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G Sinson

Publications and source records attributed to G Sinson.

At least 19 recordsLinked to original sources
PubMed2006

Neuropsychological and perfusion MR imaging correlates of revascularization in a case of moyamoya syndrome.

Serial neurocognitive and perfusion MR imaging findings are described in the perioperative course of a 48-year-old woman with a superficial temporal artery to middle cerebral artery bypass for right hemispheric ischemia due to moyamoya syndrome. Neurocognitive testing reflected both global and focal cerebrovascular dysfunction, which suggests that perfusion augmentation following surgical revascularization may engender cognitive and neurologic improvement beyond focal regions of established ischemia.

Cerebral Revascularization↗
PubMed2001

Fatal rebleeding following coil embolization of cerebral aneurysms: the role of long-term systemic anticoagulation.

Embolization of cerebral aneurysms has become a common technique. Its impact on subsequent medical management of the patient is not well known. We report two patients who presented in a poor neurological grade after subarachnoid hemorrhage from posterior communicating artery aneurysms. Both were treated by coil embolization and both developed subclavian vein thrombosis, requiring systemic anticoagulation, initiated 11 and 21 days after embolization, respectively. Both developed a large, fatal intracranial hemorrhage adjacent to the embolized aneurysm in the fourth week of anticoagulation. Systemic anticoagulation of patients who have had a ruptured aneurysm treated by coil embolization may carry a significant risk of rebleeding. Alternate management strategies should be considered in these patients.

Aged↗
PubMed2001

Neuroprotective and behavioral efficacy of nerve growth factor-transfected hippocampal progenitor cell transplants after experimental traumatic brain injury.

OBJECT: Immortalized neural progenitor cells derived from embryonic rat hippocampus (HiB5), were transduced ex vivo with the gene for mouse nerve growth factor (NGF) to secrete NGF (NGF-HiB5) at 2 ng/hr/10(5) cells in culture. METHODS: Fifty-nine male Wistar rats weighing 300 to 370 g each were anesthetized with 60 mg/kg sodium pentobarbital and subjected to lateral fluid-percussion brain injury of moderate severity (2.3-2.4 atm, 34 rats) or sham injury (25 rats). At 24 hours postinjury, 2 microl (150,000 cells/microl) of [3H]thymidine-labeled NGF-HiB5 cells were transplanted stereotactically into three individual sites in the cerebral cortex adjacent to the injury site (14 rats). Separate groups of brain-injured rats received nontransfected (naive [n])-HiB5 cells (12 animals) or cell suspension vehicle (eight animals). One week postinjury, animals underwent neurological evaluation for motor function and cognition (Morris water maze) and were killed for histological, autoradiographic, and immunocytochemical analysis. Viable HiB5 cell grafts were identified in all animals, together with reactive microglia and macrophages located throughout the periinjured parenchyma and grafts (OX-42 immunohistochemistry). Brain-injured animals transplanted with either NGF-HiB5 or n-HiB5 cells displayed significantly improved neuromotor function (p < 0.05) and spatial learning behavior (p < 0.005) compared with brain-injured animals receiving microinjections of vehicle alone. A significant reduction in hippocampal CA3 cell death was observed in brain-injured animals receiving transplants of NGF-HiB5 cells compared with those receiving n-HiB5 cells or vehicle (p < 0.025). CONCLUSIONS: This study demonstrates that immortalized neural stem cells that have been retrovirally transduced to produce NGF can markedly improve cognitive and neuromotor function and rescue hippocampal CA3 neurons when transplanted into the injured brain during the acute posttraumatic period.

Animals↗
PubMed2001

Magnetization transfer imaging and proton MR spectroscopy in the evaluation of axonal injury: correlation with clinical outcome after traumatic brain injury.

