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Classification of Seizures and Epilepsy
Published in Stanley R. Resor, Henn Kutt, The Medical Treatment of Epilepsy, 2020
The subtypes of temporal lobe and frontal lobe epilepsies are really anatomic specifications of seizures, not epileptic syndromes. And while temporal lobe epilepsy is surely a welcome addition as the most common syndrome encountered in adults and is additionally supported by a wealth of clinical data, the other various anatomic subtypes, especially of the frontal lobe epilepsies, can hardly be justified by the available information and, in any event, depend almost entirely for recognition upon availability of intracranial epidural or depth electrodes. A simple distinction between “temporal lobe epilepsy” and “extratemporal symptomatic epilepsy” might have been wiser, more practical, and easier to support with information now available. Finally, the appendix listing “Symptomatic generalized epilepsies of specific etiologics” is illogical and out of date. Why separate out different forms of neuronal ceriod lipofuchsinosis but not do the same for the various variants of the gangliosidoses or sialodoses? The mitochondrial disorders, now one of the best understood groups causing progressive myoclonus epilepsy, are not mentioned. And some authors, including me, do not believe Ramsay-Hunt syndrome can any longer be defended as a specific disease (17).
Neurological problems
Published in Catherine Nelson-Piercy, Handbook of Obstetric Medicine, 2020
Ramsay Hunt syndrome is herpes zoster (shingles) of the geniculate ganglion and causes a unilateral facial palsy (identical to Bell's) with herpetic vesicles in the external auditory meatus and occasionally the soft palate.
The Facial Nerve and its Non-Neoplastic Disorders
Published in John C Watkinson, Raymond W Clarke, Christopher P Aldren, Doris-Eva Bamiou, Raymond W Clarke, Richard M Irving, Haytham Kubba, Shakeel R Saeed, Paediatrics, The Ear, Skull Base, 2018
Christopher Skilbeck, Susan Standring, Michael Gleeson
The prognosis for Ramsay Hunt is worse than idiopathic facial palsy. Persistent weakness is observed in 30–50% of patients and only 10% recover completely after complete loss of function without treatment.133 Regarding management, the same controversies exist as in idiopathic palsy. Most advocate a combination of steroids and antiviral agents, but for a longer period of time, 2–3 weeks. The largest retrospective Ramsay Hunt syndrome treatment study showed a statistically significant improvement in patients treated with prednisone and acyclovir within 3 days of onset.134 The recommended regime is prednisone 1 mg/kg/day for 5 days followed by a 10-day taper, as well as intravenous acyclovir (250 mg three times daily), or oral acyclovir (800 mg five times daily). Robillard et al. 135 have shown that patients with Ramsay Hunt syndrome treated with prednisone were less likely to progress to complete facial paralysis than untreated patients. The combination of steroids and acyclovir also seems to reduce otalgia, vertigo and post-herpetic neuralgia. Surgical decompression is not indicated.
Disseminated herpes zoster in an immunocompetent young adult: A rare complication of Ramsay Hunt syndrome
Published in Acta Oto-Laryngologica Case Reports, 2023
Naoyuki Matsumoto, Makiko Toma-Hirano, Takuya Yasui, Ken Ito
Ramsay Hunt syndrome (RHS) is a complication of latent varicella-zoster virus (VZV) infection, and is considered as a form of herpes zoster occurring in the otic region. It is usually identified clinically as a triad of facial paralysis, otalgia and herpetiform vesicles on the ear or in the mouth, frequently accompanied by vestibulocochlear symptoms, such as tinnitus, sensorineural hearing loss, and vertigo [1]. Herpes zoster is caused by reactivation of VZV which may be dormant in sensory ganglia of the dorsal root ganglia after a previous varicella infection. Although grouped vesiculobullous skin lesions usually appear along only one or two dermatomes, it is occasionally disseminated hematogenously in patients with decreased immunity [2]. We report a rare case of Ramsay Hunt syndrome developing disseminated herpes zoster in an immunocompetent young adult, in whom discrimination from drug eruption was important for clinical decision-making.
The characteristics of vHIT gain and PR score in peripheral vestibular disorders
Published in Acta Oto-Laryngologica, 2021
Yi Du, Lili Ren, Xingjian Liu, Weiwei Guo, Ziming Wu, Shiming Yang
We retrospectively analyzed 386 patients admitted to the vertigo clinic at the Chinese PLA General Hospital from December 2019 to May 2020. Two authors (ZMW and LLR) carefully reviewed patients’ information, including the history, medical records, imaging results, neuro-otological examination, audiology, and vestibular function tests. Acoustic neuroma (AN) were radiologically diagnosed and went through vHIT before surgery. MD was diagnosed according to the AAO-NHS criteria [10]. Vestibular migraine (VM) patients were identified according to the Barany Society diagnostic criteria [11]. The diagnosis of benign paroxysmal positional vertigo (BPPV) is based on the Barany Society 2015 diagnostic criteria [12]. Bilateral vestibular hypofunction (BVH) is diagnosed according to the Barany Society 2017 diagnostic criteria [13]. Ramsay-Hunt syndrome (RHS) with vertigo is diagnosed with an ipsilateral herpetic eruption on the auricle and external ear canal, facial palsy, and vertigo. The diagnosis of unilateral vestibular dysfunction(UVD) was based on the history of acute sustained vertigo or imbalance, abnormal results in the caloric test (unilateral weakness >25%) and no additional central lesion signs.
Electroneurography value as an indicator of high risk for the development of moderate-to-severe synkinesis after Bell’s palsy and Ramsay Hunt syndrome
Published in Acta Oto-Laryngologica, 2019
Haruki Nakano, Shin-Ichi Haginomori, Shin-Ichi Wada, Yusuke Ayani, Ryo Kawata, Ryuichi Saura
From April 2014 to September 2016, 114 patients who had been treated for Bell’s palsy and Ramsay Hunt syndrome at our hospital were retrospectively screened. Patients who were younger than 20 years of age, older than 85 years of age, or whose conditions were complicated by other neurological diseases were excluded (n = 19). In addition, patients who underwent decompression surgery (n = 11) were excluded. According to the method many reports adopted, patients were classified into two groups based on the ENoG value: those with an ENoG value of 10%–20% were classified into Group A, and those with an ENoG value of <10% were classified into Group B [2–4]. The patients with an ENoG value of >20% (n = 45) were excluded, as we previously reported that patients with an ENoG value of >20% were cured within 4 months [5].