A Case of Dysgraphia after Cerebellar Infarction Where Functional NIRS Guided the Task Aimed at Activating the Hypoperfused Region.

BACKGROUND: Linguistic impairment following cerebellar lesions is characterized by a marked cerebellocerebral diaschisis with decreased perfusion in the left cerebral hemisphere. CASE: We report on a 60-year-old right-handed French chef who presented with linguistic deficits following a right cerebellar infarction. Neurolinguistic examinations in the acute phase showed impaired graphomotor planning, especially for kanji (Japanese morphograms). Despite the absence of any structural damage to the supratentorial brain regions, a quantitative 123I-IMP SPECT study revealed a relative hypoperfusion, mainly around the left posterior middle temporal gyrus, considered to be a crossed cerebellar-cerebral diaschisis. We performed functional near-infrared spectroscopy (fNIRS) and observed that a picture card task could increase blood perfusion in the affected area. This task was as follows: once he saw a picture card depicting a dish, the patient had to list the ingredients that make up the dish. For example, he had to name vegetables, meat, and spices upon seeing a "curry" picture card. We added this task to his daily speech-hearing therapy regimen. In the chronic phase, we confirmed symptom amelioration in linguistic performance-paralleled reduction in the level of hypoperfusion on SPECT study. Discussion. This case is the first report of an fNIRS approach used to evaluate evidence-based prospective speech-hearing tasks by observing blood flow to the hypoperfused area of the cerebral cortex surface.

Brain infarction due to vertebral artery dissection caused by a bone protrusion from the condylar fossa in a juvenile case.

A 16-year-old boy presented with multiple posterior circulation ischemic strokes resulting from vertebral artery (VA) dissection. Three-dimensional computed tomography showed aberrant sub-occipital bone protuberance, proximal to the VA dissection. Since the patient was a habitual neck cracker, VA dissection was thought to result from the impact shock of the rotational head movement. This could be due to either the osseous prominence or the compression between the prominence and the C1. Although it is a rare etiology of Bow Hunter's syndrome, VA dissection due to sub-occipital bone spur because of neck cracking should be considered in the diagnosis of Bow Hunter's syndrome in juvenile patients.

Syringomyelia due to Lumbar Spinal Fluid Drainage in the Acute Phase of Subarachnoid Hemorrhage: A Case Report.

Lumbar spinal fluid drainage is a common procedure for treating hydrocephalus and alleviating vasospasm by egesting blood in the subarachnoid cavity after subarachnoid hemorrhage. Despite being an effective and safe procedure, cerebrospinal fluid overdrainage might result in serious complications. Here we report the case of a 49-year-old man who suffered from tonsillar herniation with subsequent cervicothoracic syringomyelia in the acute phase of subarachnoid hemorrhage due to vertebral artery dissection. About 2 weeks after lumbar drainage was switched from external ventricular drainage initiated on the day of subarachnoid hemorrhage, the recovery from the disturbance of consciousness revealed tetraplegia, and magnetic resonance imaging demonstrated tonsillar herniation and syringomyelia. Removal of the spinal drain and resumption of external ventricular drainage resulted in the restoration of the herniated tonsils to the normal position and the complete disappearance of syringomyelia 11 days later. We should consider that spinal syringomyelia could develop as a complication of lumbar spinal fluid drainage in the acute phase of thick subarachnoid hemorrhage, particularly in the posterior cranial fossa.

Brain Volume Determination in Subarachnoid Hemorrhage Using Rats.

Brain edema is routinely measured using the wet-dry method. Volume, however, is the sum total of all cerebral tissues, including water. Therefore, volumetric change following injury may not be adequately quantified using percentage of edema. We thus tested the hypothesis that dried brains can be reconstituted with water and then re-measured to determine the actual volume. Subarachnoid hemorrhage (SAH) was induced by endovascular perforation in adult male Sprague-Dawley rats (n = 30). Animals were euthanized at 24 and 72 h after evaluation of neurobehavior for determination of brain water content. Dried brains were thereafter reconstituted with equal parts of water (lost from brain edema) and centrifuged to remove air bubbles. The total volume was quantified using hydrostatic (underwater) physics principles that 1 ml water (mass) = 1 cm(3) (volume). The amount of additional water needed to reach a preset level marked on 2-ml test tubes was added to that lost from brain edema, and from the brain itself, to determine the final volume. SAH significantly increased both brain water and volume while worsening neurological function in affected rats. Volumetric measurements demonstrated significant brain swelling after SAH, in addition to the brain edema approach. This modification of the "wet-dry" method permits brain volume determination using valuable post hoc dried brain tissue.

