Cranial nerve deficits in giant cavernous carotid aneurysms and their relation to aneurysm morphology and location.

BACKGROUND: Giant cavernous carotid aneurysms (GCCAs) usually exert substantial mass effect on adjacent intracavernous cranial nerves. Since predictors of cranial nerve deficits (CNDs) in patients with GCCA are unknown, we designed a study to identify associations between CND and GCCA morphology and the location of mass effect. METHODS: This study was based on data from the prospective clinical and imaging databases of the Giant Intracranial Aneurysm Registry. We used magnetic resonance imaging and digital subtraction angiography to examine GCCA volume, presence of partial thrombosis (PT), GCCA origins, and the location of mass effect. We also documented whether CND was present. RESULTS: We included 36 GCCA in 34 patients, which had been entered into the registry by eight participating centers between January 2009 and March 2016. The prevalence of CND was 69.4%, with one CND in 41.7% and more than one in 27.5%. The prevalence of PT was 33.3%. The aneurysm origin was most frequently located at the anterior genu (52.8%). The prevalence of CND did not differ between aneurysm origins (p = 0.29). Intracavernous mass effect was lateral in 58.3%, mixed medial/lateral in 27.8%, and purely medial in 13.9%. CND occurred significantly more often in GCCA with lateral (81.0%) or mixed medial/lateral (70.0%) mass effect than in GCCA with medial mass effect (20.0%; p = 0.03). After adjusting our data for the effects of the location of mass effect, we found no association between the prevalence of CND and aneurysm volume (odds ratio (OR) 1.30 (0.98-1.71); p = 0.07), the occurrence of PT (OR 0.64 (0.07-5.73); p = 0.69), or patient age (OR 1.02 (95% CI 0.95-1.09); p = 0.59). CONCLUSIONS: Distinguishing between medial versus lateral location of mass effect may be more helpful than measuring aneurysm volumes or examining aneurysm thrombosis in understanding why some patients with GCCA present with CND while others do not. CLINICAL TRIAL REGISTRATION NO: NCT02066493 ( clinicaltrials.gov ).

Anterior clinoidectomy.

BACKGROUND: The optic nerve within the optic canal, the parophthalmic segment of the carotid artery, and the oculomotor nerve in the superior orbital fissure all lay against the anterior clinoid process. Bone resection uncovers these structures. METHOD: For extradural resection of the anterior clinoid process and surrounding bone, two key steps are recommended: bony opening of the superior orbital fissure, and transection of the orbitotemporal periosteal fold. CONCLUSION: Anterior clinoidectomy is technically challenging. Following a sequence of surgical steps to expose clearly-defined surgical landmarks helps to make this procedure simple and safe. KEY POINTS: • Pterional craniotomy • Complete extradural anterior clinoidectomy • Slit dura (3 mm) to drain cerebrospinal fluid • Peel dura from orbital roof and lateral wall • Bony opening of superior orbital fissure to use it as surgical corridor • Drilling of optic canal • Transection of orbitotemporal periosteal fold • Hollow anterior clinoid process and piece-meal resection • Transection of falciforme ligament to free optic nerve • Replace falciforme ligament by extradural free pericranial flap.

Basilar artery perforator aneurysms: Report of 9 cases and review of the literature.

Basilar perforator artery aneurysms (BAPA's) are an under-recognised cause of sub-arachnoid haemorrhage (SAH). We present our single centre experience of BAPA's and review of the literature. We performed a retrospective review of our prospectively maintained database to identify all BAPA's that presented acute SAH between February 2009 and February 2018. We identified 9 patients (male = 7), each with a single aneurysm, and average age 55 ±â€¯9.7 years. All aneurysms were small, 2.1 ±â€¯0.5 mm (range 1-3 mm). Three aneurysms were not detected on initial angiography. Six aneurysms were treated with flow diversion, 3 were managed conservatively. No repeat haemorrhage occurred in the flow diverted patients. One patient treated conservatively suffered a repeat haemorrhage and died (mRS 6). Follow up imaging (n = 7), at average 5.6 months (range 3-12 months), showed complete occlusion in all the flow-diverted aneurysms and no change in one conservatively managed patient. There was no evidence of perforator infarction on the follow-up post treatment imaging. Clinical follow-up data was available in 8 patients, 6 of whom (75%) had a good outcome (mRS ≤ 2). A high index of suspicion is required to diagnose BAPA. Flow diversion can be used to treat BAPA's with acceptable risk of perforator infarction and low risk of repeat haemorrhage.

