A rare case of sacral epidural arteriovenous fistula with concomitant occult multiple lumbar epidural arteriovenous fistulas.

We describe a rare case of sacral epidural arteriovenous fistulas (edAVFs) with atypical clinical course of treatment. A 78-year-old man with a history of spinal surgery presented progressive gait disturbance and urinary incontinence. Spinal angiography demonstrated a sacral spinal AVF fed by bilateral lateral sacral arteries, draining to the venous pouch with subdural drainage. The first treatment by direct interruption of a subdural drainer was incompletely finished. Postoperative reassessment by 3D imaging analysis led to the diagnosis of sacral edAVF and 3D understanding of its angioarchitecture. The second treatment by transarterial embolization (TAE) resulted in complete occlusion of a sacral edAVF. However, spinal venous congestion didn't improve, because the recruitment of occult edAVFs at the multiple lumbar levels and complex-shaped sacral ventral epidural venous plexus (VEP) were involved in the remnant of prior subdural drainage. The third treatment was performed by TAE for three occult edAVFs and the VEP compartment connecting between a patent edAVF and subdural drainage, which resulted in complete disappearance of spinal cord edema. Endovascular embolization of VEP compartment connecting to subdural drainage in addition to fistulous occlusion may be one of the treatment options for several edAVFs at the multiple spinal levels.

Role of Endovascular Approach as Diagnostic Technique and First-Line Therapy for the Patients with Micro-Arteriovenous Malformations: A Case Report and Literature Review.

Objective: We describe a rare case report of micro-arteriovenous malformation (micro-AVM) treated by the endovascular approach in addition with literature review. Case Presentation: A 12-year-old boy presenting with a spontaneous intracerebral hematoma in the left occipital lobe underwent conventional diagnostic workups. The results of initial catheter angiography were considered to be equivocal as the AVM. Superselective angiography (SA) demonstrated a micro or small AVM (single feeder and single drainer type) with an aneurysmal dilatation. Immediate transarterial embolization (TAE) might fail to occlude the whole of nidus area completely, and subsequently, we switched to the surgical exploration of AVM lesion. Intraoperative findings demonstrated that the whole of AVM lesion had already been occluded completely, indicating the complete occlusion by TAE only. Pathological findings of the surgical specimen showed an aneurysmal dilatation was a venous aneurysm with vulnerable vascular wall structure, which was certainly the source of bleeding. Based on the above results, the retrospective revaluation of superselective angiogram permitted us to understand that the nidus of AVM was micro nidus type and TAE had resulted in the complete nidus occlusion. Conclusion: SA is the most useful diagnostic modality to clarify the angioarchitecture of micro-AVM and AVM-related aneurysms. If SA is successfully performed and relatively safe TAE is expected to be possible, the subsequent attempt to do curative embolization as a first-line treatment may be worthy of consideration. However, the surgical procedure should be fully reserved for the possible incomplete obliteration and hemorrhagic complications.

Cerebrospinal Fluid Leakage at the Lumbar Spine: A Unique Cause of Delayed Neurologic Deterioration in a Traumatic Acute Subdural Hematoma Patient.

We present a rare case of traumatic acute subdural hematoma (SDH) in which intracranial hypotension (IC) secondary to cerebrospinal fluid (CSF) leakage at the lumbar spine caused delayed neurological deterioration. A 70-year-old male sustained a head injury after ground-level fall and was brought to our institution. A brain computed tomography (CT) showed a thin acute SDH with mild brain shift, and conservative management was initiated. He exhibited neurological deterioration on the 9th hospital day, however, and a brain CT showed a change in CT density and marked an increase in hematoma volume and brain shift. It was thought that conversion from acute to subacute SDH was associated with the deterioration, and emergency hematoma evacuation was performed. Despite the surgery, neither clinical nor radiographical improvement occurred. The lack of improvement pointed to the presence of underlying IC, and a CT myelography revealed the dural sleeve of the right L2 nerve root as the source of the CSF leakage. An epidural blood patch therapy was performed on the 12th hospital day to seal the CSF leakage. The postprocedural course was uneventful, and the patient was discharged free of symptoms on the 20th hospital day. Spinal CSF leakage should be considered as a cause of delayed neurological deterioration in patients with traumatic acute SDH which exhibits conversion to subacute SDH.

