BACKGROUND: Neurovascular-compression syndrome (NCS) is described as a prominent pathological contact between cranial nerves and vessels. Trigeminal neuralgia, hemifacial spasm, and glossopharyngeal neuralgia are typical clinical entities associated with NCS. On the other hand, the hyoglossal nerve is rarely affected by NCS. CASE DESCRIPTION: We present a case of hypoglossal nerve palsy (HNP) secondary to vertebral artery (VA) compression. A 47-year-old man presented to our hospital with a 1-month history of dysarthria and dysphagia. Neurological examination revealed left HNP, with an intact swallowing reflex and no oropharyngeal or palatal weakness. Magnetic resonance imaging (constructive interference in steady state) revealed left hypoglossal nerve compression by the V4 segment of the left atherosclerotic VA. He underwent microvascular decompression (MVD) surgery. Intraoperatively, the VA was compressing the hypoglossal nerve. The left VA was moved and attached to the dura matter using a polytetrafluoroethylene (Teflon®) sheet and fibrin glue. Postoperatively, the patient exhibited gradual recovery of HNP in 3 months without dysfunction of lower cranial nerves. CONCLUSION: In patients with isolated HNP, vascular compression should be considered as a cause of these symptoms, and subsequent MVD can lead to resolution.
BACKGROUND:Neurovascular-compression syndrome (NCS) is described as a prominent pathological contact between cranial nerves and vessels. Trigeminal neuralgia, hemifacial spasm, and glossopharyngeal neuralgia are typical clinical entities associated with NCS. On the other hand, the hyoglossal nerve is rarely affected by NCS. CASE DESCRIPTION: We present a case of hypoglossal nerve palsy (HNP) secondary to vertebral artery (VA) compression. A 47-year-old man presented to our hospital with a 1-month history of dysarthria and dysphagia. Neurological examination revealed left HNP, with an intact swallowing reflex and no oropharyngeal or palatal weakness. Magnetic resonance imaging (constructive interference in steady state) revealed left hypoglossal nerve compression by the V4 segment of the left atherosclerotic VA. He underwent microvascular decompression (MVD) surgery. Intraoperatively, the VA was compressing the hypoglossal nerve. The left VA was moved and attached to the dura matter using a polytetrafluoroethylene (Teflon®) sheet and fibrin glue. Postoperatively, the patient exhibited gradual recovery of HNP in 3 months without dysfunction of lower cranial nerves. CONCLUSION: In patients with isolated HNP, vascular compression should be considered as a cause of these symptoms, and subsequent MVD can lead to resolution.