Upper Motor Neuron Diseases and Laryngeal Presentations
- PDF / 585,512 Bytes
- 6 Pages / 595.276 x 790.866 pts Page_size
- 115 Downloads / 188 Views
NEUROLARYNGOLOGY (AJ MCWHORTER AND L ADKINS, SECTION EDITORS)
Upper Motor Neuron Diseases and Laryngeal Presentations Yolanda D. Heman-Ackah 1,2,3
# Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Purpose of Review The purpose of this manuscript is to review laryngeal manifestations of upper motor neuron disease. A review of the relevant neuroanatomy is performed as well as a description of common laryngeal signs of upper motor neuron disease and the disease entities that cause them. Recent Findings Upper motor neuron lesions must occur in the brainstem or in the bilateral cerebral hemisphere in order to cause signs and symptoms in the larynx. Summary The presence of bilateral vocal fold paralysis or paresis with concurrent signs of myoclonus, tremor, rigidity, hyperactive gag reflex, and/or laryngospasm episodes should prompt an investigation for possible medullary brainstem or bilateral cerebral cortex pathology. Keywords Pseudobulbar palsy . Spastic vocal fold paralysis . Spastic laryngeal nerve paralysis . Bilateral vocal fold paralysis . Upper motor neuron disease . Dysphonia
Introduction The larynx receives its motor innervation from the Xth cranial nerve, whose upper motor neuron is part of the corticobulbar tract. The corticobulbar tract originates in the lateral aspect of the motor cortex of the frontal lobe, an area often referred to as “Brodmann’s Area 4” (Fig. 1). The corticobulbar tract contains axons of the motor divisions of cranial nerves V, VII, IX, X, XI, and XII. From the motor cortex, these axons then travel with the corticospinal tract through the internal capsule and to the brainstem. At the brainstem, the axons terminate in the This article is part of the Topical collection on Neurolaryngology Electronic supplementary material The online version of this article (https://doi.org/10.1007/s40136-020-00292-9) contains supplementary material, which is available to authorized users. * Yolanda D. Heman-Ackah [email protected] 1
Philadelphia Voice Center, PO BOX 2878, Bala Cynwyd, PA 19004, USA
2
Department of Otolaryngology-Head and Neck Surgery, Drexel University College of Medicine, Philadelphia, PA, USA
3
Department of Otolaryngology-Head and Neck Surgery, Thomas Jefferson University Sidney Kimmel Medical School, Philadelphia, PA, USA
cranial nerve nuclei contained in the medulla and pons [1, 2]. In the medulla and pons, the bilateral corticobulbar tracts from each cerebral hemisphere provide axons to each of the cranial nerve nuclei for cranial nerves V, IX, X, and XI and the upper face supplied by CN VII. The lower face (CN VII) receives innervation only from the contralateral corticobulbar tract. Thus, when an ipsilateral disruption of the corticobulbar tract occurs, oftentimes, the only motor deficit is a paresis/paralysis of the contralateral lower face [1–5]. In general, lesions that affect upper motor neurons (i.e., axons in the corticobulbar tract above the cranial nerve nuclei or in the corticospinal tracts above the anterior horn cell in the spin
Data Loading...
