Year XVII n. 4/01






Angelo Gandolfi




The dysfunction syndromes of the cranial nerves are, in the vast majority of cases, due to a vascular compression of the involved nerve, usually at the root entry/exit zone of the nerve itself at the brainstem (R.E.Z.).

The pulsatile compression may also be caused by a vein or by an association of an artery and a vein. In recent decades, microvascular decompression procedures have been perfectioned, allowing the microneurosurgeon to detach the vessel away fron the nerve, thus eliminating the pathological contact. The cure rate of these operative approaches, always performed using the operating microscope, varies, depending from duration of symptoms, previous destructive procedures carried out on the neural structures and from nature of different nerves, being possible in some cases to greatly alleviate symptomatology but not to abolish it completely. The most fascinating results are obtained in decompressing the Trigeminal Nerve in cases of tic doloureux, the Facial Nerve in cases of hemifacial spam (HFS) and the Vestibulo-Cochlear nerve in cases of vertigo associated with tinnitus (noise) in the ear. A full description of each vascular compression syndrome, symptomatology and surgical repair methodology is exposed in details, including the more uncommon vascular compressions such as those causing neurogenic arterial hypertension, spasmodic torticollis and oculogyric crises with paresis.

Symptoms of cranial nerves compression syndromes can be considered as “caricatures” and exagerated expression of a given cranial nerves physiological function.

The involved nerves are sequentially distributed in the cerebello-pontine angle (CPA), that is the recess in-between the pons and cerebellum, located in the Posterior Cranial Fossa, on both side of brainstem. The primary causative factor of these exagerated symptoms has found correct interpretation in the last three decades, especially after the widespread introduction of the operating microscope.

This tool has confirmed the existence of abnormal relationships between nerves and vessels in their respective arachnoid cysterns.

The sound demostration of this anatomical condition, has allowed the refinement of microneurotherapeutic methods apt to alleviate the conflictual situation between nerves and vessels, thus bringing effective cure to a series of invalidating clinical symptoms. The most important and well studied among these symptoms, curable using the neurovascular decompression procedure (NVD), are:


- the typical Trigeminal Neuralgia (Tic douloreux);


- the involuntary tonico-clonic contractions of one side of the face, called Hemifacial Spasm (HFS);


- Tinnitus aurium, which means a persistent, annoyng and at times unbearable noise in the ear, usually associated with Vertigo;


- Glossopharyngeal Neuralgia, that is pain in the region of the tonsilla palatina and deep in the troath on one side; - the Disabling Positional vertigo(DPV);


- the Spasmodic Torticollis;


- cases of so called Neurogenic Hypertension;


- the Cyclic Oculomotor Spasm with paresis.


The concept of neurovascular compression The binding substrate that links togheter these disturbances of neural function (causing hyperactive - hypoactive symptoms and signs), in term of primary causative factor for all of them, is the presence of a contact, abnormal with respect to its anatomical position and mechanical effects, between the emergence of the respective cranial nerve from the surface of the brainstem (Root Entry-Exit Zone, R.E.Z.) and a specific vascular structure, either arterial or venous in nature.

This abnormal contact can be described in terms of Cross Compression, a vascular-nerve cross compression, i.e. a mechanical compression of one element against the other or even a sandwich compression, that is “entrapment” of the nerve in between two vascular structures.

The vessels are mainly situated at the level of the R.E.Z., made-up of central myelin around the axons, called oligodendroglial myelin.

This myielin not only isolates the axis cylinders but allows correct transmission of neural impulses.

A short description of the brainstem is given at this point: it is made up of the mesencephalon, pons and medulla oblongata; it lies at the midline of the posterior fossa and from its lateral sides the various cranial nerves exit, if motor in nature (to reach the respective end organ), or enter, if sensitive or sensorial in nature, reaching respective nuclei for synapsing.

The Authors, mostly neurosurgeons, that have contributed to the clarification of the complex anatomical setting called neurovascular conflict (responsible of specific clinical symptoms depending on the involved nerve) have been, in order of time: Walter Dandy (3) at the beginnings of the thirdies; James Gardner (10), at the beginning of the sixthies and finally Peter J. Jannetta from Pittsburgh (11-21) in the early seventhieths.