Frequency and characteristics of traumatic brain injury in restrained drivers involved in road traffic accidents.

BACKGROUND: While seatbelt is an important device protecting drivers from traumatic brain injury (TBI), it has rarely been reported how often and in what circumstances restrained drivers sustain TBI after road traffic accident (RTA). Whole-body computed tomography (WBCT) for blunt trauma patients may provide a unique opportunity to investigate the frequency and characteristics of TBI sustained by restrained drivers. METHODS: A single-center, retrospective observational study was conducted using prospectively acquired data. Between January 2013 and December 2017, 409 restrained drivers (284 men/125 women, mean age of 45.0 ± 19.1 years) whose vehicle had been severely damaged in RTAs underwent WBCT for evaluation of injuries. Multivariate regression analysis was performed to identify variables predictive of TBI. Influence of collision patterns (frontal, lateral or rollover) on the frequency and severity of TBI was evaluated. Relationship between collision patterns and CT findings was also reviewed. RESULTS: Thirty-one restrained drivers (7.6%) sustained TBI after RTA. The distribution of Glasgow Coma Scale (GCS) scores among the 31 drivers was 15 in 9, 13-14 in 9, 9-12 in 4, and ≤ 8 in 9, indicating that the majority of TBIs were classifiable as mild. The frequency of TBI in alert and oriented drivers, i.e., those with a GCS score of 15, was 2.9%. Multivariate regression analysis showed that both altered mental status (OR, 4.933; 95% CI, 1.135-21.431) and loss of consciousness (OR, 6.492; 95% CI, 1.669-25.249) were associated with TBI. The frequency of TBI tended to be higher in drivers with rollover collision than those with frontal collision (6 vs. 13%, p = 0.07). Interhemispheric acute subdural hematoma and subcortical petechial hemorrhage seemed to be characteristic CT findings in drivers with frontal and lateral collision, respectively. CONCLUSIONS: The key finding of this study, i.e., that (1) TBI was observed in 7.6% of restrained drivers with severe vehicular damage, may provide useful information to neurosurgeons who take care of RTA victims. The majority of the TBIs were mild without need for neurosurgical intervention. While association may exist between type of collision and type of brain injury, further studies with prospective design are warranted.

Stroke while driving: Frequency and association with automobile accidents.

Background Cardiovascular events while driving have occasionally been reported. In contrast, there have been few studies on stroke while driving. Aim The objectives of this study were to (1) report the frequency of stroke while driving and (2) evaluate its association with automobile accidents. Methods Clinical data prospectively acquired between January 2011 and December 2016 on 2145 stroke patients (1301 with ischemic stroke, 585 with intracerebral hemorrhage, and 259 with subarachnoid hemorrhage) were reviewed to identify patients who sustained a stroke while driving. The ratio of driving to performing other activities was evaluated for each stroke type. Furthermore, the drivers' response to stroke was reviewed to understand how automobile accidents occurred. Results Among the 2145 patients, 85 (63 ischemic stroke, 20 intracerebral hemorrhage, and 2 subarachnoid hemorrhage) sustained a stroke while driving. The ratio of driving to performing other activities was significantly higher in ischemic stroke (4.8%) than in intracerebral hemorrhage (3.4%) or subarachnoid hemorrhage (0.8%). A majority of drivers either continued driving or pulled over to the roadside after suffering a stroke. However, 14 (16%) patients were involved in automobile accidents. In most patients, an altered mental status due to severe stroke was the presumed cause of the accident. Conclusion Stroke occurred while driving in 4.0% of all strokes and accidents occurred in 16% of these instances.

Clinical characteristics of stroke occurring in the toilet: Are older adults more vulnerable?

