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Cranial Neuropathies I, V, and VII–XII
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Brainstem: lesions are often associated with other CN deficits and long tract involvement: Stroke (lateral medullary syndrome).Multiple sclerosis (MS).Tumor (brainstem glioma, lymphoma, and metastases).Syringobulbia.Hemorrhage from hypertension, ruptured vascular anomalies.Inflammatory conditions: sarcoidosis, connective tissue diseases, and vasculitis.Infectious conditions.
6th Nerve (Abducent) Palsy
Published in K. Gupta, P. Carmichael, A. Zumla, 100 Short Cases for the MRCP, 2020
K. Gupta, P. Carmichael, A. Zumla
The lateral medullary syndrome (Wallenberg's syndrome) is characterized by the thrombosis of the vertebral or the posterior inferior cerebellar artery. The clinical features include: Numbness and impaired sensation over the half of the face (ipsilateral 5th cranial nerve damage).Loss of taste (nucleus and tractus solitarius).Dysphasia, paralysis of vocal cords and hoarseness (9th and 10th nerves). Ipsilateral cerebellar signs.Ipsilateral Horner's syndrome (sympathetic fibres).Vertigo, nystagmus, diplopia (vestibular nucleus).Contralateral loss of pain and temperature over half of the body (spinothalamic tract).
Brain regions, lesions, and stroke syndromes
Published in Christos Tziotzios, Jesse Dawson, Matthew Walters, Kennedy R Lees, Stroke in Practice, 2017
Christos Tziotzios, Jesse Dawson, Matthew Walters, Kennedy R Lees
Lateral medullary syndrome (German internist and neurologist Wallenberg’s syndrome). Ataxia, vertigo, nystagmus; nausea and vomiting; ipsilateral Horn-er’s syndrome; ipsilateral facial and body sensory loss; swallowing and speaking difficulties. Due to lateral medullary infarction.
Center of pressure velocities in patients with body lateropulsion: three case report series of Wallenberg’s syndrome
Published in Physiotherapy Theory and Practice, 2022
Hideaki Matsuo, Masafumi Kubota, Mayumi Matsumura, Mami Takayama, Yuri Mae, Yuki Kitazaki, Soichi Enomoto, Asako Ueno, Masamichi Ikawa, Tadanori Hamano, Ai Takahashi, Misao Tsubokawa, Seiichiro Shimada
Wallenberg’s syndrome, also known as a lateral medullary syndrome, is a neurological condition caused by a lateral medullary infarction. This syndrome’s symptoms are ipsilateral Horner syndrome, ipsilateral limb ataxia, superficial sensory disturbance of the ipsilateral face and contralateral limbs, dysarthria, dysphagia, and vertigo. Body lateropulsion (BL), a postural disorder characterized by the body involuntarily tilting to one side, is one of the Wallenberg syndrome’s predominant symptoms (Dieterich and Brandt, 1992, 2019; Kim et al., 2007; Maeda et al., 2005; Pérennou et al., 2008; Thömke et al., 2005; Yamaoka, Kishishita, Takayama, and Okubo, 2018). Lesions of the descending lateral vestibulospinal tract or the ascending dorsal spinocerebellar tract may induce BL (Kim et al., 2007; Maeda et al., 2005; Thömke et al., 2005). Pérennou et al. (2008) reported that patients having brainstem strokes showed severe visual vertical tilts and BL and minor or no tilts of vertical posture. This suggests that vestibular nuclear lesions interfere with postural control via direct vestibulo-spinal mechanisms rather than via a higher-order representation mechanism (Kim et al., 2007; Pérennou et al., 2008, 2014). Although pathological mechanisms that cause BL are better understood, features of postural control are not fully understood. Therefore, demonstrating these features during the recovery process of patients with BL may assist in developing effective physical therapy programs and plans of care.
An innovative approach in the treatment of trigeminal trophic syndrome
Published in Journal of Dermatological Treatment, 2022
Catherine Pisano, Matthew Fox, Jason Reichenberg
Trigeminal trophic syndrome (TTS) is a rare disorder that presents as ulceration of the nasal ala, and less often with ipsilateral cheek, cutaneous lip, and forehead involvement, following damage to the trigeminal nerve (1–6). Less than 200 cases of trigeminal trophic syndrome have been reported worldwide with the highest prevalence being in middle-aged women (1). The leading cause of TTS is believed to be insult to the trigeminal nerve following trigeminal nerve ablation or transection of the Gasserian ganglion during therapeutic treatment of trigeminal neuralgia (1). Other less common causes include strokes (particularly Wallenberg lateral medullary syndrome), intracranial neoplasms, trauma, or infection (1–3). Treatment of TTS is notoriously difficult due to the large behavioral component of this disease process in addition to the irreversible trigeminal anesthesia and paresthesia in a dermatomal distribution. Here we present a challenging case of TTS following trauma and concurrent herpes zoster infection with successful treatment using thermoplastic mask placement. Our patient presented with extensive geometric ulceration of his left medial face extending from his eyebrow to upper cutaneous lip with complete absence of his left nasal ala. Significant re-epithelization was seen after only 6 weeks of thermoplastic mask therapy. While thermoplastic mask placement is effective for TTS, there are very limited reports of its success in the United States. This case is being presented to highlight the clinical diagnosis and treatment of TTS using thermoplastic mask placement.
Audiovestibular findings in a 6 year old child with pilocytic astrocytoma – a case report
Published in International Journal of Audiology, 2020
Aravind Kumar Rajasekaran, A. Arivazhagan, Pradeep Yuvaraj, N. Shivashankar
Compromise of vestibular commissural fibres (which are part of central compensation mechanism) has been reported to cause hyper-excited response in the contralateral vestibular nuclei due to dis-inhibition (Lundy, Zapala, and Olsholt 2008). Lundy, Zapala, and Olsholt (2008) drew evidence for their postulation from the presence of commissural fibres (Uchino et al. 2001) and their affliction in patients with lateral medullary syndrome (Dieterich et al. 2005). However, this postulate can only explain the hyper-excited response on the non-lesion side and not on the lesion side, as observed in our patient.