BACKGROUND AND PURPOSE: Current imaging does not permit quantification of neural injury after traumatic brain injury (TBI) and therefore limits both the development of new treatments and the appropriate counseling of patients concerning prognosis. We evaluated the utility of magnetization transfer ratio (MTR) and proton MR spectroscopy in identifying patients with neuronal injury after TBI. METHODS: Thirty patients with TBI (21-77 years old; mean age, 42 years; admission Glasgow Coma Scale (GOS) scores 3-15; mean score, 11) were studied on a 1.5-T system with magnetization transfer imaging and MR spectroscopy of the splenium. Magnetization transfer imaging was also performed in the brain stem in all patients, and other areas of the brain were sampled in one patient. The splenium of the corpus callosum and brain stem were studied because these are often affected by diffuse axonal injury. Scans were obtained 2 to 1129 days after injury (median, 41 days). MTR was considered abnormal if it was more than 2 SD below normal. Proton MR spectroscopy was used to calculate the N-acetylaspartate (NAA)/creatine (Cr) ratio. GOS was determined at least 3 months after injury. RESULTS: In 10 patients with a GOS of 1 to 4, the mean NAA/Cr was 1.24 +/- 0.28; two of these patients had abnormal MTR in normal-appearing white matter (NAWM). In 20 patients with a GOS of 5, the mean NAA/Cr was 1.53 +/- 0.37 (P < .05); four of these patients had abnormal MTR in NAWM. MTR abnormalities in NAWM were identified in six patients, but these changes did not correlate with GOS or MR spectroscopy changes. CONCLUSION: MTR and MR spectroscopy can quantify damage after TBI, and NAA levels may be a sensitive indicator of the neuronal damage that results in a worse clinical outcome.

Aspartic Acid↗
PubMed2000

Magnetization transfer imaging of traumatic brain injury.

Magnetization transfer imaging (MTI) has been shown to be sensitive for the detection of white matter abnormalities in entities such as multiple sclerosis, progressive multifocal leukoencephalopathy, and wallerian degeneration. Our hypothesis was that MTI would detect traumatic white matter abnormalities (TWMA) and provide information additional to that obtainable with routine spin- and gradient-echo imaging. We hypothesized that the presence of TWMA defined by MTI would correlate with outcome following TBI. Twenty-eight victims of head trauma and 15 normal controls underwent magnetic resonance imaging including MTI. Magnetization transfer ratios (MTR) were calculated for areas of shearing injury and for normal-appearing white matter (NAWM) in locations frequently subject to diffuse axonal injury. Abnormal MTRs were detected in NAWM in eight patients. All eight had persistent neurologic deficits, including cognitive deficits, aphasia, and extremity weakness. Seven of the 28 patients had no abnormal findings on neurologic exam at discharge, transfer, or follow-up. None of these patients had an abnormal MTR in NAWM. In the remaining 13 patients, who had persistent neurologic deficits, no regions of abnormal MTR were detected in NAWM. MTI is a sensitive method for the detection of TWMA. Detection of abnormal MTR in NAWM that is prone to axonal injury may predict a poor patient outcome. The presence of normal MTR in NAWM in these areas does not necessarily confer a good outcome, however.

Adult↗
PubMed1999

Alterations in ionized and total blood magnesium after experimental traumatic brain injury: relationship to neurobehavioral outcome and neuroprotective efficacy of magnesium chloride.

Experimental evidence suggests that magnesium plays a role in the pathophysiological sequelae of brain injury. The present study examined the variation of blood ionized and total magnesium, as well as potassium, sodium, and ionized calcium, after experimental fluid percussion brain injury in rats. Blood ionized magnesium concentration significantly declined from 0.45 +/- 0.02 to 0.32 +/- 0.02 mM by 30 min postinjury and stayed depressed for the 24-h study period in vehicle-treated rats. Blood total magnesium concentration was 0.59 +/- 0.01 mM and remained stable over time in brain-injured vehicle-treated animals. When magnesium chloride (125 micromol/rat) was administered 1 h postinjury, ionized magnesium levels were restored by 2 h postinjury and remained at normal values up to 24 h following brain trauma. Magnesium treatment also significantly reduced posttraumatic neuromotor impairments 1 and 2 weeks after the insult, but failed to attenuate spatial learning deficits. A significant positive and linear correlation could be established between ionized magnesium levels measured 24 h postinjury and neuromotor outcome at 1 and 2 weeks. We conclude that acute ionized magnesium measurement may be a predictor of long-term neurobehavioral outcome following head injury and that delayed administration of magnesium chloride can restore blood magnesium concentration and attenuate neurological motor deficits in brain-injured rats.