Accuracy of CT-navigated pedicle screw positioning in the cervical and upper thoracic region with and without prior anterior surgery and ventral plating.

AIMS: We aimed to retrospectively assess the accuracy and safety of CT navigated pedicle screws and to compare accuracy in the cervical and thoracic spine (C2-T8) with (COMB) and without (POST) prior anterior surgery (anterior cervical discectomy or corpectomy and fusion with ventral plating: ACDF/ACCF). PATIENTS AND METHODS: A total of 592 pedicle screws, which were used in 107 consecutively operated patients (210 COMB, 382 POST), were analysed. The accuracy of positioning was determined according to the classification of Gertzbein and Robbins on post-operative CT scans. RESULTS: High accuracy was achieved in 524 screws (88.5%), 192 (87.7%) in the cervical spine and 332 (89%) in the thoracic spine, respectively. The results in the two surgical groups were compared and a logistic regression mixed model was performed to analyse the risk of low accuracy. Significantly lower accuracy was found in the COMB group with 82.9% versus 91.6% in the POST group (p = 0.036). There were no neurological complications, but two vertebral artery lesions were recorded. Three patients underwent revision surgery for malpositioning of a screw. Although the risk of malpositioning of a screw after primary anterior surgery was estimated to be 2.4-times higher than with posterior surgery alone, the overall rates of complication and revision were low. CONCLUSION: We therefore conclude that CT navigated pedicle screws can be positioned safely although greater caution must be taken in patients who have previously undergone anterior surgery. Cite this article: Bone Joint J 2017;99-B:1373-80.

Leukocyte-endothelium interactions in pial venules during the early and late reperfusion period after global cerebral ischemia in gerbils.

The contribution of leukocytes to secondary brain damage after cerebral ischemia is still under discussion. The purpose of the present study was to examine the pial microcirculation after global cerebral ischemia while focusing on leukocyte-endothelium interactions during the early and late reperfusion period of up to 4 days. A closed cranial window technique that leaves the dura mater intact was used. Global cerebral ischemia of 15 minutes' duration was induced in male Mongolian gerbils (n = 91). Pial microcirculation was observed by intravital fluorescence microscopy. Leukocyte-endothelium interactions (LEIs) in pial venules, vessel diameters, capillary density, and regional microvascular blood flow measured by laser Doppler flowmetry were quantified during 3 hours of reperfusion and in intervals up to 4 days after ischemia. Within 3 hours of reperfusion, the number of leukocytes (cells/100 microm x minute) rolling along or adhering to the venular endothelium increased from 0.1 +/- 0.2 to 28.4 +/- 17.4 (P < 0.01 vs. control) and from 0.2 +/- 0.2 to 4.0 +/- 3.8 (P < 0.05), respectively. There was no capillary plugging by leukocytes; capillary density remained unchanged. In the late reperfusion period, at 7 hours after ischemia, LEIs had returned to baseline values. Furthermore, from 12 hours to 4 days after ischemia, no LEIs were observed. Changes in regional microvascular blood flow did not correlate with LEIs. Global cerebral ischemia of 15 minutes' duration induces transient LEIs that reach a maximum within 3 hours of reperfusion and return to baseline at 7 hours after ischemia. LEIs are not related to changes in microvascular perfusion, which suggests mainly that the expression of adhesion receptors is necessary to induce LEIs rather than rheologic factors. It seems unlikely that this short-lasting activation of leukocytes can play a role in the development of secondary brain damage.

Influence of the bradykinin B1/B2-receptor-antagonist B 9430 on the cerebral microcirculation and outcome of gerbils from global cerebral ischemia.

