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Query: UMLS:C0019270 (hernia)
15,856 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty four patients with a chronic otitis were evaluated prospectively by magnetic resonance imaging (MRI) to delineate its contribution in the diagnosis of middle ear masses. The results were correlated to the CT and the surgical and pathological findings. MRI permitted to differentiate the inflammatory tissues from either cholesteatoma, cholesterol granuloma and cerebromeningeal hernia.
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PMID:[Contribution of magnetic resonance imaging in the evaluation of chronic otitis]. 206 28

A CT and MR study of a case of brain hernia within the middle ear cavity is reported. MR allows differentiation between brain tissue and other abnormalities of the ear with a similar appearance on CT.
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PMID:Brain herniation into the middle ear cavity: MR imaging. 274 98

Symptomatic cholesterol granuloma developed in the middle ear cavities in three cases. At computed tomography (CT) after the administration of contrast material, the granulomas appeared as nonspecific, nonenhanced soft-tissue masses with variable bone erosion. These features are indistinguishable from those of other similar clinical entities, especially cholesteatoma, paraganglioma, and endaural brain hernia. At magnetic resonance (MR) imaging, cholesterol granulomas had a more characteristic appearance. In two cases, the granulomas were depicted as areas of high signal intensity with both T1- and T2-weighted sequences. In the third case, an expansile mastoid cholesterol cyst exhibited medium signal intensity on T1-weighted images, with only a small hyperintense area and a hypointense area located in the cystic wall. Correlations between CT, MR, and microscopic findings show that MR imaging is far superior to CT in tumoral characterization, which is crucial for planning surgical approaches. MR imaging has limitations, however, particularly its inability to depict subtle bone abnormalities.
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PMID:Cholesterol granulomas of the middle ear cavities: MR imaging. 274 35

A pulsion hernia of the tympanic membrane is an outwardly bulging, thin, atrophic area of the tympanic membrane. Those patients who develop pulsion hernias repeatedly autoinflate the middle ear and consequently maintain a positive middle ear pressure, which pushes the thin atrophic portion of the tympanic membrane laterally beyond the normal plane of the tympanic membrane. The thinness of the tympanic membrane over the pulsion hernia suggests that the herniation has developed through a pre-existing area of weakness where the fibrous middle layer has disappeared.
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PMID:Pulsion hernias of the tympanic membrane. 359 58

A case of spontaneous brain hernia into the middle ear cleft is described. Even without preceding infection, trauma or surgery of the mastoid, dural and cerebral tissue may protrude into the antrum or middle ear space. The pathology of this rare disease is discussed.
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PMID:[Spontaneous hernia of the brain into the temporal bone]. 673 Sep 55

Herniation of meningeal and/or encephalic tissue into the middle ear is a pathology which, even if rarely found by the otologist, can be life-threatening for the patient because of eventual infective intracranial complications. Four different etiological types are possible, infective, post-surgical, traumatic and spontaneous. From a pathogenic point of view, all types are characterized by a bony and dural defect localized in the tegmen through which meningeal and encephalic tissue can herniate. Symptomatology is often non-specific so that some cases are diagnosed during surgery. When there is strong suspicion of herniation neuroradiological assessment procedures must be carried out in order to make a correct pre-operative diagnosis, High Resolution Computed Tomography (HRCT) of the temporal bone in particular, can show the exact limits and location of the bone defect, while Magnetic Resonance Imaging (MRI) allows the nature of the tissue in the middle ear to be determined. Surgery is the only appropriate therapy. Different approaches have been described amongst which the transmastoid with or without temporal minicraniotomy and the middle cranial fossa (MCF) are the most frequently reported literature. From June 1982 to March 1994, 27 consecutive cases underwent surgery at the Gruppo Otologico, Piacenza. As a result of the occurrence of postoperative meningitis in one case, a new surgical technique through the MCF was standardized. The main step of this procedure consist in leaving the herniated tissue in situ so as to make a barrier between the middle ear and subdural space. The technique is indicated either in the case of large, multiple or very anteriorly located bony defects or when there is an infection in the middle ear.
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PMID:[Meningoencephalic herniation into the middle ear]. 892 63

Herniation of the brain into the middle ear is a rare, but potentially life-threatening complication of chronic otitis media. Fifty patients with a tegmen defect associated with chronic otitis media were operated on between 1985 and 1998. Among these 50, 15 patients presented brain herniation associated with the bony defect. Fourteen patients had undergone previous mastoid surgery for chronic otitis media. Neurological symptoms were encountered in five patients. In 10, magnetic resonance imaging (MRI) was performed before surgery, and a diagnosis of brain herniation could be made. The hernia was repaired in all patients using a middle fossa craniotomy, combined with a transmastoid approach in 11 cases where a large hernia, and/or inflammatory tissues were present in the mastoid. The herniated brain tissue was resected in all, and the dural and bony defects were closed with fascia and bone. No complication or recurrence occurred, during a mean follow-up of 2 years. In conclusion, the occurrence of severe neurological complications as a consequence of brain herniation emphasizes the necessity for recognition and appropriate management of this disease. Computerized tomography (CT) scanning allows the suspicion of brain herniation, but a definitive diagnosis can best be established with an MRI study. The hernia should be repaired using a middle fossa craniotomy, combined with a transmastoid approach in one or two stages, when necessary.
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PMID:Brain herniation and chronic otitis media: diagnosis and surgical management. 1101 52

