Trigeminal Neuralgia Due to Pontine Infarction

Peker, Selçuk; Akansel, Gür; Sun, Ibrahim; Pamir, Necmettin

doi:10.1111/j.1526-4610.2004.4200_1.x

Cited by 35 publications

(27 citation statements)

References 13 publications

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“…These findings indicate that trigeminal neuralgia in cases with vascular compression is due to demyelination. Recently, Peker et al [36] described a case of secondary TN due to pontine infarction which supports the central origin. De Ridder et al [12] supported the central theory and suggested a correlation between the length of the central segment of a cranial nerve and incidence of vascular compression.…”

Section: Discussionmentioning

confidence: 99%

Microvascular Decompression in Trigeminal Neuralgia with No Vascular Compression

Baechli

Gratzl²

2007

Eur Surg Res

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Background: Microvascular decompression (MVD) is a well-known surgical procedure with one of the best long-term results in the therapy of trigeminal neuralgia. But the exact pathophysiology of this disease has not yet been elucidated. Cases with undetectable vascular compression who are cured after MVD make this dilemma clear. Autopsy studies have also shown vascular compression in asymptomatic cases. Methods:Five of 40 cases with TN treated with MVD in our clinic had no visible vascular compression. Diagnosis was made with MRI and MRA. Results: Surprisingly all of these 5 patients were cured with MVD. Two of them needed only one operation to become pain free and 3 a second operation. Conclusion: We think that the therapeutic effect of MVD is due to minimal trauma of the nerve. It seems that MVD is a good alternative strategy with low complication rates in comparison to ablative procedures.

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Section: Discussionmentioning

confidence: 99%

Microvascular Decompression in Trigeminal Neuralgia with No Vascular Compression

Baechli

Gratzl²

2007

Eur Surg Res

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“…In the present case, the involvement of the pontine trigeminal entry zone (which has been implicated in the pathogenesis of trigeminal neuralgia [21] and SUNCT-like headache [22]) may also have led to the attacks of pain and, during severe attacks, to autonomic symptoms by the activation of collaterals of second-order trigeminal neurones to the superior salivatory nucleus. Alternatively, the partial ischemic damage to the spinal trigeminal tract or nucleus (causing ipsilateral facial hypesthesia for pain and temperature) may have led to an aberrant signal transmission to higher-order pain centres.…”

Section: Discussionmentioning

confidence: 98%

Trigemino-autonomic headache related to Gasperini syndrome

et al. 2010

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We report the association of ipsilateral trigemino-autonomic headache to a case of right-sided nuclear facial and abducens palsy (Gasperini syndrome), ipsilateral hypacusis and right hemiataxia, caused by the occlusion of the right anterior inferior cerebellar artery. Short-lasting attacks of mild to moderate ipsilateral fronto-periorbital head pain, accompanied by lacrimation and mild conjunctival injection during more severe attacks, were present from the onset of symptoms, with a gradual worsening over the next few months and remitting during naproxen therapy. Magnetic resonance imaging showed an infarct in the right cerebellar peduncle, extending toward the pontine tegmentum, also involving the ipsilateral spinal trigeminal nucleus and tract and the trigeminal entry zone. Gasperini syndrome may be accompanied by ipsilateral trigemino-autonomic head pain.

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“…One could be demyelination, which would cause electrophysiological alterations in the trigeminal system leading to ephaptic transmission, spontaneous firing, and mechanosensitivity, both before and after discharge. 3,4 The other could be the anatomical structure of trigeminal pathways. In general, the spinal trigeminal nucleus that controls the craniocervical part of algesthesia exists more caudal in the brainstem compared with the other nuclei of the trigeminal nerve.…”

Section: Discussionmentioning

confidence: 99%