The influence of the bradykinin B1/B2 antagonist B 9430 on the cerebral microcirculation following global cerebral ischemia was investigated in a closed cranial window preparation in Mongolian gerbils by intravital fluorescence microscopy. Global cerebral ischemia (GCI) was induced by occlusion of both common carotid arteries for 15 min. Leukocyte-endothelium interactions, vessel diameters, and the segmental microvascular blood flow were observed by intravital microscopy before and up to three hours after global cerebral ischemia. Following the early reperfusion period the animals survived up to 4 days after ischemia. The neurological deficit and the body weight were assessed daily. On day 4 animals were subjected to perfusion fixation and the brain was removed. Nerve cell damage from ischemia was quantified histologically in cortex, hippocampus, and striatum. Animals with treatment received the bradykinin B1/B2 receptor antagonist B 9430 before (i.v.), during, and after ischemia (s.c.) until the end of the experiment. The frequency of leukocytes (cells/100 microns x min) rolling along the venular endothelium post ischemia was significantly decreased (p < 0.05) in treated animals as compared to untreated controls (33.0 +/- 6.2 vs. 8.5 +/- 2.3) as well as the number of leukocytes attached to the endothelial surface (7.2 +/- 3.0 vs. 2.0 +/- 1.0, n.s.). The neuroscore on day 4 (pre-ischemic control: 22 points) was reduced to 13.4 +/- 3.2 in untreated animals, while to 4.7 +/- 3.2 points in the treatment group. No differences between animals with and without treatment were found as to the number of viable neurons. Although bradykinin is released in the brain during global cerebral ischemia, its antagonisation does not improve outcome despite the effective inhibition of leukocyte-endothelium interactions.

Leukocyte-endothelium interactions in global cerebral ischemia.

A closed cranial window was implanted in male Mongolian Gerbils to investigate leukocyte-endothelium interactions (LEI) at the brain surface in global cerebral ischemia (GCI) by intravital fluorescence microscopy. Four days after 15 min of bilateral common carotid artery occlusion the ischemic tissue damage was histologically analysed in selectively vulnerable areas of the brain. The frequency of Rhodamine 6G labeled leukocytes rolling along ("roller") and firmly attached ("sticker") to postcapillary endothelium was assessed before and up to 180 min after GCI. As compared to the sham operated control animals induction of LEI was found in animals with GCI, following a steady increase up to a significant level attained at 60 min (rollers) or at 120 min of reperfusion (sticker), respectively (p < 0.05). In animals with cerebral ischemia histological assessment revealed a significant decrease of viable neurons in the CA1-sector of hippocampus (neurons/mm2 +/- SEM: 1308 +/- 71 vs. 829 +/- 106), in parietal neocortex (727 +/- 17 vs. 542 +/- 49), and in striatum (547 +/- 26 vs. 352 +/- 49; p < 0.01), respectively. A significant correlation between the extent of irreversible neuronal damage and the frequency of leukocyte adherence to the endothelium could not be established. Nevertheless a direct correlation between the number of surviving neurons and of rolling leukocytes was observed, which may be suggestive of a protective potential of leukocyte rolling.

Late bacterial granuloma at an intrathecal drug delivery catheter.

In the case reported, neurological complaints were pain and dysaesthesiae in the lower back and thigh, as well as paresis of the ileopsoas muscle. MRI of the lumbar spine showed an intradural-extramedullary mass at the level of L1 homogeneously enhancing with gadolinium. This mass was situated at the tip of an intrathecal catheter implanted 11 years before for a morphine trial infusion as therapy for phantom pain after amputation of the right arm. Now, removal of the catheter was performed. Cultures of lumbar CSF and the catheter tip demonstrated coagulase negative staphylococcus. Antibiotic medication with cephalosporines was given for 6 weeks. After removal of the catheter, the patient was free of pain and he progressively regained full neurological function. Although most catheter-associated granulomas reported so far were sterile in nature, bacterial infection should still be considered even years after catheter placement.