A Rare Case of Dysphagia with Palatal Tremor
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CLINICAL CONUNDRUM
A Rare Case of Dysphagia with Palatal Tremor Tao Xiang1 · Feng Wang2 · Yingyue Yang1 · Juan Li1 Received: 15 July 2020 / Accepted: 24 August 2020 © The Author(s) 2020
Case Presentation
Diagnosis
A 77-year-old man with a known history of long-standing hypertension experienced a left cerebellar hemorrhage 9 months ago, then a right cerebellar hemorrhage 3 months prior to his presentation. The patient had noticeable dysphagia that required placing a nasogastric tube for nasal feeding. The standardized swallowing assessment revealed that he had an impairment in lip closure, head, and trunk control, pharyngeal reflex, as well as independent coughing. To observe the pathophysiological changes of the pharynx and larynx, a fiberoptic laryngoscope was inserted prior to the video fluoroscopic swallowing study (VFSS), which showed that there was no pathophysiological change. VFSS detected the rhythmic tremor of the soft palate and epiglottis, with residues displayed in the vallecula and pyriform sinuses. Magnetic resonance imaging (MRI) depicted bilateral long T2 signal shadows in the cerebellum, enlargement of the bilateral olivary nucleus, with a longer T2-weighted signal change. The T2 FLAIR image demonstrated an increased signal change, with the right inferior olivary nucleus (ION) obviously larger than the left. (Fig. 1) (9 months after the left cerebellar hemorrhage, 3 months after the right cerebellar hemorrhage).
The patient presented with a palatal tremor (PT) after two episodes of cerebellar hemorrhage. MRI indicated bilateral hypertrophic degeneration of the olivary nucleus, especially on the left side. These findings taken together confirmed a diagnosis of hypertrophic olivary degeneration (HOD). HOD is a rare neurological condition characterized by trans-synaptic degeneration that occurs secondary to focal lesions disrupting the normal function of the afferent fibers to the ION as part of the dentate–rubro–olivary pathways (Guillain–Mollaret triangle, GMT) [1]. Possible etiologies for this condition include infarction, toxicosis, trauma, surgery, tumors, vascular malformations or hemorrhage. In this case, the patient developed HOD secondary to cerebellar hemorrhage [2].
* Tao Xiang [email protected] Feng Wang [email protected] Yingyue Yang [email protected] Juan Li [email protected] 1
Department of Rehabilitation Medicine, Chengdu Second People’s Hospital, No. 10 Qingyunnan Street, Jinjiang District, Chengdu 610017, Sichuan, China
Department of Neurology, Chengdu Second People’s Hospital, Chengdu 610017, Sichuan, China
2
Discussion GMT is composed of the contralateral dentate nucleus (DN), the ipsilateral red nucleus (RN) and the ipsilateral ION. DN, RN, and ION form an afferent and efferent loop pathway. The fibers from the DN are crossed by the superior cerebellar foot and reach the contralateral midbrain red nucleus. The red nucleus sends fibers descending through the central tegmental bundle to the ipsilateral ION for relay. The ION is then emitted from fibers passing through the
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