Trigeminal Sectioning

Neurology. 2005 Nov 22;65(10):1650-1.

Tearing without pain after trigeminal root section for cluster headache.

The cranial autonomic symptoms (CAS) in patients with cluster headache (CH) are considered to occur as a result of intense ophthalmic division pain. Five CH patients underwent transection of the trigeminal nerve root but continued to experience periodic CAS without pain, whereas another five patients continued to experience typical cluster headaches. These findings confirm that CH is generated by a central pacemaker and the pain may be expressed without activation of the peripheral trigeminovascular network.

PMID: 16301498

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Neurology. 2003 Apr 22;60(8):1360-2.

Outcome of trigeminal nerve section in the treatment of chronic cluster headache.

Departments of Neurology, Mayo Clinic, Rochester, MN, USA.

Chronic cluster headache accounts for 10 to 15% of all patients with cluster headache and is often resistant to medical management. The authors followed 17 patients with intractable chronic cluster headache who underwent trigeminal nerve section. They found that trigeminal nerve section is an effective treatment with acceptable morbidity for a carefully selected group of patients.

PMID: 12707445

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Brain 2002 May;125(Pt 5):976-84

Persistence of attacks of cluster headache after trigeminal nerve root section.

Matharu MS, Goadsby PJ.

Headache Group, Institute of Neurology, University College London, UK.

Cluster headache is a strictly unilateral headache that occurs in association with cranial autonomic features. We report a patient with a trigeminal nerve section who continued to have attacks. A 59-year-old man described a 14-year history of left-sided episodes of excruciating pain centred on the retro-orbital and orbital regions. These episodes lasted 1-4 h, recurring 2-3 times daily. The attacks were associated with ipsilateral ptosis, conjunctival injection, lacrimation, rhinorrhoea and facial flushing. From 1986 to 1988, he had trials of medications without any benefit. In February 1988, he had complete surgical section of the left trigeminal sensory root that shortened the attacks in length for 1 month without change in their frequency or character. In April 1988, he had further surgical exploration and the root was found to be completely excised; post-operatively, there was no change in the symptoms. From 1988 to 1999, he had a number of medications, including verapamil and indomethacin, all of which were ineffective. Prednisolone 30 mg orally daily rendered the patient completely pain free. Sumatriptan 100 mg orally and 6 mg subcutaneously aborted the attack after approximately 45 and 15 min, respectively. He was completely anaesthetic over the entire left trigeminal distribution. Left corneal reflex was absent. Motor function of the left trigeminal nerve was preserved. Neurological and physical examination was otherwise normal. MRI scan showed a marked reduction in the calibre of the left trigeminal nerve from the nerve root exit zone in the pons to Meckel's cave. An ECG-gated three-dimensional multislab MRI inflow angiogram was performed. No dilatation was observed in the left internal carotid artery during the cluster attack. Blink reflexes were elicited with a standard electrode and stimulus. Stimulation of the left supraorbital nerve produced neither ipsilateral nor contralateral blink reflex response. Stimulation of the right supraorbital nerve produced an ipsilateral response with a mean R2 onset latency of 36 ms and a contralateral response with a mean R2 onset latency of 32 ms. Lack of ipsilateral vessel dilatation makes the role of vascular factors in the initiation of cluster attacks questionable. With complete section of the left trigeminal sensory root the brain would perceive neither vasodilatation nor a peripheral neural inflammatory process; however, the patient continued to have an excellent response to sumatriptan. The case illustrates that cluster headache may be generated primarily from within the brain, and that triptans may have anti-headache effects through an entirely central mechanism.

PMID: 11960888

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Br J Neurosurg. 1993;7(5):483-90.

Trigeminal nerve section for chronic migrainous neuralgia.  (now known as Cluster Headache)

Kirkpatrick PJ, O'Brien MD, MacCabe JJ.

Department of Neurosurgery, Addenbrooke's Hospital, Cambridge, UK.

We report a series of 14 patients who underwent partial or complete trigeminal nerve root section for chronic unremitting migrainous neuralgia. They had all suffered attacks with severe pain for over 18 months without remission (mean duration 5.5 years). Symptoms were refractory to extended medical intervention and had caused prolonged disruption of lifestyle. The sensory root was completely divided in two cases with complete relief of pain (mean follow-up period 5.6 years). In the other 12 patients, 50-90% of the superomedial portion of the sensory root was divided. Of these, five received no further surgery, and experienced complete (n = 2), near complete (n = 2), or incomplete (n = 1) relief of neuralgia (mean follow-up 5.5 years). The remaining seven patients in the partially divided group were not relieved of pain after operation (n = 5) or suffered early recurrence of pain (n = 2). They showed incomplete sensory loss in the first trigeminal division (V1) and had a second operation to extend the nerve division. V1 anaesthesia was established in all cases after the second procedure, and as a result, four are currently completely free of pain and one has near complete relief of pain. The remaining two patients are still experiencing severe neuralgia (mean follow up 4.1 years). Twelve out of 14 patients (85.7%) receiving surgery for chronic migrainous neuralgia experienced adequate pain relief and are able to follow a normal life (mean follow up 5.6 years). Corneal abrasion was the commonest long-term complication, occurring in three cases (28.5%) and progressing to chronic keratitis in one. We conclude that total trigeminal nerve root section is an effective treatment for patients suffering from chronic migrainous neuralgia and can be safely offered as a primary surgical treatment.

PMID: 7505590

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Page Last Updated:  04/02/2008