Spinal genesis of Mayer waves.

Variability in cardiovascular spectra was first described by Stephan Hales in 1733. Traube and Hering initially noted respirophasic variation of the arterial pressure waveform in 1865 and Sigmund Mayer noted a lower frequency oscillation of the same in anesthetized rabbits in 1876. Very low frequency oscillations were noted by Barcroft and Nisimaru in 1932, likely representing vasogenic autorhythmicity. While the origins of Traube Hering and very low frequency oscillatory variability in cardiovascular spectra are well described, genesis mechanisms and functional significance of Mayer waves remain in controversy. Various theories have posited baroreflex and central supraspinal mechanisms for genesis of Mayer waves. Several studies have demonstrated the persistence of Mayer waves following high cervical transection, indicating a spinal capacity for genesis of these oscillations. We suggest a general tendency for central sympathetic neurons to oscillate at the Mayer wave frequency, the presence of multiple Mayer wave oscillators throughout the brainstem and spinal cord, and possible contemporaneous genesis by baroreflex and vasomotor mechanisms.

WITHDRAWN: Multimodal treatment and microsurgical resection of basal ganglionic and thalamic arteriovenous malformations.

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WITHDRAWN: Hybrid surgical endovascular theatres in the treatment of arteriovenous malformations.

This article has been withdrawn at the request of the author(s) and/or editor. The Publisher apologizes for any inconvenience this may cause. The full Elsevier Policy on Article Withdrawal can be found at https://www.elsevier.com/about/our-business/policies/article-withdrawal.

Intracranial Venous Hypertension in Craniosynostosis: Mechanistic Underpinnings and Therapeutic Implications.

Patients with complex, multisutural, and syndromic craniosynostosis (CSO) frequently exhibit intracranial hypertension. The intracranial hypertension cannot be entirely attributed to the craniocephalic disproportion with calvarial restriction because cranial vault expansion has not consistently alleviated elevated intracranial pressure. Evidence has most strongly supported a multifactorial interaction, including venous hypertension along with other pathogenic processes. Patients with CSO exhibit marked venous anomalies, including stenosis of the jugular-sigmoid complex, transverse sinuses, and extensive transosseous venous collaterals. These abnormal intracranial-extracranial occipital venous collaterals might represent anomalous development, with persistence and subsequent enlargement of channels normally present in the fetus, either as a primary defect or as nonregression in response to failure of the development of the jugular-sigmoid complexes. It has been suggested by some investigators that venous hypertension in patients with CSO could be treated directly via jugular foraminoplasty, venous stenting, or jugular venous bypass, although these options are not in common clinical practice. Obstructive sleep apnea, occurring as a consequence of midface hypoplasia, can also contribute to intracranial hypertension in patients with syndromic CSO. Thus, correction of facial deformities, as well as posterior fossa decompression, could also play important roles in the treatment of intracranial hypertension. Determining the precise mechanistic underpinnings underlying intracranial hypertension in any given patient with CSO requires individualized evaluation and management.

Intracavernous internal carotid artery mycotic aneurysms: comprehensive review and evaluation of the role of endovascular treatment.

Mycotic aneurysms may arise in the setting of many local or systemic infections. Those of the intracranial circulation are especially worrisome due to their potential to compress vital neural structures and their propensity for rupture with consequent hemorrhage. Mycotic aneurysms of the intracavernous internal carotid artery (ICA) represent an exceedingly rare clinical entity, described in less than fifty published cases. Typically presenting as a cavernous sinus syndrome with signs and symptoms of the underlying infection, they are often missed initially, with diagnosis and treatment commencing for the triggering infection or confused with cavernous sinus thrombophlebitis, which may be additionally coexistent, confounding timely diagnosis of the aneurysmal disease. Compared to non-mycotic aneurysms of the intracavernous ICA, which typically have a benign course, the infectious etiology of the mycotic variety increases their tendency to rupture, precludes surgical clipping as a viable treatment option, and requires institution of prolonged antibiotic therapy prior to definitive intervention. Their critical location, friability, and propensity to occur bilaterally result in an unpredictable risk of rapid neurological decline and death, making the timing and specific nature of treatment a unique dilemma facing the treating physician. This review seeks to discuss the natural history of and management strategies for mycotic aneurysms of the intracavernous ICA with special emphasis on the role, safety, and efficacy of endovascular therapies.