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|Year : 2000 | Volume
| Issue : 4 | Page : 330-2
Percutaneous trigeminal ganglion balloon compression : experience in 40 patients.
Department of Neurosurgery, K.G. Hospital, Coimbatore, India.
Department of Neurosurgery, K.G. Hospital, Coimbatore, India.
Forty patients of trigeminal neuralgia were treated with percutaneous trigeminal ganglion balloon compression. Symptoms had been present since six months to twenty years. The age ranged between 23 years and 73 years. All the patients had immediate relief from pain. Two had already undergone trigeminal cistern rhizolysis. One patient had foramen ovale stenosis. After the procedure, all the patients had mild to moderate degree of ipsilateral facial sensory loss which included buccal mucosa and anterior 2/3rd of the tongue. Facial dysaesthesia (anaesthesia dolorosa) was seen in only one case, who had mild involvement lasting one week. Thirty patients had altered taste sensation, probably due to general somatic sensory loss. Five patients had herpes perioralis. In this study group, two patients had already undergone microvascular decompression. All the patients were followed for a period ranging from one to eighteen months. Balloon compression technique seems to be better than injection of alcohol, glycerol or radio frequency lesion. Recurrence of pain was noted in 3 patients after one year.
|How to cite this article:|
Natarajan M. Percutaneous trigeminal ganglion balloon compression : experience in 40 patients. Neurol India 2000;48:330
The exact cause of trigeminal neuralgia is not known. Hence, various types of treatment modalities like ethyl alcohol, butyl alcohol injection into the ganglion, glycerol injection into the trigeminal cistern (TCGI), peripheral nerve divisions, radio frequency lesion of preganglionic fibres, open ganglionic compression, tearing of the ganglion, fraziers fractional root section,
Dandy's procedure of sectioning sensory root in the posterior fossa, Sjoqvist operation and micro vascular decompression have been advocated. Patients may get relief from pain for varying periods with each method of treatment. Among the available methods, microvascular decompression appears to be more physiological and does not result in facial sensory loss. Manipulations in and around trigeminal ganglion resulting in pain relief is well known. Sheldon had published a large series on open compression of trigeminal ganglion in 1955, with good success rate.
Forty patients, who presented with classical symptoms of trigeminal neuralgia, from September 1997 to February 1999 were included. There were 23 female and 17 male patients. The youngest patient was 23 years and the oldest 73 years old. Duration of the symptoms ranged from 6 months to 20 years. 35 patients were referred primarily after the failure of medical therapy. All the patients were taking carbamazepine 600 mg to 1200 mg daily. Three patients were taking additional phenytoin sodium and gabapentin. Three patients had already undergone TCGI and had developed recurrence of pain. They had mild sensory loss over the face, along with classic electric shock like pain in the mandibular and maxillary divisions. Two patients had undergone microvascular decompression elsewhere, 6 months and 18 months earlier respectively. 35 patients, who presented for the first time, did not have any focal neurological deficit. No patient in this study had bilateral trigeminal neuralgia. CT scan was done in 35 cases and MRI brain in 5 cases. Two patients had associated ectatic basilar artery. One patient had undergone DSA and showed a fusiform aneurysm of vertebral and basilar artery. Eight patients were suffering from diabetes mellitus and were on oral hypoglycaemic drugs. 32 patients had associated hypertension. Twelve patients had additional coronary artery disease (CAD).
Procedure of percutaneous trigeminal balloon compression (PTBC)
All patients were thoroughly evaluated for fitness for general anaesthesia. Antiseptic mouthwash was advised a day before surgery. Under general anaesthesia, a wide bore needle was passed into foramen ovale using the classical Hakanson's technique. Biomed balloon catheter was introduced through the needle and pushed 1 cm beyond and navigated into the Meckel's cave. The position of tip was confirmed by using a C arm image intensifier in both antero-posterior and lateral views. 0.5ml of iohexol (water soluble contrast) was injected to inflate the balloon. Usually the balloon is of the shape of a 'pear' when inside the Meckel's cave. X-rays were taken [Figure. 1]. Balloon was deflated and withdrawn. The entire procedure lasted less than 20 minutes.
In all patients except one, the needle could be introduced easily. The only exception was the patient with foramen ovale stenosis, in whom, the needle just fitted in the foramen. This patient had already undergone TCGI. She had relief for six months, and then pain recurred. Accidental carotid artery puncture was not encountered in any of these patients.