Peter Jannetta perfectioned the concept of neurovascular compression, applied sistematically the microscope to the clinical use and made considerable effort over the world to make these entities well known, after his first pioneering experience in Los Angeles togheter with Robert Rand.

Peter Jannetta has also the merit to have sistematized and divulged a microsurgical, retromastoid approach in the lateral decubitus position, for the best approach to the CPA and site of the conflict.

It is also his own merit to have had numerous “serendipitous” intuitions about the entire “panorama” of this pathology, so that an innumerable “schiera” of other surgeons all over the world, in Italy also the Author (1,2,6-9,27-29), were able to apply his method and, mostly important, to fully confirm his hypotheses and intraoperative findings. The Concept of Neuro-Vascular Decompression has herein been introduced, which refers to the act of separating a blood vessel from a neural structure with which the former is found to be in “conflictual” situation, bringing about a mechanical disturbance to the nerve. P.J. Jannetta has described the various morphological anomalies brought about by a vessel on or in a nerve: deforming effect and angulation of nerve bundles (Bending effect); impingement by the vessel on the nerve substance, with myelin discoloration and ‘grooving’ on nerve surface; separation of nerve bundles by vascular loops penetrating inside nerve thickness, with distortion and stretching of fibers and so on. P. Jannetta specifically refers to a “pulsatile cross compression”, at the level of the root entry or exit zone from brainstem.

Typical trigeminal neuralgia or ‘tic doloureux’ The per year incidence of this syndrome is reported to be about 3,4 among 100.000 male subjects and 5,9 on the same number of female subjects (28). Age of onset of symptoms is generally around the fourth decade. Pain is more requent on the right side of the face, especially in women and it affects the middle or lower third of the face, less often the superior third, around the eye.

Patients afflicted by this disease do experience one of the more devastating pains occurring in Nature: pain attacks are sudden in onset and of very brief duration, like ‘lightining pains’ in the face: they may appear several time during daytime, also during the night: they are characterized by a lancinating, unexpected , stabwound pain or an electric shock. Intensity of pain is extreme.

The patient, as time goes by, becomes absolutely conditioned by his pains: he does not eat anymore because is afraid of eliciting pain attack; he does not wash his face nor brush his teeth; he slowly becomes an human relict.

Often, he keeps his face protected with some towel or heat bag and lives in the continuous expectation of a ‘punishing’ pain.

There are in facts certain cutaneous or mucous areas, called trigger points, whose even mild tactile irritation (also from the air of a blowing wind) open up the door for the acute and lancinating pain.

Trigger zones are most frequently localized around the nose and superior lip and in the gengival mucosa.

As already mentioned, air or cold/warm water may endanger the fragile pain -free situation of the patient. Chewing, talking, touching the palate and moving the tongue during swallowing, snoring may suddenly trigger an attack.

At the end of the critical pain, it often disappears completely, or it may remain in a milder, dull, but always disturbing steady state.

Medical treatment at the beginning of attacks is usually effective in preventing the pains, but may be ineffective in a long range control of the symptom. It is usually an antiepileptic drug that affects the pain of trigeminal neuralgia, which originates from the braistem nucleus where the main sensory root fibers of the nerve terminates.

When control is not avilable with medications, surgery becomes necessary, as the only way to effectively abate pain attacks.

Several methods of surgical control of trigeminal pain are available to the neurosurgeon, all of them well experimented, but none of them going stright to the etiological factor involved,that is the vascular compression of the nerve, generally at the brainstem root entry zone.

