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Background: Brain protection and cosmetic aspects are the major indications of cranioplasty (CP) after decompressive craniectomy. CP can avoid the recurrence of brain damage, achieve the plastic effect, protect the patient from seizures, and relieve the syndrome of trephine. Materials and Methods: This was a prospective, observational study done over a period of 2 years from April 2017 to April 2019 in the Department of Neurosurgery at Sri Venkateswara Institute of Medical Sciences (SVIMS), Tirupati. Patients of age group 20-60 years who underwent CP after decompressive craniectomy for traumatic brain injury or cerebrovascular accidents with refractory intracranial hypertension were included. The study population was divided into two groups: early and late CP groups. Neurocognitive assessment was done 72 h before and 3 months after CP by mini-mental state examination (MMSE), Glasgow outcome score (GOS), and PGI battery of brain dysfunction (PGIBBD) scores. Cerebral glucose metabolism was assessed by 18F-FDG PET scan. Results: In both early and late CP groups, there was a highly significant difference between the mean pre- and postoperative values of MMSE, GOS, and PGIBBD, suggesting significant improvement in neurocognitive parameters of patients postoperatively. There was no significant difference between early and late CP groups for mean standard uptake values (SUVs) on PET scan for both affected (P-value- 0.40) and nonaffected (P-value- 0.30) sides. Conclusion: CP improves the cerebral metabolism and neurocognitive outcome, weather it is done early or late. Keywords: Cognitive outcome, cranioplasty, decompressive craniectomy, PET scan, standard uptake values (SUVs), Author(s): Vivek Sharma [1]; Venkata Vemula Rameshchandra [2]; Bodapati Chandramouliswara Prasad [2]; Rinu Dwivedi (corresponding author) [3] Key Message: Cranioplasty after decompressive craniectomy does improve cerebral glucose metabolism however timing [...]

Urban stormwater is responsible for recurrent mortality events of coho salmon (Oncorhynchus kisutch) documented in the US Pacific Northwest. Currently, the toxic mode of action is unknown; however, mortality is often associated with large increases in hematocrit (Hct). We found that hemoconcentration and red cell swelling may offer a partial explanation for increased Hct, based on increased total hemoglobin and reduced mean cell hemoglobin concentration of the blood in runoff-exposed juvenile coho salmon, relative to controls. No significant changes were seen in plasma total thiols or antioxidant power, discounting osmoregulatory dysfunction and plasma dehydration as a driver of hemoconcentration. To test for plasma leakage, we injected Evans blue dye complexed with bovine serum albumin (EBD-BSA) intracardially and circulated for 5 min, followed by a 15 min washout with saline. Coho salmon exposed to roadway runoff showed significant accumulation of EBD-BSA in brain and olfactory rosette regions compared with controls, demonstrating plasma leakage from the cerebrovasculature. Our results suggest blood-brain barrier disruption underlies symptom development in coho salmon exposed to roadway runoff. Les eaux de ruissellement urbaines sont responsables d'episodes de mortalite de saumons cohos (Oncorhynchus kisutch) recurrents documentes dans les eaux des Etats du nord-ouest des Etats-Unis. Si le mode d'action toxique est actuellement inconnu, la mortalite est souvent associee a de fortes augmentations de l'hematocrite (Hct). Nous avons constate que l'hemoconcentration et le gonflement des globules rouges pourraient partiellement expliquer l'Hct accrue, a la lumiere de l'augmentation de l'hemoglobine totale et de la diminution de la concentration moyenne d'hemoglobine des cellules du sang de saumons cohos juveniles exposes au ruissellement par rapport aux valeurs de temoins. Aucun changement significatif des thiols plasmatiques totaux ou du pouvoir antioxydant n'a ete observe, ce qui exclut une dysfonction de l'osmoregulation et la deshydratation du plasma comme causes de l'hemoconcentration. Pour verifier s'il y a fuite de plasma, du colorant bleu d'Evans complexe a de l'albumine serique bovine (EBD-BSA) a ete injecte par voie intracardiaque et a circule pendant 5 min, suivi d'un lavage de 15 min avec de la solution saline. Les saumons cohos exposes a des eaux de ruissellement de routes presentaient une accumulation significative d'EBD-BSA dans les regions du cerveau et de la rosette olfactive comparativement aux temoins, ce qui demontre une fuite de plasma du systeme vasculaire cerebral. Nos resultats indiqueraient qu'une perturbation de la barriere hemato-encephalique sous-tend l'apparition de symptomes chez les saumons cohos exposes a des eaux de ruissellement de routes. [Traduit par la Redaction], Introduction Urban stormwater runoff is a well-recognized global threat to freshwater biodiversity and ecosystem function (Walsh et al. 2005). Coho salmon (Oncorhynchus kisutch) are a sensitive-species indicator for nonpoint source [...]