Animals↗
PubMed1998

Suprasellar osteolipoma: case report.

BACKGROUND: Osteolipomas are distinguished from other intracranial lipomas by their arrangement of central adipose and peripheral osseous tissues and by characteristically arising in the suprasellar/interpeduncular region. METHODS: We report computed tomography (CT), magnetic resonance imaging (MRI), and pathology findings from this 34-year-old man who underwent surgical removal of this benign lesion. RESULTS: This case displays the distinctive histopathology that has been reported in 13 of 31 (42%) lipomas in this region. In contrast, ossification of lipomas at other intracranial sites is relatively rare. CONCLUSIONS: Ossification should be expected in many suprasellar/interpeduncular lipomas, and osteolipoma should be included in the radiologic differential diagnosis of fat-intensity masses with calcification in this region.

Adult↗
PubMed1998

Case of the month: March 1998--48 year old man with back pain and weakness.

A 48 year old man with long history of end stage renal disease (ESRD) and secondary hyperparathyroidism presented with back pain and incontinence. MRI and CT showed T2 expansion with bony destruction and spinal cord compression. Other vertebral bodies showed destructive lesions as well. Microscopic examination showed a brown tumor composed of multinucleated giant cells and bone uninvolved by tumor showed "tunneling" resorption. Brown tumors are an exaggerated form of "local" osteitis fibrosa cystica in patients with ESRD and secondary hyperparathyroidism, but spinal cord compression is rare.

Back Pain↗
PubMed1998

Dementia resulting from dural arteriovenous fistulas: the pathologic findings of venous hypertensive encephalopathy.

PURPOSE: Dural arteriovenous fistulas (DAVFs) are acquired arteriovenous shunts located within the dura. The highly variable natural history and symptomatology of DAVFs range from subjective bruit to intracranial hemorrhage and are related to the lesion's pattern of venous drainage and its effect on the drainage of adjacent brain. We examined the prevalence and features of DAVFs in patients with progressive dementia or encephalopathy. METHODS: The records and radiologic studies of 40 consecutive patients with DAVFs treated at our institution were reviewed. RESULTS: Five (12.5%) of 40 consecutive patients with DAVFs had encephalopathy or dementia. In each patient, high flow through the arteriovenous shunt combined with venous outflow obstruction caused impairment of cerebral venous drainage. Hemodynamically, the result was widespread venous hypertension causing diffuse ischemia and progressive dysfunction of brain parenchyma. Results of CT or MR imaging revealed abnormalities in each patient, reflecting the impaired parenchymal venous drainage. Pathologic findings in one patient confirmed the mechanism of cerebral dysfunction as venous hypertension. The hemodynamic mechanism and resulting abnormality appeared identical to that seen in progressive chronic myelopathy resulting from a spinal DAVF (Foix-Alajouanine syndrome). Remission of cognitive symptoms occurred in each patient after embolization. CONCLUSION: Venous hypertensive encephalopathy resulting from a DAVF should be considered a potentially reversible cause of vascular dementia in patients with progressive cognitive deficits.

Aged↗
PubMed1997

Metabolic quantification of lesion volume following experimental traumatic brain injury in the rat.