AIM: While autonomic imbalance during defecation/micturition can cause hemodynamic instability, stroke occurring in the toilet has rarely been investigated. The objective of the present study was to clarify the frequency and clinical characteristics of toilet-related stroke. METHODS: Clinical data prospectively acquired between January 2011 and December 2015 on 1939 patients with acute stroke (1224 cerebral infarctions [CI], 505 intracerebral hemorrhages [ICH] and 210 subarachnoid hemorrhages [SAH]) were reviewed to identify patients with a toilet-related stroke. For each stroke type, the ratios of stroke occurring during defecation/micturition to those occurring during other activities were calculated. Subsequently, how patients with toilet-related stroke were brought to medical attention was investigated. Whether older patients (aged >65 years) had an elevated ratio of toilet-related stroke was investigated in each stroke type. RESULTS: A total of 108 patients (41 CI, 37 ICH and 30 subarachnoid hemorrhages) sustained a stroke in the toilet. The ratio of toilet-related stroke was highest in subarachnoid hemorrhages (14.3%), followed by ICH (7.3%). Circadian differences existed among the three stroke types: toilet-related CI were more likely to occur in the night-time than ICH. Patients with toilet-related CI were significantly more likely to sustain cardioembolic stroke. In all three stroke types, <40% of patients could call for help by themselves. Older patients showed a significantly higher proportion of toilet-related stroke in CI, but not in hemorrhagic strokes. CONCLUSIONS: The toilet is a closed space where stroke occurs disproportionately frequently. Effort to reduce the incidence of toilet-related strokes is warranted, as early patient detection is not always feasible. Geriatr Gerontol Int 2018; 18: 250-255.

Clinical Characteristics of Stroke Occurring while Bathing.

BACKGROUND: Stroke can occur during any human activity. Although cardiac arrests or drowning accidents while bathing have been studied extensively, there are few studies focusing on stroke occurring while bathing. The objectives of this study were to evaluate the clinical characteristics of stroke occurring while bathing and the association between stroke and drowning accidents. METHODS: Clinical data prospectively acquired between January 2011 and December 2015 on 1939 patients with stroke (1224 cerebral infarctions [CIs], 505 intracerebral hemorrhages [ICHs], and 210 subarachnoid hemorrhages [SAHs]) were reviewed to identify patients who sustained a stroke while bathing. The ratio of bathing-related strokes to strokes occurring during other activities was evaluated. Moreover, the demographics of these 2 groups were compared in each stroke type. RESULTS: Among the 1939 patients, 78 (CI, 32; ICH, 28; and SAH, 18) sustained a stroke while bathing. The ratio of bathing to other activities in the SAH group was the highest (8.6%), followed by the ICH group (5.5%), whereas that in the CI group was the lowest (2.6%). Regardless of stroke type, only a minority of patients were found to have collapsed inside the bathtub. CONCLUSIONS: The higher ratio of bathing in hemorrhagic strokes may indicate that there is a small risk of hemorrhagic stroke while bathing in vulnerable subjects. This retrospective study did not establish a causal relationship between bathing and stroke nor identify risk factors, which means that future prospective studies are warranted. The finding that the great majority of bathing-related stroke patients were found to have collapsed outside the bathtub suggests that the involvement of stroke in drowning accidents in the bathtub may be small.

Subarachnoid hemorrhage complicated with neurogenic pulmonary edema and takotsubo-like cardiomyopathy.

Patients with poor-grade subarachnoid hemorrhage (SAH) are often complicated with acute cardiopulmonary dysfunctions, particularly neurogenic pulmonary edema (NPE) and takotsubo-like cardiomyopathy (TCM). This study retrospectively investigated the incidence, demographics, clinical characteristics, and outcomes of patients with SAH complicated with both NPE and TCM (NPE-TCM). The effects of aneurysm location and other clinical variables on the incidence of NPE-TCM were also investigated. Among 234 SAH patients treated during 5-year period, 16 (7%) presented with NPE, and transthoracic ultrasonography revealed that 14 of these 16 patients (88%) also had TCM. All 14 patients with NPE-TCM had poor-grade SAH (World Federation of Neurosurgical Societies grades IV and V). Ruptured posterior circulation aneurysm was predictive of NPE-TCM, but other clinical variables were not. Eight of the 14 patients with NPE-TCM could undergo treatment for ruptured aneurysm. Long-term outcomes were favorable in 5 of the 8 patients. Grade IV SAH patients had significantly better outcomes than grade V patients. TCM develops frequently in SAH patients presenting with NPE, and transthoracic ultrasonography should be conducted routinely in that population. Patients with ruptured posterior circulation aneurysm may have elevated risk of developing NPE-TCM. Endovascular obliteration of the aneurysm may be preferable to open surgery, but the optimal treatment modality needs to be evaluated further. Considering the limited number of SAH patients complicated with NPE-TCM, a multi-center cooperative study may be required.