Astrocytes have multiple functions in the brain, including affecting blood vessel (BV) homeostasis and function. However, the underlying mechanisms remain elusive. Here, we provide evidence that astrocytic neogenin (NEO1), a member of deleted in colorectal cancer (DCC) family netrin receptors, is involved in blood vessel homeostasis and function. Mice with Neo1 depletion in astrocytes exhibited clustered astrocyte distribution and increased BVs in their cortices. These BVs were leaky, with reduced blood flow, disrupted vascular basement membranes (vBMs), decreased pericytes, impaired endothelial cell (EC) barrier, and elevated tip EC proliferation. Increased proliferation was also detected in cultured ECs exposed to the conditioned medium (CM) of NEO1-depleted astrocytes. Further screening for angiogenetic factors in the CM identified netrin-1 (NTN1), whose expression was decreased in NEO1-depleted cortical astrocytes. Adding NTN1 into the CM of NEO1-depleted astrocytes attenuated EC proliferation. Expressing NTN1 in NEO1 mutant cortical astrocytes ameliorated phenotypes in blood-brain barrier (BBB), EC, and astrocyte distribution. NTN1 depletion in astrocytes resulted in BV/BBB deficits in the cortex similar to those in Neo1 mutant mice. In aggregate, these results uncovered an unrecognized pathway, astrocytic NEO1 to NTN1, not only regulating astrocyte distribution, but also promoting cortical BV homeostasis and function., Introduction The brain, the organ that consumes the most energy, depends on a cerebral blood supply to obtain oxygen and nutrients for neuronal function. Malformation or dysfunction of blood vessels [...]

Byline: Amit. Bhatti, Niranjan. Mahajan, Devashish. Vyas, Mudasir. Shah, Vikram. Huded Context: Recanalization failure rate in mechanical thrombectomy (MT) for large vessel occlusions is up to 30%. Outcome greatly depends [...]

Byline: Neha. Gupta, Vipin. Singh, Shobhna. Jafa Background: In brain injury patients, positive end-expiratory pressure (PEEP) may potentially increase the intracranial pressure (ICP). ICP can be noninvasively assessed from the [...]

Purpose Nicorandil has dual properties and acts as a nitric oxide donor and an ATP-sensitive potassium (K.sub.ATP) channel opener. Considering its pharmacological profile, nicorandil might exert protective effects on the brain as well as on the heart. The purpose of this study was to directly evaluate the effect of nicorandil on cerebral blood flow (CBF) in mice using a transcranial Doppler method. Methods Under general anesthesia, the nicorandil groups received a single-bolus intraperitoneal injection of the respective doses of nicorandil (1, 5, or 10 mg/kg), while the control group received vehicle only. CBF was measured using a transcranial Doppler flowmeter. N.sup.G-nitro-l-arginine methyl ester and glibenclamide were used to elucidate the underlying mechanisms. Results A single-bolus injection of 1 mg/kg of nicorandil increased the CBF (11.6 ± 3.6 vs. 0.5 ± 0.7%, p < 0.001) without affecting the heart rate and blood pressure. On the contrary, 5 and 10 mg/kg of nicorandil significantly decreased the cerebral blood flow by decreasing the mean blood pressure below the cerebral autoregulation range. The positive effect of 1 mg/kg of nicorandil on the cerebral blood flow was inhibited by co-administration of either N.sup.G-nitro-l-arginine methyl ester or glibenclamide. Conclusions A clinical dose of nicorandil increases CBF without affecting systemic hemodynamics. The positive effect of nicorandil on CBF is most likely caused via both the nitric oxide pathway and K.sub.ATP channel opening., Author(s): Masakazu Kotoda [sup.1] , Tadahiko Ishiyama [sup.2] , Kazuha Mitsui [sup.1] , Sohei Hishiyama [sup.1] , Takashi Matsukawa [sup.1] Author Affiliations: (Aff1) 0000 0001 0291 3581, grid.267500.6, Department of [...]

