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Lipoma of the floor of the mouth. A case report and literature review  [PDF]
Hellenic Archives of Oral and Maxillofacial Surgery , 2012,
Abstract: Lipomas are slowly growing benign tumors of the adipose tissue which may occur in the whole human body. They are rarely found in the oral maxillofacial region; their incidence in the oral cavity is about 1-4 %. Intraorally, lipomas can occur at the buccal mucosa, the tongue, the vestibule, the lips, the palate and the floor of the mouth. In the majority of the cases, treatment does not cause serious concern. However, when the tumor is adjacent to important anatomical structures, like the floor of the mouth, then possibility of complication should be considered by the maxillofacial surgeon.This paper reports a case of lipoma of the mouth floor,its surgical treatment and a short review of the literature.
Epidermoid cyst of the floor of the mouth. A case report and literature review
Navas-Aparicio MC,Rojas-Madrigal A,Cubero-Brenes E
Revista de la Sociedad Otorrinolaringológica de Castilla y León, Cantabria y La Rioja , 2012,
Abstract: Dermoid and epidermoid cysts are cystic benign, slightly common malformations that may be found in the area of head and neck between 1.6 and 7 %, representing less than 0.01 % of all the cysts of the oral cavity. This pathology is important of the knowledge of the professional in dentistry and medicine to be able to do the early diagnose and the respective treatment. The purpose of this study is the review of the relevant literature of the dermoid and epidermoid cysts and the presentation of a case of epidermoid cyst in floor of mouth in a patient of 13 years and 5 months of age.
Cerebral amyloid angiopathy presenting as a posterior leukoencephalopathy: A case report and review of the literature  [cached]
Maramattom Boby Varkey,Maramattom Leena Varkey
Neurology India , 2004,
Abstract: Cerebral amyloid angiopathy (CAA) is well known to present with lobar intracerebral hemorrhage, dementia or transient neurological events. White matter changes with CAA have only been recently described and can be seen with either sporadic or familial CAA. We present a 50-year-old man with rapidly progressive dementia in whom MRI brain showed symmetrical white matter changes in the parieto-occipital regions. Brain biopsy revealed changes of CAA along with features of Alzheimer′s disease. Immunohistochemistry revealed amyloid beta protein. The subcortical lesions were thought to occur from hypoperfusion of the distal white matter. The role of amyloid in the pathogenesis of CAA and the mechanism of leukoencephalopathy are discussed.
Cerebral amyloid angiopathy-related inflammation presenting with steroid-responsive higher brain dysfunction: case report and review of the literature
Hideya Sakaguchi, Akihiko Ueda, Takayuki Kosaka, Satoshi Yamashita, En Kimura, Taro Yamashita, Yasushi Maeda, Teruyuki Hirano, Makoto Uchino
Journal of Neuroinflammation , 2011, DOI: 10.1186/1742-2094-8-116
Abstract: CAA-related inflammation is a rare disease, defined by the deposition of amyloid proteins within the leptomeningeal and cortical arteries associated with vasculitis or perivasculitis. Here we report a patient with CAA-related inflammation who showed higher brain dysfunction that improved with steroid therapy. In cases with atypical radiological lesions like our case, cerebral biopsy with histological confirmation remains necessary for an accurate diagnosis.Cerebral amyloid angiopathy (CAA) is a common pathology in the elderly characterized by the deposition of amyloid proteins within the leptomeningeal and cortical arteries [1]. Recently, coexisting inflammations in CAA patients, such as vasculitis or perivasculitis, which clinically resemble central nervous system vasculitis, have been recognized as CAA-related inflammation [2,3]. The inflammation typically responds well to steroid therapy [4], and recent studies have pointed out its similarities with meningoencephalitis induced by immunization to Aβ in Alzheimer disease patients [4-6]. Herein we report a patient with CAA-related