Traumatic aneurysm of the supraclinoid internal carotid artery-case report-.

A 23-year-old male was admitted after a motor vehicle accident with acute epidural hematoma, diffuse subarachnoid hemorrhage (SAH) in the basal cistern, and fractures at the anterior cranial base. Angiography revealed an aneurysm of the right supraclinoid internal carotid artery (ICA). His consciousness suddenly worsened on the 23rd day. Expansion of the SAH in the basal cistern and two hump aneurysms were detected. He underwent endovascular embolization of these aneurysms and the right ICA with Guglielmi detachable coil. Traumatic aneurysms are difficult to diagnose in the early period after injury and are associated with a high mortality. Endovascular treatments for traumatic aneurysms have lower mortality rate, and can be performed under local anesthesia.

Progression of pre-existing Chiari type I malformation secondary to cerebellar hemorrhage: case report.

A previously healthy 32-year-old man was surgically treated under a diagnosis of right subcortical hematoma. Magnetic resonance imaging incidentally demonstrated tonsillar herniation. Thirty-two months later, he was readmitted with complaints of occipital, neck, and shoulder pain as well as cerebellar ataxia. Subsequent magnetic resonance imaging demonstrated cerebellar hemorrhage and progression in the downward herniation of the tonsils. Conservative treatment resulted in spontaneous disappearance of the cerebellar hematoma, and the clinical signs and radiological findings improved. Patients with Chiari type I malformation require neuroimaging follow up because the downward herniation of the tonsils can progress in association with subsequent pathophysiological disorders.

Acute treatment with rosuvastatin protects insulin resistant (C57BL/6J ob/ob) mice against transient cerebral ischemia.

The purpose of this study was to investigate the short-term effects of rosuvastatin (RSV), a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, on transient, focal cerebral ischemia in C57BL/6J ob/ob mice with insulin resistance (IR). Male ob/ob, lean, or wild-type (WT) mice were treated with RSV (10 mg/kg per day, i.p.) or vehicle for 3 days. Ischemia was induced by 60 mins of middle cerebral artery occlusion (MCAO) and cortical blood flow (CBF) was monitored by laser-Doppler flowmetry. Infarct volumes were measured 24 h after reperfusion. IR mice exhibited a higher infarct volume compared with Lean or WT mice, and RSV reduced infarct volume only in obese mice (40%+/-3% versus 32%+/-3%, P<0.05). Blood cholesterol and insulin levels were elevated in ob/ob mice but were unaffected by RSV. The CBF reductions during MCAO were similar in all groups and were not affected by RSV. Although RSV did not increase cortical endothelial NO synthase (eNOS) levels in the ob/ob mice, it attenuated the increased cortical expression of intracellular adhesion molecule-1 (ICAM-1) after MCAO from ob/ob mice. Thus, RSV protects against stroke in IR mice by a mechanism independent of effects on the lipid profile, CBF, or eNOS but dependent on suppression of post-MCAO ICAM-1 expression.

Systemic administration of diazoxide induces delayed preconditioning against transient focal cerebral ischemia in rats.

