Presentation on theme: "Clinical Program for Cerebrovascular Disorders Mount Sinai Medical Center Intracerebral Hemorrhage and A Comprehensive Overview of the Malignant Gliomas."— Presentation transcript:
Clinical Program for Cerebrovascular Disorders Mount Sinai Medical Center Intracerebral Hemorrhage and A Comprehensive Overview of the Malignant Gliomas and Their Treatment Clinical Case Presentation Clara Raquel Epstein, MD Fellow
Intracerebral Hemorrhage and Neoplasms- Pathogenesis Mechanism is unclear –Growing neoplasms develop new blood vessels to keep pace with expansion (angiographic blush) –Intracranial malignant neoplasms contain vasculature distinctive from normal cerebral blood vessels –Three patterns – Axial, Retiform, Glomeruloid Retiform is associated with increased tumor related hemorrhage Tortuous and convoluted course High incidence in Gliomas
Intracerebral Hemorrhage and Neoplasms- Pathogenesis Mechanism is unclear (continued) –Primary brain tumors have neovessels which are immature, fenestrated, and lack tight junctions – More permeable than normal and more vulnerable –Tendency to bleed b/c of increased vascular fragility and reduced mechanical support from surrounding tissue –Invasion of vessel walls further compromise vascular integrity –Tumor necrosis increases incidence of hemorrhage
Intracerebral Hemorrhage and Neoplasms- Epidemiology
Intracerebral Hemorrhage and Neoplasms- Presentation Stroke-like presentation –Lateralizing signs and abrupt change in level of alertness occurs in 24% to 62% of patients –May present in coma (25%-54%) –Progressive development of neurologic signs over several days (33%-62%) –Overall the proportion of patients with acute, subacute, or clinically silent intratumoral hemorrhage varies among different series, depending on means of diagnosis (imaging vs. autopsy)
Intracerebral Hemorrhage and Neoplasms- Diagnosis
Intracerebral Hemorrhage and Neoplasms Clinical Case Presentation A 72 year old right handed Hispanic female with a history of hypertension, depression and treated tuberculosis presented on 12/4/99 with complaints of acute onset of headache associated with flashing lights, and an episode of vomiting. In addition, the patient reported difficulty with her left visual field. Per history the patient was in her usual state of health until approximately 10 PM the evening prior to admission.
Hospital Course Initially the patient was doing well with minimal neurologic impairment with the exception of a left visual field cut. The patient was started on Dilantin for seizure prophylaxis. However, the patient’s course in the stroke unit was significant for progressive neurologic deterioration with a progression of left hemiparesis and left facial palsy despite steroid therapy. In addition, the infectious disease service was consulted for a positive RPR titer and a decision to treat the patient with a three week course of Penicillin IM was initiated.
Hospital Course On admission a CT scan was obtained which showed evidence of a an area of increased attenuation consistent with an intracerebral hematoma in the right parietal lobe with surrounding edema and effacement of the cortical sulci in the right frontoparietal region. Some compression of the right ventricular atrium and mild dilation of the temporal horn was seen, as well as slight mass effect on the 3 rd ventricle. No significant shift of the midline structures at this time was evident. In the posterior fossa the 4 th ventricle was normal in size and midline. It was suggested that this could represent an underlying neoplastic lesion such as a Glioblastoma multiforme.
Hospital Course A CT of the chest, abdomen and pelvis was obtained as part of the metastatic workup. A soft tissue mass in the right subpleural midlung field with irregular prominent soft tissue surrounding the right mid lobe bronchus suggested a possible neoplastic foci. In addition, nodules were seen at the right apex for which the suggestion of neoplasm could not be excluded.The pulmonary service was consulted for evaluation. It was felt that the changes may be a related to her history of tuberculosis and further diagnostic workup was deferred.
Hospital Course After significant neurologic deterioration, on 12/14/99, a repeat CT scan was obtained which showed evidence of increasing vasogenic edema surrounding the previously described right parietal hematoma. There was also greater mass effect with an increase in compression of the lateral cerebral ventricles and a mild right to left midline shift. The trapped temporal horn of the right lateral cerebral ventricle had enlarged since the previous studies as well. Neurosurgery was consulted and on 12/16/99 the patient will undergo excision of the underlying lesion utilizing frameless stereotaxy.
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