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LETTERS to the EDITOR Calf Muscle Hypertrophy Clinical Neuropathology, Vol. 37 – No. 3/2018 – Letters to the editor 146 LETTERS TO THE EDITOR sias in the right foot and continuous calf pain. Routine blood tests, including sedimentation rate, C-reactive protein, eosinophil count, Calf muscle hypertrophy thyroid hormones, liver enzymes, and cry- following S1 radiculopathy: ocrit were within normal ranges. ANA-ENA screening and search for neurotrophic vi- Letter A stress disorder caused by ruses were negative. Serum creatine kinase ©2018 Dustri-Verlag Dr. K. Feistle hyperactivity with variable (CK) was increased (520 UI/L). ISSN 0722-5091 response to treatment Needle electromyography (EMG) showed DOI 10.5414/NP301093 e-pub: February 16, 2018 marked abnormalities consisting of continu- Nila Volpi1,2, Federica Ginanneschi1,2, ous complex repetitive discharges (CRDs), Alfonso Cerase1,3, Salvatore Francesco polyphasic motor unit potentials with reduced Carbone4, Margherita Aglianò1, voluntary recruitment in the right gastroc- Paola Lorenzoni1, Matteo Bellini3, nemius muscle. EMG recordings of right Sabina Bartalini2, Giovanni Di Pietro5, tibialis anterior, quadriceps femoris, gluteus and Alessandro Rossi1,2 maximum, and adductor magnus muscles were unremarkable. 1Department of Medical, Surgical, and Magnetic resonance imaging (MRI) (Fig- Neurological Sciences, University of ure 1) showed a volume increase of right leg Siena, 2Unit of Neurology and Clinical posterior muscles, more evident on soleus Neurophysiology, 3Unit of Neuroradiology, and medial gastrocnemius, with intrafascial 4Unit of Diagnostic Imaging, and edema and mild hypervascularization of hy- 5Unit of Neurosurgery, University pertrophic muscles. Hospital Santa Maria alle Scotte, Lumbosacral spinal MRI and computed Siena, Italy tomography (Figure 1) evidenced diffuse de- generative disease of the lumbar spine and a L5-S1 right paramedian posterior disc herni- Sir, – Neurogenic focal muscle hyper- ation compressing the ipsilateral S1 radicular trophy (NMH) is a rare event in different sheath and S1 nerve root. instances of impaired nerve conduction: ac- A biopsy of the medial right gastroc- quired and inherited polyneuropathies/mul- nemius muscle (Figure 2) showed grossly tineuropathies [1, 2], post-polio syndromes hypertrophic fibers, grouped atrophy, and [3], spinal stenosis, spinal muscle atrophies, sparse myonecroses. Target lesions indicat- radiculopathies [4]. Unilateral calf hypertro- ed denervation in most hypertrophic fibers. phy is an uncommon, but not unique, finding Inflammation consisted of scattered foci of in S1 radiculopathy [5]. Muscle histology mononuclear cells surrounding necrotic fi- shows denervation, with atrophic as well as bers. MHC-I (HLA-ABC) neolocalization hypertrophic fibers, and frequent coexistence was restricted to necrotic/regenerating fibers. of inflammatory changes. Nevertheless, clin- Focal increase of acid phosphatase (AP) ac- ical presentation and responsiveness to treat- tivity and cytoplasmic patchy deposits of ment are not uniform. We report a 65-year- complement terminal complex (membrane old man, who presented with a 2-month attack complex: MAC) were detected in history of painful progressive enlargement the largest fibers with myofibrillar disarray. of the right calf, which started 5 months af- Immunohistochemistry for myosin heavy ter an acute lumbago, causing pain of poste- chains (MyHC) showed reactivity of all fi- rior right thigh, leg, and heel. The right calf bers for the slow isoform, with a milder stain was markedly enlarged (7.5 cm right > left), in fibers coexpressing fast myosin, resulting tense, and sensitive to touch/pressure, with in transitional hybrid fibers (~ 40%). Recur- no skin/subcutaneous changes, no involve- rent regenerating fibers coexpressed neona- ment of the regional lymph nodes (Figure 1). tal/fast/slow myosin. By morphometric Neurological examination detected weak- analysis, the frequency peak of fiber equiva- ness of right foot plantar flexion (3/5 MRC lent diameters was observed at ~ 100 µm, scale) and absence of right ankle jerk reflex; with recurrent elements being larger than the patient complained of tingling paresthe- 200 µm. Clinical Neuropathology, Vol. 37 – No. 3/2018 – Letters to the editor 147 Figure 1. Top left: grossly hypertrophic right calf. Top right: lumbar spine neuroimaging. T1- (A) and T2- weighted (B) sagittal, T2-weighted consecutive axial (C) MRI, and axial CT (D): disc and facet joints degen- erative disease at right side of L5-S1 level, including zygapophyseal osteophytes (white closed arrow) and paramedian disc herniation (open arrows) in the right S1 lateral recess, compressing ipsilateral S1 root (black closed arrow). Bottom: MRI of the legs. T1-weighted image (A): volume increase