1/191. magnetic resonance imaging in the diagnosis of asymmetrical bilateral masseteric hypertrophy.Asymmetrical bilateral masseteric hypertrophy or unilateral masseteric hypertrophy may present a diagnostic dilemma. While the history and clinical examination are important in differentiating this benign condition from parotid and dental pathology, they cannot necessarily exclude rarer malignant lesions of or within the muscle itself. We present a case where MRI provided clear and elegant confirmation of our provisional clinical diagnosis by illustrating both the soft tissue features and the logical corresponding bony features of this condition, thus obviating the need for further invasive investigations.- - - - - - - - - - ranking = 1keywords = muscle (Clic here for more details about this article) |
2/191. hypertrophy and pseudohypertrophy of the lower leg following chronic radiculopathy and neuropathy: imaging findings in two patients.Enlargement of the ipsilateral muscle compartment is an exceptional finding in patients with chronic radiculopathy, peripheral nerve injury, anterior horn cell diseases, or acquired peripheral neuropathy. We report radiographic, ultrasonographic, CT and MRI findings in a patient with chronic S1 radiculopathy and another with chronic neuropathy of the common fibular nerve (L4-S2), both presenting with painless enlargement of the calf muscles.- - - - - - - - - - ranking = 2keywords = muscle (Clic here for more details about this article) |
3/191. Moebius syndrome: the new finding of hypertrophy of the coronoid process.The first detailed description of congenital facial paralysis was reported by Moebius in 1888. It is characterized by either unilateral or bilateral paralysis of the facial muscles and an associated abducens palsy. The present report is of two patients with Moebius syndrome, who were also diagnosed with trismus at birth. Each patient also demonstrated bilateral hypertrophy of the coronoid process of the mandible. In effect, the zygoma obstructed the excursion of the mandible because of a "coronoid block." A three-dimensional computed tomography scan demonstrated normal temporomandibular joints but bilateral hypertrophy of the coronoid processes and micrognathia. Both patients demonstrated less than 10 mm of oral excursion. Bilateral coronoidectomies were performed through an intraoral approach. The oral excursions after surgery increased to at least 20 mm. In each of these patients, the coronoid process was enlarged relative to the zygoma, which was of normal size and configuration. The trismus was associated with blocking of the coronoid by the anterior zygoma, preventing open or full excursion of the hypoplastic mandibles. Moebius syndrome can have a variable presentation at birth. In two patients, the authors describe a new finding of hypertrophy of the coronoid process and trismus secondary to obstruction of the coronoid by the hypertrophic zygomas during oral excursions. Each patient is described, and a review of the literature is discussed.- - - - - - - - - - ranking = 1keywords = muscle (Clic here for more details about this article) |
4/191. Progressive pulmonary vascular disease after pulmonary artery banding and total correction in a case of ventricular septal defect and pulmonary hypertension.A 7-month-old infant with ventricular septal defect and pulmonary hypertension underwent pulmonary artery banding, which resulted in a decrease in the pulmonary arterial peak pressure from 102 to 54 mmHg. lung biopsy findings showed at most an early grade 3 Heath-Edwards classification, and an index of pulmonary vascular disease of 1.4, both of which indicated operability for total correction. Small pulmonary arteries less than 100 microns in diameter, however, showed marked hydropic changes in the medial smooth muscle cells. Total correction was performed at the age of 2 years, but the pulmonary arterial pressure failed to decrease. A lung biopsy taken just after the closure of the ventricular septal defect contraindicated operability due to progressive pulmonary vascular disease at a grade 6 Heath-Edwards classification and an index of pulmonary vascular disease of 2.4. The patient died at 8 months after the operation, and an autopsy revealed still more advanced pulmonary vascular disease at a grade 6 Heath-Edwards classification and an index of pulmonary vascular disease of 2.8. The pathogenesis of arterial changes is discussed.- - - - - - - - - - ranking = 1keywords = muscle (Clic here for more details about this article) |
5/191. Complex repetitive discharges: cause or effect of neurogenic muscle hypertrophy?We report a patient with adult-onset spinal muscular atrophy (SMA) of the scapulohumeral type with neurogenic muscle hypertrophy (NMH) in markedly weakened biceps muscles in association with continuous complex repetitive discharges (CRDs). This is an apparently unique case due to the bilaterality of the NMH associated with CRDs as well as the well-circumscribed symmetric upper extremity distribution of the hypertrophy. The possible mechanisms of NMH in association with spontaneous motor activity are discussed.- - - - - - - - - - ranking = 6keywords = muscle (Clic here for more details about this article) |
6/191. The development of hypertrophic pyloric stenosis in a patient with prostaglandin-induced foveolar hyperplasia.BACKGROUND: Hypertrophic pyloric stenosis (HPS) has been described in association with several obstructive antropyloric lesions including idiopathic foveolar hyperplasia (gastric mucosal hypertrophy), feeding tubes, eosinophilic gastroenteritis, and hypertrophic antral polyps. Non obstructive antral webs have also been described with HPS. PATIENT AND methods: We present a case of gastric-outlet obstruction in association with HPS, namely, prostaglandin-induced foveolar hyperplasia. This entity has been previously described, but rarely in association with HPS. We report a female infant requiring prostaglandin therapy for pulmonary atresia who developed dose-related prostaglandin-induced foveolar hyperplasia and symptoms of progressive non-bilious vomiting. RESULTS: Initially, ultrasonography demonstrated evidence of antral mucosal hypertrophy as the cause for gastric-outlet obstruction. The patient subsequently developed progressive thickening of the antropyloric muscle, resulting in sonographic appearances of hypertrophic pyloric stenosis. Pyloromyotomy was eventually required for treatment of HPS. CONCLUSION: A common denominator of most of the above-described entities is thickening and/or hypertrophy of the antral mucosa. We suggest that the antropyloric musculature may hypertrophy in an effort to overcome the gastric-outlet obstruction caused by the adjacent thickened antral mucosa. In other words, these entities may represent examples of "secondary" hypertrophic pyloric stenosis.- - - - - - - - - - ranking = 1keywords = muscle (Clic here for more details about this article) |