Stroke is one of the most common diseases and a leading cause of death and disability. Cessation of cerebral blood flow (CBF) leads to cell death in the infarct core, but tissue surrounding the core has the potential to recover if local reductions in CBF are restored. In these areas, detrimental peri-infarct depolarizations (PIDs) contribute to secondary infarct growth and negatively affect stroke outcome. However, the cellular pathways underlying PIDs have remained unclear. Here, we have used in vivo multiphoton microscopy, laser speckle imaging of CBF, and electrophysiological recordings in a mouse model of focal ischemia to demonstrate that PIDs are associated with a strong increase of intracellular calcium in astrocytes and neurons. We found that astroglial calcium elevations during PIDs are mediated by inositol triphosphate receptor type 2-dependent (IP3R2-dependent) release from internal stores. Importantly, Ip3r2-deficient mice displayed a reduction of PID frequency and overall PID burden and showed increased neuronal survival after stroke. These effects were not related to local CBF changes in response to PIDs. However, we showed that the release and extracellular accumulation of glutamate during PIDs is strongly curtailed in Ip3r2-deficient mice, resulting in ameliorated calcium overload in neurons and astrocytes. Together, these data implicate astroglial calcium pathways as potential targets for stroke therapy., Introduction Stroke is a leading cause of death and disability and is associated with an enormous socioeconomic burden. In the infarct core, a dramatic reduction of cerebral blood flow (CBF) [...]

Background Aortic stiffness is closely linked with cardiovascular diseases (CVDs), but recent studies suggest that it is also a risk factor for cognitive decline and dementia. However, the brain changes underlying this risk are unclear. We examined whether aortic stiffening during a 4-year follow-up in mid-to-late life was associated with brain structure and cognition in the Whitehall II Imaging Sub-study. Methods and findings The Whitehall II Imaging cohort is a randomly selected subset of the ongoing Whitehall II Study, for which participants have received clinical follow-ups for 30 years, across 12 phases. Aortic pulse wave velocity (PWV) was measured in 2007-2009 (Phase 9) and at a 4-year follow-up in 2012-2013 (Phase 11). Between 2012 and 2016 (Imaging Phase), participants received a multimodal 3T brain magnetic resonance imaging (MRI) scan and cognitive tests. Participants were selected if they had no clinical diagnosis of dementia and no gross brain structural abnormalities. Voxel-based analyses were used to assess grey matter (GM) volume, white matter (WM) microstructure (fractional anisotropy (FA) and diffusivity), white matter lesions (WMLs), and cerebral blood flow (CBF). Cognitive outcomes were performance on verbal memory, semantic fluency, working memory, and executive function tests. Of 542 participants, 444 (81.9%) were men. The mean (SD) age was 63.9 (5.2) years at the baseline Phase 9 examination, 68.0 (5.2) at Phase 11, and 69.8 (5.2) at the Imaging Phase. Voxel-based analysis revealed that faster rates of aortic stiffening in mid-to-late life were associated with poor WM microstructure, viz. lower FA, higher mean, and radial diffusivity (RD) in 23.9%, 11.8%, and 22.2% of WM tracts, respectively, including the corpus callosum, corona radiata, superior longitudinal fasciculus, and corticospinal tracts. Similar voxel-wise associations were also observed with follow-up aortic stiffness. Moreover, lower mean global FA was associated with faster rates of aortic stiffening (B = -5.65, 95% CI -9.75, -1.54, Bonferroni-corrected p < 0.0125) and higher follow-up aortic stiffness (B = -1.12, 95% CI -1.95, -0.29, Bonferroni-corrected p < 0.0125). In a subset of 112 participants who received arterial spin labelling scans, faster aortic stiffening was also related to lower cerebral perfusion in 18.4% of GM, with associations surviving Bonferroni corrections in the frontal (B = -10.85, 95% CI -17.91, -3.79, p < 0.0125) and parietal lobes (B = -12.75, 95% CI -21.58, -3.91, p < 0.0125). No associations with GM volume or WMLs were observed. Further, higher baseline aortic stiffness was associated with poor semantic fluency (B = -0.47, 95% CI -0.76 to -0.18, Bonferroni-corrected p < 0.007) and verbal learning outcomes (B = -0.36, 95% CI -0.60 to -0.12, Bonferroni-corrected p < 0.007). As with all observational studies, it was not possible to infer causal associations. The generalisability of the findings may be limited by the gender imbalance, high educational attainment, survival bias, and lack of ethnic and socioeconomic diversity in this cohort. Conclusions Our findings indicate that faster rates of aortic stiffening in mid-to-late life were associated with poor brain WM microstructural integrity and reduced cerebral perfusion, likely due to increased transmission of pulsatile energy to the delicate cerebral microvasculature. Strategies to prevent arterial stiffening prior to this point may be required to offer cognitive benefit in older age. Trial registration ClinicalTrials.gov NCT03335696, Author(s): Sana Suri 1,2,*, Scott T. Chiesa 3, Eniko Zsoldos 1,2, Clare E. Mackay 1,2, Nicola Filippini 1,2, Ludovica Griffanti 1,2, Abda Mahmood 1, Archana Singh-Manoux 4,5, Martin J. Shipley [...]