Cannabinoid Receptor Type 2 Agonist Attenuates Acute Neurogenic Pulmonary Edema by Preventing Neutrophil Migration after Subarachnoid Hemorrhage in Rats.

We evaluated whether JWH133, a selective cannabinoid type 2 receptor (CB2R) agonist, prevented neurogenic pulmonary edema (NPE) after subarachnoid hemorrhage (SAH) by attenuating inflammation. Adult male rats were assigned to six groups: sham-operated, SAH with vehicle, SAH with JWH133 (0.3, 1.0, or 3.0 mg/kg) treatment 1 h after surgery, and SAH with JWH133 (1.0 mg/kg) at 1 h with a selective CB2R antagonist, SR144528 (3.0 mg/kg). The perforation model of SAH was performed and pulmonary wet-to-dry weight ratio was evaluated 24 and 72 h after surgery. Western blot analyses and immunohistochemistry were evaluated 24 h after surgery. JWH133 (1.0 mg/kg) significantly and most strongly improved lung edema 24 h after SAH. SR144528 administration significantly reversed the effects of JWH133 (1.0 mg/kg). SAH-induced increasing levels of myeloperoxidase (MPO) and decreasing levels of a tight junction (TJ) protein, junctional adhesion molecule (JAM)-A, were ameliorated by JWH133 (1.0 mg/kg) administration 24 h after SAH. Immunohistochemical assessment also confirmed substantial leukocyte infiltration in the outside of vessels in SAH, which were attenuated by JWH133 (1.0 mg/kg) injection. CB2R agonist ameliorated lung permeability by inhibiting leukocyte trafficking and protecting tight junction proteins in the lung of NPE after SAH.

Subarachnoid Hemorrhage-Triggered Acute Hypotension Is Associated with Left Ventricular Cardiomyocyte Apoptosis in a Rat Model.

Whether hypotension that occurs due to neurogenic stunned myocardium after subarachnoid hemorrhage (SAH) is associated with cardiomyocyte apoptotic cell death remains unknown. In this study, 18 male rats were subjected to sham or the endovascular perforation model of SAH surgery. Based on the mean arterial pressure (MAP) after SAH, rats were separated into SAH with hypotension (SAH hypotension) or SAH with blood pressure preservation (SAH BP preservation) groups. All animals were euthanized 2 h after the surgical procedure. Hearts were removed and separated transversely into base and apex parts, then Western blot analyses and immunohistochemistry were performed only in the apex part. One rat died as a result of severe SAH and two rats with mild SAH were excluded. We analyzed data from 15 rats that were divided into three groups: sham, SAH hypotension, and SAH BP preservation (n = 5, each). There was a significantly higher cleaved caspase-3/caspase-3 ratio in the SAH hypotension group compared with sham and the SAH BP preservation group. Cardiomyocyte apoptosis was demonstrated in the SAH rats. This is the first experimental report that describes SAH-induced neurogenic stunned myocardium with ensuing hypotension may result from the acute apoptotic cardiomyocyte cell death in the left ventricle.

Cannabinoid receptor type 2 agonist attenuates apoptosis by activation of phosphorylated CREB-Bcl-2 pathway after subarachnoid hemorrhage in rats.

