The Variable Appearance of Third Ventricular Colloid Cysts: Correlation with Histopathology and the Risk of Obstructive Ventriculomegaly.

BACKGROUND AND PURPOSE: While third ventricular colloid cysts may present as an incidental finding, they also harbor the potential to cause ventricular obstruction and sudden death. Herein we analyze the relationship between imaging appearance and the risk of obstructive ventriculomegaly. MATERIALS AND METHODS: This is a retrospective review of the MR imaging appearance of 64 patients with colloid cysts, 46 of whom also had a CT scan, obtained by a tertiary hospital imaging report data base search over a 10-year period. Cysts were categorized by appearance on T2-FLAIR and correlated with patient age, cyst size, and the risk of obstructive ventriculomegaly. Histopathologic correlation was available for 28 cases. RESULTS: The 64-patient cohort was 52% female, median age 50 years (range 10 to 99 years). Cysts hyperintense on T2-FLAIR (53.1%) were larger (P <.001), occurred in younger patients (P = .01), and had a higher risk of obstructive ventriculomegaly than homogeneously hypointense cysts (relative risk 6.18, 95% CI [2.04, 18.67]). Three patterns of T2 hyperintensity were identified: homogeneously hyperintense, hyperintense rim, and cysts with "dot sign." Although "dot sign" cysts were larger (P < .001), there was no significant difference in patient age or the risk of ventricular obstruction among T2 hyperintense cysts. Cyst wall histopathology did not vary with imaging appearance. CONCLUSIONS: Hyperintensity on T2-FLAIR, whether homogeneous, rim, or "dot sign," is associated with larger cyst size and younger patient age, and is an imaging risk factor for obstructive ventriculomegaly. The hyperintense rim does not represent a thickened cyst wall.

Massage therapy in the workplace: reducing employee strain and blood pressure.

AIM: Assess the effects of workplace-based massage therapy on physiological and psychological outcomes. METHODS: We used afield experiment in which 28 participants were randomly assigned into either an experimental (n = 14) or control (n = 14) group. The experimental group received weekly massage treatments at work for a four week period while the control group did not. RESULTS: Both strain and blood pressure were significantly reduced during treatment for the experimental group but not for the control group. CONCLUSIONS: This study provides initial support for the effectiveness of workplace-based massage therapy as part of a comprehensive workplace health strategy.

Estrogens decrease reperfusion-associated cortical ischemic damage: an MRI analysis in a transient focal ischemia model.

BACKGROUND AND PURPOSE: Early identification of irreversible cerebral ischemia is critical in defining strategies that influence neuronal survival after stroke. We used MRI to investigate the effects of 17beta-estradiol (E2) on the temporal evolution of focal ischemia. METHODS: Female rats were ovariectomized and divided into 1 of 2 groups: ovariectomy alone (OVX; n=4) or ovariectomy with estrogen replacement (OVX+E2; n=3). Both groups were then subjected to 1-hour middle cerebral artery occlusion (MCAO), with the use of a standardized endovascular monofilament model, followed by reperfusion. Sequential diffusion-weighted (DWI) and T2-weighted (T2WI) MRI were obtained during and after the MCAO. In separate groups of animals (n=5 for OVX and OVX+E2), cerebral blood flow (CBF) was measured by laser-Doppler methods before, during, and after occlusion. RESULTS: DWI detected similar lesion characteristics during MCAO in both groups. In the OVX group, lesion size did not change during reperfusion, but the signal intensity ratio increased early and stabilized during the latter stages. In contrast, DWI lesion size decreased during reperfusion in OVX+E2 rats by 50% to 60% (P<0.05), a size reduction almost exclusively limited to cortical regions. During MCAO, the signal intensity ratio in OVX+E2 rats was reduced compared with OVX rats. Reperfusion further attenuated the signal intensity ratio in cortical but not subcortical regions (P<0.05 versus OVX). T2WI revealed no lesions in either group during MCAO, but it detected lesion sizes similar to that of DWI during reperfusion. Furthermore, similar patterns and magnitudes of estrogen treatment-related decrease in lesion size were noted after reperfusion. T2WI demonstrated less intense signal intensity ratio changes in both groups compared with DWI. There were no differences in CBF between groups either during occlusion, early reperfusion, or 1 day after reperfusion. CONCLUSIONS: This study strongly suggests that estrogens selectively protect cortical tissue from ischemic damage during MCAO and that this protection is exerted during both the occlusion and reperfusion phases of ischemia and does not involve an estrogen-related change in CBF.