Diazoxide is the prototypical opener of mitochondrial ATP-sensitive potassium channels (mitoK(ATP)) and protects neurons in vivo and in vitro against chemical and anoxic stresses. While we have previously shown that diazoxide administration induces acute preconditioning against transient cerebral ischemia in rats, the potential for delayed preconditioning of diazoxide has not been examined. The purpose of this study was to determine whether diazoxide promotes delayed preconditioning following 90 min of middle cerebral artery occlusion (MCAO) in male Wistar rats. Diazoxide (10 mg/kg) or vehicle was injected intraperitoneally 24 h before MCAO. Infarct volumes were measured 72 h after reperfusion. In animals anesthetized with halothane, treatment with diazoxide exhibited a 35% reduction (48.3+/-3.0% to 31.3+/-4.8%) and 18% reduction (35.1+/-2.2% to 28.9+/-2.1%) in cortical and subcortical infarct volumes, respectively. Administration of the mitoK(ATP) blocker 5-hydroxydecanoate attenuated this beneficial effect. In contrast, diazoxide did not induce delayed preconditioning in isoflurane-anesthetized rats. These findings support the concept that diazoxide produces delayed preconditioning via mitoK(ATP) activation but that physiological status can affect induction of preconditioning.

Neuronal preconditioning with the antianginal drug, bepridil.

It has recently been shown that the antianginal drug bepridil (BEP) activates mitochondrial ATP-sensitive potassium (mitoK(ATP)) channels and thus confers cardioprotection. Our aim was to investigate whether BEP could induce preconditioning in cultured rat cortical neurons. Although BEP depolarized isolated and in situ mitochondria and increased reactive oxygen species generation, no acute protection was observed. However, a 3-day BEP-treatment elicited dose-dependent delayed neuroprotection against 180 min of oxygen-glucose deprivation (cell viability: untreated, 52.5 +/- 0.85%; BEP 1 micromol/L, 59.6 +/- 1.53%*; BEP 2.5 micromol/L, 71.9 +/- 1.23%*; BEP 5 micromol/L, 95.3 +/- 0.89%*; mean +/- SEM; *p < 0.05 vs. untreated) and 60 min of glutamate excitotoxicity (200 micromol/L; cell viability: untreated, 54.1 +/- 0.69%; BEP 1 micromol/L, 61.2 +/- 1.19%*; BEP 2.5 micromol/L, 78.1 +/- 1.67%*; BEP 5 micromol/L, 91.2 +/- 1.20%*; mean +/- SEM; *p < 0.05 vs. untreated), and inhibited the reactive oxygen species surge upon glutamate exposure. The protection was antagonized with co-application of the superoxide dismutase mimetic M40401, but not with reduced glutathione, catalase, or with the mitoK(ATP) blocker 5-hydroxydecanoate. Furthermore, BEP treatment resulted in increased levels of phosphorylated protein kinase C, manganese-dependent superoxide dismutase, glutathione peroxidase, and Bcl-2. Our results indicate that BEP induces delayed neuronal preconditioning which is dependent on superoxide generation but perhaps not on direct mitoK(ATP) activation.

The mitochondrial K(ATP) channel opener BMS-191095 reduces neuronal damage after transient focal cerebral ischemia in rats.

Activation of mitochondrial ATP-sensitive potassium (mitoK(ATP)) channels protects the brain against ischemic or chemical challenge. Unfortunately, the prototype mitoK(ATP) channel opener, diazoxide, has mitoK(ATP) channel-independent actions. We examined the effects of BMS-191095, a novel selective mitoK(ATP) channel opener, on transient ischemia induced by middle cerebral artery occlusion (MCAO) in rats. Male Wister rats were subjected to 90 mins of MCAO. BMS-191095 (25 microg; estimated brain concentration of 40 micromol/L) or vehicle was infused intraventricularly before the onset of ischemia. In addition, the effects of BMS-191095 on plasma and mitochondrial membrane potentials and reactive oxygen species (ROS) production in cultured neurons were examined. Finally, we determined the effects of BMS-191095 on cerebral blood flow (CBF) and potassium currents in cerebrovascular myocytes. Treatment with BMS-191095 24 h before the onset of ischemia reduced total infarct volume by 32% and cortical infarct volume by 38%. However, BMS-191095 administered 30 or 60 mins before MCAO had no effect. The protective effects of BMS-191095 were prevented by co-treatment with 5-hydroxydecanoate (5-HD), a mitoK(ATP) channel antagonist. In cultured neurons, BMS-191095 (40 micromol/L) depolarized the mitochondria without affecting ROS levels, and this effect was inhibited by 5-HD. BMS-191095, similar to the vehicle, caused an unexplained but modest reduction in the CBF. Importantly, BMS-191095 did not affect either the potassium currents in cerebrovascular myocytes or the plasma membrane potential of neurons. Thus, BMS-191095 afforded protection against cerebral ischemia by delayed preconditioning via selective opening of mitoK(ATP) channels and without ROS generation.