Early brain injury (EBI) which comprises of vasogenic edema and apoptotic cell death is an important component of subarachnoid hemorrhage (SAH) pathophysiology. This study evaluated whether cannabinoid receptor type 2 (CB2R) agonist, JWH133, attenuates EBI after SAH and whether CB2R stimulation reduces pro-apoptotic caspase-3 via up-regulation of cAMP response element-binding protein (CREB)-Bcl-2 signaling pathway. Male Sprague-Dawley rats (n=123) were subjected to SAH by endovascular perforation. Rats received vehicle or JWH133 at 1h after SAH. Neurological deficits and brain water content were evaluated at 24h after SAH. Western blot was performed to quantify phosphorylated CREB (pCREB), Bcl-2, and cleaved caspase-3 levels. Neuronal cell death was evaluated with terminal deoxynucleotidyl transferase-mediated uridine 5'-triphosphate-biotin nick end-labeling staining. Additionally, CREB siRNA was administered to manipulate the proposed pathway. JWH133 (1.0mg/kg) improved neurological deficits and reduced brain water content in left hemisphere 24h after SAH. JWH133 significantly increased activated CREB (pCREB) and Bcl-2 levels and significantly decreased cleaved caspase-3 levels in left hemisphere 24h after SAH. CREB siRNA reversed the effects of treatment. TUNEL positive neurons in the cortex were reduced with JWH133 treatment. Thus, CB2R stimulation attenuated EBI after SAH possibly through activation of pCREB-Bcl-2 pathway.

Cannabinoid type 2 receptor stimulation attenuates brain edema by reducing cerebral leukocyte infiltration following subarachnoid hemorrhage in rats.

Early brain injury (EBI), following subarachnoid hemorrhage (SAH), comprises blood-brain barrier (BBB) disruption and consequent edema formation. Peripheral leukocytes can infiltrate the injured brain, thereby aggravating BBB leakage and neuroinflammation. Thus, anti-inflammatory pharmacotherapies may ameliorate EBI and provide neuroprotection after SAH. Cannabinoid type 2 receptor (CB2R) agonism has been shown to reduce neuroinflammation; however, the precise protective mechanisms remain to be elucidated. This study aimed to evaluate whether the selective CB2R agonist, JWH133 can ameliorate EBI by reducing brain-infiltrated leukocytes after SAH. Adult male Sprague-Dawley rats were randomly assigned to the following groups: sham-operated, SAH with vehicle, SAH with JWH133 (1.0mg/kg), or SAH with a co-administration of JWH133 and selective CB2R antagonist SR144528 (3.0mg/kg). SAH was induced by endovascular perforation, and JWH133 was administered 1h after surgery. Neurological deficits, brain water content, Evans blue dye extravasation, and Western blot assays were evaluated at 24h after surgery. JWH133 improved neurological scores and reduced brain water content; however, SR144528 reversed these treatment effects. JWH133 reduced Evans blue dye extravasation after SAH. Furthermore, JWH133 treatment significantly increased TGF-ß1 expression and prevented an SAH-induced increase in E-selectin and myeloperoxidase. Lastly, SAH resulted in a decreased expression of the tight junction protein zonula occludens-1 (ZO-1); however, JWH133 treatment increased the ZO-1 expression. We suggest that CB2R stimulation attenuates neurological outcome and brain edema, by suppressing leukocyte infiltration into the brain through TGF-ß1 up-regulation and E-selectin reduction, resulting in protection of the BBB after SAH.

Early brain injury, an evolving frontier in subarachnoid hemorrhage research.

Subarachnoid hemorrhage (SAH), predominantly caused by a ruptured aneurysm, is a devastating neurological disease that has a morbidity and mortality rate higher than 50%. Most of the traditional in vivo research has focused on the pathophysiological or morphological changes of large-arteries after intracisternal blood injection. This was due to a widely held assumption that delayed vasospasm following SAH was the major cause of delayed cerebral ischemia and poor outcome. However, the results of the CONSCIOUS-1 trial implicated some other pathophysiological factors, independent of angiographic vasospasm, in contributing to the poor clinical outcome. The term early brain injury (EBI) has been coined and describes the immediate injury to the brain after SAH, before onset of delayed vasospasm. During the EBI period, a ruptured aneurysm brings on many physiological derangements such as increasing intracranial pressure (ICP), decreased cerebral blood flow (CBF), and global cerebral ischemia. These events initiate secondary injuries such as blood-brain barrier disruption, inflammation, and oxidative cascades that all ultimately lead to cell death. Given the fact that the reversal of vasospasm does not appear to improve patient outcome, it could be argued that the treatment of EBI may successfully attenuate some of the devastating secondary injuries and improve the outcome of patients with SAH. In this review, we provide an overview of the major advances in EBI after SAH research.