A reliable and rapid method for quantifying lesion volume following traumatic brain injury (TBI) has vast potential in brain injury research. Staining with 2, 3, 5-triphenyltetrazolium chloride (TTC) provides for demarcation of damaged or infarcted tissue from normal, viable cerebral tissue, in which a red formazan product is formed by reduction during cellular respiration of mitochondrial dehydrogenase enzymes. The present study evaluated the use of TTC staining to quantify the cortical lesion volume in rats undergoing fluid-percussion (FP) brain injury. Male Sprague-Dawley rats (350-450 g, n = 27) were anesthetized (sodium pentobarbital, 60 mg/kg, ip) and subjected to lateral FP brain injury of mild (1.1-1.3 atm, n = 5), moderate (2.0-2.3 atm, n = 9), or high (2.4-2.6 atm, n = 8) severity, while sham (noninjured) animals (n = 5) were anesthetized and surgically prepared without injury. Forty-eight hours after injury animals were sacrificed, brains were stained with TTC, and lesion volumes were calculated. A highly significant correlation was found between cerebral cortical lesion volume (mm3) and severity of brain injury (r = 0.85; p < 0.0001). The mean (+/-SD) lesion volumes were 12.1 (+/-4.5) mm3 following mild injury, 33.8 (+/-8.6) mm3 following moderate injury, and 45.1 (+/-14.0) mm3 following severe injury. A significant difference was observed between all injury groups using a t test with Bonferroni correction (p < 0.05). These results suggest that the TTC staining technique is a useful, rapid, and reproducible method for quantification of lesion volume following lateral FP brain injury.

Animals↗
PubMed1997

Delayed administration of basic fibroblast growth factor (bFGF) attenuates cognitive dysfunction following parasagittal fluid percussion brain injury in the rat.

The present study evaluates the therapeutic effects of delayed administration of bFGF on cognitive dysfunction and histopathological damage following lateral fluid-percussion (FP) brain injury. Male Sprague-Dawley rats were trained to learn a visuospatial task in a Morris Water Maze (MWM) paradigm and then were anesthetized and subjected to either FP brain injury of moderate severity (2.5-2.8 atm, n = 32) or surgery without brain injury (n = 10). Twenty-four hours postinjury, an infusion cannula connected to a mini-osmotic pump was implanted into the area of maximal cortical injury to continuously infuse either bFGF (2.0 g) or vehicle for 7 days. Treatment with bFGF significantly attenuated posttraumatic memory dysfunction in the MWM at 8 days postinjury when compared to vehicle treatment (p < 0.05). The cortical lesion and significant cell loss in the ipsilateral CA3 region of the hippocampus, produced by FP injury, was not affected by bFGF treatment. However, immunohistochemical evaluation of glial fibrillary acidic protein revealed a trend toward increased astrocytosis in the injured cortex of bFGF-treated animals compared to vehicle-treated animals (p < 0.1). These results indicate that bFGF may be efficacious in attenuating cognitive dysfunction associated with traumatic brain injury.

Analysis of Variance↗
PubMed1997

Improvement of cognitive deficits and decreased cholinergic neuronal cell loss and apoptotic cell death following neurotrophin infusion after experimental traumatic brain injury.

This study explores the effects of infusion of nerve growth factor (NGF) on behavioral outcome and cell death in the septal region using the clinically relevant model of fluid-percussion brain injury in the rat. Animals were subjected to fluid-percussion brain injury and 24 hours later a miniosmotic pump was implanted to infuse NGF (12 animals) or vehicle (12 animals) directly into the region of maximum injury for 2 weeks. Four weeks postinjury the animals were tested for cognitive function using a Morris Water Maze paradigm. Neurological motor function was evaluated over a 4-week postinjury period. The rats receiving NGF infusions had significantly higher memory scores than vehicle-treated animals. Examination of the cholinergic neurons in the medial septal region using choline acetyltransferase immunohistochemistry demonstrated significant cell loss after injury. Infusion of NGF significantly attenuated loss of these cholinergic neurons. A second group of animals was subjected to fluid-percussion brain injury alone (23 rats) or injury followed by NGF infusion (18 rats). These animals were killed between 24 hours and 2 weeks postinjury and the septal region was examined for the presence of apoptotic cells using the terminal deoxynucleotidyl transferase-mediated biotinylated-deoxyuridinetriphosphate nick-end labeling technique. Apoptotic cells were identified as early as 24 hours postinjury; their numbers peaked at 4 and 7 days, and then declined by 14 days. The NGF-treated animals had some apoptotic cells; however, even at 7 days there were significantly fewer of these cells. No significant motor differences were observed between the NGF- and vehicle-treated groups. These data indicate that NGF administration beginning 24 hours after fluid-percussion brain injury has a beneficial effect on cognition and results in sparing of cholinergic septal neurons. These improvements persist after cessation of NGF administration. The beneficial effects of NGF may be related to its ability to attenuate traumatically induced apoptotic cell death.

