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.

Delayed re-opening of an STA-MCA bypass graft.

We describe the case of a 47-year-old female with symptomatic right MCA stenosis who had undergone cerebral revascularization through a superficial temporal artery-to-middle cerebral artery (STA-MCA) bypass. Despite clear patency in the operating room, post-operative angiography showed no flow in the bypass. Her ipsilateral internal carotid artery (ICA) was widely patent. She remained asymptomatic and follow-up angiography four years later showed a widely patent bypass graft in the setting of critical stenosis of the ipsilateral ICA. That the graft was found opened up and supplying the hemisphere was presumably stimulated by an increased "demand" and flow gradient promoting its patency.

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.

Chronic and acute stressors among military personnel: do coping styles buffer their negative impact on health?

This study examined the moderating impact of positive and negative coping styles on the relationship of acute and chronic job stressors with self-reported health symptoms of 521 military personnel. The number of acute work-related events was associated with a high frequency of self-reported symptoms. Similarly, role ambiguity, overload, and lack of job stimulation were associated with increased symptoms. Only the negative coping styles (i.e., venting of negative emotions and denial/disengagement) were uniquely associated with symptoms. Only 5 of the 13 proposed Stressor x Coping interactions were significant, and they all involved the negative coping styles. That is, instead of alleviating the negative outcomes of work stressors, these coping styles were associated with high strain, regardless of the amount of stressor, and, in some cases, these coping styles exacerbated the negative effect of the stressor on the strain outcomes.

The journal as a guide for the healing journey.

The healing influence of the journal is now being recognized through research and in the practices of those who are using this modality. The journal is an important tool because it works as a catalyst for self-discovery and self-reflection. As nurses practice holistic living, the journal is a friend that helps nurture the self and lifts others to higher levels of empowerment on the journey of healing and wellness.

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.

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.

Estradiol exerts neuroprotective effects when administered after ischemic insult.

BACKGROUND AND PURPOSE: 17beta-Estradiol (E2) has been reported to exert neuroprotective effects when administered before an ischemic insult. This study was designed to determine whether E2 treatment after ischemia exerts the same effects and, if so, how long this therapeutic window remains open, and whether the effects are related to changes in cerebral blood flow (CBF). METHODS: Female Sprague-Dawley rats were subjected to permanent middle cerebral artery occlusion (MCAO). In protocol 1, E2 was administered (100 microg/kg IV followed immediately by subcutaneous implantation of crystalline E2 in a silicone elastomer tube) to ovariectomized females (OVX+E2) at 0.5 (n=8), 1 (n=6), 2 (n=7), 3 (n=6), or 4 (n=9) hours after MCAO. Intact (INT; n=6) and ovariectomized females (OVX; n=12) were subjected to MCAO and received vehicle instead of E2. Two days after MCAO the animals were killed, and ischemic lesion volume was determined by 2,3,5-triphenyltetrazolium chloride staining. In protocol 2, CBF was monitored before and at 1, 24, and 48 hours in a group of animals receiving E2 or vehicle 0.5 hour after ischemia induction (INT, n=6; OVX, n=8; OVX+E2, n=6). RESULTS: Lesion volume was 20.9+/-2.2% and 21.8+/-1.2% in the INT and OVX groups, respectively. E2 was found to decrease lesion volume significantly when administered within 3 hours after MCAO. The lesion volumes were 6.3+/-0.5%, 10.3+/-2.1%, 11.8+/-1.8%, 13.5+/-1.6%, and 17.9+/-2.8% when E2 was administered at 0.5, 1, 2, 3, or 4 hours after MCAO, respectively. CBF decreased to 43.1+/-2.2% and 25.4+/-1.0% in the INT and OVX animals, respectively, at 5 minutes after MCAO. In comparison to OVX rats, CBF was not different at 1 hour after E2 administration but was increased significantly in the OVX+E2 group 1 and 2 days after E2 administration. CONCLUSIONS: E2 exerts neuroprotective effects when administered after ischemia, with a therapeutic window in a permanent focal cerebral ischemia model of approximately 3 hours. This effect of estradiol was associated with no immediate change in blood flow but with a delayed increase in CBF.

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.

Experimental model of small deep infarcts involving the hypothalamus in rats: changes in body temperature and postural reflex.

