Biomedical subjects
Publications and source records attributed to J Zyroff.
Magnetic resonance imaging findings in three patients with diskogenic vertebral sclerosis of the lumbar spine are presented. Increased signal intensity within the vertebral bodies was observed on T2-weighted images that corresponded to areas of bony sclerosis on plain radiography. Decreased signal intensity within the disk space on T2-weighted images serves to differentiate diskogenic sclerosis from infectious spondylitis.
A patient with biopsy-proven primary mucocele of the anterior clinoid process is presented. Gadolinium-DTPA enhanced magnetic resonance imaging revealed a nonenhancing lesion isointense to gray matter. Computed tomography revealed well corticated bony margins without direct involvement of the sphenoid sinus.
The capacity of intracarotid infusion of urokinase to salvage neurologic function in a baboon model of acute thrombotic stroke has been studied. The model consists of reversible eccentric balloon compression (3 hours) of the right middle cerebral artery (MCA) proximal to the take-off of the lenticulostriate arteries (LSA), resulting in in situ thrombosis of perforating branches supplying the right corpus striatum. Neurologic endpoints included quantitative assessment of neurologic function (NE), estimation of cerebral infarction volume by computerized tomographic (CT) scan, and carotid angiography. In untreated acute stroke control animals (n = 6), a persistent decrease in functional score (from 100 to 36 +/- 11) at 14 days and a defined region of cerebral infarction (volume = 3.2 +/- 1.5) were detected at 10 days. Intracarotid urokinase administered to five animals (1.2 X 10(6) IU over 60 min) following the 3 hour period of MCA occlusion improved neurologic function (NE = 50, 55, 85, 100, 100) and reduced infarction size (0.3, 0.5, 0.8, 0.7, 1.1 cm3, respectively) without evidence of intracranial hemorrhage. Systemic fibrinogenolysis was produced in all five treated animals. We conclude that thrombolytic therapy given within 3 hours of experimental thrombotic occlusion may salvage neurologic function and reduce cerebral infarction volume without CT scan detectable intracranial bleeding.
To study the effects of antithrombotic therapy in experimental stroke, we have characterized a baboon model of acute cerebrovascular thrombosis. In this model an inflatable silastic balloon cuff has been implanted by transorbital approach around the right middle cerebral artery (MCA), proximal to the take-off of the lenticulostriate arteries (LSA). Inflation of the balloon for 3 hours in six animals produced a stereotypic sustained stroke syndrome characterized by contralateral hemiparesis. An infarction volume of 3.2 +/- 1.5 cm3 in the ipsilateral corpus striatum was documented by computerized tomographic (CT) scanning at 10 days following stroke induction and 3.9 +/- 1.9 cm3 (n = 4) at 14 days by morphometric neuropathologic determinations of brain specimens fixed in situ by pressure-perfusion with 10% buffered formalin. Immediate pressure-perfusion fixation following deflation of the balloon was performed in 16 additional animals given Evans blue dye intravenously prior to the 3 hour MCA balloon occlusion. Light microscopy and transmission electron microscopy consistently confirmed the presence of thrombotic material occluding microcirculatory branches of the right LSA in the region of Evans blue stain, but not those of the contralateral corpus striatum. When autologous 111In-platelets were infused intravenously in four animals from the above group prior to the transient 3 hour occlusion of the right MCA, gamma scintillation camera imaging of each perfused-fixed whole brain demonstrated the presence of a single residual focus of 111In-platelet activity involving only the Evans blue-stained right corpus striatum. Focal right hemispheric activity was equivalent to 0.55 +/- 0.49 ml of whole blood, and the occlusion score derived from histologic examination of the microcirculation of the Evans blue-stained corpus striatum averaged 34.8 +/- 2.8. Similar 111In-platelet imaging and histologic scoring experiments carried out in four animals pretreated with the antithrombotic combination heparin and ticlopidine showed marked reduction of both 111In-platelet activity (0.01 +/- 0.03 ml vs. 0.55 +/- 0.49 ml; p less than 0.01) and thrombotic occlusion of the microcirculation (10.8 +/- 7.4 units vs. 34.8 +/- 2.8 units; p less than 0.01) in the right corpus striatum following 3 hours of MCA occlusion. In separate control experiments 111In-labeled autologous platelets were infused after the 3 hour period of right MCA occlusion and subsequent balloon deflation in two animals; no focus of 111In-platelet activity was demonstrated in fixed whole brain.(ABSTRACT TRUNCATED AT 400 WORDS)
The purpose of this investigation was to describe gadopentetate-dimeglumine-enhanced MR findings in metastatic disease to the pial lining of the spinal cord. Correlation was made with clinical data, other radiologic studies, and pathologic findings. Eighty-six patients with a known malignancy and unexplained neurologic signs or symptoms were studied with pre- and postcontrast T1-weighted images. In seven of these patients, abnormal enhancement of the pial lining of the cord was seen on the sagittal postcontrast T1-weighted images. This appeared as a thin rim of enhancement along the surface of the cord in six patients and as a focal, thick rim of enhancement in addition to the thin rim of enhancement in the seventh patient. Axial images confirmed the location along the pial lining in each case. Precontrast T1-weighted images in all seven cases and precontrast T2-weighted images in five cases failed to detect any focal abnormalities of the pial lining of the cord. Pathologic confirmation was available in five of the seven patients. Primary malignancies in these patients included breast carcinoma (two), lymphoma (one), leukemia (one), adenocarcinoma of the lung (one), prostate carcinoma (one), and malignant melanoma (one). Three of seven patients had metastatic disease evident only within the CNS, while four patients had widespread disease outside the CNS. We conclude that contrast-enhanced MR imaging is useful in the diagnosis of pial spread of metastatic disease in patients with a known primary malignancy and unexplained neurologic signs or symptoms.
PURPOSE: To evaluate the clinical and MR findings of metastatic lesions involving the cerebellopontine angle (CPA), which may be useful in differentiating them from the more commonly occurring benign CPA lesions. METHODS: Clinical and MR findings of 14 patients with clinical/radiologic (seven) or pathologic (seven) diagnoses of CPA metastasis were retrospectively reviewed. RESULTS: Useful clinical findings included acute onset and rapid progression of cranial nerve symptoms, especially 7th and/or 8th cranial nerve deficits (92.9%). Cranial nerve symptoms could be unilateral (50%) and frequently involved multiple cranial nerves (64.3%). MR findings showed significantly more extensive disease than suggested by clinical presentation, with 100% of patients having multiple cranial nerve involvement and 85.7% bilateral. Useful MR findings included small and/or bilateral CPA-enhancing lesions with relative isointensity to brain parenchyma on precontrast MR, with associated findings of multiple and/or bilateral cranial nerve and/or leptomeningeal lesions. CONCLUSIONS: These associated findings suggest that cerebrospinal fluid dissemination and/or leptomeningeal extension may be an important pathway for metastatic spread to the CPA. Because the CPA metastasis may be the initial or only site of metastasis, and may occur many years after the initial diagnosis of malignancy, MR findings with clinical correlation are not only useful for the detection of CPA metastases, but also for their differentiation from the more common benign CPA tumors.