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CASE REPORTS
TRIGEMINAL NEURALGIA DUE TO ECTATIC DILATION OF VERTEBRAL ARTERY
KAVITA K KRISHNA*, BENOJ DANIEL**, MM JAIN***
A 70 year old man presented with left sided trigeminal neuralgia refractory to optimal medical therapy. His CT scan revealed vascular compression of left side of pons as the cause. He responded to surgical therapy using Harknel’s procedure (radio frequency neuroablation).
INTRODUCTIONThe pain produced by trigeminal neuralgia (TN) is excruciating, perhaps the worst pain known to human beings. The pathophysiologic mechanisms responsible for the paroxysmal pain of TN remain unknown despite extensive research directed towards the study of neurophysiology of the trigeminal system. Various researchers have implicated central mechanisms in patients with TN, others have argued for a peripheral mechanism. Clinical observation supporting a peripheral mechanism include the occurrence of TN as the manifestation of a mass lesion (tumour, dolicoectatic basilar artery or aneurysm) compressing the preganglionic trigeminal root in the posterior or middle cranial fossa. We present a case of TN where the cause was ectatic dilatation of the left vertebral artery.
CASE HISTORY
A male aged 70 years presented with excruciating episodic pain in the left half of the face since 3 months accompanied by tics and watering of the left eye. The pain radiated from frontal to mandibular region, increased on exposure to cold, washing of face and mastication. On examination, he had intermittent tics on left periorbital area. There was no sensorimotor deficit. His haematological and biochemical investigations were within normal limits. CT scan brain revealed ectatic dilatation of the left vertebral artery causing indentation over the left pontine region (Fig. 1). The patient was treated with increasing doses of Carbamezapine (800 mg/day in divided doses) and Gabapentine (600 mg/day). However, there was no relief of symptoms after 8 weeks. He was subjected to radiofrequency neuroablation therapy (Harknel’s procedure). He developed loss of pain sensation over left half of face, but is happy as he is completely relieved of the excruciating pain.
DISCUSSION
In 1934, Dandy outlined the theory of vascular compression as a cause of TN. He identified the major compression vessel as the anterior inferior cerebellar artery.1 Jannetta affirms that TN is a painful condition caused by 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 aging process, or by a cross compressing vein, or by both. He identified the vessels involved in 1204 consecutive previously unoperated sides, in patient with typical TN. The most frequently involved was superior cerebellar artery (75.5%), followed by anterior inferior cerebellar artery (9.6%), vertebral artery (1.7%), posterior inferior cerebellar artery (0.7%); 55.7%, had compression by veins also.2 Peter and Thomas also confirm that vascular compression of the fifth cranial nerve is an anatomical abnormality specific to TN.3 The evidence supporting a central mechanism for TN relates to the provocation of a severe discharge of pain by minimal tactile stimuli, the prolongation of pain spasm after its onset and the development of a positive refractory period in which local stimuli do not trigger ‘pain’. In this manner the pain is somewhat like as seizure or epileptic event.4All patients of TN should be given adequate trial of medical therapy. Failure to make the patient completely painfree and out of fear of recurrent attacks is an indication for surgery. Prior to surgical intervention. MRI scan of the posterior fossa to look for mass lesions, large ectatic vascular or other vascular malformations should be done. Radiofrequency neuroablation consists of inserting a probe through the foramen ovale, applying a radiofrequency current to destroy all the thinly myelinated smallest nerve fibres which carry pain sensation and sparing the heavily myelinated fibres carrying other modalities of sensations. However, there is permanent numbness in the area for the pain which can result in accidentally biting of tongue cheek, etc. Three to five per cent of treated cases may be afflicted with anaesthesia dolorosa - a constant, severe, painful, burning sensation in the treated area, which fails to respond to any treatment and is usually permanent.
Microvascular decompression (MVD) is extraordinarily effective in relieving the pain and has the major advantage of sparing facial sensation and avoid dysaesthetic sensation. Through an incision 2.5-6 cm long, posterior to the mastoid process, a craniectomy is performed high and lateral in the posterior fossa. The arachnoid is opened anteromedial to the vein exposing the trigeminal nerve. The vessel loop related to the root entry zone, is entirely teased out from between the trigeminal nerve and the pons into a horizontal position, a teflon implant is placed between the vessel and the nerve. The operative complications include operative death, brain stem infarct, cerebellar haematoma, cerebellar oedema, hydrocephalus, facial paresis, hearing loss, extra-ocular muscle palsies, cerebrospinal fluid leak, pseudomeningocoele, bacterial meningitis and severe post operative headache. Following failed MVD, glycerol rhizolysis or radiofrequency may be the treatment of choice.
The purpose of presenting this case report was to emphasize the importance of surgical treatment in TN when refractory to medical treatment. Microvascular compression is an important cause of trigeminal neuralgia. Though our patient was not subjected to MVD and responded to neuroablation, in centres where the expertise and facilities exist, MVD should be the procedure of choice.
REFERENCES
1. Dandy WE. Concerning cause of trigeminal neuralgia. Am J Surg 1934; 24 : 447-55.
2. Jannetta PJ. Microvascular decompression of the trigeminal nerve for tic doloreux. In: Youmans ed. Neurological surgery 4th edn. WB Saunders Co. Philadelphia. 1996: 3404-15.
3. Hamlyn PJ, King TT. Neurovascular compression in trigeminal neuralgia :a clinical and anatomical study. J Neurosurgery 1992; 76 : 948-54.
4. Cruccu G. Idiopathic and symptomatic trigeminal pain. J Neurol Neurosurgery Psychiatry 1990; 53 : 1034-42.
5. Radiofrequency ablation. http://www.medhelp.org/per16/neuro/archive/245.htm.
6. Tavares MP. Trigeminal neuralgia - microvascular decompression. http://www.medstudents.com.br/neuroc/neuroc2.htm.