Hyperbaric oxygen preconditioning attenuates hyperglycemia-enhanced hemorrhagic transformation by inhibiting matrix metalloproteinases in focal cerebral ischemia in rats.

Hyperglycemia dramatically aggravates brain infarct and hemorrhagic transformation (HT) after ischemic stroke. Oxidative stress and matrix metalloproteinases (MMPs) play an important role in the pathophysiology of HT. Hyperbaric oxygen preconditioning (HBO-PC) has been proved to decrease oxidative stress and has been demonstrated to be neuroprotective in experimental stroke models. The present study determined whether HBO-PC would ameliorate HT by a pre-ischemic increase of reactive oxygen species (ROS) generation, and a suppression of MMP-2 and MMP-9 in hyperglycemic middle cerebral artery occlusion (MCAO) rats. Rats were pretreated with HBO (100% O2, 2.5 atmosphere absolutes) 1 h daily for 5 days before MCAO. Acute hyperglycemia was induced by an injection of 50% dextrose. Neurological deficits, infarction volume and hemorrhagic volume were assessed 24 h and 7 days after ischemia. ROS scavenger n-acetyl cysteine (NAC), hypoxia-inducible factor-1α (HIF-1α), inhibitor 2-methoxyestradiol (2ME2) and activator cobalt chloride (CoCl2), and MMP inhibitor SB-3CT were administrated for mechanism study. The activity of MMP-2 and MMP-9, and the expression HIF-1α were measured. HBO-PC improved neurological deficits, and reduced hemorrhagic volume; the expression of HIF-1α was significantly decreased, and the activity of MMP-2 and MMP-9 was reduced by HBO-PC compared with vehicle group. Our results suggested that HBO-PC attenuated HT via decreasing HIF-1α and its downstream MMP-2 and MMP-9 in hyperglycemic MCAO rats.

Role of SCH79797 in maintaining vascular integrity in rat model of subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: Plasma thrombin concentration is increased after subarachnoid hemorrhage (SAH). However, the role of thrombin receptor (protease-activated receptor-1 [PAR-1]) in endothelial barrier disruption has not been studied. The aims of this study were to investigate the role of PAR-1 in orchestrating vascular permeability and to assess the potential therapeutics of a PAR-1 antagonist, SCH79797, through maintaining vascular integrity. METHODS: SCH79797 was injected intraperitoneally into male Sprauge-Dawley rats undergoing SAH by endovascular perforation. Assessment was conducted at 24 hours after SAH for brain water content, Evans blue content, and neurobehavioral testing. To explore the role of PAR-1 activation and the specific mechanism of SCH79797's effect after SAH, Western blot, immunoprecipitation, and immunofluorescence of hippocampus tissue were performed. A p21-activated kinase-1 (PAK1) inhibitor, IPA-3, was used to explore the underlying protective mechanism of SCH79797. RESULTS: At 24 hours after SAH, animals treated with SCH79797 demonstrated a reduction in brain water content, Evans blue content, and neurobehavioral deficits. SCH79797 also attenuated PAR-1 expression and maintained the level of vascular endothelial-cadherin, an important component of adherens junctions. Downstream to PAR-1, c-Src-dependent activation of p21-activated kinase-1 led to an increased serine/threonine phosphorylation of vascular endothelial-cadherin; immunoprecipitation results revealed an enhanced binding of phosphorylated vascular endothelial-cadherin with endocytosis orchestrator ß-arrestin-2. These pathological states were suppressed after SCH79797 treatment. CONCLUSIONS: PAR-1 activation after SAH increases microvascular permeability, at least, partly through a PAR-1-c-Src-p21-activated kinase-1-vascular endothelial-cadherin phosphorylation pathway. Through suppressing PAR-1 activity, SCH79797 plays a protective role in maintaining microvascular integrity after SAH.

Transition of research focus from vasospasm to early brain injury after subarachnoid hemorrhage.