17-beta estradiol can reduce secondary ischemic damage and mortality of subarachnoid hemorrhage.

Subarachnoid hemorrhage (SAH) is a unique disorder commonly occurring when an aneurysm ruptures, leading to bleeding and clot formation, with a higher incidence in females. To evaluate the influence of 17-beta estradiol (E2) in the outcome of subarachnoid hemorrhage, SAH was induced by endovascular puncture of the intracranial segment of internal carotid artery in 15 intact females (INT), 19 ovariectomized females (OVX), and 13 ovariectomized female rats with E2 replacement (OVX + E2). Cerebral blood flow was recorded before and after SAH. All animals were decapitated immediately after death or 24 hours after SAH for clot area analysis. Brains were sliced and stained with 2,3,5-triphenyltetrazolium chloride (TTC) for secondary ischemic lesion analysis. The cortical cerebral blood flow (CBF), which was measured by a laser-Doppler flowmeter, decreased to 29.6%+/-17.7%, 22.8%+/-8.3%, and 43.5%+/-22.9% on the ipsilateral side (P = 0.01), and decreased to 63.4%+/-14.1%, 57.4%+/-11.0%, and 66.6%+/-17.9% on the contralateral side (P = 0.26) in INT, OVX, and OVX + E2, respectively. The subcortical CBF, which were measured by the H2 clearance method, were 7.77+/-12.03, 7.80+/-8.65, and 20.58+/-8.96 mL 100 g(-1) min(-1) on the ipsilateral side (P < 0.01), and 21.53+/-2.94, 25.13+/-3.01, and 25.30+/-3.23 mL 100 g(-1) min(-1) on the contralateral side in INT, OVX, and OVX + E2, respectively. The mortality was 53.3%, 68.4%, and 15.4% in INT, OVX, and OVX + E2, respectively (P = 0.01), whereas no significant difference in clot area was noted among the groups. The secondary ischemic lesion volume was 9.3%+/-8.4%, 24.3%+/-16.3%. and 7.0%+/-6.4% in INT, OVX, and OVX + E2, respectively (P < 0.01). This study demonstrated that E2 can reduce the mortality and secondary ischemic damage in a SAH model without affecting the clot volume.

The effect of corpus callosum lesions on unilateral neglect in monkeys.

The cerebral hemispheres may be mutually inhibitory. An injured hemisphere may continue to be inhibited while the uninjured hemisphere is released from inhibition, inducing attentional bias. Patients with neglect might therefore benefit from transection of the corpus callosum. To test this hypothesis, we ablated the frontal arcuate gyrus alone or several months after corpus callosum transection in monkeys. Neglect was significantly worse in animals with a corpus callosum transection. Therefore, the hemispheres may be mutually excitatory or compensatory, and a callosal transection would not be therapeutic. Because the rate of recovery in the two groups was not different, recovery seemed to be an intrahemispheric phenomenon.

Treatment of visual loss in pseudotumor cerebri associated with uremia.

Ten patients with pseudotumor cerebri associated with renal insufficiency had papilledema and elevated intracranial pressure, but neurologic examinations and CT were normal. The 40% frequency of severe visual loss, 20/100 or worse, was higher than expected for pseudotumor cerebri. While furosemide was effective in 3 patients with renal transplants, administration of corticosteroids to 2 other patients did not halt progressive loss of vision. The visual function of 2 patients deteriorated even after lumboperitoneal shunting. Five patients underwent fenestration of the optic nerve sheath. This procedure improved the visual acuity of 3 patients and stabilized vision in the others. While the pathogenesis of pseudotumor cerebri in renal insufficiency is unknown, optic nerve sheath fenestration is the surgical treatment of choice for visual loss unresponsive to medical therapy.

