Spontaneous Intraventricular Hemorrhage: A Rare Presentation of a Skull Base Mesenchymal Chondrosarcoma

2017 ◽  
Vol 99 ◽  
pp. 811.e1-811.e5 ◽  
Author(s):  
Altaf Ali Laghari ◽  
Gohar Javed ◽  
Muhammad Faheem Khan ◽  
Syed Ijlal Ahmed ◽  
Karim Rizwan Nathani ◽  
...  
2018 ◽  
Vol 5 (4) ◽  
pp. 99-103
Author(s):  
Yuta Murakami ◽  
Shinya Jinguji ◽  
Yugo Kishida ◽  
Masahiro Ichikawa ◽  
Taku Sato ◽  
...  

2000 ◽  
Vol 46 (2) ◽  
pp. 75-77
Author(s):  
Toshiya OKO ◽  
Kazuhiro MORIHANA ◽  
Motoki OOTSUKA ◽  
Manabu FUJIOKA ◽  
Hiroyuki SAKIYAMA ◽  
...  

2018 ◽  
Vol 2018 ◽  
pp. 1-4
Author(s):  
Mark A. Dobish ◽  
David A. Wyler ◽  
Christopher J. Farrell ◽  
Hermandeep S. Dhami ◽  
Victor M. Romo ◽  
...  

This report displays a rare presentation of lactic acidosis in the setting of status epilepticus (SE). The differential diagnosis of lactic acidosis is broad and typically originates from states of shock; however, this report highlights an alternative and rare etiology, SE, due to chronic skull base erosion from temporomandibular joint (TMJ) disease. Lactic acidosis is defined by a pH below 7.35 in the setting of lactate values greater than 5 mmol/L. Two broad classifications of lactic acidosis exist: a type A lactic acidosis which stems from global or localized tissue hypoxia or a type B lactic acidosis which occurs once mitochondrial oxidative capacity is unable to match glucose metabolism. SE is an example of a type A lactic acidosis in which oxygen delivery is unable to meet increased cellular energy requirements. This report is consistent with a prior case series that consists of five patients experiencing generalized tonic-clonic (GTC) seizures and lactic acidosis. These patients presented with a pH range of 6.8-7.41 and lactate range of 3.8-22.4 mmol/L. Although severe lactic acidosis following GTC has been described, this is the first report in the literature of chronic skull base erosion from TMJ disease causing SE.


2013 ◽  
Vol 32 (09) ◽  
pp. 393-398 ◽  
Author(s):  
Sumit Thakar ◽  
Ravi Dadlani ◽  
Sunil V. Furtado ◽  
Nandita Ghosal ◽  
Alangar S. Hegde

2021 ◽  
Vol 21 ◽  
pp. 101020
Author(s):  
Amee D. Azad ◽  
Connie M. Sears ◽  
Peter H. Hwang ◽  
Ahmed Mohyeldin ◽  
Juan Fernandez-Miranda ◽  
...  

2018 ◽  
Vol 45 (11) ◽  
pp. 2025-2025 ◽  
Author(s):  
Nicolas Louarn ◽  
Quentin Alias ◽  
Laurène Aupin ◽  
Nicolas Benoist ◽  
Marine Desroches ◽  
...  

2013 ◽  
Vol 4 (8) ◽  
pp. 561
Author(s):  
Shobha Sudarshan Shetty ◽  
Ramaprakasha S ◽  
Glaxon Alex ◽  
Sandheep George Villoth

2013 ◽  
Vol 2013 ◽  
pp. 1-3 ◽  
Author(s):  
Musaed Alzahrani ◽  
Louis Gaboury ◽  
Issam Saliba

A 48-year-old woman presented with unilateral hearing loss and tinnitus for three years associated with middle ear effusion. Previous treatments, including antibiotics, corticoids, and transtympanic tube, were ineffective. Otomicroscopy showed a greyish retrotympanic mass associated with middle ear effusion. High resolution CT scan of the mastoid was in favor of chronic oto-mastoiditis without any evidence of tegmen dehiscence. Surgical exploration revealed a polypoid greyish mass filling the tympanic cavity. Histological examination postoperatively revealed a meningothelial meningioma. Postoperative magnetic resonance imaging (MRI) was obtained and showed a large skull base meningioma, extending from the clivus anteriorly to the porus acusticus posteriorly with middle ear invasion. After discussion with the multidisciplinary tumor board, it was managed by stereotactic radiotherapy due to the high surgical associated neurovascular risks. In conclusion, middle ear meningioma, although still a rare presentation, should be suspected in the presence of atypical chronic OME.


2021 ◽  
Vol 14 (1) ◽  
pp. e237105
Author(s):  
Iman Usama Hosni ◽  
Bhavesh Karbhari ◽  
Robert Orr ◽  
Neil Opie

We present a rare case of sarcoidosis with extensive bony destruction of the maxillofacial and skull base bones. A 65-year-old woman was referred with an asymptomatic, non-healing dental socket. Examination revealed an oroantral fistula that was biopsied and repaired under general anaesthesia. Investigations included plain and cross-sectional imaging. Serological tests, in particular ACE, were normal. Histology showed benign florid granulomatous inflammation. At 6 months, the patient remained asymptomatic. She was re-referred 3 years later with further bony destruction of her maxilla and mandible. Repeat imaging showed intrathoracic lymphadenopathy and skull base involvement. Repeat biopsy confirmed granulomatous inflammation. Given the pulmonary, histological and radiological findings, a sarcoidosis diagnosis was made. Following multidisciplinary team meetings, the patient was treated with methotrexate and arrangements made for close monitoring. This case highlights the need for a consensus in identifying, treating and developing a follow-up protocol in such patients.


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