Meningoencephalic hernia of the middle ear, due to the advent of antibiotics, the surgical microscope, and the new surgical techniques for the treatment of chronic otitis media, is an infrequent pathology in the presents days. The goal of this paper is to present four cases of meningoencephalic hernia of the middle ear, three of then postsurgical and the remaining of inflammatory origin. Diagnosis, treatment and complications are discussed. Meningoencephalic hernia of the middle ear is usually asymptomatic and diagnosis is accidental. Immediate surgical treatment is indicated in order to avoid the potential complications of this disease. Transmastoid approach has been used for three cases and a middle cranial fossa approach was used in the fourth patient.
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PMID:[Post-surgical and post-infectious meningoencephalic herniation in the middle ear]. 1152 61

Mucopolysaccharidosis type I (MPS I) is caused by a deficiency of the lysosomal hydrolase a-L-Iduronidase leading to accumulation of the GAGs, dermatan sulfate, and heparan sulphate, The disease spectrum includes a disorder with severe involvement and CNS disease Hurler disease (HPS I H) a chronic disease without CNS disease Scheie disease (HPS I S5) and the intermediate Hurler/Scheie disease(HPS I HIS).The urine GAGs pattern. confirmed by Iduronidase enzyme assay is diagnostic. Over 200 mutations exist. Genotype / phenotype correlation is poor but two nonsense mutations results in Hurler disease.The skeletal disease dysostosis multiplex (DM) is seen in severe variants of MPS I. The hypoplastic odontoid putting these patients at high risk of cervical cord damage. MPS IH (Hurler Disease) affected infants develop a spinal 'gibbus' deformity, persistent nasal discharge, middle ear effusions and frequent upper respiratory infection. They have "coarse", facial features, and an enlarged tongue. . Progressive upper airway disease leads to obstructive sleep apnoea. Corneal clouding and cognitive impairment appears, growth ceases. Joint stiffness and contractures limit mobility. Cardiac disease is universal. Death occurs before 10 years. SCHEIE patients are diagnosed as teenagers with hepatomegaly, joint contractures, cardiac valve abnormalities and corneal clouding . Prolonged survival with considerable disability without cognitive impairment is usual. MPS IH/S Hurler/Scheie. is diagnosed by 6.5 years, with variable skeletal and visceral manifestations without cognitive involvement. Joint stiffness, corneal clouding, , umbilical hernia, abnormal facies, hepatomegaly, joint contractures, and cervical myelopathy occur. Patients die in their 20s .Haematopoietic stem cell transplantation (HSCT) the standard treatment of MPS IH for 30 years is unpredictable .When performed before 2 years it can stabilize cognitive impairment. Hepatosplenomegaly, urine GAGs excretion, upper airways obstruction and cardiomyopathy improve . The coarse hair and facial features soften and corneas partly clear,but dysostosis multiplex and cervical instability are not improved. Enzyme replacement therapy (ERT) in patients with MPS IH is associated with improved GAG excretion, left ventricular hypertrophy,sleep studies and liver size. The standard treatment of MPS IHIS and MIPS IS is ERT a-L-Iduronidase, laronidase, a life-long therapy. GAG excretion is reduced, respiratory function and physical endurance improve. Joint mobility improves but not dural thickening, cardiac valve lesions or eye changes. MPS I mice have been successfully treated with IDUA-expressing mesenchymaf stem cells . Gene therapy may be developed for MPS I, via an ex vivo approach demonstrated to improve even skeletal outcomes in animal models.
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PMID:Mucopolysaccharidosis type I. 2534 91

A 75-year-old patient complained of mastication-induced clicking tinnitus on the left side, and otoendoscopic examination revealed that the left tympanic membraneTM was outwardly bulged by clenching her teeth. Temporal bone computed tomography demonstrated that the posteromedial bony wall of the glenoid was partially dehiscent, allowing herniation of soft tissue contents of temporomandibular joint into the middle ear. Increased middle ear pressure due to soft tissue herniation can induce left tympanic membrane bulging and accompanying clicking tinnitus. Herniation of temporomandibular joint soft tissue into the middle ear should be considered as a differential diagnosis when clicking tinnitus is evoked by mastication.
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PMID:Temporomandibular joint herniation into the middle ear: A rare cause of mastication-induced tinnitus. 3179 59


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