The effect of duodenojejunal alimentation on gastric pH and hormones in intensive care unit patients.

We evaluated effects of duodenojejunal (DJ) feeding on gastric pH and selected gastrointestinal hormones in 13 randomly selected patients in an intensive care unit (ICU). To obtain baseline values for gastric pH, a nasogastric (NG) tube was placed in each patient and gastric pH was measured every 30 minutes for 2 hours. To obtain control values, a Dobbhoff tube was placed fluoroscopically and 0.45 percent saline solution (NaCl), 75 ml, was infused for 1 hour and gastric pH was measured again; the previously placed NG tube was left in position. Then, by randomization, either 0.45 percent NaCl (pH = 5) was continued (n = 6) or a high-nitrogen, isotonic, enteral feeding solution (Osmolite HN, pH = 6.4) (n = 7) was infused, both at 75 ml/h. Gastric pH was noted hourly for 96 hours; antacid (Maalox TC, 15-ml aliquots) was given by NG tube when the pH was 4 or less. After 96 hours, the infusion was stopped and gastric pH was noted for 4 additional hours. Before and during initial saline solution infusion; after 24, 48, 72, and 96 hours of continuous infusion; and 4 hours after stopping the infusion, peripheral venous blood was obtained for measurement of plasma gastric inhibitory polypeptide (GIP) and serum gastrin. Data were analyzed by ANOVA (RMD), Fishers' exact test, and the unpaired t-test. Groups did not differ demographically. Throughout the infusion, gastric pH tended to be higher with the enteral feeding solution than with saline solution, but this was significant only at 24 hours. Less antacid was required with the enteral feeding solution at 24 and 48 hours than with saline solution. Plasma GIP levels were significantly higher with the enteral feeding solution than with saline solution during most of the infusion. Serum gastrin levels did not differ between the groups. In this cohort, infusion of the enteral feeding solution tended to maintain a gastric pH of more than 4 and was associated with increased plasma GIP levels, which may inhibit gastric acid secretion. Early enteral feeding may benefit certain ICU patients.

Systemic administration of a calpain inhibitor reduces behavioral deficits and blood-brain barrier permeability changes after experimental subarachnoid hemorrhage in the rat.

Increases in intracellular calcium and subsequent activation of calcium-activated proteases (e.g., calpains) may play a critical role in central nervous system injury. Several studies have implicated calpain activation following subarachnoid hemorrhage (SAH). This study evaluated the effect of a calpain inhibitor administration following SAH in the rat on behavioral deficits (postinjury days 1-5, employing a battery of well-characterized assessment tasks), and blood-brain barrier permeability changes (48 h post-SAH, quantifying the microvascular alterations according to the extravasation of protein-bound Evans Blue using a spectrophotofluorimetric technique). Rats were injected with 400 microl of autologous blood into the cisterna magna to induce SAH. Within 5 min after the surgical procedure, Calpain Inhibitor II or vehicle was continuously administered intravenously for 2 days. Results indicated that Calpain Inhibitor II treatment after SAH significantly improved (a) beam balance time (day 1, p < 0.05), but not beam balance score, (b) latency to traverse the beam on days 1-4 (day 1-3, p < 0.001; day 4, p < 0.01), and (c) loss in body weight on days 4-5 (p < 0.05). Evans Blue dye extravasation was significantly less in SAH Calpain Inhibitor II-treated rats compared to SAH vehicle-treated rats in seven out of the eight brain regions studied (p < 0.001, 0.01, and 0.05). These results suggest that pharmacological inhibition of a relatively selective, membrane-permeant calpain inhibitor can significantly reduce some pathophysiological SAH consequences, and indicate that the inhibition of calpain may be a beneficial therapeutic approach to reduce post-SAH global brain dysfunction.