As soon as the balloon was inflated, all patients developed bradycardia. Heart rate decreased to 54 to 60, for few seconds and then normalised. Oxygen saturation remained normal. One patient, who had mild diabetes, developed intra procedural myocardial infarction, acute left ventricular failure and pulmonary oedema. This event was recognised immediately as the pulse oximetry showed steep reduction inspite of 100% oxygenation using anaesthetic Boyles apparatus. The patient could be saved and later cardiac evaluation revealed acute lateral wall ischaemia with elevated CPK (MB fraction).
Compression Time varied between one to ten minutes. 5 patients who had TCGI and MVD earlier were given compression for 10 minutes. Compression time was 10 minutes in 16 (40%) cases, 5 minutes in 10 (25%) cases, 2 minute in 8 (20%) cases and 1 minute in 6 (15%) cases.
Thorough neurological examination was carried out the very next day after PTBC and before discharge. Patients were followed up for a period ranging between 1 month and 18 months. 100% pain relief was observed in all patients. Only one patient who was a diabetic had facial dysaesthesia. Facial sensory blunting was noticed immediately in 33 (82.5%) patients. 15 of them improved in 6 months. In other patients, though a mild degree of facial numbness was persistent, it was acceptable. Corneal sensory blunting was noted in 35 (87.5%) patients. All these patients recovered within one month. Five patients developed masticator weakness which resolved within a week. 30 patients developed diminished taste sensation, probably due to decreased general somatic sensation. One patient had subjective feeling of excess saltish taste in the food. Five patients developed herpetic lesions around the angle of mouth. Probably these patients endorse the theory of herpes simplex infection lying dormant in the gasserian ganglion. Three patients developed cheek haematoma which subsided with cold compression.
Manoeuvres in and around trigeminal nerve pathway result in relief from pain in trigeminal neuralgia. Parkinson described a patient where trigeminal nerve could not be identified in the middle cranial fossa. During surgery, cautery was used liberally and lot of packing was done. The pain relief lasted 35 years in him. In microvascular decompression, nerve root is gently handled while separating the vessel and while interpositioning the graft. This handling of root may be responsible for the relief of pain in these cases. In this study, 40% of patients had 10 minutes compression. They were less than 60 years of age. None had recurrence of pain. Longer the duration of compression, more denser the facial sensory loss. With lesser compression time, recovery from facial numbness was quicker. Corneal sensation also was retained. Although Lichtor and Mullan recorded prolonged masticatory weakness, only 5 patients (12.5%) had weakness lasting for one week. Patient with ectatic basilar artery and the one with fusiform aneurysm of the vertebral artery had total pain relief after PTBC. The relief of pain in these cases, through PTBC, may confirm that manoeuvring the trigeminal ganglion gives pain relief.
In this study group, no patient developed ocular nerve palsy, carotid artery injury or carotico cavernous fistula. Recurrence of pain was experienced by three patients after one year. Two had undergone TCGI and both were severely diabetic. One had foramen ovale stenosis and thus the ballooning could not be done. All patients developed mild bradycardia (vasodepressor reflex) while balloon was inflated. This was counteracted with injection of atropine. In 20% of patients, a slight fall in BP (10mm of systolic) was noted. Except for one patient who developed intra operative myocardial infarction, no other serious untoward incident was encountered. Facial dyaesthaesia is really a menacing complication following TCGI or RF lesions. Sometimes, it is worse than the trigeminal neuralgic pain. Many times the patient feels that half of his face is missing. But after PTBC, no such dense sensory loss was encountered. Corneal ulceration has been noted following TCGI, however, the same was not seen in this study.
There is some correlation between duration of the disease and the relief by PTBC. Shorter the duration, better is the PTBC response. An interesting observation was made in three patients of less than 30 years of age. They had complete relief from pain. Usually microvascular decompression is recommended in younger patients.
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|3.||Brown JA, Gouda JJ : Percutaneous balloon compression of the trigeminal nerve. Neurosurg Clin N America1997; 8 : 1. |
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|5.||Lichtor T, Mullan JF : A 10 year follow up review of percutaneous micro compression of the trigeminal ganglion. J Neurosurg1990; 72 : 49-54. |
|6.||Mullan S, Licntor T : Percutaneous micro compression of the trigeminal ganglion for trigeminal neuralgia. J Neurosurg 1983; 59 : 1007-1012. |