Muscle hypertrophy following acquired neurogenic injury: systematic review and analysis of existing literature

Author:

Strano Camilla MM123ORCID,Bosco Luca123,Laurini Christian13,Sferruzza Giacomo4,Butera Carla5,Falzone Yuri M.12,Sorrenti Benedetta13,Ratti Adele13,Tufano Laura6,Leonardi Luca7,Merlonghi Gloria6,Morino Stefania7,Gerevini Simonetta8,Del Carro Ubaldo5,Garibaldi Matteo67ORCID,Filippi Massimo1345ORCID,Previtali Stefano C12

Affiliation:

1. Neurology Unit IRCCS San Raffaele Scientific Institute Milan Italy

2. Neuromuscular Repair Unit, Institute of Experimental Neurology (INSPE) IRCCS San Raffaele Scientific Institute Milan Italy

3. Vita‐Salute San Raffaele University Milan Italy

4. Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience IRCCS San Raffaele Scientific Institute Milan Italy

5. Neurophysiology Unit IRCCS San Raffaele Scientific Institute Milan Italy

6. Department of Neuroscience, Mental Health and Sensory Organs (NESMOS), Faculty of Medicine and Psychology SAPIENZA University of Rome Rome Italy

7. Neurophysiology Unit Sant'Andrea Hospital Rome Italy

8. Unit of Neuroradiology Papa Giovanni XXIII Hospital Bergamo Italy

Abstract

AbstractObjectivesNeurogenic muscle hypertrophy (NMH) is a rare condition characterized by focal muscle hypertrophy caused by chronic partial nervous injury. Given its infrequency, underlying mechanisms remain poorly understood. Inspired by two clinical cases, we conducted a systematic review to gain insights into the different aspects of NMH.MethodsWe systematically searched online databases up until May 30, 2023, for reports of muscle hypertrophy attributed to acquired neurogenic factors. We conducted an exploratory analysis to identify commonly associated features. We also report two representative clinical cases.ResultsOur search identified 63 reports, describing 93 NMH cases, to which we added our two cases. NMH predominantly affects patients with compressive radiculopathy (68.4%), negligible muscular weakness (93.3%), and a chronic increase in muscle bulk. A striking finding in most neurophysiological studies (60.0%) is profuse spontaneous discharges, often hindering the analysis of voluntary traces. Some patients exhibited features consistent with more significant muscle damage, including higher creatine phosphokinase levels, muscle pain, and inflammatory muscle infiltration. These patients are sometimes referred to in literature as “focal myositis.” Treatment encompassed corticosteroid, Botulinum Toxin A, decompressive surgery, antiepileptic medications, and nerve blocks, demonstrating varying degrees of efficacy. Botulinum Toxin A yielded the most favorable response in terms of reducing spontaneous discharges.InterpretationThis systematic review aims to provide a clear description and categorization of this uncommon presentation of an often‐overlooked neurological disorder. Though questions remain about the underlying mechanism, evidence suggests that aberrant fiber overstimulation along with increased workload that promotes focal damage may result in muscle hypertrophy. This may serve as a guide for therapeutic interventions.

Publisher

Wiley

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