21 research outputs found

    Does intravenous administration of recombinant tissue plasminogen activator for ischemic stroke can cause inferior myocardial infarction?

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    Recombinant tissue plasminogen activator (rTPA) is one of the main portions of acute ischemic stroke management, but unfortunately has some complications. Myocardial infarction (MI) is a hazardous complication of administration of intravenous rTPA that has been reported recently. A 78-year-old lady was admitted for elective coronary artery bypass graft surgery. On the second day of admission, she developed acute left hemiparesis and intravenous rTPA was administered within 120 minutes. Three hours later, she has had chest pain. Rescue percutaneous coronary intervention was performed on right coronary artery due to diagnosis of inferior MI, and the symptoms were resolved. © M. Almasi et al. 2016 Licensee PAGEPress, Italy

    Atherosclerosis in patients with endometriosis

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    Endometriosis refers to endometrial tissue implantation including stromal and epithelial tissue outside the uterus. It is an often painful disorder that involves the ovaries and fallopian tubes. The association between endometriosis and atherosclerosis is interesting. The present study was conducted to assess the Doppler findings of the carotid artery in patients with and without endometriosis. In this study that included 30 patients with endometriosis and 30 control subjects, all patients underwent carotid ultrasonography, and the measurement of intima-media thickness (IMT) was done in the distal common carotid artery, proximal to the origin of the carotid bulb, and finally, we compare the IMT in two groups. This study revealed that there are no differences in the IMT between patients with and without Endometriosis. © Copyright A.H. Habibi, et al., 2019

    Pantothenate kinase-associated neurodegeneration: Clinical aspects, diangnosis and treatments

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    Pantothenate Kinase-Associated, Neurodegeneration (PKAN) is an autosomal, recessive disorder characterized by a, mutation in the PANK2 gene. The clinical, presentation may range from only speech, disorder to severe generalized dystonia, spasticity, Visual loss, dysphagia and, dementia. The hallmark of this disease is, eyes of the tiger signs in the medial aspect, of bilateral globus pallidus on T2-weighted, MRI that is a hyperintense lesion surrounded, by hypointensity. Common treatments, for PKAN disease include anticholinergics, botulinum toxin, Oral and Intrathecal, baclofen, Iron chelation drugs and surgical, procedures such as ablative pallidotomy or, thalamotomy, Deep brain stimulation., There are many controversies about the, pathogenesis and treatment of this disease, and in recent years interesting studies have, been done on PKAN disease and other similar, diseases. This review summarizes the, clinical presentation, etiology, imaging, modalities and treatment. © S. Razmeh et al

    Pantothenate kinase-associated neurodegeneration: Clinical aspects, diangnosis and treatments

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    Pantothenate Kinase-Associated, Neurodegeneration (PKAN) is an autosomal, recessive disorder characterized by a, mutation in the PANK2 gene. The clinical, presentation may range from only speech, disorder to severe generalized dystonia, spasticity, Visual loss, dysphagia and, dementia. The hallmark of this disease is, eyes of the tiger signs in the medial aspect, of bilateral globus pallidus on T2-weighted, MRI that is a hyperintense lesion surrounded, by hypointensity. Common treatments, for PKAN disease include anticholinergics, botulinum toxin, Oral and Intrathecal, baclofen, Iron chelation drugs and surgical, procedures such as ablative pallidotomy or, thalamotomy, Deep brain stimulation., There are many controversies about the, pathogenesis and treatment of this disease, and in recent years interesting studies have, been done on PKAN disease and other similar, diseases. This review summarizes the, clinical presentation, etiology, imaging, modalities and treatment. © S. Razmeh et al

    A novel homozygous variation in the PANK2 gene in two Persian siblings with atypical pantothenate kinase associated neurodegeneration

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    Pantothenate Kinase-associated Neurodegeneration (PKAN) is an autosomal recessive disorder that is caused by variation in pantothenate kinase-2 gene (PANK2) gene on chromosome 20. The common presentation of this disease includes progressive dystonia, Parkinsonism, retinopathy, cognitive impairment, and spasticity. The typical magnetic resonance imaging finding is eye of the tiger sign in globus pallidus and not pathogenic and not found in all patients. In the present study, we describe two siblings who have a novel variation of the PANK2 gene. These patients with the same genotype, have different ages at the onset of disease and also the various severity of the disease. The description of these cases helps to understand this disease, its symptoms, pathogenesis, and its treatment. © A.H. Habibi et al., 2019

    Closure of palatal fistula with buccal fat pad flap

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    Palatal fistula as a complication of palatal surgery is difficult to manage due to the presence of fibrotic and scarred tissue and the absence of local virgin tissue. Recurrence rates are high. To investigate the efficacy of repairing small and medium sized palatal fistulas using the buccal fat pad (BFP), 20 patients (aged 2.5-19 years) with palatal fistula (10-20 mm) underwent closure surgery using a pedicled BFP flap. The nasal layer was closed by a local mucosal flap (turn down flap) and the pedicled BFP flap was used for oral lining. Full epithelialization of the BFP layer was observed within 4 weeks in all patients. A 2 mm defect in the anterior part of the previous fistula location remained in one case, which spontaneously healed after 2 months; all others closed successfully. Mild pain and cheek swelling occurred in 10 patients, which disappeared within 5 days with no surgical intervention. This study suggests the pedicled BFP flap is a simple and relatively secure method for palatal fistula management. It is recommended for fistulas less than 20 mm in length located in the posterior two-thirds of the palate. © 2010 International Association of Oral and Maxillofacial Surgeons

    Toward shortening interoperation period in two-stage cross facial nerve graft with muscle transfer

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    Cross facial nerve graft with free muscle transfer is a well-accepted method to deal with the long-standing facial paralysis, which is usually carried out in 2 separate operations including the nerve graft in first operation followed by a muscle transfer 10 to 12 months later. However, delayed rehabilitation of the nerve graft because of its long length leads to considerable interval between first and second operations.Nine patients with long-standing unilateral facial paralysis underwent 2-stage cross facial nerve graft with some modifications in techniques. In this new technique, by placing the end of the nerve graft in nasolabial fold in the first stage, we used shorter nerve grafts and reduced the interval between operations from 3.5 to 5 months. We believe that by using shorter nerve grafts in this technique, we can perform second-stage operation pretty earlier, and placing the end of nerve graft in nasolabial fold reduces the risk of nerve graft traumatization in preauricular dissection during the second stage. © 2008 by Lippincott Williams & Wilkins

    Cross-facial nerve graft: A report of chronically paralyzed facial muscle neurotization by a nerve graft

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    A 21-year-old housewife with long-standing hemifacial paralysis on the left side decided to undergo the classic two-stage cross-facial nerve graft with muscle transfer. The first stage of the operation was performed successfully with the use of a sural nerve graft. After the appearance of Tinel's sign 8 months later, gain of function in the muscles of the paralyzed side was observed and negated the need for the second-stage muscle transfer. © 2007 Springer Science+Business Media, LLC
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