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"en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Limbus vertebra: (A) lateral radiograph of lumbar spine. The image shows the irregularity of the superior and anterior corners of the vertebral body at lumbar 3 (L3). The L2–L3 intervertebral space is narrowed. There are small anterior osteophytic formations at L2 and L4. The density of the vertebral bodies is conserved; (B) computed tomography with sagittal multiplanar reconstruction, in which the irregularity of the anterosuperior margin of L3 vertebral body can be seen in greater detail. Sclerosis can be observed both in the recessed vertebral endplates and around the osseous fragments separated from the rest of the bone. Listhesis can also be detected at L3–sacral 1 (S1) and Schmorl's node in the superior endplate at L1; (C) magnetic resonance imaging (MRI) of sagittal spin-echo T1-weighted (SET1) sequences. The intensity of the vertebral bodies is conserved and the osseous fragment separated from the L3 body has the same signal intensity has the rest of the bone; (D) MRI of sagittal spin-echo T2-weighted sequences. The findings complement what can be observed in the SET1 sequence. There is a decrease in height and signal of intervertebral discs at L2–L3, L3–L4 and L5–S1 in relation to dehydration in the setting of a degenerative disc disease. There is also a posterior central disc herniation at L5–S1, that migrated cranially, accompanied by listhesis; (E) MRI sagittal SET1 sequences in-phase and out-of-phase. In these sequences, the signal of the disc cartilage is high and bright. It can be seen how it is introduced between the osseous fragment and the foremost region of the superior L3 endplate; (F) drawing representing the changes observed in the images to the left. It can be seen that the L2–L3 intervertebral disc is introduced through the anterior surface of the L3 vertebral body. A Schmorl node can also be seen in the superior endplate of L1 and a protrusion of the L5–S1 disc, with a posterior central disc herniation, accompanied by listhesis at L5–S1.</p>"
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"en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">(A) Increase in the volume of right leg. (B, C) Longitudinal and cross-sectional magnetic resonance imaging of both lower limbs. (D) Muscle biopsy of the patient reported here (hematoxylin–eosin 10×). (E) For comparison, a normal muscle biopsy of medial gastrocnemius (10×).</p>"
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"textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">An increase in the volume of an anatomical region is not a common reason for being sent to a rheumatology department. We report the case of a patient with a progressive increase in the circumference of her right leg. She was referred to us to rule out a possible rheumatic disease.</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Case Report</span><p id="par0010" class="elsevierStylePara elsevierViewall">The patient was a 67-year-old woman who, in January 2012, was sent from general surgery to be studied for a possible myopathy. She had a history of non-insulin-dependent diabetes mellitus and chronic low back pain secondary to disc herniation surgery at lumbar 5–sacral 1 (L5–S1) more than 30 years ago. She had the feeling that the thickness of her right calf had been increasing progressively for more than a year, and associated it with a more significant gradual weakening in recent months. The physical examination found no evidence of connective tissue disease. She had negative results on sciatic tests and a painless increase in the circumference of right calf region (45<span class="elsevierStyleHsp" style=""></span>cm) with respect to the left side (39<span class="elsevierStyleHsp" style=""></span>cm). She found it difficult to maintain her right foot in a tiptoe posture and right Achilles reflex was abolished (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>A). We also performed an analytical study, both general (complete blood count, laboratory findings including liver function, creatine phosphokinase, aldolase, erythrocyte sedimentation rate and C-reactive protein) and immunological (rheumatoid factor, anti-cyclic citrullinated peptide antibodies, antinuclear antibodies, extractable nuclear antigen autoantibodies and antineutrophil cytoplasmic antibodies), with normal results. An electromyogram of lower limbs showed severe chronic neurogenic changes in right S1 myotome. There were no signs of active denervation, and magnetic resonance imaging (MRI) of the lower limbs revealed marked atrophy of medial gastrocnemius and soleus muscle and partial atrophy of the lateral gastrocnemius muscle. The latter were nearly totally replaced and generated a diffuse signal, which appeared to behave with a signal similar to that of connective tissue fat in all the pulse sequences, compatible with areas of fat replacement (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>B and C). Muscle biopsy revealed no dystrophic changes, necrosis, regeneration or histological evidence of active denervation. There was a slight variability in the size of the fibers, and marked infiltration of adipose tissue and, less pronounced, of connective tissue in both the endomyseum and perimyseum (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>D). The study was completed with MRI of the lumbar spine, which showed degenerative discovertebral changes at L5–S1, with right foraminal stenosis and slight swelling of the root, probably secondary to radicular involvement. With no evidence of malignancy or of autoimmune or metabolic disease, and in the absence of symptoms implicating the sciatic nerve and of significant low back pain, we opted for a conservative approach. There have been no changes in the course of the follow-up of our patient to date.