Fig. 01 : Retrosigmoid approach. Observe the position and incision ( red line ). Observe the area of craniectomy ( black shading ).
The pain produced by trigeminal neuralgia ( TN ) is excruciating, perhaps the worst pain know to human beings. Walter Dandy pioneered the posterior fossa approach for the treatment of TN. In 1934, Dandy (1) outlined his theory of vascular compression as a cause of TN, and pointed to the main problem with that theory; namely, that vascular contact occasionally occurs without the production of pain and may be absent when neuralgia is present. Dandy identified the major compressing vessel as the anterior inferior cerebellar artery. Peter Jannetta (2) was the first neurosurgeon to apply the operating microscope to the problem of TN. He observed the almost universal occurrence of vascular channels compressing the trigeminal nerve in patients with TN and devised a technique for nondestructive microvascular decompression of the nerve.
The pathophysiology mechanisms responsible for the paroxysmal pain of TN remains unknown, despite extensive research directed toward the study of neurophysiology of the trigeminal system. Various researches have implicated central mechanisms in patients with TN; others have argued for a peripheral mechanism. Clinical observations supporting a peripheral mechanism include the occurrence of TN as the manifestation of a mass lesion ( tumor, dolichoectatic basilar artery, or aneurysm ) compressely the preganglionic trigeminal root in the posterior or middle cranial fossa. Barker II and cols. (3) studied 26 patients, during a period of 20 years, with typical symptoms of TN and with posterior fossa tumors at operation. These tumors included 14 meningiomas, 8 acoustic neurinomas, 2 epidermoide tumors, 1 angiolipoma, and 1 ependymoma. At the operation, the root entry zone of the trigeminal nerve was examined for vascular cross-compression in 21 patients. Vessels compressing the nerve at the root entry zone were observed in all patients examined. Probable this peripheric mechanism is the correct one. Janetta affirms that TN is a painful condition caused by a abnormality of the root entry zone of the trigeminal nerve, and that the abnormality may be associated with cross-compression by an artery loop that has imposed upon the nerve as a result of vascular elongation secondary to the aging process, or by a cross-compressing vein, or by both. Jannetta identified the vessels involved in 1.204 consecutive, previously unoperated sides, in patients with typical TN ( Table 01 )
Table 01 : Vessel found to compress the Trigeminal nerve in 1.204 consecutive previously unoperated sides in patients with typical TN (2).
_____________________________________________________ Superior cerebellar artery ---------------- 75,5% Anterior inferior cerebellar artery -------- 9,6% Posterior inferior cerebellar artery ------- 0,7% Vertebral artery --------------------------- 1,6% Basilar artery ----------------------------- 0,7% Labyrinthine artery ------------------------ 0,2% Unnamed small artery ----------------------- 15,4% Vein --------------------------------------- 68,2% Vein only ---------------------------------- 12,5% Vein and artery ---------------------------- 55,7% Unnamed small artery or vein only ---------- 18,5% ______________________________________________________
The evidence supporting a central mechanism relates to the provocation of a severe discharge of pain by minimal tactile stimulation, the prolongation of pain spasm after it onset, and the development of a posited refractory period in which local stimuli do not trigger the pain. In this manner the pain is somewhat like a seizure or epileptic event (4).
Several criteria must be met before arriving at a recommendation of surgery - Microvascular decompression ( MVD ). First and for most is the certainly of diagnosis. Patients uniformly complain of severe, instant-onset, relatively brief ( tics ) , very intense paroxysms of electric shock like lancinating pain confined to the territory of one or more contiguous branches of the trigeminal nerve ( table 02 ). The pain may occur spontaneously but is usually triggered by light, non noxious, tactile stimuli such as moving the face while talking, touching the face, wind on the face, kissing, eating, or brushing the teeth. Its infrequently nocturnal.
Table 02 : Spatial distribution of symptoms in TN, in 1.204 patients operated on by Jannetta.(2)
__________________________________________________________ Division involved : First ( V1 ) only ----------------------- 2,8% Second ( V2 ) only ---------------------- 17,7% Third ( V3) only ------------------------ 14,6% V1 + V2 --------------------------------- 17,2% V2 + V3 --------------------------------- 35,4% V1 + V3 --------------------------------- 0 V1 + V2 + V3 ---------------------------- 12,3% ___________________________________________________________
Patients with TN frequently have mild sensory loss in the pure distribution of trigeminal nerve. The Trigeminal reflex ( corneal reflex, blink reflex, masseter inhibitory periods, jaw-jerk ) have abnormalities (4).The corneal reflex may be decreased, especially in neuralgia of first division trigeminal nerve, and it may be decreased in only part of the cornea, especially the upper half. These changes revert to normal gradually after MVD of the nerve.
TN predominates in middle and old age. The correlation of tics with arteriosclerosis is clear. This correlates well with the arteriosclerotic tortuous elongation of arteries - loops. The predominance is in women. The reasons for the predominance in women are not clear. It may be explained by the fact that the posterior fossa is smaller in women than in men. It is also possible that the effect of estrogen, which causes elongation of arteries, may be the reason for this increased incidence. This is only conjecture, and better information in needed.
