Cases reported "Hypertrophy"

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1/140. 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.
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2/140. 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.
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3/140. Chronic inflammatory demyelinating polyneuropathy with multiple hypertrophic nerves in intracranial, and intra- and extra-spinal segments.

    Hypertrophic nerves have occasionally been seen in chronic inflammatory demyelinating polyneuropathy (CIDP), but most are in the cauda equina. We report a case with CIDP in whom magnetic resonance imaging (MRI) with gadolinium diethylene triamine penta-acetic acid (Gd-DTPA) enhancement demonstrated hypertrophy of various peripheral nerves including multiple cranial nerves. Interestingly, none showed neurological signs corresponding to the lesions, except for clinical signs consistent with CIDP. MRI can be useful for the detection of silent, but abnormal nerve involvement in CIDP.
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4/140. Hippocampal sclerosis with hypertrophy of end folium pyramidal cells.

    Mesial temporal lobectomy for the treatment of intractable temporal lobe seizures may show dual pathologies for example hippocampal sclerosis (HCS) combined with a malformation. In a lobectomy specimen from a 40-year-old female with typical radiological and pathological features of HCS, an additional histopathological finding was the presence of hypertrophic pyramidal cells in the dentate hilus, in which cytoplasmic accumulations of phosphorylated neurofilament were demonstrated. Although these cells closely resembled dysplastic nerve cells of cortical dysplasia, we argue that the cytoskeletal abnormalities observed are a result of ongoing alterations to hippocampal circuitry in an evolving HCS.
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5/140. An asymptomatic hypertrophic pacchionian granulation simulating osteolytic lesion of the calvaria.

    Osteolytic lesions can be seen in various diseases. We present a rare case of symptomatic hypertrophic pacchionian granulation mimicking bone tumor in the calvaria. A 50-year-old woman suffered from a previous VII cranial nerve peripheral paresis accompanied by headache. A plain radiograph revealed a punched-out paramedial occipital lesion. Precontrast-enhanced computed tomographic scans demonstrated a hypodense mass, with a defect of both tables of the left occipital bone. magnetic resonance imaging (MRI) demonstrated a hypointense mass on the T1-weighted image and isointense to cerebrospinal fluid on the T2-weighted image, with capsule-like contrast enhancement by gadolinium. A biopsy was performed. Histologically, hypertrophic pacchionian granulation was diagnosed. The patient has had no growth for 2 years. This case suggests the need to include hypertrophic pacchionian granulation in the differential diagnosis of punched-out lesions.
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6/140. 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).
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7/140. Idiopathic hypertrophic cranial pachymeningitis: clinicoradiological spectrum and therapeutic options.

    OBJECTIVE: Idiopathic hypertrophic cranial pachymeningitis is a rare disease, of undetermined pathogenesis, that is characterized by inflammation and fibrosis of the dura mater. methods: We encountered six patients with idiopathic hypertrophic cranial pachymeningitis and analyzed their clinical presentations, radiological findings, and treatment. RESULTS: In the six patients, the main manifestations were cranial nerve palsies and headache. Three associations were present, namely optic neuropathy, tolosa-hunt syndrome, and diabetes insipidus. gadolinium-enhanced magnetic resonance imaging was diagnostic, showing intense dural enhancement in a linear or nodular pattern. The responses to corticosteroid therapy were better for patients who exhibited linear, rather than nodular, dural enhancement. For one patient, surgical decompression of the superior orbital fissure provided lasting relief. The course of the disease followed one of three patterns, i.e., sustained remission, relapse with corticosteroid independence, or relapse with corticosteroid dependence. pulse corticosteroid therapy provided significant relief, while reducing the daily corticosteroid requirement and avoiding side effects, for a corticosteroid-dependent relapsing patient. CONCLUSION: Idiopathic hypertrophic cranial pachymeningitis exhibits varied clinical courses. It is important to prevent irreversible cranial neuropathy during the active phase of the disease, using daily administration of corticosteroids, pulse corticosteroid therapy, or surgical decompression.
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8/140. Chronic demyelinating hypertrophic brachial plexus neuropathy.

    A patient with unilateral, painless, chronic progressive upper limb sensorimotor deficit showed electrophysiological evidence of a focal demyelinating neuropathy with almost complete conduction block across the brachial plexus. magnetic resonance imaging disclosed marked brachial plexus hypertrophy. Intravenous immunoglobulin led to fast and complete recovery, maintained by intermittent perfusions. Hypertrophic brachial plexus neuropathy can be a presentation of focal chronic inflammatory demyelinating polyradiculoneuropathy. Objective and quantitative assessment of hand function is useful to evaluate treatment results and to optimize treatment regimens.
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9/140. 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.
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10/140. Hypertrophic dens resulting in cervical myelopathy: histologic features of the hypertrophic dens.

    STUDY DESIGN: A case report of a 43-year-old woman who had hypertrophic dens in the developmentally narrow atlas ring that resulted in cervical myelopathy. OBJECTIVES: To present histologic findings of the hypertrophic dens, which was excised en block the transoral approach, and to discuss the pathogenesis of the hypertrophic change of the dens. SUMMARY OF BACKGROUND DATA: Few cases have been reported of cervical myelopathy associated with hypertrophic dens, and there have been no previous reports describing the histologic features of hypertrophic dens. methods: Clinical data were reviewed from the patient's chart, and histologic features of the hypertrophic dens were examined in the sagittally cut section. RESULTS: After posterior decompression surgery, cervical myelopathy in the patient subsided. Myelopathy reappeared 4 years after surgery. Imaging studies showed osteoarthritis of the atlantodental joint, hypertrophic dens, and degeneration of the cruciate ligament. In the second surgery, transoral removal of the dens with posterior occipitocervical fusion was performed. Histologic studies showed thickening of the cortical bone of the anterior and cranial parts of the dens. The apical portion, which was the insertion portion of the ala ligaments, showed degenerative changes of tide marks. CONCLUSION: Atlantoaxial instability and enthesopathy were probably the causes of the hypertrophic changes of the dens in this case.
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