of soleus and medial gas- trocnemius muscles (white arrows). Fat-suppressed T2-weighted image: edema, with interfascial component (arrows). No fat involution was detectable by T1/T2 images. Regular popliteal artery run-off excluded vascu- lar impairment (C). Steady-state post-contrast T1-weighted image (D): muscle masses showed homoge- neous enhancement (*) because of increased interstitial spaces due to inflammatory components. Steroid treatment was carried out with articular zygapophyseal infiltration of the prednisone 50 mg/day for 3 weeks, with no right L5-S1 root with a mix of local anes- clinical remission. Consequently, the patient thetic (Ropivacain, 2 mg) and corticosteroid was submitted to CT-guided percutaneous (Triamcinolon, 40 mg), with considerable transforaminal periganglionic, and trans- clinical remission: shortly after the proce- Clinical Neuropathology, Vol. 37 – No. 3/2018 – Letters to the editor 148 Figure 2. Medial right gastrocnemius muscle: biopsy findings. Hematoxylin-eosin: myonecrosis with mononuclear invasion (*); atrophic/hypertrophic fibers, internalized nuclei; target lesions as hypereosino- philic areas. Histogram of fiber equivalent diameter: high percentage of diameters > 100 µm; > 15% small atrophic fibers. MHC-I (HLA-ABC) IP: only necrotic (*) and sparse degenerating/regenerating (**) fibers show neolocalization. NADH-TR: target lesions as areas devoid of enzymatic activity with peripheral hy- perreactive rim and coarse architectural changes. MAC IP: patchy cytoplasmic spots on target fibers (suc- cessive sections*), contrasting with uniform cytoplasmic stain in necrotic fibers invaded by mononuclear cells (arrowhead). CD4 – CD8 IP on successive sections: only necrotic fibers present with infiltrates. Acid phosphatase hyperactivity in a grossly hypertrophic fiber, with severe disruption of myofibrillar organiza- tion, as shown in successive section stained for NADH-TR. Serial MyHCs IP: all fibers express slow MyHC, target lesions show a hyperreactive rim; variable intensity of MyHC slow stain in grouped fast fibers (arrowhead). Regenerating fibers (*) coexpress neonatal, slow, and fast isoforms. (NADH-TR = reduced nicotinamide adenine dinucleotide-tetrazolium reductase; AP = acid phosphatase; IP = immunoperoxi- dase; scale bar: 50 µm). Clinical Neuropathology, Vol. 37 – No. 3/2018 – Letters to the editor 149 dure, pain and muscle tenderness decreased changes. However, the varying response to and within 4 weeks a 2.5-cm reduction of steroids does not strictly correlate with in- the right calf circumference was discern- flammation, neither in FM [9] nor in radic- ible. Nevertheless, 2 months later, pain and ulopathy-associated NMH [6], suggesting, swelling recurred so that surgical discectomy besides a direct action on radicular compres- was performed. Three months later, the right sion, a steroid activity on the suppression of calf circumference, although still hypertro- the membrane excitability. phied, was 3.5 cm less. Clinical examina- Genetic factors or selective axon vul- tion showed full recovery of the right plantar nerability have been suggested to be re- flexion (MRC: 5), a sharp decrease of the sponsible for the uncommon occurrence of foot paresthesia, and a reduction of the calf large “atrophy-resistant” fibers in muscle of tension. EMG demonstrated a reduction of subjects with spinal cord injuries [13]; yet, CRDs with improved muscular recruitment. unrecognized motoneuron/muscle molecular Coexisting inflammatory changes have features might also explain the low preva- led to inclusion of NMH into the domain of lence of NMH associated with the relatively focal myositis (FM) [5, 6], a benign pseudo- frequent S1 radiculopathy. tumor lesion within a single skeletal muscle, A transitional “hybrid” fiber phenotype, predominant at the lower limbs, possibly re- coexpressing different isoforms of myosin current or evolving into diffuse myositis [7]. and other contractile proteins, has been re- Unlike the present case, histology of pure ported in denervated muscle, with a shift to FM usually shows no neurogenic changes fast type 2 fibers [14], whereas a fast-to-slow and a prominent inflammation [8, 9]. shift occurs following electric stimulation or In most calf NMH cases, increased CK excessive exercise [15]. Our finding of an plasma levels and focal inflammation likely ongoing major transition to the slow phe- represent a reactive response to degeneration notype suggests that histotype shift, from remodeling of denervated fibers [5]. Corre- continuous muscle activity, might cause the spondingly, MHC-I upregulation and T-cell reported type 1 predominance in gastrocne- deposits were extremely limited in our pa- mius NMH [3]. Serial MyHC immunohis- tient’s gastrocnemius muscle, in contrast to tology
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