Varicella zoster virus (VZV) can invade the brainstem or brain via the glossopharyngeal, vagus , or facial nerve, resulting in brainstem inflammation or encephalitis. We report the case of a 66-year-old male patient with a primary manifestation of medulla injury of the glossopharyngeal and vagus nerves, combined with a medulla lesion, who was misdiagnosed with lateral medullary syndrome. Facial nerve injury and earache subsequently occurred and human herpes virus 3 (VZV) was detected by second-generation sequencing of the cerebrospinal fluid. The final diagnosis was varicella zoster encephalitis, which improved after antiviral therapy.

Cerebral fat embolism (CFE) syndrome is relatively rare in clinical practice. Currently, there is no uniform standard of magnetic resonance imaging for the diagnosis of the disease. In this report, we present head computed tomography and magnetic resonance images (T2-weighted images, fluid-attenuated inversion recovery images, diffusion-weighted images, and susceptibility-weighted images) in a case of CFE. This report explains the imaging characteristics of CFE and improves the clinician’s understanding of this disease and its etiology.

Rationale:Study reported an extremely rare case of trigeminal neuralgia, vestibular paroxysmia, and hemifacial spasm successively occurring in a patient with vertebrobasilar dolichoectasia (VBD).Patient concerns:A 66-year-old female patient presented with episodic vertigo for 20 days before she was admitted to our hospital. Vertigo suddenly occurred when the patient rotated her head 20 days ago, the symptoms of vertigo were improved after continuous 1 to 3 seconds, and similar symptoms were repeated in sleep and rest, with a frequency of 30 to 40 times per day. The patient had a history of hypertension with poor blood pressure control for more than 20 years.Diagnoses:The final diagnosis was vertebrobasilar dolichectasia, right trigeminal neuralgia, and vestibular paroxysmia.Interventions:Vitamin B1 (10 mg), methylcobalamin (0.5 mg), and carbamazepine (0.1 g) were given orally 3 times a day to relieve the symptoms.Outcomes:On the seventh day of drug treatment, the symptoms of paroxysmal vertigo and trigeminal neuralgia were completely relieved, but occasional episodes occurred during the follow-up period. Five months after discharge, right hemifacial spasm appeared in the patient, which did not affect the quality of life of the patient, so the patient did not choose further treatment. Six months after discharge, the patient was lost to follow-up.Lessons:Comprehensive treatment to control VBD risk factors, delay the progression of VBD, and improve clinical symptoms may have a better effect on such patients. However, further research is needed.

The Papez circuit is an important brain structure that is closely associated with learning and memory. In this report, we present four patients with anterograde amnesia as the main manifestation induced by Papez circuit infarction. In addition, we review the distribution of the responsible arteries in key and rare regions to investigate the pathogenesis of these infarctions.

Aims: To evaluate the clinical, pathological, and genetic features of patients with riboflavin-responsive multiple acyl-CoA dehydrogenase deficiency (RR-MADD). Methods: Thirty-one patients with RR-MADD admitted to our hospital from January 2005 to November 2020 were enrolled, and their clinical data were collected. Pathological characteristics of the muscle tissue and possible pathogenic gene mutations were analyzed. Results: The most common clinical features in all patients were symmetrical proximal muscle weakness. Laboratory examination revealed elevated levels of creatine kinase, homocysteine, and uric acid, acylcarnitines, and organic acid. The muscle biopsy revealed typical pathological changes like lipid deposition. Genetic analysis identified ETFDH mutations in 29 patients, among which one had homozygotes, 19 had compound heterozygotes, 7 had heterozygous mutations, and 2 had heterozygous mutations of both ETFDH and ETFA. Two patients had no pathogenic gene mutations. All patients were treated with riboflavin, and their symptoms improved, which was consistent with the diagnosis of RR-MADD. Conclusion: The clinical manifestations and genetic test results of patients with RR-MADD are heterogeneous. Therefore, a comprehensive analysis of clinical, pathological, and genetic testing is essential for the early diagnosis of RR-MADD.