RESUMO
BACKGROUND: Thalamic aphasia is an unusual clinical presentation of brain neoplasm with few cases reported. Herein, we present a case of an adult woman with thalamic aphasia due to glioblastoma of the thalamus. CASE PRESENTATION: A 57-year-old female patient presented with difficulty walking, slow speech and cognition and altered mental status. At baseline, she was conversant and interactive. Physical examination showed right hemiparesis in addition to word finding difficulties, an impaired naming of objects and semantic paraphasia but preserved repetition and comprehension. The remaining neurological exam was otherwise unremarkable. Brain CT and brain MRI scans showed a left thalamic lesion that is centrally necrotic and peripherally enhancing suggestive of a high-grade neoplasm. Eventually, histopathological examination of brain biopsy confirmed the diagnosis of glioblastoma multiforme. Thalamic aphasia was proposed as an explanation for the neurological symptoms observed in this patient. CONCLUSIONS: This patient demonstrates an unusual presentation of glioblastoma multiforme as thalamic aphasia. It may also point to the potential contribution of the understanding of how thalamic aphasia evolves to characterize the role of the thalamus in language functions.
Assuntos
Afasia/patologia , Neoplasias Encefálicas/patologia , Glioblastoma/patologia , Tálamo/patologia , Adulto , Encéfalo/patologia , Feminino , Humanos , Idioma , Masculino , Pessoa de Meia-Idade , Exame NeurológicoRESUMO
BACKGROUND: Air embolism is an extremely rare complication that can follow gastrointestinal endoscopy. The most accepted treatment of cerebral air embolism (CAE) is hyperbaric oxygen (HBO). Limited evidence suggests that lidocaine may have a neuroprotective effect. The exact mechanism does not appear to be well elucidated. METHODS: We conducted a literature search using multiple combinations of keywords from PubMed and Ovid Medline databases according to the PRISMA guidelines. We included articles with cases of air embolism caused by an esophagogastroduodenoscopy (EGD). We excluded cases related to other procedures e.g. colonoscopy, endoscopic retrograde cholangiopancreatography, cholangioscopy, Kasai procedure, bronchoscopy, laparoscopy or thoracoscopy. We were able to identify 30 cases of CAE associated with EGD. We included our experience in treating one patient with CAE after elective EGD. RESULTS: Given the results of our literature search and this patient's characteristics, we chose to treat our patient with HBO and lidocaine infusion. Our case series consists of 31 patients of post EGD CAE, the mean age was 63.7 ± 11.14 years, 38.7% of the patients were women (nâ¯=â¯12). 38.7% of the cases underwent esophageal dilatation (nâ¯=â¯12), while 19.35% had EGD biopsy (nâ¯=â¯6), 9.6% had variceal ligation (nâ¯=â¯3), and 3.22% had variceal banding (nâ¯=â¯1). In 20 out of 31 cases, echocardiography has been documented, 20% of those patients (nâ¯=â¯4) had patent foramen ovale. HBO was used in treatment of 48% of cases (nâ¯=â¯15), among the included patients, 61% survived (nâ¯=â¯19). Our patient showed significant neurological improvement. CONCLUSIONS: Despite the rare incidence of CAE during or after EGD, physicians should be aware of this potential complication. In patients who develop sudden acute neurological symptoms, early diagnosis and intervention may prevent devastating neurological injury and death. The most accepted emergent treatment for CAE includes HBO, consideration of lidocaine, and work-up of source of the air embolism.