Case report: Trigeminal neuralgia misdiagnosed as glossopharyngeal neuralgia.

Background: Trigeminal neuralgia (TN) and glossopharyngeal neuralgia (GPN) are cranial nerve neuralgias with the same clinical manifestations, pathological features, and trigger factors; their affected sites are adjacent. Performing a magnetic resonance imaging (MRI) examination alone can easily lead to a misdiagnosis. Case presentation: A 72-year-old man had visited another hospital with severe left-sided tongue pain. On MRI, vascular compression of the glossopharyngeal nerve had been visible, with unclear evidence of trigeminal nerve involvement. He had been diagnosed with left-sided GPN and underwent microvascular decompression (MVD) of the left glossopharyngeal nerve. However, no improvement was observed after surgery. During a second surgery at our hospital, MVD of the trigeminal nerve was performed, and the trigeminal nerve was fully explored and separated. The patient's pain resolved after surgery. Ultimately, the patient was definitively diagnosed with left-sided TN. Discussion and conclusion: MVD is currently the most efficacious surgical option for treating cranial nerve neuralgia. To select patients for MVD, having an MRI criteria for identifying true neurovascular compression will be helpful. However, clinicians should focus more on a patient's clinical symptoms and not rely solely on MRI findings. This patient's case can help clinicians distinguish between TN and GPN, improve the understanding of these diseases, avoid misdiagnosis, and reduce the possibility of secondary damage.

Zolpidem arouses patients in vegetative state after brain injury: quantitative evaluation and indications.

BACKGROUND: To investigate the efficacy and indications of zolpidem, a nonbenzodiazepine hypnotic, inducing arousal in vegetative state patients after brain injury. METHODS: One hundred sixty-five patients were divided into 4 groups, according to area of brain damage and injury mechanism. All patients' brains were imaged by Tc-ECD single-photon emission computerized tomography (SPECT), before and 1 hour after treatment with 10 mg of zolpidem. Simultaneously, 3 quantitative indicators of brain function and damage were obtained using cerebral state monitor. Thirty-eight patients withdrew from the study after the first zolpidem dose. The remaining 127 patients received a daily dose of 10 mg of zolpidem for 1 week and were monitored again at the end of this week. RESULTS: One hour after treatment with zolpidem, cerebral state index was increased and burst suppression reduced in both brain contrecoup contusion and space-occupying brain compression groups (P < 0.05). SPECT showed, 1 hour after medication, that cerebral perfusion was improved in both brain contrecoup contusion and space-occupying brain compression groups, but no changes were seen in primary and secondary brain stem injury groups. In the 127 patients' group, after 1 week of zolpidem treatment, all parameters obtained from cerebral state monitor were not statistically different compared with those after the initial medication (P > 0.05). CONCLUSIONS: Zolpidem is an effective medicine to restore brain function in patients in vegetative state after brain injury, especially for those whose brain injuries are mainly in non-brain-stem areas. Improvement of brain function is sudden rather than gradual.