Hypoperfusion induces overexpression of beta-amyloid precursor protein mRNA in a focal ischemic rodent model.

Silent stroke is one of the risk factors of dementia. In the present study, we used a novel focal ischemic animal model to investigate the effects of comparatively small changes of cerebral blood flow (CBF) on the expression of beta-amyloid precursor protein (APP) mRNA. Focal ischemia was achieved by introducing a 4-0 monofilament to the bifurcation of anterior and middle cerebral arteries. Brain samples were harvested from ischemic core and penumbra of cortices at 1, 4 and 7 days following ischemia. The expression of APP mRNA was assessed by RT-PCR. The CBF was decreased to 50% for 1 day after stroke and recovered to 90% at the fourth day after stroke. The changes of CBF were accompanied by an increase in the expression of APP mRNA. APP mRNA increased to 208% and 152% in the penumbra and core ischemic regions, respectively, on the fourth day after MCAO and remained high through the seventh day of ischemia. This study suggests brain hypoperfusion enhances APP mRNA expression and may contribute to the progression of cognitive impairment after silent stroke.

Estrogen attenuates over-expression of beta-amyloid precursor protein messager RNA in an animal model of focal ischemia.

Cerebral ischemia is a risk factor for late onset Alzheimer's disease. Since estrogen replacement therapy benefits the outcome of cerebral stroke in post-menopausal women, we designed the present study to investigate the effects of estrogen on the expression of beta-amyloid precursor protein (APP) mRNA following focal ischemia in female rats. Female rats were ovariectomized (OVX) for two weeks. A single dose of 17 beta-estradiol (E2) (100 microgram/kg) was injected s.c. two hours before a unilateral middle cerebral artery (MCA) occlusion. Brain samples were harvested from ischemic core and penumbra of cortices at one hour and twenty-four hours following MCA occlusion. The expression of APP mRNA was assessed by RT-PCR. At one hour after MCA occlusion, OVX rats had a 67.9% (p<0.05) increase in APP mRNA in the penumbra. E2 treatment reduced this APP mRNA over-expression by 26.3% at that region. At twenty four hours following MCA occlusion, OVX rats had increases in APP mRNA of 52.9% and 57.0% (p<0.05) in the core and penumbra, respectively. E2 treatment reduced the APP mRNA over-expression by 61.0% and 48.6% (p<0.05) in these two regions, respectively. These effects appeared to reflect an interaction between hormonal environment and ischemia, since in the absence of MCA occlusion, there were no significant differences in APP mRNA expression among OVX, OVX-E2 treated and intact female rats. The present study demonstrates that estrogen may have an important role in reducing the over-expression of APP mRNA following focal ischemia.

Effects of gender and estradiol treatment on focal brain ischemia.

The present studies were undertaken to investigate the effects of gender and estrogen treatment on focal cerebral ischemia in male and female rats. Focal ischemia was created by inserting a 3-0 surgical suture through the left cervical internal carotid artery to obstruct the blood flow into the middle cerebral artery (MCA). The MCA was reperfused by removing the suture in 40 min. All rats were sacrificed for measurement of infarct area after 24 h. In the first study, mortalities from MAC occlusion were 12.5% (2/16) each for intact male rats and intact female rats, and 23.5% (4/17) for ovariectomized (OVX) female rats. The coronal infarct area (mean+/-S. E.M.) was 9.5+/-1.0% for intact female rats, 16.6+/-1.6% for intact male rats (p=0.0001 vs. intact female rats), and 16.0+/-1.4% for OVX female rats (p=0.0002 vs. intact female rats). In a second experiment, OVX-female rats were administrated either 17beta-estradiol (E2) or its vehicle, hydroxypropyl-beta-cyclodextrin (HPCD), at 40 min after the onset of MCA occlusion. Mortalities were 40% (4/10) for vehicle treated OVX rats and 0% for E2 treated OVX rats. The coronal infarct area (mean+/-S.E.M.) was 19.3+/-1.8% for vehicle treated rats vs. 8.0+/-1. 2% for E2 treated rats (p<0.01). Serum estrogen levels for vehicle treated OVX rats were 14.5+/-1.2% pg/ml vs. 142.7+/-23.6 pg/ml for E2 treated OVX rats (p<0.01). These results strongly suggest that the level of circulating estrogens play an important role in protecting brain tissues against ischemia induced by MCA occlusion.