Using the microneurosurgical operation called neurovascular decompression, the pulsatile cross compression of a blood vessel against the nerve is definitely resolved. Postoperative results are optimal in 95% of the cases in typical cases of ‘tic doloureux’. There is complete disappearance of the pains, as soon as the patient awakens from anesthesia. At times some medication is still necessary in the first postoperative days, in order to fully control the pain. In the minority of trigeminal neuralgia cases, etiology is not a blood vessel but it is represented by a tumor proper of the nerve or close to it, such a neurinoma, a meningioma, dermoid cyst or foci of demyelination inside main sensory root or in the brainstem close to it. In these cases, of course, neurovascular compression as described above is not the causative factor. There may be a vessel impinging and grooving on nerve substance, held against the nerve by the compressive effect of the tumor. In these cases not only tumor must be removed but also the vessel must be decompressed, in order to achieve pain suppression. In the large case series of P. Jannetta and other Authors relapsing of neuralgic pain after microvascular decompression is reported. The latter may happen shortly after operation, because the correct causative vessel is not decompressed or they may appear after as many as 10 to 15 years after first decompression.

In this case, either because a reorganization of neurovascular relationships has taken place or because there has been a slippering of the insulating teflon felts, neuro vascular conflict does form again. In any case, treatment of trigeminal neuralgia with the method of neurovascular decompression is the one that offers the best and stable results, with respect to other forms of surgical approach to trigeminal nerve, which may end up in the so called ‘disesthesia dolorosa’, due to definitive destruction or devascularization of nerve fibers.

If adequately carried out, microvascular decompression mantain normal sensory modalities in the face and normal corneal sensitivity.

Hemifacial spasm (HFS) This disturbance of motor facial nerve activity shows an incidence of 0,74 per 100.000 male people and 0,81 among 100.000 female people (28).

It appears at the level of facial muscles on one side, has a typical and an atypical variant.

The typical hemifacial spasm is characterized by involuntary,spasmodic contractions arising from the muscle around the eye, gradually spreading, over time, toward musculature of the middle and lower part of the face, even involving the platysma muscle in the neck. The spasms,in the advanced phases of the disease,alternate with tonic contractions of the same muscles.

Steady contractions (tonic phenomenon) is of variable duration, at times sustained and with evident hemi-face deformity. In the atypical variant of hemifacial spasm, it primarily arises in the lower half of the face, progressively spreading to involve upper face and orbicularis oculi.