Byline: Praveen. Kesav, Deepak. Menon, K. Vysakha, Chandrasekaran. Kesavadas, Sapna. Sreedharan, Sankara. Sarma, P. Sylaja Background: Cerebral microbleed (CMB) is a novel neuroimaging marker of cerebral small vessel disease. Objective: [...]

Postural tachycardia syndrome (POTS), a chronic form of orthostatic intolerance, has signs and symptoms of lightheadedness, loss of vision, headache, fatigue, and neurocognitive deficits consistent with reductions in cerebrovascular perfusion. We hypothesized that young, normocapnic POTS patients exhibit abnormal cerebral autoregulation (CA) that results in decreased static and dynamic cerebral blood flow (CBF) autoregulation. All subjects had continuous recordings of mean arterial pressure (MAP) and CBF velocity (CBFV) using transcranial Doppler sonography in both the supine supine position and during a 70[degrees] head-up tilt. During tilt, POTS patients (n = 9) demonstrated a higher heart rate than controls (n = 7) (109 [+ or -] 6 vs. 80 [+ or -] 2 beats/min, P < 0.05), whereas controls demonstrated a higher MAP than POTS (87 [+ or -] 2 vs. 77 [+ or -] 3 mmHg, P < 0.05). Also during tilt, mean CBFV decreased 19.5 [+ or -] 2.6% in POTS patients versus 10.3 [+ or -] 2.0% in controls (P < 0.05). We then used a transfer function analysis of MAP and CFBV in the frequency domain to quantify these changes. The low-frequency (LF; 0.04-0.15 Hz) component of CBFV variability increased during tilt in POTS patients (supine: 3 [+ or -] 0.9 vs. tilt: 9 [+ or -] 2, P < 0.02). In POTS patients, there was an increase in LF and high-frequency coherence between MAP and CBFV, an increase in LF gain, and a lack of significant change in phase. Static CA may be less effective in POTS patients compared with controls, since immediately after tilt CBFV decreased more in POTS patients and was highly oscillatory and autoregulation did not restore CBFV to baseline values until the subjects became supine. Dynamic CA may be less effective in POTS patients because MAP and CBFV during tilt became almost perfectly synchronous. We conclude that dynamic and static autoregulation of CBF are less effective in POTS patients compared with control subjects during orthostatic challenge. chronic orthostasis; coherence; transcranial Doppler

