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Litchy, William J.

https://orcid.org/0000-0002-0483-442X

Mayo Clinic

Mayo Clinic

Citations 82

In memorium: Jasper Daube MD
Litchy, William J. , Albers, James W., Phillips, Lawrence H.

Muscle & Nerve | May 11, 2020 | Volume: 62 | Issue: 2 | Pages: 149-151

10.1002/mus.26916 Get It

Neuromuscular transmission defects in myopathies
Liewluck, Teerin , Laughlin, Ruple S. , Litchy, William J. , Milone, Margherita , Liewluck, T

Muscle & Nerve | May 3, 2019 | Volume: 60 | Issue: 1 | Pages: No page available

10.1002/mus.26503 Get It

Neuromuscular transmission defects in myopathies: Rare but worth searching for
Elahi, Behzad , Laughlin, Ruple S. , Litchy, William J. , Milone, Margherita , Liewluck, Teerin , Liewluck, T

Muscle & Nerve | December 8, 2018 | Volume: 59 | Issue: 4 | Pages: 475-478

10.1002/mus.26393 Get It

ABSTRACTIntroduction: Decremental responses in repetitive nerve stimulation have been reported in a few hereditary myopathies. We examined the frequency of decrement in a cohort of myopathy patients. Methods: We reviewed all patients referred for myopathy who underwent repetitive nerve stimulation between January 2007 and May 2017. We included patients with decrement (>10%) and either a pathological or molecular diagnosis of myopathy. Results: Among 157 patients with myopathies, 4 patients had decrement (2 hydroxychloroquine‐associated vacuolar myopathy, 1 centronuclear myopathy, and 1 distal myopathy). One hydroxychloroquine‐associated vacuolar myopathy patient also had inflammatory myopathy. Pyridostigmine improved weakness in the centronuclear myopathy patient, but not in the distal myopathy patient. No patient with an acquired myopathy received pyridostigmine. Conclusions: Despite the rare occurrence of decrement in myopathy, its presence may urge consideration of pharmacological intervention. Muscle Nerve 59:475–478, 2019
A tropomyosin-receptor kinase-fused gene mutation associates with vacuolar myopathy
Madigan, Nicolas N. , Tracy, Jennifer A., Litchy, William J. , Niu, Zhiyv , Chen, Chunhua , Ling, Kun , Milone, Margherita , Niu, Zhiyv

Neurology Genetics | November 7, 2018 | Volume: 4 | Issue: 6 | Pages: No page available

10.1212/nxg.0000000000000287 Get It

Blink R1 latency utility in diagnosis and treatment assessment of polyradiculoneuropathy‐organomegaly‐endocrinopathy‐monoclonal protein‐skin changes and chronic inflammatory demyelinating polyradiculoneuropathy
Wang, Wei , Litchy, William J. , Mauermann, Michelle L. , Dyck, P. James B. , Mandrekar, Jay , Klein, Christopher J. , Dispenzieri, Angela , Klein, Christopher J , Mauermann, Michelle L

Muscle & Nerve | June 24, 2017 | Volume: 57 | Issue: 1 | Pages: No page available

10.1002/mus.25731 Get It

ABSTRACTIntroduction: In polyradiculoneuropathy‐organomegaly‐endocrinopathy‐monoclonal protein‐skin changes (POEMS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), limb nerve conduction studies (NCSs) are limited in identifying demyelination and in detecting treatment effects in severely affected patients. Blink R1 latency may improve these assessments. Methods: POEMS and CIDP patients who had undergone NCS and blink reflex were identified. Correlations among R1 latency, limb NCS, and neuropathy impairment scores (NIS) were compared. Results: Among 182 patients (124 POEMS, 58 CIDP) who were identified, R1 prolongation (>13 ms) occurred in 64.3% (65.3% POEMS, 62.1% CIDP). R1 prolongation correlated with more severely affected NCS in both POEMS (ulnar CMAP 2.6 mV vs. 4.5 mV, P = 0.001) and CIDP (2.0 mV vs. 6.1 mV, P < 0.001). In severely affected patients (ulnar CMAP ≤0.5 mV [10%:18/182]), R1 (>13 ms) helped establish demyelination. In 31 patients (16 POEMS, 15 CIDP), the R1 latency changes were concordant with NIS changes in 94% of patients with POEMS and 60% of patients with CIDP. Discussion: Blink R1 latencies are valuable in defining demyelination and detecting improvement in severely affected POEMS and CIDP patients. Muscle Nerve 57: E8–E13, 2018
Assessing mNIS+7Ionis and international neurologists' proficiency in a familial amyloidotic polyneuropathy trial
Dyck, Peter J., Dyck, Peter J., Kincaid, John C., Dyck, P. James B. , Chaudhry, Vinay , Goyal, Namita , Alves, Christina , Salhi, Hayet, Wiesman, Janice F. , Labeyrie, Céline , Robinson‐Papp, Jessica , Cardoso, Márcio , Laurá, Matilde , Ruzhansky, Katherine , Cortese, Andrea , Brannagan, Thomas H., Khoury, Julie, Khella, Sami, Ferreira, João , Wang, Annabel K., Pinto, Marcus Vinícius , Ayache, Samar S. , Benson, Merrill D., Coelho, Teresa , Polydefkis, Michael , Gorevic, Peter D., Planté‐Bordeneuve, Violaine , Whelan, Carol , Merlini, Giampaolo , Drachman, Brian, Conceição, Isabel , Klein, Christopher J. , Ackermann, Elizabeth J., Hughes, Steven G. , Mauermann, Michelle L. , Bergemann, R , Lodermeier, Karen A., Davies, Jenny L., Carter, Rickey E. , Litchy, William J. , Dyck, Peter J., Dyck, Peter J., Waddington‐Cruz, Márcia , Berk, John L. , Adams, David , Heitner, Stephen B. , Gertz, Morie A. , Merlini, Giampaolo , Pinto, Marcus V , Klein, Christopher J , Brannagan, T H , Carter, Rickey E , Conceição, Isabel , Mauermann, Michelle L

