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Trigeminal neuralgia induced by brainstem infarction treated with pontine descending tractotomy: illustrative case

Rachyl M. Shanker, Miri Kim, Chloe Verducci, Elhaum G. Rezaii, Kerry Steed, Atul K. Mallik, and Douglas E. Anderson

Trigeminal neuralgia (TN) most commonly presents as neuropathic pain secondary to neurovascular compression (NVC) at the nerve root entry zone (NREZ) 1 , 2 or as a result of a space-occupying lesion impacting the trigeminal nerve. 3 However, there exists a subset of patients in whom trigeminal pain is induced by brainstem ischemia, interrupting the NREZ, spinal trigeminal nucleus, or descending spinal trigeminal tract (SpTV). While cases of TN induced by a brainstem infarct have been reported, there are no clear treatment recommendations for this

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Computational hemodynamic analysis of the offending vertebral artery at the site of neurovascular contact in a case of hemifacial spasm associated with subclavian steal syndrome: illustrative case

Keita Tominaga, Hidenori Endo, Shin-ichiro Sugiyama, Shin-ichiro Osawa, Kuniyasu Niizuma, and Teiji Tominaga

Neurovascular compression syndromes such as hemifacial spasm (HFS) and trigeminal neuralgia (TN) are generally caused by neurovascular contact between the vascular structure and the cranial nerves. In HFS, neurovascular compression occurs along the root exit zone (REZ) of the facial nerve, most commonly by either the anterior inferior cerebellar artery or the posterior inferior cerebellar artery (PICA) and rarely by vertebral artery (VA). Microvascular decompression (MVD) is an effective microsurgical treatment option for HFS through releasing the contact of

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Microvascular decompression for developmental venous anomaly causing hemifacial spasm: illustrative case

Margaret Tugend and Raymond F Sekula Jr.

DVA or a decrease in outflow from the DVA. Symptoms from flow-related causes include headache, neurological deficit, seizures, and coma secondary to hemorrhage or infarction. Mechanical causes include obstructive hydrocephalus and nerve compression, causing trigeminal neuralgia and HFS. Cases with symptoms attributed to DVA, such as headache, but with no identifiable patho-mechanism, are classified as idiopathic. 5 Here, we present an example of mechanical compression of the facial nerve by a pontine DVA ostensibly causing HFS. Although the patient ultimately had a