Decreased cerebral blood flow (CBF) has been observed following the resuscitation from neonatal hypoxic-ischemic injury, but its mechanism is not known. We address the hypothesis that reduced CBF is due to a change in nitric oxide (NO) and superoxide anion [O.sup.-.sub.2] balance secondary to endothelial NO synthase (eNOS) uncoupling with vascular injury. Wistar rats (7 day old) were subjected to cerebral hypoxia-ischemia by unilateral carotid occlusion under isoflurane anesthesia followed by hypoxia with hyperoxic or normoxic resuscitation. Expired C[O.sub.2] was determined during the period of hyperoxic or normoxic resuscitation. Laser-Doppler flowmetry was used with isoflurane anesthesia to monitor CBF, and cerebral perivascular NO and [O.sup.-.sub.2] were determined using fluorescent dyes with fluorescence microscopy. The effect of tetrahydrobiopterin supplementation on each of these measurements and the effect of apocynin and [N.sup.[omega]]-nitro-L-arginine methyl ester (L-NAME) administration on NO and 02 were determined. As a result, CBF in the ischemic cortex declined following the onset of resuscitation with 100% [O.sub.2] (hyperoxic resuscitation) but not room air (normoxic resuscitation). Expired C[O.sub.2] was decreased at the onset of resuscitation, but recovery was the same in normoxic and hyperoxic resuscitated groups. Perivascular NO-induced fluorescence intensity declined, and [O.sup.-.sub.2]-induced fluorescence increased in the ischemic cortex after hyperoxic resuscitation up to 24 h postischemia. L-NAME treatment reduced 02 relative to the nonischemic cortex. Apocynin treatment increased NO and reduced [O.sup.-.sub.2] relative to the nonischemic cortex. The administration of tetrahydrobiopterin following the injury increased perivascular NO, reduced perivascular [O.sup.-.sub.2], and increased CBF during hyperoxic resuscitation. These results demonstrate that reduced CBF follows hyperoxic resuscitation but not normoxic resuscitation after neonatal hypoxic-ischemic injury, accompanied by a reduction in perivascular production of NO and an increase in [O.sub.2]. The finding that tetrahydrobiopterin, apocynin, and L-NAME normalized radical production suggests that the uncoupling of perivascular NOS, probably eNOS, due to acquired relative tetrahydrobiopterin deficiency occurs after neonatal hypoxic-ischemic brain injury. It appears that both NOS uncoupling and the activation of NADPH oxidase participate in the changes of reactive oxygen concentrations seen in cerebral hypoxic-ischemic injury. apocynin; neonatal rat; vasculature; [N.sup.[omega]]-nitro-L-arginine methyl ester

We hypothesize that cerebral ischemia leads to enhanced expression of endothelin (ET), 5-hydroxytryptamine (5-HT), and angiotensin II (ANG II) receptors in the vascular smooth muscle cells. Our aim is to correlate the upregulation of cerebrovascular receptors and the underlying molecular mechanisms with the reduction in regional and global cerebral blood flow (CBF) after subarachnoid hemorrhage (SAH). SAH was induced by injecting 250 [micro]l blood into the prechiasmatic cistern in rats. The cerebral arteries were removed 0, 1, 3, 6, 12, 24, and 48 h after the SAH for functional and molecular studies. The contractile responses to ET-1. 5-carboxamidotryptamine (5-CT), and ANG II were investigated with myograph. The receptor mRNA and protein levels were analyzed by quantitative real-lime PCR and immunohistochemistry, respectively. In addition, regional and global CBFs were measured by an autoradiographic method. As a result, SAH resulted in enhanced contractions to ET-1 and 5-CT. ANG II [via ANG II type 1 ([AT.sub.1]) receptors] induced increased contractile responses [in the presence of the ANG II type 2 ([AT.sub.2]) receptor antagonist PD-123319]. In parallel the [ET.sub.B], [5-HT.sub.1B], and [AT.sub.1] receptor, mRNA and protein levels were elevated by time. The regional and global CBF showed a successive reduction with time after SAH. In conclusion, the results demonstrate for the first time that SAH induces the upregulation of [ET.sub.B], [5-HT.sub.1B], and [AT.sub.1] receptors in a time-dependent manner both at functional, mRNA, and protein levels. These changes occur in parallel with a successive decrease in CBF. Thus there is a temporal correlation between the changes in receptor expression and CBF reduction, suggesting a linkage. cerebral blood flow; cerebral ischemia

