Eric Anthony Nash, MD
Clinical Assistant Professor, Otolaryngology (Head and Neck Surgery)
Bio
Dr. Eric Nash is a board-certified otolaryngologist with Stanford Health Care. He is also a clinical assistant professor in the Department of Otolaryngology – Head and Neck Surgery at Stanford University School of Medicine.
Dr. Nash specializes in treating laryngeal and voice disorders and laryngeal, nasal, and ear disease; managing head and neck tumors; and performing surgery for sinus disorders.
Dr. Nash’s research interests include spasmodic dysphonia (a voice disorder that causes involuntary spasms of the vocal cords) and treatments for voice disorders.
Dr. Nash has published research in top scientific journals, including The Laryngoscope, Neurological Disease and Therapy, Otolaryngology–Head and Neck Surgery, and more.
Dr. Nash is a member of the American Medical Association, California Otolaryngology Society, and American Academy of Otolaryngology–Head and Neck Surgery.
Clinical Focus
- Otolaryngology
Academic Appointments
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Clinical Assistant Professor, Otolaryngology (Head and Neck Surgery)
Honors & Awards
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Palm Springs Top Physicians, Castle Connolly & Palm Springs Life Magazine (2008–2018)
Boards, Advisory Committees, Professional Organizations
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Fellow, American Academy of Otolaryngology–Head and Neck Surgery (AAO-HNS) (2001 - Present)
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Member, American Medical Association (2001 - Present)
Professional Education
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Residency: University of California at Irvine School of Medicine (1997) CA
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Medical Education: UCLA David Geffen School Of Medicine (1989) CA
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Board Certification: American Board of Otolaryngology, Otolaryngology (2001)
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Internship: Harbor UCLA Medical Center (1991) CA
All Publications
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Effects of stimulus intensity on laryngeal long latency responses in awake humans.
Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery
1997; 117 (5): 521-9
Abstract
Percutaneous electrical stimulation applied to the internal branch of the superior laryngeal nerve (ISLN) results in two long latency laryngeal adductor responses in awake humans: an ipsilateral thyroarytenoid (TA) R1 muscle response at 16 ms, and later bilateral TA R2 muscle responses at 60 ms. The purpose of this study was to determine whether a functional relationship existed between the R1 and R2 responses by gradually increasing the level of electrical stimulation from threshold to supramaximal levels. R1 amplitude increased linearly with stimulation intensity in 9 of the 11 subjects, whereas R2 only had a positive linear relationship in 3 subjects and a negative relationship with stimulation intensity in 1 subject. Significant negative relationships were found between response latency and stimulation intensity in 3 subjects for the R1 responses and 3 other subjects for the R2 responses. Overall, R1 amplitudes increased systematically, whereas R2 responses varied in latency and amplitude with increasing stimulus intensity. Neither the latencies nor the amplitudes of the two responses were related after adjusting for stimulation intensity within subjects by using partial correlation coefficients. The R1 and R2 responses were functionally unrelated and most likely have different neural components.
View details for DOI 10.1016/S0194-59989770025-1
View details for PubMedID 9374178
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Laryngeal muscle activity during speech breaks in adductor spasmodic dysphonia.
The Laryngoscope
1996; 106 (4): 484-9
Abstract
To determine the laryngeal muscle activation abnormalities that are associated with speech symptoms in adductor spasmodic dysphonia (ADSD), electromyographic measures of extrinsic and intrinsic laryngeal muscles during speech compared 1) muscle activity when ADSD patients had breaks in words with when they produced the same words without breaks; and 2) muscle activity in ADSD patients during speech without voice breaks with normal control producing phonetically similar words. Simultaneous electromyographic recordings were made from the thyroarytenoid (TA), cricothyroid (CT), sternothyroid (ST), thyrohyoid (TH) and the posterior cricoarytenoid (PCA) muscles during speech testing in 11 ADSD patients and 10 control subjects. Speech breaks were identified and mean muscle activity measured starting 100 ms preceding a voice break and for the remainder of the word. Mean muscle activity level was significantly greater on break than non break words in ADSD patients only for the thyroarytenoid muscle (p<.001). No significant differences were found between the ADSD and control subjects during non break words for any of the laryngeal muscles studied. The results demonstrated that 1) only the thyroarytenoid, of the muscles tested, was affected in ADSD, 2) that muscle activation abnormalities were spasmodic, only appearing when symptoms occurred and 3) no imbalances of muscle tone were evident when speech disruptions did not appear.
View details for DOI 10.1097/00005537-199604000-00017
View details for PubMedID 8614226
- Laryngeal muscle activation in abductor spasmodic dysphonia Otolaryngology--Head and Neck Surgery 115 (2). 1996 P141-P142
- Botulinum toxin injection for adductor spasmodic dysphonia NEUROLOGICAL DISEASE AND THERAPY 25. 1994 437-437