This variant is quite less common than the typical one. In the typical HFS, the vessel compressing the facial nerve is located ventrally and anteriorly to the REZ, whereas in the atypical variant it is located superiorly and posteriorly. It is common experience in this disease that the clinical manifestations become disabling with time and produce an heavy derangement of the psycological status of the afflicted, who avoids social contacts and common day-life relations. In these cases, the Jannetta operation is the most indicated to obtain resolution of symptoms, even immediately after surgery (11, 12, 15,21,22,25). To perform a neurovascular decompression for HFS the craniectomy site must be a bit lower than that used in cases of TN. The microneurosurgical techniques is the same as already described, aside that meticulous attention has to be given to the acoustico-vestibular nerve,which need to be lifted off and apart in order to gain full sight on the facial nerve REZ and carry out the decompression. Intraoperative auditory evoked potentials recording, even elicited from the surface of the nerve, is mandatory,with the aim to avoid auditory damage. Monitoring from the facial nerve itself and from the muscles of the face, according with the full description given by Aage Moller, is another adjuvant neurophysiologic tool, in order to ‘catch’ the correct vessel that need to be decompressed. If the surgeons lifts off the nerve the correct vessel, the spasm immediately disappears; if the same vessel is left to fall again on the nerve, the spasmodic activity reappears in the involved facial musculature, as recorded by needle electromiography. HFS is usually seen in earlier ages than trigeminal neuralgia (TN) , it prefers the female sex and the left side of the face. Complete resolution of symptoms is obtained in 95% of cases. Permanent paralysis of facial nerve function following operation is less than 2,5% . Tinnitus (noise in the ear) eventually associated with Vertigo and progressive sensorineural hearing loss. In the cases where tumor processes are responsible for the symptoms of tinnitus and vertigo and when a strictly peripheral end organ disease has been excluded (at the level of the cochlea and vestibule), these symptoms are related to “hyperfunction” of the auditory and vestibular nerves (11,16-18,27). Central, oligodendroglial myelin, the thin covering of nerve fibers, is represented in a long tract of the stato-acoustic nerve and this is the reason why compression by an offending vessel may be found either at the REZ of the VIII nerve or at its extreme peryphery, even at the level of the internal auditory canal. Tinnitus indeed, when not generated by an inner ear disease, can be elicited by vascular compression all along the nerve trunk. Vertigo, on the other hand, is often produced by conflictual situations located next to the pons, on the vestibular division of the nerve. Frequently, in these cases, togheter with vertigo, disequilibrium is also present. If only disequilibrium is the symptom, in absence of true vertigo, the vessel is found at the level of the nerve REZ, on its vestibular partition. Positional vertigo aggravated by head movements and the accompanying tinnitus, if associated with detectable lenghtening of the 1-3 interval of the brainstem auditory potentials (not due to a tumor), does represent an indication not to sectioning the vestibular nerve but to decompress its root entry zone. At this level, most often, veins instead of arteries are found. In decompression operations performed with the aim of alleviating only the tinnitus aurium, the latter may not be benefited in a complete manner, although patients are happy to notice its diminution. The effects of neurovascular decom-pression for tinnitus may require even 18 months before a beneficial effetct is obtained. Of course the operation entails hearing preservation of the affected nerve. Remission of disequilibrium and vertigo, even weeks or months after the time of operation, can be expected in 90% of cases, remission of tinnitus, even months after the operation as already told, in 60% of cases. These operations may be carried out on both nerves, in cases where symptomatology is bilateral. Glossopharyngeal neuralgia The syndrome is characterized by an unbearable, shock-like pain at the level of the tonsillar fossa and surrounding region, on one side. It recognizes, as trigger mechanisms, chewing and, mostly, swallowing. It is often accompanied by a background pain in the throat and in the deepest part of the ear. Even the passage of saliva during involuntary and mechanical swallowing mechanisms may acutely trigger such miserable pain.The patient does not eat any more, is very limited in drinking whatever kind of beverages. Pain may radiate to the external ear, in the region of the pinna,in front of the ear, in the mastoid region. Diagnosis is at times very difficult. There is clear indication to microneurosurgical vascular decompression of the 9th nerve in this syndrome. Exposure of the nerve follows the same route as the one employed in neurovascular surgery of eight nerve hyperactive syndromes. If operation is carried on the left side, there may be a cardiovascular response with hypertension. Bradycardia or even syncope may be expected in nerve. the non operated glossopharyngeal neuralgia, because of hyperactivity of Hering nerve fibers, coursing with the 9th Disabling Positional Vertigo (DPV) This syndrome has been identified and systematized in recent years by Margareta and Aage Moller, together with P.J.Jannetta at the University of Pittsburgh (14,18,23). From the standpoint of symptomatology, it consists of the following characteristics: vertigo and disequilibrium of severe entity and almost continuous in time (no paroxysms of vertigo or fluctuation of hearing like in Meniere’s disease); vertigo and or disequilibrium typically ensuing following whatever kind of head movement and not subject to the phenomenon of “fatigue”; vertigo may be objective in nature, becoming worse when certain head or body positions are assumed; there is a sensation of “ondulation”, like stayng on a boat (this all may even become better following movements), the gait shows enlarged base, walking is a like a “drunck”; it is sometime staggering, incerto e barcollante; the patients are constantly nauseated and may vomit during movement of the head; they may have tinnitus aurium, with pain in the ear. Occasionally there is a short duration “twithching around the eye”. The syndrome, so particular but definite in its overall clinical picture, has been treated by neurovascular decompression of the eight nerve at the brainstem, due to the associated abnormalities in the early part of the brainstem auditory potentials. In certain cases it has been noted how the vessel did create on the surface of the eight nerve, both on the vestibular and the cochlear partitions, an indentation, a real groove, especially on the vestibular fibers contingent. Resolution of symptoms is gradual in time, first disappearing vestibular signs, later the tinnitus. Neurogenic Hypertension There are selected cases of so called ‘essential’ hypertension, caused by a vascular loop of the vertebral or basilar artery, which