Estrogen appears to enhance cerebral blood flow (CBF). An association between CBF and physiologically altered hormonal levels due to menstrual cycle, menopause, or exogenous manipulations such as ovariectomy or hormone replacement therapy has been demonstrated. The purpose of this study was to determine the association between ovarian stimulation and CBF in vivo by measuring blood flow in the internal carotid artery (ICA) after pituitary suppression and during controlled ovarian stimulation in women undergoing in vitro fertilization treatment cycles. ICA volume flows were measured by angle-independent dual-beam ultrasound Doppler in 12 women undergoing controlled ovarian stimulation. Measurements were performed after pituitary/ovarian suppression, in the late follicular phase, and at midluteal phase. Blood flow in the ICA increased by 22.2% and 32% in the late follicular and midluteal phases compared with the respective values obtained during ovarian suppression (P < 0.0005 and P < 0.0001, respectively). There was a significant correlation between increments in estrogen levels and increments in CBF when the late follicular phase was compared with the ovarian suppression period (r = 0.8, P < 0,001). Mean blood flow velocity significantly increased (by 15.7% and 16.9%, respectively) and cerebral vascular resistance significantly decreased (by 17.6% and 26.5%) during the late follicular and midluteal phases compared with respective measures during ovarian suppression. There was a significant correlation between an increase in estrogen levels and a decrease in cerebral vascular resistance when the late follicular phase was compared with the ovarian suppression period (r = -0.6, P < 0.05). These changes imply sex hormone-associated intracranial vasodilation leading to increased CBF during controlled ovarian stimulation. estrogen; progesterone; angle-independent Doppler; in vitro fertilization

The purpose of this study was to characterize vascular responses and to examine mechanisms of vascular dysfunction in TallyHo mice, a new polygenic model of Type II diabetes. Responses of cerebral arterioles and carotid arteries were examined in vivo by using a cranial window and in vitro by using tissue baths, respectively. Dilatation of cerebral arterioles (baseline diameter = 33 [+ or -] [micro]m) in response to acetylcholine, but not to nitroprusside, was markedly reduced (P < 0.05) in TallyHo mice. Responses of cerebral arterioles to acetylcholine in TallyHo mice were restored to normal with polyethylene glycol-superoxide dismutase (100 U/ml; a superoxide scavenger). Responses to acetylcholine were also greatly impaired (P < 0.05) in the carotid arteries from TallyHo mice. Phenylephrine- and serotonin-, but not to KCl- or U46619-, induced contraction was increased two- to fourfold (P < 0.05) in carotid arteries of TallyHo mice. Responses to phenylephrine and serotonin were reduced to similar levels in the presence of Y-27632 (an inhibitor of Rho kinase; 3 [micro]mo1/1). These findings provide the first evidence that vascular dysfunction is present in TallyHo mice and that oxidative stress and enhanced activity of Rho kinase may contribute to altered vascular function in this genetic model of Type II diabetes. carotid artery; cerebral circulation; endothelium; microcirculation

To purchase or authenticate to the full-text of this article, please visit this link: http://dx.doi.org/10.1111/j.1552-6569.2006.00024.x Byline: Afshin A. Divani (1), Adnan I. Qureshi (1), Kenneth R. Hoffman (1), M. Fareed K. Suri (1), Jawad F. Kirmani (1) Keywords: Angiography; cerebral blood flow; ischemic stroke; perfusion; stenosis; SPECT Abstract: ABSTRACT Background and Purpose. Recently, endovascular techniques have gained significant therapeutic potential for both treatment and prevention of stroke. Cerebral angiography, which is an essential component of these procedures, has been used to provide morphological information regarding condition of blood vessels. In this study, we propose to determine the possibility of acquiring information regarding cerebral blood flow (CBF) in addition to morphologic information from data routinely available during angiography. Methods. Digital subtraction angiography sequences were obtained for eight patients having occlusive disease in internal carotid artery (ICA) territories. Two regions-of-interest (ROIs) corresponding to the two brain hemispheres on AP view were delineated. For each image, the average pixel value within each ROI was calculated and used to generate time-density curves. Indices obtained from each curve were compared with each other and with the results obtained from the single photon emission computed tomography (SPECT) studies performed a pre- or postangiography procedure. Results. Comparison between ICA stenosis and cerebral perfusion measurements revealed that cerebral perfusion deficit can be independent of arterial occlusive disease. The indices obtained from the time-density curves exhibit a correlating trend with the results from SPECT studies. However, lack of sufficient sample data prevented any meaningful statistical analysis to be conducted. Conclusions. We have developed a technique for utilizing the angiographic data for the important task of routinely and easily measuring CBF. Availability of CBF measurements during cerebral angiography may favorably impact upon the appropriate use of endovascular procedures and potentially contribute to the reduction of morbidity and mortality associated with stroke. Author Affiliation: (1)From the Imaging Core Laboratory, Zeenat Qureshi Stroke Research Center, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark, New Jersey (AAD, AIQ, MFKS, JFK), and Department of Neurosurgery and Toshiba Stroke Research Center, School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Buffalo, New York (KRH). Article History: Received July 12, 2005, and in revised form October 25, 2005. Accepted for publication November 7, 2005. Article note: Address Correspondence to Dr Afshin A. Divani, Zeenat Qureshi Stroke Research Center, UMDNJ New Jersey Medical School, Medical Science Building, H506, 185 South Orange Ave, Newark, NJ 07103. E-mail: divaniaa@umdnj.edu.