inflammation who showed convulsion in the left lower extremity and higher brain dysfunction; both were dramatically improved by steroid therapy.A 56-year-old man first noticed discomfort in his left lower limb in January 2010. After 7 days, convulsion in the left lower limb suddenly occurred, and he was transported to the emergency hospital. Magnetic resonance imaging (MRI) showed increased white matter intensities in the right parietal lobe on T2-weighted and fluid attenuated inversion-recovery (FLAIR) images. T1-weighted gadolinium (Gd)-enhanced images revealed enhanced leptomeningeal lesions along the parietal sulci (Figure 1A-B). No microhemorrhages were observed with Gradient-recalled echo (GRE)-T2* imaging (1.5T). He was referred to our institution.On admission, neurological exam showed mild hyperesthesia in the left lower limb and mild hypalgesia in the left crus. No other abnormal
Quistes epidermoides del suelo de boca: presentación de dos casos y revisión de la literatura Epidermoid cysts of the floor of the mouth: presentation of two cases and review of the literature  [cached]
Lorena Sanz,Francisco J. Gamboa,Teresa Rivera
Revista Espa?ola de Cirugía Oral y Maxilofacial , 2010,
Abstract: Los quistes epidermoides son una patología frecuente, pero su localización en la cavidad oral es excepcional. Para el abordaje quirúrgico son factores determinantes su tama o y las relaciones anatómicas. Presentamos dos casos clínicos diagnosticados en el servicio de ORL entre 1999 y 2007, que consultaron por tumoración de crecimiento progresivo en el suelo de boca. Se realiza una revisión acerca del diagnóstico y de los abordajes quirúrgicos de los quistes epidermoides para intentar estandarizar su tratamiento. Epidermoid cysts are a frequent pathology; nevertheless their location in the oral cavity is exceptional. Their size and anatomical location are determining factors in the surgical approach. We present two cases diagnosed in our ENT Department between 1999 and 2007, which were referred to us due to slow growing masses on the floor of the mouth. A literature review was made on the diagnosis, surgical techniques and management of epidermoid cysts in an attempt to standardise their management.
The cerebrovascular basement membrane: role in the clearance of β-amyloid and cerebral amyloid angiopathy  [PDF]
Cheryl A. Hawkes
Frontiers in Aging Neuroscience , 2014, DOI: 10.3389/fnagi.2014.00251
Abstract: Cerebral amyloid angiopathy (CAA), the accumulation of β-amyloid (Aβ) peptides in the walls of cerebral blood vessels, is observed in the majority of Alzheimer’s disease brains and is thought to be due to a failure of the aging brain to clear Aβ. Perivascular drainage of Aβ along cerebrovascular basement membranes (CVBMs) is one of the mechanisms by which Aβ is removed from the brain. CVBMs are specialized sheets of extracellular matrix that provide structural and functional support for cerebral blood vessels. Changes in CVBM composition and structure are observed in the aged and Alzheimer’s disease brain and may contribute to the development and progression of CAA. This review summarizes the properties of the CVBM, its role in mediating clearance of interstitial fluids and solutes from the brain, and evidence supporting a role for CVBM in the etiology of CAA.
Screening for Familial APP Mutations in Sporadic Cerebral Amyloid Angiopathy  [PDF]
Alessandro Biffi,Anna Plourde,Yiping Shen,Robert Onofrio,Eric E. Smith,Matthew Frosch,Claudia M. Prada,James Gusella,Steven M. Greenberg,Jonathan Rosand
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0013949
Abstract: Advances in genetic technology have revealed that variation in the same gene can cause both rare familial and common sporadic forms of the same disease. Cerebral amyloid angiopathy (CAA), a common cause of symptomatic intracerebral hemorrhage (ICH) in the elderly, can also occur in families in an autosomal dominant pattern. The majority of affected families harbor mutations in the Beta amyloid Peptide (Aβ) coding region of the gene for amyloid precursor protein (APP) or have duplications of chromosomal segments containing APP.
