The incidence of anatomic variations of the vertebral artery V2 segment is high. Potentially dangerous conditions can be detected on preoperative imaging.
Pathophysiological processes following subarachnoid hemorrhage (SAH) present survivors of the initial bleeding with a high risk of morbidity and mortality during the course of the disease. As angiographic vasospasm is strongly associated with delayed cerebral ischemia (DCI) and clinical outcome, clinical trials in the last few decades focused on prevention of these angiographic spasms. Despite all efforts, no new pharmacological agents have shown to improve patient outcome. As such, it has become clear that our understanding of the pathophysiology of SAH is incomplete and we need to reevaluate our concepts on the complex pathophysiological process following SAH. Angiographic vasospasm is probably important. However, a unifying theory for the pathophysiological changes following SAH has yet not been described. Some of these changes may be causally connected or present themselves as an epiphenomenon of an associated process. A causal connection between DCI and early brain injury (EBI) would mean that future therapies should address EBI more specifically. If the mechanisms following SAH display no causal pathophysiological connection but are rather evoked by the subarachnoid blood and its degradation production, multiple treatment strategies addressing the different pathophysiological mechanisms are required. The discrepancy between experimental and clinical SAH could be one reason for unsuccessful translational results.
Bow hunter's syndrome (BHS) is defined as symptomatic, vertebro-basilar insufficiency caused by mechanical occlusion of the vertebral artery (VA) at the atlanto-axial level during head rotation. In the literature, about 40 cases have been reported. However, due to the rarity of this pathology, there are no guidelines for diagnosis and treatment. Conservative, surgical, and endovascular concepts have been proposed. In order to work out an algorithm, we performed a systematic review of the literature and a retrospective analysis of patients, which have been treated in our institutions over the last decade. The clinical series was comprised of five patients. The symptoms ranged from transient vertigo to posterior circulation stroke. Diagnosis was established by dynamic angiography. In all patients, the VA was decompressed; one patient required additional fusion. The clinical and radiological results were good, and the treatment-related morbidity was low. The literature review demonstrated that Bow hunter's syndrome is a rare pathology but associated with a pathognomonic and serious clinical presentation. The gold standard of diagnosis is dynamic angiography, and patients were well managed with tailored vertebral artery decompression. By this management, clinical and radiological results were excellent and the treatment-related morbidity was low.
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OBJECTIVE:
We describe our surgical technique of exposure, control, and transposition of the third segment of the vertebral artery (VA V3 segment).
METHODS:
The VA V3 segment extends from the C2 transverse foramen to the dura mater of the foramen magnum. It initially courses vertically between the C2 and C1 transverse foramens, then runs horizontally over the atlas groove, and finally obliquely upwards before piercing the dura mater. Exposure of the VA V3 segment through an antero-lateral approach is performed by passing medially to the ster-nomastoid muscle. After exposure and protection of the spinal accessory nerve, the C1 transverse process is identified below and in front of the mastoid tip. The small muscles that insert on it are cut to expose the C1-C2 portion. The inferior aspect of the horizontal portion is safely separated from the atlas groove by elevating the subperiosteal plane and the superior aspect is freed by a cut a few millimeters above the VA on the occipital condyle. Complete unroofing of the C1 transverse foramen is achieved by resecting the bone while leaving intact the subperiosteal plane. The VA then can be transposed. Venous bleedings during the dissection from periosteal sheath tearing can be controlled by direct bipolar coagulation.
RESULTS:
The control of the VA V3 segment is essentially used for lesions in the VA vicinity and to improve the surgical exposure at the craniocervical junction level. Indications therefore are tumoral removal, VA decompression, and rarely, nowadays, VA revascularization.
CONCLUSION:
Perfect knowledge of the anatomy and the surgical technique permits a safe exposure, control, and transposition of the VA V3 segment. This is the first step of many surgical procedures.
Augmentation of pedicle screws in general significantly increased the number of load cycles and failure load comparing to the nonaugmented control group. For the augmentation technique (cement first, in situ augmented, percutaneously application) no effect could be exhibited on the failure of the pedicle screws. By the cranio-caudal cyclic loading failure of the pedicle screws occurred by screw cut through the superior endplate and the characteristic "windshield-wiper effect", typically observed in clinical practice, could be reproduced.
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