create a ‘niche’ and a real indentation on the surface of brainstem parenchima, at the level of lateral fossette of the medulla oblongata (so called retro-olivary sulcus), on the left side (2, 15,16,21). The pulsatile, chronic vascular compression and its mechanical effects, induce a deregulation of physiologic heart controlling mechanisms responsible for maintenance of systemic pressure tone and causing “facilitation” of the inotropic stimulation of heart mucle fibers. After decompression of the vessel from the surface of distorted brainstem,the values of the blood pressure gradually return to normal. The first clinical experience carried out by P.J. Jannetta and others (2) are confirmed in an experimental model, essentially constituted by a enflatable, pulsatile balloon at the level of the supposed vascular compression site, in baboons. Further experimental evidence of the underlyng phenomena responsible for this neurogenic hypertension and, most of all, further clinical positive results are needed. Spasmodic Torticollis Among the rarest manifestations of vascular compression-induced syndromes, the torticollis spasmodicus is the one (4,25,26). This manifestation, when not a part of Dystonia syndromes due to pathology of basal ganglia such as pallidum and putamen or subthalamic nucleus of Louis, may gain benefit by bilateral decompression (generally from P.I.C.A. loops) of the emerging point of spinal accessory nerve roots at the level of upper cervical cord. Expectancy of marked reduction of this invalidating disturbance or even complete resolution can reasonably be expected within three years from completion of the operation. Cyclic Oculomotor Spasm with Paresis The pathophysiology of cyclic oculomotor spasm with paresis, which is an extremely rare disease, is similar to hemifacial spasm in that it seems to be caused by compression of a portion of the oculomotor (III) nerve while being, at the same time, a disorder of the motor nucleus of cranial nerve IIIrd (reported by Moller, ref. 26) The procedure of neurovascular decompression The clear-cut example of the surgical procedure (N.V.D.) needed in the described hyperactive-hypoactive cranial nerves syndromes, is the one used in relieving Trigeminal neuralgia. The operation is performed in general anesthesia. It entails a small craniectomy behind the ear (“a minima craniectomy”), with exposure and subsequent incision of the dura mater close to the sigmoid and transverse sinus.The cerebello-pontine angle is exposed searching in its upward direction for the cisterna of the trigeminal nerve. Once the nerve is recognized, the cisterna is opened and full exposure of the course of the nerve is obtained, from the REZ to the entrance into the Ganglion Gasseri. The nerve may partially or totally be hidden by the presence of the Dandy’s vein coursing toward superior petrosal sinus. In this case, either the vein is gently dispalced, or one of its branches microcoagulated and cut or the vein cut in toto. From this stage on, searching of the compressing vessel is carried out along all the surface of the nerve. Either cranial or caudal branching of superior cerebellar artery or even its main trunk is responsible for the pulsating, compressive effect and, at times, distortion or bending or grooving of the nerve course and substance may occur. The responsible vessel is gently detached or avulsed from inside the nerve substance and held away, with careful attention and meticulous care not to damage perforating vessels coursing to braistem surface and substance. At this point, after complete and gentle freeing off, the vessel is isolated from the nerve, keeping the two structures separated, using shredded teflon felts. At times it is possible to mantain the decompression using both teflon felts or string of silk which held the wall of the vessel away from nerve and is then glued to the tentorial dura with fibrin glue in a stable manner (Figg. 1-3, 4-6, 7-9, 10-12). Before deciding to close up definitely the surgical field, further exploration of the vascular network and its relationship to the nerve is carried out, to check for possible different compressing vessels, either arteries or veins.The same operative technique, with slightly diverging technical points in relation to the precise nerve to be reached, are also used for decompressive procedures to be adopted in the other syndromes previously described, such as Vertigo with accompanying Tinnitus (figg. 15,16) or Glossopharyngeal Neuralgia (Fig. 17). The most sparkling results are obtained in treating Tic doloureux, hemifacial spasm and vestibulo-cochlear nerve the presence of a tumor has been carried out. In the case of Hemifacial Spasm, with the aim to minimize the disorders, when auditory damage possibly resulting from cerebellar retraction using the posterior retrosigmoid approach, it has recently been perfectioned by Zini-Gandolfi a technique to perform the decompression through the enlarged middle cranial fossa approach (6, 7,28,29). This approach allows full visualization, from above, of the entire cerebello-pontine angle and in particular the cochleo-vestibular bundle and the facial nerve in front of them, using a quite limited “temporal craniotomy”. With this surgical view no retraction or displacement of the VIII nerve is required and the REZ of facial nerve is entirely under control, still separated, emerging from brainsetm, with respect to neighboring neural structures (Figg. 13, 14). Availability of such surgical view, facilitates manipulation of the VII nerve REZ, with no interfering effect on structure, function and vascular supply of the auditory or vestibular nerves. Conclusive remarks The concept of “neurovascular decompression” is well established nowadays. It represents a method to cure or at least to markedly alleviate several manifestations of posterior fossa cranial nerve hyperfunction/dysfunction syndromes. Recent results by Aage Moller of the University of Texas at Dallas underlie the fact that, concomitant with the anatomical and mechanical event (which is the primum movens of the final clinical picture in vascular compression syndromes) represented by the pulsatile cross compression of the vessel directly on the nerve there must be, at least with certainty in TN and HFS, a kind of facilitating effect on the central nuclei of these same cranial nerve. This facilitation is brought about and established with the mechanism of “Kindling”. The vascular compression would brought about an epileptic-like reorganization of the central nuclei (themselves subject to suprasegmental facilitations o inhibitions) apt to autonomize these nuclei in their “firing” properties. There must be another facilitating factor, a kind of “suitable substrate”, maybe congenital and still unknown, an “opening gate” for the emerging symptoms, making it possible for these symptoms to take place and to be clinically manifest. This concept would help to explain why a neurovascular contact in some people is apt to induce, by the kindling phenomenon, reorganization of the central nucleus and why in other subjects, equally bearing a clear cut contact between a nerve and a vessel, no one symptoms among those previously described is going to ensue (26).