Reduced MK801 binding in neocortical neurons after AAV-mediated transfections with NMDA-R1 antisense cDNA.

Two adeno-associated virus (AAV)-derived plasmids were constructed with portions of the N-methyl-d-aspartic acid-R1 (NMDA-R1) receptor subunit downstream from the AAV p40-(pJDT95dlk-aR1) or cytomegalovirus (CMV) promoter (pTRUF3-aR1) in an antisense orientation. Each plasmid drove expression of antisense NMDA-R1 in primary rat neocortical neuronal cultures 4 days after transfection as detected by reverse transcriptase-polymerase chain reaction (RT-PCR). Transfection with pTRUF3-aR1 (2x4 microgram) but not with pJDT95dlk-aR1 decreased neuronal [3H]MK-801 binding in a dose-dependent manner.

Testosterone increases and estradiol decreases middle cerebral artery occlusion lesion size in male rats.

This study was undertaken to determine the effects of estrogen and testosterone on cerebral ischemic lesion size induced by middle cerebral artery (MCA) occlusion in male rats. Rats were gonadectomized and treated with testosterone, estrogen, or testosterone plus estrogen filled Silastic pellets. The animals were divided into 6 groups: intact, intact + estrogen (E2), castrate, castrate + testosterone (T), castrate + E2, and castrate + T + E2. One week after treatment, cerebral ischemia was induced by MCA occlusion for 40 min, followed by reperfusion. After 24 h, rats were sacrificed and slices were then stained to assess lesion size. The presence of testosterone increased and the removal of testosterone decreased lesion size. A strong positive correlation (r2 = 0.922) between plasma testosterone concentrations and ischemic lesion size was observed. Estradiol treatment reduced ischemic area. In summary, the present study provides evidence that testosterone exacerbates and estrogens ameliorate ischemic brain damage in an animal model of cerebral ischemia.

Nicotinic alpha 7 receptors protect against glutamate neurotoxicity and neuronal ischemic damage.

The alpha7 receptor agonist dimethoxybenzylidene anabaseine (DMXB) protected rat neocortical neurons against excitotoxicity administered 24 h before, but not concomitantly with, NMDA. This action was blocked by nicotinic but not muscarinic antagonists. DMXB (1 mg/kg i.p.) also reduced infarct size in rats when injected 24 h before, but not during, focal ischemic insults. In a mecamylamine-sensitive manner, alpha7 receptors appear neuroprotective in non-apoptotic model.

Contralateral trochlear nerve paresis and ipsilateral Horner's syndrome.

Two patients had paresis of the trochlear nerve contralateral to the site of lesions in the brainstem. Both patients had ipsilateral blepharoptosis and miosis suggesting oculosympathetic paresis from involvement of the descending sympathetic tract, adjacent to the fourth cranial nerve nucleus and its fascicles, in the caudal mesencephalon. Cerebral antiography documented an arteriovenous malformation of the brainstem in Case 1. Magnetic resonance imaging disclosed a lesion of high signal intensity on T2-weighted images involving the dorsal mesencephalon in Case 2. Involvement of the superior cerebellar peduncle produced ipsilateral dysmetria and ataxia. Lesions involving the fourth cranial nerve nucleus or its fascicles, before decussation in the superior medullary velum, and adjacent sympathetic fibers may produce an ipsilateral Horner's syndrome and contralateral superior oblique muscle paresis.