Transient glucose and amino acid deprivation induces delayed preconditioning in cultured rat cortical neurons.

Several studies have demonstrated that glucose deprivation, combined either with anoxia or with the inhibition of oxidative phosphorylation, leads to the development of ischemic tolerance in neurons. The aim of our experiments was to investigate whether similar effects could be achieved by transient energy deprivation without either anoxia or the inhibition of the electron transfer chain. Preconditioning was carried out by incubating primary rat cortical neuronal cultures for 3, 6 or 9 h in a glucose- and amino acid-free balanced salt solution supplemented with B27 in normoxic conditions. After 24 h, neuronal cultures were exposed to oxygen-glucose deprivation, glutamate or hydrogen peroxide. Cell viability was measured 24 h after the lethal insults. Potential mechanisms that can influence free radical production were also examined. Energy deprivation protected neuronal cells against lethal stimuli (e.g. cell survival after oxygen-glucose deprivation was 33.1 +/- 0.52% in the untreated group and 80.1 +/- 1.27% in the 9-h energy deprivation group), reduced mitochondrial membrane potential, decreased free radical formation, attenuated the intracellular free calcium surge upon glutamate receptor stimulation, and resulted in an elevated level of GSH. Our findings show that transient energy deprivation induces delayed preconditioning and prevents oxidative injuries and neuronal cell death.

Impaired endothelin-induced vasoconstriction in coronary arteries of Zucker obese rats is associated with uncoupling of [Ca2+]i signaling.

Although insulin resistance (IR) is a major risk factor for coronary artery disease, little is known about the regulation of coronary vascular tone in IR by endothelin-1 (ET-1). We examined ET-1 and PGF(2alpha)-induced vasoconstriction in isolated small coronary arteries (SCAs; approximately 250 microM) of Zucker obese (ZO) rats and control Zucker lean (ZL) rats. ET-1 response was assessed in the absence and presence of endothelin type A (ET(A); BQ-123), type B (ET(B); BQ-788), or both receptor inhibitors. ZO arteries displayed reduced contraction to ET-1 compared with ZL arteries. In contrast, PGF(2alpha) elicited similar vasoconstriction in both groups. ET(A) inhibition diminished the ET-1 response in both groups. ET(B) inhibition alone or in combination with ET(A) blockade, however, restored the ET-1 response in ZO arteries to the level of ZL arteries. Similarly, inhibition of endothelial nitric oxide (NO) synthase with N(omega)-nitro-l-arginine methyl ester (l-NAME) enhanced the contraction to ET-1 and abolished the difference between ZO and ZL arteries. In vascular smooth muscle cells from ZO, ET-1-induced elevation of myoplasmic intracellular free calcium concentration ([Ca2+]i) (measured by fluo-4 AM fluorescence), and maximal contractions were diminished compared with ZL, both in the presence and absence of l-NAME. However, increases in [Ca2+]i elicited similar contractions of the vascular smooth muscle cells in both groups. Analysis of protein and total RNA from SCA of ZO and ZL revealed equal expression of ET-1 and the ET(A) and ET(B) receptors. Thus coronary arteries from ZO rats exhibit reduced ET-1-induced vasoconstriction resulting from increased ET(B)-mediated generation of NO and diminished elevation of myoplasmic [Ca2+]i.

Rebleeding from a primary brain tumor manifesting as intracerebral hemorrhage (CNN 04/077, revised version).

