Eight-and-a-half syndrome caused by tuberculous meningitis: a case report
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LETTER TO THE EDITOR
Eight‑and‑a‑half syndrome caused by tuberculous meningitis: a case report Kai Shao1,2 · Fangming Dong1,2 · Shangzun Guo2,3 · Jianhua Wang1,2 · Zhanyong Sun1,2 Received: 29 August 2020 / Accepted: 20 October 2020 © Belgian Neurological Society 2020
Keywords Tuberculous meningitis · Central nervous system infection · Eight-and-a-half syndrome · One-and-a-half syndrome · Facial nerve palsy · Internuclear opthalmoplegia
Introduction Eight-and-a-half syndrome is recognized as one-and-a-half syndrome with the addition of peripheral facial nerve palsy, often caused by ischemic strokes, demyelinating lesions, tumors and arteriovenous malformations [1]. There are no documented cases in the literature of a patient with tuberculous meningitis (TBM) presenting with eight-and-a-half syndrome. Here we report, to the best of our knowledge, the first case of TBM with eight-and-a-half syndrome.
Case presentation A 46-year-old man was admitted to the hospital with a one-month history of right facial weakness and a twoweek history of abrupt-onset diplopia when looking to the right. These symptoms were accompanied by complaints of * Zhanyong Sun [email protected] Kai Shao [email protected] Fangming Dong [email protected] Shangzun Guo [email protected] Jianhua Wang [email protected] 1
Department of Neurology, Hebei Medical University, Shijiazhuang 050017, China
2
Department of Neurology, Hebei General Hospital, Shijiazhuang 050051, China
3
Department of Graduate College, Hebei North University, Zhangjiakou 075000, China
headache, dizziness, low-grade fever, anorexia and fatigue for the past month. He had been diagnosed with hypertension one month prior. Neurological examination on admission revealed right horizontal conjugate gaze palsy, limited adduction of the right eye, and horizontal nystagmus of the left eye upon abduction. Vertical eye movements were normal, and pupils were symmetrical and reactive to light. He also had right peripheral facial palsy and right Horner’s syndrome. No hemiparesis or hemisensory deficit was found and deep tendon reflexes were normal. No pathological reflection of Babinski’s sign was induced. There was no sign of meningeal irritation. Laboratory investigations showed a high white blood count (9.44 × 109/L, 75.10% neutrophils) and high C-reactive protein levels (17.26 mg/L). Chest X-ray and CT showed no remarkable findings. Brain T2-weighted magnetic resonance imaging showed hyperintense lesions in the right medulla oblongata and pons (Fig. 1a, b). Brain gadolinium (Gd)-enhanced T1-weighted images revealed contrast enhancement in the medulla oblongata, pons, and leptomeninges (Fig. 1c, d). A lumbar puncture was performed to collect cerebrospinal fluid (CSF). The CSF was colorless and transparent, weakly positive on the Pandy test (qualitative test of elevated protein), negative in acid-fast bacilli (AFB) staining, ink staining, virus polymerase chain reaction, and bacterial culture. CSF findings during the period of hospitalization are listed in Table 1. Olig
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