, 20 (14%) patients underwent ventriculoperitoneal (VP) shunt replacement secondary to chronic hydrocephalus. In the present study, we found that the following factors were significantly related to the need of VP shunting: increasing age, the presence of acute hydrocephalus, preoperative CSF diversion, low admission Hunt and Hess grades, and poor Fisher's SAH grades. No patient was readmitted for shunt replacement at our hospital later than 117 days after hemorrhage. Acute hydrocephalus was combined with high mortality (28%) at our follow-up review. Ten of 29 (34%) patients with acute hydrocephalus required definite shunt replacement. However, less than 10% of patients without acute hydrocephalus needed shunting postoperatively. We recommend that patients with aneurysmal SAH should be followed up at least 6 months after the hemorrhage, especially in those patients with high risks of developing chronic hydrocephalus.

Attenuation of basilar artery spasm after experimental subarachnoid hemorrhage in rabbit by potassium channel activator cromakalim--a preliminary result.

Cerebral vasospasm associated with aneurysmal subarachnoid hemorrhage (SAH) remains a major complication in patients suffering from SAH. Regulation of membrane potential of arterial smooth muscle through activation or inhibition of potassium (K+) channel activity provides an important mechanism to dilate or constrict arteries. The present study examined the effect of a K+ channel activator, cromakalim, on cerebral vasospasm following experimental SAH. By the route of topical application and intra-arterial injection, basilar arteries were exposed transclivally and measured on-line using videomicroscopic camera. Continuous microinjection from right vertebral artery was given after the result of application was observed. Basilar artery spasm induced by SAH was released by topical or intra-arterial administration of cromakalim, and this beneficial effect against cerebral vasospasm was dose-dependent. There was no significant difference between topical and intra-arterial administration of cromakalim. These results indicate that K+ channel activator may play an important role for ameliorating cerebral vasospasm. An important goal of future studies will be to carefully evaluate the possibility and effect of intra-arterial administration of cromakalim to treat angiographic vasospasm.

Prognosis of spontaneous intracerebral hemorrhage in hemodialysis patients.

During an 8-year period, 32 consecutive patients with chronic renal failure on maintenance hemodialysis were diagnosed to have cerebral hemorrhage. The outcome was determined using the activity of daily life (ADL) at 6 months after hemorrhage. The overall mortality was 64%. Of the 12 surviving patients, no one made a good recovery (back to normality), 5 recovered to ADL grade II, 4 to grade III, 1 to grade IV, and 2 to grade V. Up to 91% of the patients had a history of hypertension. On admission, Glasgow coma scale (GCS) was 15 in 8 cases, 8-14 in 10, and below 8 in 14. The poor prognostic factors showing statistical significance included a poor admission GCS, age above 65 years, and blood sugar level of more than 200 mg/dl. Other factors which apparently were not related to the outcome included sex, history of stroke, acute myocardial infarction, hypertension, and diabetes mellitus, the locations of hemorrhage, the duration of hemodialysis, treatment modality (surgery vs non-surgery), and the laboratory data (blood urea nitrogen, creatinine, platelet count, hemoglobin, prothromin time, and partial thromboplastin time). This study confirmed a poor prognosis for hemodialysis patients with cerebral hemorrhage. More attention should be paid to the control of blood sugar in this group to improve the outcome of cerebral hemorrhage in hemodialysis patients, especially in elderly patients with poor admission GCS.

Hemolysate induces structural and functional injury to cultured cerebral endothelial cells.

Damage to the vascular endothelium is considered an important feature in the development of cerebral vasospasm following subarachnoid hemorrhage. The present study examined this issue by testing the effects of hemolysate on the morphology and barrier function of cultured Bovine Middle Cerebral Artery Endothelial Cells (BMCA-ECs). Hemolysate elicited a dose-dependent loss of cells in confluent cultures of BMCA-ECs. The shape of the surviving cells changed from a typical cobblestone appearance to a spindle-like appearance with increased vacuolization. Hemolysate-induced damage was reduced by co-incubation with bovine calf serum (BCS) in a concentration-dependent manner. The early impact of hemolysate on endothelial cells was evaluated using a permeability assay in which the passage of 14C-sucrose across a BMCA-EC monolayer was analyzed. Hemolysate significantly increased the permeability of 14C-sucrose across the endothelial barrier. In contrast to its protective effects against cell loss, BCS did not block the early hemolysate-induced increase in transcellular permeability. These findings further implicate erythrocyte contents in the pathogenesis of structural and functional damage to the endothelium following subarachnoid hemorrhage.