(traduzione dell'Autore)


Angelo Gandolfi

Docente di Neurochirurgia

Università di Parma






Fig.1-3 Nevralgia del Trigemino destro. Sequenze successive di decompressione neuro-vascolare. Si vedono le strutture vascolari e nervose circostanti il nervo trigemino, ma non è subito evidente la ‘compressione’ neuro-vascolare. Si inizia poi ad allontanare il ramo principale dell’arteria cerebellare superiore dall’emergenza del nervo Trigemino; sono state posizionate le prime falde di Teflon, dette di ‘sicurezza’. Alla fine della microdissezione chirurgica, i due rami di divisione dell’arteria sono visibili alla sinistra del nervo Trigemino, allontanati stabilmente da falde di Teflon soffice. La vena (di colore blu) non esercita alcun effetto compressivo.

Right Trigeminal Neuralgia. The vascular structures around the trigeminal nerve are seen, but the neurovascular compression is still not visible. The main trunk of S.C.A. (superior cerebellar artery) is started to be moved away from the trigeminal nerve root entry zone. Shredded Teflon felts have been positioned at this stage, with the aim of an ‘early security’ decompressive effect. Following microsurgical dissection, the two main divisions of the S.C.A. are visible at the left side of the trigeminal main sensory root, themselves definitely taken away from the nerve with Teflon. The blue colored large vein does not determine any compression on the sensory root.



Figg. 4-6 Nevralgia trigeminale destra. Sequenze successive di distacco dei due rami di divisione della S.C.A. dalla radice sensitiva primaria del nervo trigemino. I due rami verranno ‘incollati’ alla membrana del tentorio e stabilmente fissati con falde di Teflon e colla di fibrina: le falde non verranno tuttavia a contatto con la superficie della radice sensitiva, lasciandola completamente libera da ogni contatto. In Fig.6 si evidenzia il primo agglomerato di Teflon che, posizionato, sposta i vasi ‘via dal nervo’, in direzione del tentorio.

Right Trigeminal Neuralgia. Progressive sequences of detachment of the two main division branches of the S.C,.A. away from main sensory root of the trigeminal nerve. The two branched vessels will be ‘attached’ with fibrin glue on shredded teflon felts to the surface of the tentorium and fixed in situ. The teflon felts will not enter into any contact with the surface of the sensory trigeminal root. Fig.6 shows the first Teflon agglomerate, positioned to keep vessels ‘away’ from the nerve, gently pushing them against tent.