Animals↗
PubMed1996

Intraoperative endovascular surgery for cerebral aneurysms.

The application of a number of procedures that can be considered intraoperative endovascular neurosurgery has enhanced our ability to treat cerebral aneurysms from the abluminal surface. This study identifies a role for these techniques in the management of difficult aneurysms. A review of the last 1202 aneurysms undergoing direct clipping by the authors disclosed that these methods were used in 62 cases. Of these aneurysms, 36 arose from the internal carotid artery, 12 from the middle cerebral artery, eight from the vertebrobasilar distribution, and six from the anterior cerebral artery. The indications for applying these methods were large size (12-60 mm), intraluminal thrombus, broad neck, plaque at the neck, the potential compromise of branches at the base of the aneurysm, or a combination of these problems. The most frequently chosen intraoperative technique was suction decompression with direct removal of plaque and thrombus using suction, dissection, and/or ultrasonic aspiration. The application of temporary clips was required in all cases in which the aneurysm was opened before definitive clipping. No special pharmacological cerebral protective regimen was used. In one case in which a greater occlusion time was anticipated, cardiopulmonary bypass with profound hypothermia was performed. A favorable outcome was achieved in 73% of these difficult cases. An increased neurological deficit after surgery was seen in 11%, and the mortality rate was 8%. These methods should be considered and can be anticipated before surgery for unusual aneurysms. Many cases now being considered for embolization may be more suitable for definitive surgical obliteration.

Adult↗
PubMed1996

Combined fetal neural transplantation and nerve growth factor infusion: effects on neurological outcome following fluid-percussion brain injury in the rat.

This study was designed to evaluate the histological and behavioral impact of fetal neural transplantation with and without neurotrophin infusion in rats subjected to traumatic brain injury using a clinically relevant model of lateral fluid-percussion brain injury. Adult male Sprague-Dawley rats received lateral fluid-percussion brain injury of moderate severity (2.1-2.3 atm). Twenty-four hours after injury, minced fetal cortical grafts (E16) were stereotactically transplanted into the site of injury cavity formation (in 32 rats). Ten control animals received injections of saline. A third group of 29 animals that received transplants also underwent placement of a miniosmotic pump (immediately after transplantation) to continuously infuse nerve growth factor (NGF) directly into the region of graft placement for the duration of the experiment. A fourth group of eight animals underwent transplantation of fetal cortical cells that had been dissociated and placed in suspension. Animals were evaluated at 72 hours, 1 week, and 2 weeks after injury for cognitive function (using the Morris water maze), posttraumatic motor dysfunction, and transplant survival and morphology (using Nissl and modified Palmgren's silver staining techniques). Robust survival of whole-tissue transplants was seen in 65.5% of animals and was not increased in animals receiving NGF infusion. Animals receiving transplants of cell suspension had no surviving grafts. Brain-injured animals receiving transplants showed significant cognitive improvements compared with controls at the 2-week evaluation. Significantly improved memory scores were seen at all evaluation times in animals receiving both NGF and transplants compared with injured controls and compared with animals receiving transplants alone at the 72-hour and 1-week evaluations. Neurological motor function scores were significantly improved in animals receiving transplants alone and those receiving transplants with NGF infusion. Histological evaluation demonstrated differentiation of grafted cells, decreased glial scarring around transplants when compared with control animals, and the presence of neuronal fibers bridging the interface between graft and host. This study demonstrates that fetal cortical cells transplanted into the injured cortex of the adult rat can improve both posttraumatic cognitive and motor function and interact with the injured host brain.

Analysis of Variance↗