Vascular Compression Of Cranial Nerves Research Articles

Microvascular compression of the vestibulocochlear nerve

PURPOSE Vascular compression of cranial nerves has been widely accepted as a cause for trigeminal neuralgia and hemifacial spasm. In contrast, vascular compression of the vestibulocochlear nerve remains controversial. METHOD A comprehensive literature review including 175 articles between 1960 and 2020 was performed in an attempt to summarise the published hypotheses of the pathophysiological mechanisms of vascular compression of the vestibulocochlear nerve and their management strategies. RESULTS Vascular loops in the cerebellopontine angle (CPA) and internal auditory meatus (IAM) are very common and should be regarded primarily as a normal variant. Advances in anatomical understanding with the development of models for the tonotopy of the vestibulocochlear nerve help explain the complexity of symptoms created by possible neurovascular interaction. CONCLUSION Widely accepted, validated and sensitive diagnostic criteria and outcome measures need to be established in order to evaluate the role of surgery in vestibulocochlear nerve vascular compression.

Microvascular transposition using Teflon sling technique

Microvascular decompression is a well-established technique used to relieve abnormal vascular compression of cranial nerves and associated pain. Here the authors describe three cases in which a sling technique was used in the treatment of cranial nerve pain syndromes: trigeminal neuralgia with predominant V2 distribution, hemifacial spasm, and geniculate neuralgia and right-sided ear pain. In each case, the artery was mobilized from the nerve and tethered with a sling. All three patients had reduction of symptoms within 6 weeks.The video can be found here: https://youtu.be/iM7gukvPz6E

Cranial Nerves Compression Syndromes

Definition: Vascular compression of cranial nerves has been related to disorders such as trigeminal neuralgia, glossopharyngeal neuralgia, hemifacial spasm, disabling positional vertigo, geniculate neuralgia, spasmodic torticollis, cyclic oculomotor spasm, superior oblique myokymia, and arterial hypertension.

Neurovascular Compression Syndromes

Neurovascular compression syndromes are a group of pathological conditions caused by vascular compression of cranial nerves in the cerebellopontine angle. These syndromes include trigeminal neuralgia, hemifacial spasm, disabling positional vertigo, tinnitus, and glossopharyngeal neuralgia.

Neurovascular Compression Syndromes

Neurovascular compression syndromes are a group of pathological conditions caused by vascular compression of cranial nerves in the cerebellopontine angle. These syndromes include trigeminal neuralgia, hemifacial spasm, disabling positional vertigo, tinnitus, and glossopharyngeal neuralgia. Historical Background: In 1773, Fothergill gave a clear description of trigeminal neuralgia while in 1888 Gowers described hemifacial spasm as a disease entity. In the 1930s Dandy first observed abnormal contacts between vessels and the trigeminal nerve in patients suffering from trigeminal neuralgia. In the 1940s, Sunderland observed abnormal neurovascular relationships in the brains of elderly cadavers. In the 1960s Gardner performed vascular decompression in patients with hemifacial spasm and trigeminal neuralgia. In the 1970s and in the 1980s, Jannetta and Moller greatly contributed to clarifying the concept of neurovascular compression and to developing definitive microsurgical procedures aimed at treating these symptoms. Surgery: Microvascular decompression is a surgical procedure used to separate the offending vessel(s) from the affected cranial nerve. Usually, a piece of Teflon is placed between the blood vessel and the nerve to prevent recontact. Treatment of vascular compression syndromes by microvascular decompression is effective with a consistently high cure rate. In Parma and in Marseille the decompression was performed via a minimally invasive retrosigmoid approach in the majority of cases. The use of the endoscope (Magnan, 1993) allows a safe and reliable identification of the offending vessel(s) and confirms the correct position of Teflon before closure. The enlarged middle cranial fossa approach was used in Parma to treat hemifacial spasm. A chemical product called mesna facilitates elevation of the compressing vascular loop from the affected cranial nerve. To perform the so-called “chemically assisted dissection” (CADISS®) we use the common mechanical instruments opportunely modified in order to deliver the mesna solution on the tip of the instruments and, therefore, directly in contact with the tissues to be detached, thus reducing its inappropriate diffusion. The authors will present the surgical technique of microvascular decompression and the results obtained in 500 decompression procedures.

Tic convulsivo doloroso y toxina botulínica

Painful tic convulsif is a rare disorder that associates trigeminal neuralgia (TN) and ipsilateral hemifacial spasm (HFS). These two disorders are the most common examples of hyperactive cranial rhizopathy and are frequently caused by vascular compression of these cranial nerves at the nerve root entry and exit zone in the brain stem, which leads to paroxysmal ephaptic transmission.We report the cases of four patients with combined TN and HFS out of a total of 247 patients with HFS who were treated with botulinum toxin. One patient had TN that was contralateral to the HFS, while the other three were ipsilateral, and one of these had bilateral HFS. In all four cases both the HFS and the TN improved with botulinum toxin treatment.These four patients with TN and HFS suggest a common aetiology for the two disorders, due either to central neuronal hyperactivity or to vascular compression of several cranial nerves. The beneficial effect of botulinum toxin in both disorders supports the idea of this toxin having a central mechanism of action that acts by controlling neuronal hyperactivity in the brain stem, as well as its peripheral action.