To purchase or authenticate to the full-text of this article, please visit this link: http://dx.doi.org/10.1177/1051228405001468 Byline: Soichiro Shimizu (1), Haruo Hanyu (1), Toshihiko Iwamoto (1), Kiyoshi Koizumi (1), Kimihiko Abe (1) Keywords: Regional cerebral blood flow; single-photon emission computed tomography; frontal lobe; Donepezil; Alzheimer's disease Abstract: ABSTRACT Background and Purpose. Treatment with acetylcholinesterase inhibitors (AchEIs) is beneficial for patients with Alzheimer's disease (AD). But the clinical response varies. Functional neuroimaging techniques might allow objective evaluation of the topographic correlates of the effect of therapy on brain functioning. We attempted to evaluate the possible correlation between regional cerebral blood flow (rCBF) differences in patients with AD and response to donepezil hydrochloride (Donepezil) therapy. Methods. The subjects of this study were 51 consecutive patients with AD receiving Donepezil who underwent SPECT at baseline and 10-14 months later. We divided the patients into stabilized (n= 19) and nonstabilized (n= 32) subgroups based on changes in the Mini Mental State Examination (MMSE) score. Analysis of single-photon emission computed tomography (SPECT) data was done using 3-dimensional stereotactic surface projections (3D-SSP) and the stereotactic extraction estimation (SEE) method. We compared differences in rCBF between the two subgroups at baseline and follow-up, and between the baseline and follow-up in each subgroup. Results. Signifi cant correlation was recognized between the mean Z score changes of the left frontal lobe, left limbic lobe, and MMSE change. There were no significant baseline differences in rCBF in any region of the brain between the two subgroups. At the study endpoint, the nonstabilized subgroup showed lower rCBF in the lateral and medial frontal lobes, limbic lobe, lower lateral temporal lobe, and cingulate gyrus compared to the stabilized subgroup. Both patient groups showed a significant post-treatment increase over baseline values in the frontal lobe, and the stabilized group had more extensive and intense increases in the lateral and medial frontal lobes and orbital surface. Conclusions. Our study suggests that the diversity of clinical responses to Donepezil therapy in patients with AD is associated with rCBF changes, mainly in the frontal lobe. SPECT may be a promising tool to assess the impact of AchEI therapy on the brain function of patients with AD. Author Affiliation: (1)From the Department of Geriatric Medicine, Tokyo Medical University, 6-7-1 Nishishinjuku, Shinjuku-ku, Tokyo 160-0023, Japan (SS, HH, TI); Department of Radiology (KK, KA), Tokyo Medical University, Tokyo 160-0023, Japan. Article History: Received October 8, 2004, and in revised form September 13, 2005. Accepted for publication September 20, 2005. Article note: Address correspondence to Soichiro Shimizu, Department of Geriatric Medicine, Tokyo Medical University, 6-7-1 Nishishinjuku, Shinjuku-ku, Tokyo 160-0023, Japan. E-mail: soichiro_s@hotmail.com.