Muscle & Nerve | January 7, 2017 | Volume: 56 | Issue: 5 | Pages: 901-911

10.1002/mus.25563 Get It

ABSTRACTIntroductionPolyneuropathy signs (Neuropathy Impairment Score, NIS), neurophysiologic tests (m+7Ionis), disability, and health scores were assessed in baseline evaluations of 100 patients entered into an oligonucleotide familial amyloidotic polyneuropathy (FAP) trial.MethodsWe assessed: (1) Proficiency of grading neurologic signs and correlation with neurophysiologic tests, and (2) clinometric performance of modified NIS+7 neurophysiologic tests (mNIS+7Ionis) and its subscores and correlation with disability and health scores.ResultsThe mNIS+7Ionis sensitively detected, characterized, and broadly scaled diverse polyneuropathy impairments. Polyneuropathy signs (NIS and subscores) correlated with neurophysiology tests, disability, and health scores. Smart Somatotopic Quantitative Sensation Testing of heat as pain 5 provided a needed measure of small fiber involvement not adequately assessed by other tests.ConclusionsSpecially trained neurologists accurately assessed neuropathy signs as compared to referenced neurophysiologic tests. The score, mNIS+7Ionis, broadly detected, characterized, and scaled polyneuropathy abnormality in FAP, which correlated with disability and health scores. Muscle Nerve 56: 901–911, 2017
Epidermal Nerve Fiber Quantification in Patients With Erythromelalgia
Mantyh, William G. , Dyck, P. James B. , Engelstad, JaNean , Litchy, William J. , Sandroni, Paola , Davis, Mark D.P.

JAMA Dermatology | December 7, 2016 | Volume: 153 | Issue: 2 | Pages: 162

10.1001/jamadermatol.2016.4404 Get It

Blink reflex role in algorithmic genetic testing of inherited polyneuropathies
Wang, Wei , Litchy, William J. , Mandrekar, Jay , Dyck, P. James B. , Klein, Christopher J. , Klein, Christopher J

Muscle & Nerve | July 16, 2016 | Volume: 55 | Issue: 3 | Pages: 316-322

10.1002/mus.25250 Get It

Rapsyn congenital myasthenic syndrome worsened by fluoxetine
Visser, Amy , Laughlin, Ruple S. , Litchy, William J. , Benarroch, Eduardo E. , Milone, Margherita , Visser, Amy C

Muscle & Nerve | July 11, 2016 | Volume: 55 | Issue: 1 | Pages: 131-135

10.1002/mus.25244 Get It

ABSTRACTIntroduction: Fluoxetine is a selective serotonin reuptake inhibitor and long‐lived open channel blocker of the acetylcholine receptor, often used in the treatment of slow‐channel congenital myasthenic syndromes (CMS). Methods: We report a 42‐year‐old woman who had a history of episodic limb weakness that worsened after initiation of fluoxetine for treatment of depression. Genetic testing for CMS revealed a homozygous pathogenic mutation in the rapsyn (RAPSN) gene (p.Asn88Lys). Electrodiagnostic testing was performed before and 1 month after discontinuation of fluoxetine. Results: The 2 Hz repetitive nerve stimulation of the fibular and spinal accessory nerves showed a baseline decrement of 36% and 14%, respectively. One month after discontinuing fluoxetine, the spinal accessory nerve decrement was no longer present, and the decrement in the fibular nerve was improved at 17%. Conclusions: This case demonstrates worsening of both clinical and electrophysiologic findings in a patient with CMS secondary to a RAPSN mutation treated with fluoxetine. Muscle Nerve 55: 131–135, 2017