Symptomatic spontaneous intratumoral hemorrhage is a rare event in a patient with a brain tumor (BT). Although the treatment of choice in such a case is surgical removal of both the tumor and the hemorrhage, the optimal timing for surgical intervention has not been clearly established, particularly in those who present with minimal neurological deficits and a small hemorrhage volume. Two cases of primary BTs manifesting as an intracerebral hemorrhage (ICH) are described, in which rebleeding from the tumor occurred shortly after the initial hemorrhage. The patients each presented with the sudden onset of a headache and minimal neurological deficits, and the neuroradiological workup was consistent with a diagnosis of hemorrhagic BT. Each patient remained neurologically stable, and elective surgery had been planned within 7 days of their admission, but rebleeding occurred 5 and 6 days, respectively, after admission. A BT manifesting as an ICH may rebleed shortly after the initial bleeding, and should be treated on an emergency basis instead of an elective basis regardless of the patient's neurological status on admission or hematoma volume on the initial CT scans.

Predicting the overall management outcome in patients with a subarachnoid hemorrhage accompanied by a massive intracerebral or full-packed intraventricular hemorrhage: a 15-year retrospective study.

BACKGROUND: Patients with a subarachnoid hemorrhage (SAH) accompanied by a massive intracerebral hemorrhage (ICH) or a full-packed intraventricular hemorrhage (IVH) have poor outcomes. We evaluated the clinical factors to predict the overall outcome in such patients. METHODS: Data on nontraumatic SAH patients were collected and classified into 3 groups: the pure SAH group (SAH accompanied with neither ICH nor IVH), the ICH group (SAH accompanied with a massive ICH; hematoma 30 mL), and the IVH group (SAH and all ventricles were full-packed with hematoma). One hundred seventy-nine patients were in the ICH group and 109 in the IVH group. We evaluated clinical factors, such as the Hunt & Hess (H&H) score on admission, age, sex, history, rebleeding ratio, and the computerized tomography findings (SAH score). RESULTS: The result of multivariate logistic regression analysis of clinical variables in the ICH group, good and intermediate H&H grades, younger age (<70), no rebleeding, and lower SAH score were associated with a favorable outcome. In the result of the multivariate logistic regression analysis of clinical variables in the IVH group, only a higher SAH score was associated with an unfavorable outcome. CONCLUSIONS: In the ICH group, factors that could be used to predict a favorable outcome included good and intermediate H&H scores (1, 2, and 3) on admission, younger age (<70), and a lower SAH score. In the IVH group, the main factor that could be used to predict a favorable outcome was a lower SAH score.

Treatment of spontaneous intracranial hypotension secondary to C-2 meningeal cyst by surgical packing--case report.

A 41-year-old man presented with progressive worsening of postural headache. Computed tomography (CT) showed bilateral subdural hematomas without prior history of trauma. The diagnosis was spontaneous intracranial hypotension (SIH). Conservative treatment with oral steroids failed to prevent gradual deterioration of the patient's consciousness. CT myelography revealed massive cerebrospinal fluid (CSF) leakage between the C-1 and C-2 levels. The leak was repaired surgically via a laminectomy. A cyst, thought to be a meningeal cyst, was discovered adjacent to the right C-2 nerve root, and CSF was seen seeping out from around the cyst after a Valsalva maneuver. The presumed dural defect of the cyst was sealed by packing with muscle fragments and fibrin glue. The symptoms disappeared soon after surgery. He was discharged 1 month after surgery without deficits. Most SIH cases are benign and can be managed conservatively, or by the epidural blood patch method. Surgery is more invasive than the epidural blood patch method, but should be performed in patients with a high cervical lesion and massive CSF leakage.

Cerebellar hemorrhage secondary to cranial metastasis of prostate cancer--case report.

A 77-year-old man with a 9-year history of prostate cancer presented with high fever and dysphagia. The initial diagnosis was aspiration pneumonia, but the patient became comatose 2 days after admission, and neuroradiological workup revealed cerebellar hemorrhage, obstructive hydrocephalus, and extensive destruction of the occipital bone secondary to cranial metastasis. The diagnosis was cerebellar hemorrhage secondary to cranial metastasis of prostate cancer. Tumor resection was abandoned because of the patient's poor health. Shunt surgery and palliative radiotherapy were temporarily effective in restoring his consciousness, but he died of systemic infection 3 weeks after surgery. Metastasis of prostate cancer to the cranium, particularly to the skull base, rarely causes lower cranial nerve paresis, and awareness of this sign may lead to earlier detection of the cranial metastasis and prevention of cerebellar hemorrhage.