Spontaneous intracerebral hemorrhage in children.

We reviewed our experience in 42 children younger than 16 years with spontaneous intracerebral hemorrhage (ICH) treated between January 1989 and December 1997. Glasgow coma scale (GCS) on admission was 15 in 21 (50%) patients. The most frequent presenting symptoms were headache in 28 (67%) patients, followed by loss of consciousness in 22 (52%) patients and vomiting in 21 (50%) patients. Three cases were diagnosed initially as meningitis and two cases as common cold. The locations of ICH were lobar (26 patients) and cerebellar (7). Cerebral angiographies were performed on 28 patients, and were diagnostic in 19 (68%). Magnetic resonance imaging (MRI) scans revealed two cases of cavernous angiomas, which were confirmed by the pathologic studies of surgical specimens. Laboratory examinations detected two cases of acute leukemia. Four categories of the causes of ICH were determined in 23 (55%) patients. The leading cause of bleeding was arteriovenous malformations (AVMs). The in-hospital survival rate of all patients in this study was 79%. Patients with GCS 3-5 on admission and ICH located at brain stem, cerebellum, and multiple subcortical areas had higher mortality rates. On the follow-up (mean 42 months), seventy percent of our cases had made a good recovery, 21% a fair recovery, 3% a poor recovery, and 6% had died. Children with ICH recover motor function more rapidly than adults. However, visual deficits always persist at our long-term follow-up examinations. A physician should keep in mind the diagnosis of ICH in children, even though the presenting symptoms may be non-specific and the incidence of ICH is very low in children.

Outcome of spontaneous subarachnoid hemorrhage of unknown etiology.

During a 7-year period, 56 patients with a verified subarachnoid hemorrhage (SAH) in whom neuroradiological investigations failed to reveal a reasonable cause of the bleeding were evaluated. Forty-six patients who survived the SAH were interviewed at a follow-up examination from 10 to 82 months (mean 37 months) after the bleeding. Early prognosis of an unfavorable outcome was possible on the basis of two clinical variables: the poor Glasgow coma scale (GCS < = 11) at admission and the Fisher's SAH grade of greater than II on brain computerized tomographic scans. Other clinical variables in the acute stage, including age, sex, a history of hypertension and the complications of SAH, such as vasospasm, hydrocephalus, and rebleeding, were not related to the early outcome. GCS on discharge was predictive of activity of daily life at follow-up review. On the follow-up, 80% of the patients experienced a good recovery. Rebleeding episode occurred in a patient 5 years after the bleeding. The overall rebleeding rate was 2.2% (equivalent to an annual recurrence of 0.7%). This study confirmed a good prognosis for patients with SAH of unknown cause. We recommend that after thorough panangiography, those patients with SAH of unknown etiology should be encouraged to return to a normal life style without any restriction.

[Birth weight percentiles of premature infants needs to be updated]. / Percentielgrenzen voor geboortegewicht van vroeggeborenen moeten worden herzien.

OBJECTIVE: To analyse whether the conventional so-called Kloosterman charts for birthweight of preterm infants based on data from 1931-1965 are still valid. DESIGN: Descriptive investigation. LOCATION: The Netherlands. METHOD: Data were obtained from the 'project of the premature and small for gestational age' (POPS) survey in 1983. The population consisted of 855 Caucasian infants born after a pregnancy of 24-31 weeks. RESULTS: In nearly all gestational age categories the percentages of small-for-gestational age infants were higher than the 10% they should have been by definition; the percentages of large-for-gestational age infants were much lower than 10%. After exclusion of elective births the percentages remained different. CONCLUSION: These shifts in the birthweight distribution are probably the result of changes in obstetrics. The birthweight percentiles for preterm births will have to be updated.