Most patients respond to carbamazepine; so failure to achieve benefit from those medication in adequate doses ( 600 to 800 mg/day in divided doses ) should lead to reassessment of diagnosis. Patients who are candidates for surgery should have an adequate trial of medical therapy. By starting at a low dosage and gradually increasing the medication, most patients can be brought to and adequate therapy. By starting at a low dosage and gradually increasing medication, most patients can be brought too an adequate level. Side effects include sedation, trouble concentration, feeling like a zombie , and hematologic and hepatotoxic effects have also been reported, so patients need to be monitored carefully while on this medication. Nevertheless, it is effective initially in close to 90 percent of patients with TN (5).
Fenitoin is the next most effective drug and is appropriate either alone or with carbamazepine in those patients who are not well controlled with carbamazepine . Failure to completely control the pain, so that the patient is pain free and does not live in the fear of recurrence attacks is an indication for MVD.
Prior to considering surgery, all patients should have magnetic Resonance Imaging ( MRI ) scan, with close attention being paid to the posterior fossa. This is done to rule out other causes of compression of the trigeminal nerve such as mass lesions, large catatic vessels , or other vascular malformations.
The MVD is extraordinarily effective in reliving the pain and has the major advantage of sparing facial sensation and avoid dysesthetic sensation.
A number of positions are satisfactory in allowing the surgeon to gain access to the posterior fossa using a high lateral approach. Patients can be operated on in the prone position, lateral decubitus position, and supine position with the head rotated, as well as in the siting position. The latter affords a uniform anatomical orientation that is easily conceptualized by the surgeon.
The patient is anesthetized , intubated, and placed in a chosen position with the head fixed in a pin head holder ( Fig. 01 ).
Fig. 01 : Retrosigmoid approach. Observe the position and incision ( red line ). Observe the area of craniectomy ( black shading ).
A craniectomy ( usually 2.5 to 3.0 cm in size ) is performed high and laterally in the posterior fossa, exposing in the caudal edge of the lateral sinus and its junction with the sigmoid sinus and extending into the mastoid air cells laterally if necessary. Any open air cells are waxed heavily. An incision is made in the dura mater under the lateral sinus and extends caudally. The superolateral dura flap is incised to the lateral sinus, and the dura is sutured to the galea to tent the lateral sinus up and away. During the dura mater dislocation and opening is necessary to make valsava maneuver to avoid air embolism (Fig.02 ).
Fig. 02 : Craniectomy and dural opening that parallels the transverse and sigmoid sinuses. Opened mastoid cells are immediately covered over with wax ( green )
The operating binocular microscope is introduced. The superior petrosal vein is identified and coagulated. Afterwards its divided. So the retractor is placed over the ala of the cerebellum, with usually covers the trigeminal nerve superolaterally at the pons. The arachnoid is opened anteromedial to the vein, exposing the trigeminal nerve. After sharp and blunt dissection of the arachnoid from the trigeminal nerve is possible of identifying the vessel related to the root entry zone ( Fig. 03 ). The vessel loop are gently teased out from between the trigeminal nerve and the pons into a horizontal position. The vessel loop may be quite adherent to the nerve or may be easily separated from it.
Fig. 03 : Retrosigmoid approach to the area of the trigeminal nerve in vascular compression syndrome. Observe the relations between the trigeminal nerve, brain stem and local vessels. (1) Cerebellum ; (2) superior cerebellar artery; (3) trigeminal nerve; (4) petrosal vein; (5) abducens nerve; (6) anterior inferior cerebellar artery; (7) labyrinthine artery; (8) facial nerve; (9) statoacustic nerve; and, (10) cerebellar flocculus.
An implant made of one or multiple pieces of Teflon felt have been shredded and rolled to appropriate size and configuration is put into position. Placement is made while the vessel is held in its new position away from the nerve. The implant is placed between the vessel and the nerve. The valsalva maneuver is performed several times under the control of the anesthetist to determine whether the relationship are stable and ensure hemostasis.
The retractor is removed, and the dura is closed. A Methylmethacrylate cranioplasty can be performed . The incision is closed in layers, and a small dry dressing is applied.
The operative complications include operative death, brain stem infarct, cerebellar hematoma, cerebellar edema, hydrocephalus, facial paresis, hearing loss, extra-ocular muscle palsies, cerebrospinal fluid leak, pseudomeningocele, bacterial meningitis, severe postoperative headache.
Peter and Thomas (6) confirm that vascular compression of the fifth cranial nerve is an anatomical abnormality specific to TN. The MVD of the trigeminal nerve has a high rate of satisfaction between the patients who underwent this treatment in relation to symptom relief (7). In patients who reoccurrence occur a subsequent MVD seems to have good long-term results. However, because of the incidence of the significantly high incidence of complications, the indication for subsequent operation should be restricted to younger patients to avoid destructive procedures. In general, glycerol rhizolisis or radiofrequency may be the treatment of choice after failed MVD (8).
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