Figg. 7-9 Nevralgia trigeminale destra. Sequenze di decompressione neurovascolare. Conflitto tra radice sensitiva primaria del nervo trigemino ed entrambi i rami di biforcazione dell’arteria cerebellare superiore (S.C.A.). Questi vengono‘sgusciati’ dalla ‘spalla’ del trigemino ed allontanati dal nervo con Teflon.

Right Trigeminal neuralgia. Sequences of neurovascular decompression manouvers. There is a ‘conflict’ between the trigeminal nerve main sensory root and both bifurcating branches of the superior cerebellar artery (S.C.A.). These two branches are ‘enucleated’ from their niche inside and against nerve ‘shoulder’ and taken definitely away using Teflon.



Figg. 10-12 Nevralgia trigeminale sinistra. Fasi successive di distacco-allontanamento (‘decompressione’) ed inserzione di Teflon tra una voluminosa vena del ponte e la radice emergente del nervo Trigemino. Caso di nevralgia della 2a branca trigeminale sinistra.

Subsequent phases of micro-detachment and decompression with Teflon felts insertion between trigeminal nerve and a large pontine vein coursing against and bending the sensory root at the brainstem. This was a case of 2nd division left trigeminal neuralgia.



Figg. 13-14 Caso di emispasmo facciale tipico. Viene mostrato in due sequenze il distacco (cioè la ‘decompressione’) con dissettore smusso dell’ansa dell’arteria cerebellare media (A. I.C.A.) dal contatto col nervo. Le falde di Teflon saranno inserite nello spazio creato tra le due strutture.

‘Typical’ hemifacial spasm., right side of the face. Surgical field, as seen from above using the middle cranial fossa approach, shows, in sequence, the detachement of A.I.C.A.(anterior inferior cerebellar artery) from anterior ventral surface of the nerve. Teflon felts will be inserted in between the artery and the surface of the nerve to stabilize the neurovascular decompression.



Figg. 15-16 Angolo ponto-cerebellare sinistro; emergenza del nervo acustico-vestibolare. La ‘loop’ dell’A.I.C.A., arteria cerebellare media, era aderente e ‘pulsante’ contro la superficie del nervo, incarcerato a ‘sandwich’ tra l’arteria stessa ed un secondo vaso arterioso disposto cranialmente e lateralmente ad esso; le sequenze mostrano le arterie che sono state decompresse mediante Teflon dalla superficie di contatto col nervo; in questo caso erano presenti vertigine e acufene(fischio all’orecchio).

Left cerebello-pontine angle; eight nerve emerging from brainstem. Loop of A.I.C.A., anterior inferior cerebellar artery, caudal to it, is adherent and pulsating against surface of the nerve, which, in this case, was incarcerated in a sandwich position between the decompressed AICA and another large artery, lying on its cranial and lateral surface; the sequence shows the vessels decompressed by means of Teflon felts from their contact with the nerve. This was a case with vertigo and tinnitus.



Fig. 17 Si evidenzia l’arteria vertebrale destra, che esercita un effetto di ‘bending’, cioè incurvamento dei nervi glossofaringeo e vago nell’angolo ponto-cerebellare. Una ‘loop’ (convoluzione arteriosa) dell’arteria cerebellare inferiore e’ in posizione arcuata nello spazio tra i nervi cranici acustico-vestibolare (in alto) ed il complesso glossofaringeo-vago. Questo e’ un caso di nevralgia del Glossofaringeo, trattato mediante decompressione neuro vascolare.

Right vertebral artery is shown, slightly bending the complex of ninth and tenth cranial nerves in front of their surface and originating a conspicuous PICA loop, arcuating in the space between stato-acoustic and glossopharyngeal/vagal nerve complex. This was a case of glossopharyngeal neuralgia, treated succesfully by means of microvascular decompression of vertebral artery from its contact with the above mentioned lower cranial nerves.