Subarachnoid hemorrhage is a devastating disease that can be difficult to manage. Not only is the initial bleeding and rebleeding associated with high mortality, but a large fraction of patients also develop a delayed neurological deficit even when the aneurysm was successfully secured with clipping or coiling. Past research effort has traditionally been focused on vasospasm, which was conceived to be the sole factor for delayed neurological deficit. The failure of anti-vasospastic drugs to improve outcome in clinical trials has brought into focus the significance of early brain injury. The immediate events associated with subarachnoid hemorrhage, including increased intracranial pressure, decreased cerebral blood flow and global ischemia initiate a cascade of pathological changes that occur before the onset of delayed vasospasm. These pathological changes in the very early stage of the hemorrhage propagate and cause blood-brain barrier disruption, inflammation, oxidative stress and cell death. Focusing only on the treatment of vasospasm with complete disregard for early brain injury is insufficient for the management of subarachnoid hemorrhage. Instead, a therapeutic intervention has to aim at stopping the molecular cascades of early brain injury that may lead to long-term deficits in addition to vasospasm. We review the pathological mechanisms of early brain injury, which may reveal new therapeutic avenues that can be exploited to serve as combination therapy with anti-vasospasm medications in the future.

Isoflurane attenuates blood-brain barrier disruption in ipsilateral hemisphere after subarachnoid hemorrhage in mice.

BACKGROUND AND PURPOSE: We examined effects of isoflurane, volatile anesthetics, on blood-brain barrier disruption in the endovascular perforation model of subarachnoid hemorrhage (SAH) in mice. METHODS: Animals were assigned to sham-operated, SAH+vehicle-air, SAH+1%, or 2% isoflurane groups. Neurobehavioral function, brain water content, Evans blue dye extravasation, and Western blotting for sphingosine kinases, occludin, claudin-5, junctional adhesion molecule, and vascular endothelial cadherin were evaluated at 24 hours post-SAH. Effects of sphingosine kinase (N,N-dimethylsphingosine) or sphingosine-1-phosphate receptor-1/3 (S1P1/3) inhibitors (VPC23019) on isoflurane's action were also examined. RESULTS: SAH aggravated neurological scores, brain edema, and blood-brain barrier permeability, which were prevented by 2% but not 1% isoflurane posttreatment. Two percent isoflurane increased sphingosine kinase-1 expression and prevented a post-SAH decrease in expressions of the blood-brain barrier-related proteins. Both N,N-dimethylsphingosine and VPC23019 abolished the beneficial effects of isoflurane. CONCLUSIONS: Two percent isoflurane can suppress post-SAH blood-brain barrier disruption, which may be mediated by sphingosine kinase 1 expression and sphingosine-1-phosphate receptor-1/3 activation.

Hyperbaric oxygen preconditioning attenuates hyperglycemia enhanced hemorrhagic transformation after transient MCAO in rats.

BACKGROUND: Hemorrhagic transformation (HT) can be a devastating complication of ischemic stroke. Hyperbaric oxygen preconditioning (HBO-PC) has been shown to improve blood-brain barrier (BBB) permeability in stroke models. The purpose of this study is to examine whether HBO-PC attenuates HT after focal cerebral ischemia, and to investigate whether the mechanism of HBO-PC against HT includes up-regulation of antioxidants in hyperglycemic rats. METHODS: Male Sprague-Dawley rats (280-320 g) were divided into the following groups: sham, middle cerebral artery occlusion (MCAO) for 2 h, and MCAO treated with HBO-PC. HBO-PC was conducted giving 100% oxygen at 2.5 atm absolute (ATA), for 1 h at every 24 h interval for 5 days. At 24 h after the last session of HBO-PC, rats received an injection of 50% glucose (6 ml/kg intraperitoneally) and were subjected to MCAO 15 min later. At 24 h after MCAO, neurological behavior tests, infarct volume, blood-brain barrier permeability, and hemoglobin content were measured to evaluate the effect of HBO-PC. Western blot analysis of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) was evaluated at multiple time-points before and after MCAO. RESULTS: HBO-PC improved neurological behavior test, and reduced infarction volume, HT and Evans blue extravasation in the ipsilateral hemisphere at 24 h after MCAO. Western blot analysis failed to demonstrate up-regulation of Nrf2 in HBO-PC group before and after MCAO. Paradoxically, HBO-PC decreased HO-1 expression at 24 h after MCAO, as compared with htMCAO group. CONCLUSIONS: HBO-PC improved neurological deficits, infarction volume, BBB disruption, and HT after focal cerebral ischemia. However, its mechanism against focal cerebral ischemia and HT may not include activation of Nrf2 and subsequent HO-1 expression.