BACKGROUND AND PURPOSE: Intraluminal middle cerebral artery (MCA) occlusion in rats has been reported to cause hyperthermia assumed to be caused by hypothalamic damage. To clarify the effects of hypothalamic ischemia on body temperature and to obtain a model simulating lacunar infarction, we attempted to produce small infarcts in deep structures (including the hypothalamus). METHODS: A surgical suture was advanced to occlude the origin of the hypothalamic (HTA) and/or anterior choroidal arteries (AChA) without compromise of the anterior or middle cerebral artery origins. After treatment, rectal temperature and postural reflex were examined repeatedly for 3 days under nonanesthetic conditions. The AChA and HTA and their link with small deep infarction were then confirmed by TTC, hematoxylin and eosin, and TUNEL stains and by microsurgical dissection after colored silicone perfusion into the cerebral arteries. RESULTS: Advancement of the suture near to but not occluding the MCA origin (0.5 to 1.9 mm proximal) produced small, deep, nonneocortical strokes in 25 of 36 animals without producing MCA ischemic changes. These infarctions mainly affected the hypothalamus in 13 animals (HTA area: infarct volume 6+/-1 mm(3)) and involved both the internal capsule and hypothalamus in 12 animals (HTA+AChA area infarct volume 48+/-10 mm(3)). Rats with HTA infarction alone exhibited persistent hyperthermia for 72 hours; some also had transient mild postural abnormality. The AChA+HTA infarct group showed a transient elevation of body temperature for 24 hours and definitive postural abnormality. In the remaining 11 animals, the suture was inadvertently advanced across the MCA origin, producing a large infarct that affected both the neocortex (MCA territory) and nonneocortical structures (volume 381+/-30 mm(3), n=11). The MCA infarct group displayed a transient hyperthermia and severe postural abnormality. CONCLUSIONS: When properly positioned, the intraluminal suture method permits selective AChA and/or HTA obstruction without inducing MCA territory ischemia. This model confirms that selective hypothalamic infarction produces significant and sustained temperature regulation abnormalities. The model also may be useful in investigating the pathophysiology of small, deep, end-vessel infarction.

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.

Cloning and characterization of Gallus and Xenopus ferrochelatases: presence of the [2Fe-2S] cluster in nonmammalian ferrochelatase.

Ferrochelatase (EC 4.99.1.1) catalyzes the insertion of ferrous iron into protoporphyrin IX to form protoheme IX. This membrane-bound enzyme has been cloned from a variety of bacteria, plants, mammals, and yeast. Interestingly, only in mammals has the enzyme been found to contain a [2Fe-2S] cluster. Since the presence of this feature only in mammals would have significant evolutionary implications and because there have been no nonmammalian animal ferrochelatases cloned, expressed, and characterized, we report here the cloning and characterization of ferrochelatase from chicken (Gallus gallus) and an amphibian (Xenopus laevis). The cDNAs for both of these ferrochelatases were cloned by complementation of an Escherichia coli DeltahemH strain. The expressed and purified enzymes were characterized biochemically and both were found to contain [2Fe-2S] clusters. These clusters have spectral characteristics essentially identical to those of human ferrochelatase, although their EPR spectra are recognizably distinct from the human one. The [2Fe-2S] clusters of both chicken and amphibian ferrochelatases are readily destroyed by NO. Sequence analysis of the 3' UTR of both chicken and amphibian cDNAs show that while both have poly(A) tails neither have a consensus polyadenylation signal. The 5' UTR of Xenopus as isolated contained 135 bp and possesses no identifiable stem-loop structure.

Surgical treatment of paraclinoid and ophthalmic aneurysms.

Paraclinoid aneurysms include those arising from the ophthalmic segment and from the distal cavernous carotid artery or clinoid segment. Three aneurysm variants originate from the ophthalmic segment: ophthalmic artery, superior hypophyseal artery, and dorsal types. Clinoidal segment aneurysms arise from the carotid artery in the interval between the carotid oculomotor membrane proximally and the dural ring distally, and include anterior-lateral and medial variants. With proper exposure and a firm understanding of the parasellar osseous, dural, and vascular anatomy, most paraclinoid aneurysms are occluded with low risk to the brain or visual apparatus.

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.

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.