7/191. S-1 radiculopathy as a possible predisposing factor in focal myositis with unilateral hypertrophy of the calf muscles.Associated with chronic S-1 radiculopathy, a 44-year-old man developed unilateral hypertrophy of the calf muscles. electromyography revealed neurogenic alterations in the corresponding limb compatible with S-1 radiculopathy. In addition, MR-tomographic and bioptic findings were consistent with a focal inflammatory myopathy of the enlarged right gastrocnemius muscle. Predisposing factors for the localisation of a focal myositis are unknown. This case report highlights the diagnostic difficulties in distinguishing focal myositis and denervation hypertrophy following S-1 radiculopathy or secondary inflammation related to denervation. We consider the possibility that in our case the inflammatory process might have been triggered by electromyographically proven chronic denervation related to radiculopathy.- - - - - - - - - - ranking = 6keywords = muscle (Clic here for more details about this article) |
8/191. Hypertrophic inflammatory neuropathy involving bilateral brachial plexus.BACKGROUND: The present case is an example of hypertrophic inflammatory neuropathy (HIN). This entity is a rare tumor-like, chronic inflammatory, focal or multifocal, mainly demyelinating neuropathy of unknown origin, most frequently involving the brachial plexus. CASE DESCRIPTION: The authors describe a 67-year-old man presenting with a nodular mass in his right supraclavicular fossa. A nodular mass grossly resembling a schwannoma originating from a single nerve fascicle was surgically removed from the right C6 spinal nerve. Histologically, endoneurial edema, fibrosis, focal chronic inflammation, and extensive "onion bulb" formation were seen. Electron microscopy studies and immunohistochemistry proved that the onion bulb-forming cells were schwannian in nature and that the whorls of onion bulbs surrounded a generally demyelinated axon. Three months following surgery the patient developed acute painless paralysis of his right biceps brachii muscle that rapidly reversed; after that he remained neurologically asymptomatic. MRI revealed multiple fusiform mass lesions involving the brachial plexus bilaterally. Electrophysiologic studies demonstrated a bilateral, asymmetrical, mainly demyelinating neuropathy involving the brachial plexus; they failed to reveal any abnormality suggestive of generalized neuropathy. CONCLUSION: HIN is different from other focal tumor-like neuropathies and in particular from localized hypertrophic neuropathy (LHN).- - - - - - - - - - ranking = 1keywords = muscle (Clic here for more details about this article) |
9/191. An early onset muscular dystrophy with diaphragmatic involvement, early respiratory failure and secondary alpha2 laminin deficiency unlinked to the LAMA2 locus on 6q22.We present four subjects from one family and one subject (with an affected sibling who had died) from a second, unrelated family, with early onset, Duchenne-like, muscular dystrophy who presented with proximal girdle weakness, calf and generalized muscle hypertrophy, selective wasting of the sternomastoid muscles, rigidity of the spine and contractures of the tendo Achilles. Intellect was normal. serum creatine kinase was grossly elevated and the muscle biopsies showed a dystrophic picture. All five subjects have developed early respiratory failure due to severe diaphragmatic involvement; two have already died aged 4 and 7 years of age and the remaining three are dependent on night time ventilation. There has been very little deterioration over time in the skeletal muscle function, and the survivors remain ambulant, the oldest being 11 years. Immunocytochemical studies of the muscle biopsy showed a normal pattern for dystrophin and the dystrophin-associated glycoproteins, but a reduction of the laminin alpha2 chain of merosin. magnetic resonance imaging of the brain was normal. The disease did not link to the LAMA2 locus for laminin alpha2 on chromosome 6q, so that these families seem to represent a new form of autosomal recessive muscular dystrophy with a secondary merosin deficiency. The primary protein deficiency has not yet been identified.- - - - - - - - - - ranking = 5keywords = muscle (Clic here for more details about this article) |
10/191. Hemimasticatory spasm associated with localized scleroderma and facial hemiatrophy.OBJECTIVES: To report a case and discuss the mechanism of hemimasticatory spasm. DESIGN: Case report. PATIENT: A 37-year-old woman had a 3-year history of involuntary spasms of the right masseter muscle in association with localized scleroderma and facial hemiatrophy. Electrophysiological studies revealed a normal blink reflex. However, the masseter reflex and silent period were absent on the affected side. Distal latency and compound muscle action potential of the masseter nerve were normal. Needle electromyography demonstrated irregular bursts of motor unit potentials similar to those described in hemifacial spasm. A magnetic resonance imaging scan of the head showed mild hypertrophy of the masseter muscle and atrophy of subcutaneous fatty tissues on the affected side. Local injection of botulinum toxin A into the masseter muscle resolved the patient's symptoms. CONCLUSION: On the basis of clinical and electrophysiological findings, focal demyelination of motor branches of the trigeminal nerve owing to deep tissue changes is suggested as the cause of abnormal excitatory electrical activities resulting in involuntary masticatory movement.- - - - - - - - - - ranking = 4keywords = muscle (Clic here for more details about this article) |
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