Concomitant Ectatic Posterior Communicating Artery and Tentorial Meningioma as a Source of Oculomotor Palsy: Case Report

Although non-aneurysmal vascular compression of the oculomotor nerve is rare, it should be considered in the evaluation of unilateral oculomotor palsy. A 36-year-old non-diabetic man presented with two months of intermittent retro-orbital headache and third nerve paresis caused by compression of the oculomotor nerve between an ectatic, atherosclerotic posterior communicating artery (PComA) and a small tentorial meningioma. At operation, the subarachnoid portion of the nerve, prevented from migrating posteriorly and laterally by the meningioma, was grooved by the apex of the artery's loop. Microvascular decompression (MVD) of the artery loop from the nerve and resection of the meningioma were performed. Postoperatively, the patient's retro-orbital headache and oculomotor paresis, with the exception of mild anisocoria, resolved. Tumor infiltrating the posterior tentorium and lateral cavernous sinus was treated by Cyberknife radiosurgery five months later. One year after surgery, the patient had improvement in his headaches, full extra-ocular movements, and minimal residual anisocoria. Only one other report describes MVD of the third nerve from PComA compression. A review is presented of MVD carried out for similar cases of non-aneurysmal vascular compression of the oculomotor nerve. By analogy from cases in which an aneurysm is the compressing vascular structure, prompt surgical treatment is advocated. Complete evaluation of an isolated third nerve palsy should include MRI sequences designed to detect vascular compression of cranial nerves.

Vascular compression of cranial nerves: II: Pathophysiology

The pathophysiology of trigeminal neuralgia, hemifacial spasm and other disorders that can be cured by microvascular decompression of cranial nerves, is reviewed and different hypotheses about its pathophysiology are discussed. It is found that the pathophysiology of these disorders is complex and other factors than vascular compression are necessary to cause symptoms. While the efficacy of the microvascular decompression (MVD) operation is indisputable, it is questionable if the symptoms and signs of these disorders are caused by abnormal neural activity in the respective cranial nerves that result from the compression from a blood vessel. Instead, studies point to hyperactivity and hyperexcitability of the respective nuclei as a cause of the symptoms and signs of these disorders. Results of several studies indicate that irritation of the cranial nerve in question from close contact with a blood vessel may promote such development, and it seems necessary that other factors in addition to the vascular contact must be present in order that such a condition develops. [Neurol Res 1999; 21: 439–443]

Vascular compression of cranial nerves. I. History of the microvascular decompression operation

The development of the microvascular decompression (MVO) operation is reviewed. It is stressed that a few innovative neurosurgeons discovered the role of vascular compression of cranial nerves V and VII in trigeminal neuralgia (TGN) and hemifacial spasm (HFS) and developed an operation, later to be known as the 0VO operation. While the understanding of the pathophysiology. of these disorders has improvedl the surgIcal procedure has undergone little change since Gardner described the operation about 1960. [Neural Res 1998; 20: 727–731]

Responses from the exposed human auditory nerve to pseudorandom noise

Whole-nerve responses to lowpass-filtered noise (2.5 kHz) and broadband click stimuli were recorded from the exposed intracranial portion of the eighth nerve in patients with normal hearing who were undergoing neurosurgical operations to relieve vascular compression of cranial nerves V, VII, and VIII. Cross-correlograms between the response and the noise showed a large degree of individual variation. When noise of 95 dB SPL was used, the correlograms in some patients had a large peak that represented a positive correlation between a negative nerve potential and the rarefaction phase of the sound and that peak could usually be identified at a delay that was close to the latency of the main negative peak in the response to high-intensity broadband click sounds (3.0–3.5 ms). The amplitude of these components decreased when the sound intensity was decreased, and, at stimulus intensities below 80 dB, the correlograms became dominated by components at longer delays. In other patients, peaks of a similar amplitude appeared in the cross-correlograms between delays of 2 and 12 ms in the entire range of sound intensities that were studied (65–105 dB SPL). In all patients the location of the peaks was little affected by the stimulus intensity in the range studied. All reproducible peaks that appeared at delays longer than 2.8 ms shifted towards longer delays when the recording electrode was moved from a location near the porus acusticus to a more central location (near the brainstem) on the exposed intracranial portion of the eighth nerve, indicating that components at longer delays than 2.8 ms result from propagated neural activity in the auditory nerve. It is assumed on the basis of the results that these correlograms are measures of phase-locking of neural activity to a complex stimulus sound (noise).

Mechanism of vascular compression of cranial nerves - - role of changes of vertebro-basilar vasculatures (author's transl)

Pathogenesis of hemifacial spasms is still obscure. To elucidate the etiology, 61 patients with this clinical syndrome were closely examined. Surgical findings of all patients and vertebral arteriograms of 51 patients disclosed characteristic changes of the vertebro-basilar artery system and its branches. The vertebral artery was invariably larger in diameter ipsilaterally to the affected side of the face, made a sharp or hair-pin like angulation at the origin of the third segment of the vertebral artery and gave off branches almost rectangularly from the top of this angulated part toward the internal auditory meatus. On the other hand, the S-shaped basilar artery with the abovementioned asymmetrical changes in diameter of the vertebral arteries gave off the anterior inferior cerebellar artery toward the internal auditory canal of the affected side with an absent or hypoplastic posterior inferior cerebellar artery. Operative procedures demonstrated that the facial nerve was invariably compressed by an ectated or radundant artery which showed right turn and local “arteriosclerotic” changes at its cross-compressing site. The peculiar vasculature changes of the vertebro-basilar artery and the compressing artery may be congenitally present, and subsequently, an exaggerated intraluminal blood stream or pressure of the larger sized vertebral artery is likely to apply a stronger hemodynamic force to the wall of the angulated part of the vertebral artery, resulting in ectasia or redundancy of the peripheral branches originating from this point and also wall thickening of the right-angled part of the compressing artery which just happens to lie close enough to the exit zone of the facial nerve from the brain-stem. These vasculature findings appear to provide an important key to solve the problem of why a certain artery can cross-compress the facial nerve and why the vast majority of hemifacial spasms develop on one side of the face.