Definition of the anterior choroidal artery territory in rats using intraluminal occluding technique.

This manuscript delineates the territory of the anterior choroidal artery (AChA) in rats, as defined by the induction of an AChA infarction. By advancing a 0.24-mm surgical suture up the internal carotid artery (ICA) to a point 0.5-2 mm proximal to the middle cerebral artery (MCA) origin, the AChA could be occluded and a reliable AChA distribution infarction was produced in 62% (23/37) of animals. The infarct volume, as defined by TTC staining, was 55+/-7 mm(3). Maps of the infarction, generated by measuring the entire area of overlapping coronal slices, demonstrated that the internal capsule was always damaged. Other areas that might be affected included the hippocampus, thalamus, amygdaloid complex, piriform cortex, dorsal caudatoputamen, and lateral ventricular wall. Positioning the coated suture proximal to the AChA produced a much smaller infarct involving the medial and lateral hypothalamus, preoptic region, optic chiasm, and marginal region of the internal capsule near to the lateral hypothalamus exempt from AChA territory damage. A causative relationship between AChA occlusion and a deep cerebral infarct centered on the internal capsule was further established by: (1) identifying the AChA on the non-ischemic side with colored silicone perfusion, and subsequent similar delineation on the ischemic side, and (2) delineating infarction in the silicone perfused AChA region using hematoxylin and eosin staining and the TUNEL method. The AChA usually originated from the ICA (91% of cases), 1.75+/-0.12 mm proximal to the MCA bifurcation. Approximately 27% of the AChAs had periamygdaloid branch(es) on its initial segment.

Cervical carotid artery dissection secondary to malignant fibrous histiocytoma.

A rare case of malignant fibrous histiocytoma of the cervical carotid artery is presented. Erosion of the vessel wall by this neoplasm resulted in dissection and pseudoaneurysm formation. The etiology and diagnosis of and the therapeutic alternatives for this unique disorder are discussed briefly.

The anterior subtemporal, medial transpetrosal approach to the upper basilar artery and ponto-mesencephalic junction.

OBJECTIVE: To describe and anatomically analyze the amount of exposure provided by an anterior subtemporal, medial transpetrosal approach to access the upper third of the basilar artery, ventral mesencephalon, pons, and posterior cavernous sinus. PATIENTS AND METHODS: The outcomes of six patients who underwent surgical treatment via the anterior subtemporal, medial transpetrosal approach at our institution during the past 2 years were reviewed. The series included three patients with subarachnoid hemorrhage from low-lying basilar apex aneurysms, one patient with intraparenchymal hemorrhage from a pontine cavernous malformation, and two patients with slowly progressive cranial neuropathies secondary to petroclival tumors. Thirty dry temporal bone specimens were also measured to quantify the height of petrous bone resection and added proximal basilar artery exposure. RESULTS: The surgical exposure was greatly enhanced in each instance, allowing each lesion to be treated in a straightforward manner with minimal added morbidity (one trochlear nerve palsy, one worsening of a preexistent oculomotor nerve palsy). Our subsequent morphometric analysis indicates that an additional 1 to 1.5 cm of basilar artery, clivus, and pons exposure over that of a standard anterior subtemporal approach is provided by this technique. CONCLUSION: This approach combines the wide view of the subtemporal approach with the more proximal exposure afforded by a medial petrosectomy. The widened visualization of the ventral pons and mesencephalon minimizes cranial nerve morbidity, greatly facilitates dissection of low-lying aneurysms, and provides proximal basilar artery control that would otherwise be obscured by the petrous ridge.

The argon "contact" laser scalpel: technical considerations.

The authors describe the use of a new contact argon laser scalpel designed specifically for hand-controlled cutting and hemostasis. This instrument delivers energy precisely to targeted tissue and produces minimal damage to adjacent healthy structures. Potential clinical applications are discussed.