[Slowly progressive expanding hematoma in the Basal Ganglia: a report of 3 cases and a literature review].

We demonstrate and discuss slowly progressive expanding hematoma (SPEH) in the basal ganglia, which expands over 2 weeks. To our knowledge, there have been only 5 cases of sudden-onset SPEH of the basal ganglia. To this, we add 3 cases admitted our hospitals because of putaminal hemorrhage within 1.5 hours of onset. All hematomas exhibited "2 components of hematoma sign" on initial CT scans, which we termed the "TCH sign" characterized as an anterolateral fluid portion and a posteromedial solid portion. Follow-up CT scans revealed gradual expansion of the fluid component of the hematoma without rebleeding for the subacute phase. Two cases were treated surgically. The first case, a 47-year-old man, underwent ultrasonically guided hematoma aspiration on day 17 and the second case, a 37-year-old man, underwent hematoma removal by craniotomy on day 23 after onset. Their postoperative courses were uneventful. The third case, a 57-year-old man, improved without surgical treatment and the hematoma dissolved completely within 2 months. To an extent, the TCH sign on a CT scan can be related to SPEH. We reviewed previous reports, including those an chronic expanding intracerebral hematomas and chronic encapsulated intracerebral hematomas, and concluded that it requires approximately 1 month for encapsulation of the hematoma to emerge. We suggest a possible progressive mechanism of SPEH. At first, the hematoma is divided into a fluid and a solid portion. Local generation of osmotically active molecules by clot degradation may allow intravascular fluid to escape into the fluid portion of the hematoma. Edema fluid with leakage via the disrupted blood-brain barrier may also aggravate the fluid portion of the hematoma. The continuing inflammatory response leads to the emergence of a hematoma capsule similar to the membrane observed in cases of chronic subdural hematoma, followed by the secondary causes of hematoma expansion. We discuss feasible timing and surgical treatment methods.

Inhibition of Rho kinase by hydroxyfasudil attenuates brain edema after subarachnoid hemorrhage in rats.

The blood-brain barrier (BBB) disruption and brain edema are important pathophysiologies of early brain injury after subarachnoid hemorrhage (SAH). This study is to evaluate whether Rho kinase (Rock) enhances BBB permeability via disruption of tight junction proteins during early brain injury. Adult male rats were assigned to five groups; Sham-operated, SAH treated with saline, a Rock inhibitor hydroxyfasudil (HF) (10 mg/kg) treatment at 0.5 h after SAH, HF treatment at 0.5 and 6 h (10 mg/kg, each) after SAH, and another Rock inhibitor Y27632 (10 mg/kg) treatment at 0.5 h after SAH. The perforation model of SAH was performed and neurological score and brain water content were evaluated 24 and 72 h after surgery. Evans blue extravasation, Rock activity assay, and western blotting analyses were evaluated 24 h after surgery. Treatment of HF significantly improved neurological scores 24 h after SAH. Single treatment with HF and Y27632, and two treatments with HF reduced brain water content in the ipsilateral hemisphere. HF reduced Evans blue extravasation in the ipsilateral hemisphere after SAH. Rock activity increased 24 h after SAH, and HF reversed the activity. SAH significantly decreased the levels of tight junction proteins, occludin and zonula occludens-1 (ZO-1), and HF preserved the levels of occluding and ZO-1 in ipsilateral hemisphere. In conclusion, HF attenuated BBB permeability after SAH, possibly by protection of tight junction proteins.

[Subarachnoid hemorrhage due to a ruptured intracranial vertebral artery aneurysm associated with cerebrovascular fibromuscular dysplasia: case report].

