Although percutaneous procedures offer a less invasive route to the Gasserian ganglion for rhizotomy, posterior fossa exploration offers the only opportunity to identify an offending vessel through a nondestructive procedure with a more lasting result. Regardless of the responsible etiology in the pathogenesis of this pain, MVD surgery, through mobilizing the offending vessel or performing a rhizotomy, provides an effective and durable palliative option for symptomatic relief. Lateral or caudal compression may cause V3 (mandibular division) symptoms, and rarely, cranial compression causes V1 (ophthalmic division) symptoms. Because of the lamination pattern of fibers within the nerve root, medial compression tends to cause V2 (the maxillary division) symptoms. In addition, a vein may contribute to the compression (68%), and sometimes it is the only compressing vessel (12%). The offending vessel is most often the superior cerebellar artery (75%) or the anterior inferior cerebellar artery (10%). Recently, investigators have implicated other factors (central hypothesis: hyperactivity of the trigeminal and facial nuclei), in addition to peripheral vascular conflict, as causes for the disorder. In addition, cadaveric studies have revealed an intimate relationship between the cranial nerves in the posterior fossa and the neighboring vessels, but these cadavers had no history of cranial hyperactivity syndrome before their death. However, in some patients, no compressive artery can be found during detailed exploratory posterior fossa surgery. Vascular compression of the respective nerves at the brainstem (neurovascular conflict-peripheral hypothesis) has been proposed as the principal factor involved in the genesis of cranial nerve hyperactivity through demyelination of the root entry/exit zone of the nerve (ephaptic transmission).
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The pathogenesis of cranial nerve hyperactivity syndromes, such as trigeminal neuralgia, hemifacial spasm, geniculate neuralgia, paroxysmal positional vertigo, and glossopharyngeal neuralgia, has remained elusive. However, up to 10% of patients will not respond to these drugs and will still qualify as candidates for MVD surgery if no other underlying etiology is found.
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Initially, a small dose of an antiepileptic/antineuralgic drug (such as carbamazepine), rather than an analgesic drug, can provide excellent pain relief. Peak incidence lies in people between ages 50 and 60 years, with prevalence increasing with age. Patients may undergo unnecessary, and sometimes irreversible, dental treatment before the correct diagnosis is made.Ī crude annual incidence of trigeminal neuralgia is approximately 5.7 per 100 000 women and 2.5 per 100 000 men. At first, it is often mistaken as a tooth problem because of its presentation in the two lower branches of the trigeminal nerve. The character of the pain is typically unilateral, episodic, severe, stabbing, shock-like, or lancinating, and exacerbated by cutaneous stimuli such as tactile pressure, chewing, brushing, a breeze of air, or shaving. The typical pain of trigeminal neuralgia is relatively easy to diagnose. The severity of this disabling pain and its relief through successful operative intervention have caused microvascular decompression (MVD) surgery to be recognized as one of the most satisfying operations in neurosurgery.
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Trigeminal neuralgia is considered one of the worst pains that can affect a human being. Microvascular Decompression Surgery for Trigeminal Neuralgia: Classical Intraoperative Findings