Tracing the dural tail with image-guided surgery.

OBJECTIVE: The extent of dural resection is important for preventing recurrence in meningioma management. An image-guidance assisted technique is described to perform adequate dural resection. METHODS: A universal instrument adapter system for image-guidance was used to track the dural extension of the meningioma accurately. RESULTS: The universal instrument adapter offers the surgeon the possibility to image-guide nearly any rigid instrument via the computed calibration method. In this way a surgical marking pen was used to chase and adequately mark the "dural tail". DISCUSSION: Image-guidance systems can be used to avoid incomplete resection of the affected dura that may be responsible for tumour recurrence.

Apoptosis and expression of p53 response proteins and cyclin D1 after cortical impact in rat brain.

We measured the temporal profile and cellular identification of apoptosis in rat brain after cortical contusion injury. Double staining immunohistochemistry was also used to investigate the relationship between apoptotic cell death and selective protein expression associated with DNA damage and repair (p53, Bax, MDM2, WAF1, Gadd45, PCNA) and cell cycle protein, Cyclin D1, in male Wistar rats 48 h after injury. Cortical contusion was induced in male Wistar rats with a pneumatic impactor device. The animals were sacrificed at different times after trauma (1, 2, and 14 h and 1, 2, 4, 7 and 14 days; n=4 per time point). Sham-operated rats (n=4) and normal rats not subjected to any surgical procedure (n=4) were used as controls for temporal profile determination. Additional 11 rats were used for study of protein expression. Coronal brain sections were analyzed using an in situ terminal deoxynucleotdyl transferase-mediated biotinylated deoxyuridine triphosphate nick end labeling (TUNEL), hematoxylin, and immunohistochemical double staining methods. Apoptotic cells were observed as early as 2 h after the impact. Apoptotic cell death peaked at 2 days, gradually tapering off afterward, although scattered apoptotic cells were detected at 2 weeks after the impact. The number of apoptotic cells at 2 days far exceeded their number at other times (p=0.009). Apoptotic cells were observed primarily in the cortex adjacent to the site of injury. In addition, apoptotic cells in conjunction with few injured cells were present in the ipsilateral hippocampus and localized to the granule layer of dentate gyrus. Our data indicate that DNA fragmentation is present in nearly all neurons subacutely after cortical contusion and persists for at least 2 weeks thereafter. Apoptosis is also present in neurons localized to the hilus of the dentate gyrus at a site remote from the area of injury suggesting a selective role for apoptosis in promoting secondary brain damage and dysfunction after traumatic brain injury. Using double staining, we were able to show that a great majority of apoptotic cells (>95%) were neurons and the rest were astrocytes and endothelial cells. Proteins associated with DNA damage and repair (p53, Bax, MDM2, WAF1, Gadd 45, PCNA) were expressed in the cytoplasm of normal cells of naive and sham rats. These proteins were translocated to the nuclei of apoptotic and injured cells at 48 h after cortical contusion. Cyclin D1 was not present in apoptotic cells. The differential expression of proteins associated with DNA damage, repair and the cell cycle protein Cyclin D1 in the contused brain suggest a potential role for these proteins in cell survival and apoptosis after cortical contusion.

Trigeminal nerve and brainstem catecholamine systems in cerebral vasospasm.

Cisternal blood injection in the rat and squirrel monkey produces a biphasic cerebral vasospasm, a decrease in cerebral blood flow (CBF) and an increase in glucose uptake (CMRglu) due to an anaerobic glucolysis actually representing a decrease in metabolism. Lesioning of the A2-nucleus, its ascending cathecolamine pathways or their projection site, the median eminence in the hypothalamus, prevents the occurrence of spasm. A unilateral postganglionic trigeminal lesion causes an ipsilateral constriction of the cerebral arteries while a preganglionic lesion does not affect the baseline arterial diameter. Both kinds of trigeminal lesions induce a global increase in glucose uptake of about 50% without influencing CBF. Following subarachnoid hemorrhage (SAH) the decrease in CBF in both groups of lesioned animals is similar to that seen in controls. After SAH there is no further change in CMRglu in the animals with a preganglionic lesion, while in the postganglionically lesioned animals there is an additional increase in CMRglu of about 50% as compared to controls or animals with a preganglionic lesion. Treatment with the peptidergic substance P (SP) antagonist, spantide, or gammaglobulin against SP prevents or significantly reduces the degree of spasm and the changes in flow and metabolism normally seen post-SAH. The non-peptidergic neurokinins NK1 and NK3 antagonists do not influence flow and metabolism in SAH animals. The NK2 seems to change both flow and metabolism post-SAH in rats.