Fibromuscular dysplasia (FMD) is comprised of a group of nonatherosclerotic and noninflammatory arterial diseases. Cerebrovascular FMD occurs more frequently in women, and the mean age at which it is diagnosed is 50 years. The most common angiographic pattern of cerebrovascular FMD is the "string-of-beads" deformity at the extracranial internal carotid artery. We report the case of a 52-year-old woman who presented with a sudden severe headache and went into a deep coma. She had been complaining of headaches for 2 weeks, but no specific imaging findings were obtained. A computed tomography scan obtained on admission showed a diffuse subarachnoid hemorrhage (SAH) from the cerebellomedullary cistern to the basal cistern with evidence of clot in the fourth and third ventricles. We performed digital subtraction angiography and made the diagnosis of cerebrovascular FMD. Right carotid angiography and left vertebral angiography showed the classic "string-of-beads" pattern with multiple constrictions of the lumen. Left carotid angiography showed a long segment of tubular stenosis. Right vertebral angiography also revealed the "string-of-beads" pattern and a ruptured aneurysm at the intracranial segment, which presented as a diverticulum-like outpouching. The patient was treated with conservative measures but passed away on the 23rd day of hospitalization. An autopsy was not performed. To our knowledge, during the last three decades, there are only four previous reports which showed intracerebral ruptured aneurysms of the vertebral artery or its branch in adults with cerebrovascular FMD. We demonstrate and discuss the radiologic findings here.

Efficacy of the American Heart Association/American Stroke Association guidelines for ultra-early, intentional antihypertensive therapy in intracerebral hemorrhage.

Whether the intentional antihypertensive therapy recommended by the American Heart Association/American Stroke Association (AHA/ASA) guidelines has clinical benefit for patients who have acute spontaneous intracerebral hemorrhage (ICH) has yet to be proven. We retrospectively reviewed the clinical charts of 175 patients with putaminal or thalamic ICH with acute hypertension to examine the correlation between the efficacy of antihypertensive therapy within 3 hours of onset, hematoma expansion (HE) after hospitalization and clinical outcome. The aim of the antihypertensive therapy was to achieve and maintain a systolic blood pressure of 120 mm Hg to 160 mm Hg until the second CT scan. The mean arterial pressure (MAP) after admission was the average MAP values measured every hour for the first 3 hours of hospitalization or until the second CT scan, if this was performed within the same timeframe. Thirty-two (18.3%) patients were found to have HE. Prior to the second CT scan, antihypertensive medications were administered to all patients without any major complications. A multiple logistic regression analysis revealed that a MAP of >110 mm Hg after admission was the only variable independently associated with HE (odds ratio [OR] = 3.455; 95% confidence interval [CI] = 1.510-8.412; p = 0.004). Modified Rankin Scale scores of < or = 3 on day 30 were significantly more common in those patients without HE (p = 0.002). Our findings suggest that there are clinical benefits, by the prevention of subsequent HE, in maintaining a MAP level lower than that recommended by the AHA/ASA (110 mm Hg) after hospitalization for patients who have ICH.

[Postpartum chronic subdural hematoma following spinal anesthesia: case report].

Chronic subdural hematoma is a rare complication of epidural anesthesia. This report describes the case of a 34-year-old woman who presented with postpartum headache after she received epidural anesthesia for labor pain. The anesthesiologist's record did not show any anesthesia-related complication. Two days after the delivery (on day 2), the patient complained of headache. Postdural puncture headache was diagnosed, so she was administered analgesics, hydration therapy, and bed rest. On day 4, she reported a slight improvement and was discharged. The postural headache persisted even on day 7 after delivery. During the conservative treatment, she had suffered a mild head trauma. On day 13, she started to feel a non-postural and severe throbbing headache. On day 24, she was referred to our department. Bilateral chronic subdural hematoma was confirmed by a computed tomography scan. Physical examination revealed only mild right hemiparesis. Left burr hole trepanation was performed and this was followed by uneventful postoperative course. Right chronic subdural hematoma was managed by conservative treatment, and it completely recovered after 4 weeks. Chronic subdural hematoma should be considered when postpartum patients who have received epidural anesthesia present with mild to severe, persistent, and non-postural headache.