</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Discussion</span><p id="par0015" class="elsevierStylePara elsevierViewall">Muscle atrophy due to denervation is the most characteristic consequence of a lesion affecting a nerve structure or tissue. However, although much less frequently, there can be phenomena like muscle hypertrophy and pseudohypertrophy (replacement of muscle tissue by connective and fatty tissue) associated with different situations, such as post-polio syndrome, spinal muscle atrophy and polyneuropathies, like radiculopathies. With respect to the latter, most of the reported cases usually coincide with unilateral calf hypertrophy secondary to S1 radiculopathy; no reason is provided to explain why the territory of this nerve root is more susceptible to developing this rare disorder.<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">1</span></a> Muscle pseudohypertrophy is a phenomenon classically related to hereditary muscular dystrophy and post-polio syndromes. Here it is exceptional in that it is associated with a radiculopathy, although some authors have advocated considering muscular hypertrophy and pseudohypertrophy as different stages of the same disease process, resulting from radicular injury. A review of the reported cases outlines quite a similar presentation: an increase in the circumference of the calf in patients with a history of lumbar disc disease, characterized as progressing slowly, and often painlessly, associated by limited debility, after tumor, bone and vascular diseases have been ruled out.<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">2</span></a> Nevertheless, this phenomenon is so infrequent that authors are usually obliged to opt for a pathological diagnosis. The differential diagnosis should include hereditary myopathy, spinal muscle atrophy, hypothyroidism (Werdnig–Hoffman disease) and infiltrative diseases such as focal myositis, amyloidosis, parasites and tumors, especially sarcomas. The main cause of radiculopathy is degenerative disc and lumbar disease, and cases associated with intraspinal neurinoma<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">3</span></a> and lipoma of the sacral roots,<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">4</span></a> have also been reported. Stability or even an improvement in the prognosis of hypertrophy is usually achieved with a conservative or a surgical approach. The effect of disc decompression surgery seems to have a major influence on relieving pain and alleviating debility more than on the intent to revert the muscle hypertrophy, where the postoperative improvement may be less evident. There are therapeutic experiences with steroids, radiotherapy and botulinum toxin with modest results.<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">5</span></a></p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Conclusions</span><p id="par0020" class="elsevierStylePara elsevierViewall">Muscle pseudohypertrophy secondary to radiculopathy is an exceptional finding. Most of the few cases reported to date correspond to a true muscle hypertrophy secondary to S1 radiculopathy in the setting of a degenerative disc disease of the spine. This should be considered to avoid unnecessary tests, in which the benefit of the surgical approach should be assessed for each individual.</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Ethical Disclosures</span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Protection of human and animal subjects</span><p id="par0025" class="elsevierStylePara elsevierViewall">The authors declare that no experiments were performed on humans or animals for this study.</p></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Confidentiality of data</span><p id="par0030" class="elsevierStylePara elsevierViewall">The authors declare that they have followed the protocols of their work center on the publication of patient data.</p></span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Right to privacy and informed consent</span><p id="par0035" class="elsevierStylePara elsevierViewall">The authors have obtained the written informed consent of the patients or subjects mentioned in the article. The corresponding author is in possession of this document.</p></span></span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0065">Conflicts of Interest</span><p id="par0040" class="elsevierStylePara elsevierViewall">The authors declare they have no conflicts of interest.</p></span></span>"
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"resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Calf pseudohypertrophy due to radiculopathy is an exceptional phenomenon rarely described. We report a 67 year old woman with a previous history of lumbar disc surgery consulting by progressive increase for more than a year of evolution painless right calf associated loss of strength. Electromyographic findings showed chronic S1 radiculopathy and radiologically was appreciated in the medial gastrocnemius and soleus rights substitution of normal muscle tissue by adipose tissue without evidence of myopathy or sarcomatous degeneration.</p></span>"
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"resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">La pseudohipertrofia gemelar secundaria a una radiculopatía es un fenómeno excepcional raramente descrito. Presentamos el caso de una mujer de 67<span class="elsevierStyleHsp" style=""></span>años con antecedentes de cirugía discal lumbar que consultaba por aumento progresivo de más de un año de evolución, no doloroso, de la región gemelar derecha con ligera pérdida de fuerza asociada. Los hallazgos electromiográficos evidenciaron una radiculopatía crónica S1 y radiológicamente se apreciaba, en territorio del gastrocnemio medial y sóleo derechos, una sustitución del tejido muscular normal por tejido adiposo, sin evidencia de miopatía o degeneración sarcomatosa.</p></span>"
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