Effect of deferoxamine and sympathectomy on vasospasm following subarachnoid hemorrhage.

We examined the effects of subarachnoid hemorrhage (SAH) and treatment with deferoxamine (DFO) or sympathectomy on vascular smooth muscle function, as well as the underlying mechanisms involved, by recording the responses to nor-adrenaline and serotonin in isolated carotid arteries in vitro. All studies were performed before and 7 days after SAH. An experimental subarachnoid hemorrhage model was created in rabbits by injecting autologous arterial blood into the subarachnoid space of the rabbits via cisterna magna punction. During the chronic stage of vasospasm following SAH deferoxamine (DFO) was given to the animals and cervical and periarterial sympathectomy was performed in the other groups of animals. In isolated carotid arteries noradrenaline (10(-8) to 10(-4) mol/l) and serotonin (10(-8) to 10(-4) mol/l) produced concentration-dependent contractions. These contractile responses were significantly enhanced in animals 7 days after SAH compared to controls and did not return to control values in carotid arteries obtained from animals treated with DFO or sympathectomy for 7 days after SAH. These results show that SAH causes supersensitivity in the carotid as well as cerebral arteries during the first week after SAH and could contribute to the development of cerebral vasospasm. Both treatment with DFO and sympathectomy after SAH did not reduce the contractile responses to noradrenaline and serotonin in the carotid arteries. In conclusion, treatment with DFO or sympathectomy during the chronic stage of vasospasm after SAH did not affect the vascular responses of the extradural part of the carotid artery to vasoactive substances.

Altered endothelium-mediated relaxation by sympathectomy in isolated rabbit carotid artery rings.

The influence of cervical and periarterial sympathectomy on endothelium-dependent and endothelium-independent relaxations of the mature rabbit carotid artery was studied in vitro. The responses to adenosine, vasoactive intestinal polypeptide and substance P in sympathectomized and control rabbit carotid artery rings were recorded and analyzed. The effects of endothelium removal were also investigated. The maximal relaxation achieved by substance P, which produces endothelium-dependent relaxation, was significantly inhibited in 3 weeks in postsympathectomy arterial preparations as compared to controls. Adenosine and vasoactive intestinal polypeptide, which produce endothelium-independent relaxation, elicited similar relaxation in all tissues. These results demonstrated that the response to substance P was impaired by cervical and periarterial sympathectomy. The decreased maximum response to substance P may be the result of a decreased NK-1 receptor subtype density or excitation/response coupling, or it may be due to an impaired production and/or liberation of endothelium-derived relaxing factor (EDRF).

The effect of deferoxamine on brain lipid peroxide levels and Na-K ATPase activity following experimental subarachnoid hemorrhage.

1. In the present study we have studied the effects of deferoxamine treatment on lipid peroxidation and Na-K ATPase activity after experimental induction of subarachnoid haemorrhage (SAH) in guinea pigs. 2. We assessed the extent of lipid peroxidation by measuring the level of malondialdehyde and Na-K ATPase activity in 3 different groups (sham-operated, SAH, SAH + deferoxamine). 3. There was no significant difference in lipid peroxide content between sham-operated and haemorrhagic animals, but Na-K ATPase activity decreased after SAH. 4. Deferoxamine treatment reduced the malondialdehyde content and induced the recovery of Na-K ATPase activity, exerting a brain protective role against the detrimental effects of the haemorrhage.

Pharmacologic response of endothelium to microvascular temporary clip application.

To assess the effects of microvascular temporary clip application on vessel relaxing capability and endothelial substance release, the carotid rings of rats clipped for various durations were studied via bioassay. Noradrenaline and phenylephrine produced an immediate contraction and subsequent relaxation that failed to be suppressed by lysine acetylsalicylate or nicotine in the controls and in the arteries clipped for 0.5, 1, and 5 minutes; however, this relaxation was greatly reduced when the duration was 10 minutes. The results suggest the possible role of inadequate endothelium-derived relaxing factor release following prolonged application of the clips.

Spinal cord compression due to Brucella granuloma.

Central Nervous System (CNS) involvement during the course of Brucella infection is a rare clinical condition. In this article, a patient with a progressive paraparesis syndrome with spasticity, who was treated by medical methods and surgical intervention is analysed. This patient suffered from spinal cord compression in the thoracal region caused by a Brucella granuloma. The patient had no evidence of systemic Brucella infection.