Cerebral amyloid angiopathy in the aetiology and immunotherapy of Alzheimer disease
Roy O Weller, Stephen D Preston, Malavika Subash, Roxana O Carare
Alzheimer's Research & Therapy , 2009, DOI: 10.1186/alzrt6
Abstract: Deposition of amyloid-beta (Aβ) in the walls of cerebral arteries and capillaries as cerebral amyloid angiopathy (CAA) has a prevalence of 90% to 96% in patients with Alzheimer disease (AD) [1] and is present in 30% of non-demented individuals over the age of 60 years [2]. CAA reflects an age-related failure of elimination of Aβ from the brain along perivascular lymphatic drainage pathways by which interstitial fluid (ISF) and solutes drain from the brain [3-5]. This failure may be a key factor in the aetiology of AD.Most organs have networks of lymphatic vessels that transport fluid, protein macromolecules, cells and particulate matter from tissue to lymph nodes. Lymphatic drainage along these vessels relies upon highly competent valves, an extrinsic pump action generated by external forces from surrounding tissues and an intrinsic pump generated by coordinated contractions of lymphatic muscle cells [6]. There are no conventional lymphatics in the brain. Instead, ISF and solutes drain out of the brain along narrow basement membranes in the walls of capillaries and arteries to lymph nodes in the neck [3,7], probably driven by an intrinsic pump powered by vascular pulsations [8]. The perivascular lymphatic drainage pathway for ISF and solutes from the brain is largely separate from the cerebrospinal fluid (CSF) [7,9]. With increasing age, the brain, with its almost unique lymphatic drainage system, develops problems with lymphatic drainage of Aβ and other amyloids and these problems are rarely seen in other organs. As a result, soluble and insoluble Aβs accumulate in vessel walls and in brain parenchyma.CAA in AD is a protein-elimination-failure arteriopathy (PEFA) [5,7] common to other forms of CAA in which a variety of amyloidogenic peptides accumulate in the walls of cerebral arteries. Non-Aβ forms of CAA tend to be hereditary in origin and are associated with intracerebral haemorrhage or dementia [10]. Mutated cystatin C is deposited in the walls of cerebral arte
Schwannoma in the floor of the mouth
Hamid Poursadeghi,Sayyed Mohammad Razavi
Journal of Isfahan Dental School , 2010,
Abstract: Introduction: Schwannoma or Neurilemoma is a benign neoplasm of the nervous system originating from Schwann cells. It develops from the neural sheath of peripheral motor, sensory, sympathetic, and cranial nerves except for the optic and the olfactory nerves which basically lack Shwann cell sheaths. Approximately 25% to 45% of the schwannomas occur in the head and neck region. Usually, the mass is asymptomatic, though tenderness or pain is reported in some instances. Tongue is the most common site for oral neurilemomas. Occasionally, the tumor arises centrally within the mandibular bone and thus makes jaw expansion.Case Report: A 22-year-old man presented with a mass in the right side of his mouth floor allegedly existing from six months earlier. The mass was surgically removed. Sample sections of the mass were prepared. In microscopic examination with H&E, there were two areas of wavy and spindle cells within a loose and myxomatous stroma compatible with the known Antoni A and B patterns of Schwannoma. The tumor cells showed a diffuse positive immunohistochemical reaction to S-100 which supported the diagnosis.Conclusion: Schwannoma is a benign soft tissue tumor which mostly involves tongue within oral cavity. This tumor rarely occurs in other regions such as mouth floor. Key words: Schwannoma (neurilemoma), Floor of the mouth.
Cerebral amyloid angiopathy: A clinicopathological study of three cases  [cached]
Panicker Jalesh,Nagaraja D,Chickabasaviah Yasha
Annals of Indian Academy of Neurology , 2010,
Abstract: Cerebral amyloid angiopathy (CAA) is an important cause for intracerebral hemorrhage (ICH), yet often goes undiagnosed in the absence of histological examination of the blood vessels in the clot. In this study, we report three patients who presented with ICH. Two patients had no risk factors for bleed, whereas one patient had systemic hypertension. Tissue for analysis was obtained during hematoma evacuation in two patients and necropsy in the third. Histopathology in all three patients revealed severe degree of amyloid angiopathy with extensive amyloid deposits in the vessel walls, which was diagnostic of CAA. Both medium- and small-sized leptomeningeal and cortical vessels were affected. The vascular amyloid deposits stained with Congo red and displayed characteristic birefringence under polarizing light. In addition, vessels also showed fibrinoid necrosis and vascular endothelial proliferation. Immunohistochemistry demonstrated beta-amyloid peptide in all three cases-the protein most commonly involved in sporadic CAA. Senile plaques with amyloid cores were present in all areas, whereas neurofibrillary tangles were restricted to the medial temporal region in the autopsied case. CAA is an important cause for intracerebral bleed and may be a contributory factor even when other risk factors for ICH are present. Areas of hemorrhage tend to correlate with severity of CAA changes.
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