Byline: Pinchas Halpern (1), Miri Y. Neufeld (2), Kobi Sade (3), Aviel Silbiger (4), Oded Szold (4), Natan M. Bornstein (2), Patrick Sorkine (4) Keywords: Doppler; Ultrasound; Transcranial; Middle cerebral artery; Carbon dioxide; Ventilation Abstract: Objective To define the changes in middle cerebral artery flow velocity (Vmca) and the electroencephalogram (EEG) during rapid reduction in arterial carbon dioxide (PCO.sub.2) from acute hypercapnia. Design Human volunteer study. Setting University-affiliated hospital experimental laboratory. Participants Nine healthy volunteers aged 25--35 years. Interventions Subjects rebreathed exhaled gas from a bag pre-filled with 5% carbon dioxide (CO.sub.2) in oxygen, up to an end-tidal CO.sub.2 of 10% or to the limit of discomfort, when they were disconnected. Measurements and results Middle cerebral artery blood flow velocity was continuously measured by transcranial Doppler ultrasound, quantitative EEG was recorded and hemodynamics were monitored non-invasively. Vmca closely correlated with end-tidal CO.sub.2 changes (r=0.65, p Conclusions These findings demonstrate the rapid changes occurring in cerebral blood flow during rapid declines in arterial CO.sub.2 and the consequent potential for producing brain ischemia and hemodynamic alterations if inadvertent hyperventilation occurs following institution of mechanical ventilation for acute hypercapnia. Author Affiliation: (1) Department of Emergency Medicine, Tel Aviv Sourasky Medical Center and the Sackler Faculty of Medicine , Tel Aviv University, 6 Weizman Street, 64239, Tel Aviv, Israel (2) Department of Neurology, Tel Aviv Sourasky Medical Center and the Sackler Faculty of Medicine, Tel Aviv University, 6 Weizman Street, 64239, Tel Aviv, Israel (3) Department of Pulmonary Medicine and Allergy, Tel Aviv Sourasky Medical Center and the Sackler Faculty of Medicine, Tel Aviv University, 6 Weizman Street, 64239, Tel Aviv, Israel (4) Department of Anesthesiology & Critical Care Medicine, Tel Aviv Sourasky Medical Center and the Sackler Faculty of Medicine, Tel Aviv University, 6 Weizman Street, 64239, Tel Aviv, Israel Article History: Received Date: 06/02/2003 Accepted Date: 23/06/2003 Online Date: 02/08/2003

Background: Spontaneous intracranial hypotension (SIH) is characterised by postural headache and low opening pressure at lumbar puncture without obvious cause. Cranial magnetic resonance imaging often shows small subdural collections without [...]

The article discusses the vital role that integrated care plays in the case of treatment of patients with substance abuse as well as mental illness. Some of the reasons as to why substance abuse and mental illness occur together are highlighted, and treatment methodologies that may benefit both conditions are recommended.

Byline: Lakshmi. Sudha, Bhawna. Dev, Ravindra. Kamble, Santhosh. Joseph Cranially conjoined twins (craniopagus) are regarded as one of the rarest human malformations. Craniopagus represents 2 to 6% of conjoined twins [...]

Acute intermittent porphyria is an uncommon genetic disorder. The condition results from a deficiency in the metabolism of porphyrins, a class of biochemical compounds which includes the oxygen-carrying molecule heme. Patients with acute intermittent porphyria can suffer seizures and abnormal brain function, but the cause of these neurological symptoms is not clear. Some researchers favor the notion that the metabolic defect affects brain metabolism as well, while others believe that the disorder affects the blood vessels of the brain, depriving many brain regions of adequate blood flow. Unfortunately, many of the investigations to uncover the cause of these neurological symptoms have been conducted using autopsy material; there are reasons to suspect that the dead patients are not a representative sample. With the advent of magnetic resonance imaging (MRI), however, it has become possible to look into the living brain with high resolution. In a recent case, a 20-year-old woman with acute intermittent porphyria suffered an attack which included seizures and hallucinations. Magnetic resonance images obtained during the attack revealed areas of increased signal intensity over large areas of the brain. These regions, which appear as bright areas in the MR image, returned to normal appearance after treatment successfully resolved the symptoms. The increased signal intensity visible on the images during the patient's attack does not reveal the cause of the abnormality with certainty. However, the appearance of the image is similar to that which is observed for abnormalities of the blood vessels, such as those which occur in disorders such as systemic lupus erythematosus, vasculitis, and hypertensive encephalopathy. Therefore, the observations made on this patient support the notion that the neurological symptoms that occur during attacks of acute intermittent porphyria may be due to abnormalities of the central nervous system circulation. (Consumer Summary produced by Reliance Medical Information, Inc.)