Yoshiya Nakayama

Small Chronic Hemorrhages and Ischemic Lesions in Association With Spontaneous Intracerebral Hematomas

BACKGROUND AND PURPOSE It has been speculated that the same type of hypertensive small-artery disease can cause either intracerebral hemorrhages or ischemic lesions, depending on the circumstances. METHODS To test this hypothesis, we examined the association between spontaneous intracerebral hematomas and both small chronic hemorrhages and ischemic lesions using echo planar and T2-weighted MRI. We considered a hypointense area to represent a hemorrhage and a hyperintense area to represent an ischemic lesion. RESULTS We identified small hypointense lesions in 56.7% of 30 patients with intracerebral hematomas (mean age, 62.2 years; total number of lesions, 108) and in 25.4% of 59 patients without hematomas (mean age, 67.6 years; total lesions, 28). The incidence of hypertension was 88.3% in patients with intracerebral hematomas and 42.3% in those without. The hypointense lesions were found in 56.0% of 50 patients with hypertension, whereas they were found only in 10.3% of 39 patients without hypertension. The hypointense lesions were most common in the subcortex, followed by the putamen, pons, thalamus, and cerebellum. The hyperintense lesions were of a higher grade in patients with intracerebral hematomas than in those without. The hypointense lesions were commonly surrounded by hyperintense areas. Additionally, in 3 of 3 autopsied brains, we found hemosiderin deposits around arteriosclerotic microvessels and a surrounding small infarction in areas that had appeared as small hypointense lesions surrounded by hyperintensity on MRI. One specimen also had an organized miliary pseudoaneurysm. CONCLUSIONS Our findings indicate that spontaneous intracerebral hematomas are frequently associated with small chronic hemorrhages, ischemic lesions, and hypertension. We speculate that hypertensive intracerebral hemorrhage may have the same microangiopathic basis as cerebral infarction.

Cerebral blood flow and autoregulation in normal pressure hydrocephalus.

OBJECTIVE We tried to identify indications for cerebrospinal fluid shunting in patients with normal pressure hydrocephalus. METHODS We studied the cerebral blood flow (CBF) and vascular response to acetazolamide in the white matter, cortex, and thalamus of 21 patients with normal pressure hydrocephalus, comparing patients who improved clinically after shunting with those who did not. We used xenon-enhanced computed tomography for the CBF measurements. RESULTS Preoperatively, both groups had globally reduced CBF, but the reduction was more pronounced in the unimproved patients. The vascular response was impaired only in the white matter of the patients who improved later. After shunting, restoration of CBF, more marked in the white matter, and recovery of vascular response in the white matter paralleled clinical improvement and a reduction in ventricular dilation and periventricular lucency on computed tomographic scans in nine patients. The CBF reduction, however, deteriorated in the 12 patients who did not improve clinically. CONCLUSION We conclude that the underlying disease in the improved patients was ischemia, with a loss of autoregulatory capacity in the periventricular white matter caused by cerebrospinal fluid diffusion. Those who did not improve had irreversible brain damage in which the CBF reduction was secondary to metabolic depression and autoregulation was preserved. We also conclude that patients suspected of having normal pressure hydrocephalus will improve clinically after shunting if preoperative hemispheric CBF is greater than 20 ml/100 g per minute and the vascular response to acetazolamide is impaired only in the periventricular white matter. They will not improve, however, if the preoperative CBF is less than 20 ml/100 g per minute and the vascular response to acetazolamide is intact.

Giant fusiform aneurysm of the basilar artery: Consideration of its pathogenesis

BACKGROUND We tried to determine the pathogenesis of a fusiform aneurysm of the basilar artery based on the findings of two patients who had pontine infarctions due to thrombosis within the aneurysm. CASE REPORT The patients were female, aged 75 and 62 years. At autopsy of the first case, the dilated basilar artery was filled with fresh and old thrombus. The wall was extremely thin on the left side, where a fresh red thrombus was evident, and thick on the right side, where an old white thrombus appeared. The thick wall had a thickened and hyalinized intima, and a deposition of atheromatous plaque disrupted both the internal elastic lamina and muscle layer. The left vertebral artery was atherosclerotic and its lumen was severely compromised, but the right vertebral artery was hypoplastic. On angiogram of the second case, the dilated basilar artery presumably was filled with thrombus on the left side, contralateral to the dilated and tortuous vertebral artery. The left vertebral artery was hypoplastic. CONCLUSION Atherosclerosis may be the essential factor in the pathogenesis of a fusiform aneurysm of the basilar artery in elderly patients. The disrupted internal elastic lamina and muscle layer may be susceptible to mechanical injury by hemodynamic strain, causing progressive attenuation of the arterial wall. Stenosis of the vertebral artery on the dominant side probably produces a jet stream within the basilar artery on the stenotic side and a stagnant zone on the opposite side, promoting the initial thrombus formation.

Cerebral blood flow and intracranial pressure in chronic subdural hematomas

BACKGROUND We examined the cerebral blood flow (CBF) and intracranial pressure (ICP) in 15 patients with chronic subdural hematomas to clarify the clinical pathophysiology of this disorder. METHODS All patients had hemiparesis and/or mental disturbance, including confusion or lethargy, and demonstrated either midline shift or herniation on computed tomography (CT) scans. CBF was measured using xenon-enhanced CT preoperatively, 1 day postoperatively, and 3-4 weeks later. ICP was monitored continuously for 24 hours both before and after surgery. RESULTS The CBF was severely reduced on both sides. It stayed at the preoperative level 1 day after surgery, when all patients improved clinically, but returned to subnormal levels in 3-4 weeks. Acetazolamide-enhanced CBF values that were abnormally elevated in each region preoperatively stayed the same during each stage in the hemisphere and cortex despite the different baseline values. However, these measurements increased gradually after surgery in the thalamus and putamen. The ICP was moderately high preoperatively (14.2-25.3 mmHg; mean: 19.4 +/- 3.7 mmHg) and remained high (13.4-31.7 mmHg; mean: 21.4 +/- 6.0 mmHg) 1 day postoperatively. There was no correlation between the CBF values and ICP values in any region either before surgery or 1 day after surgery. CONCLUSIONS We conclude that chronic subdural hematomas may induce neurologic dysfunction primarily through a mechanical distortion of central brain regions such as the thalamus with a secondary influence on remote regions due to transneural depression. The effect of a subdural hematoma on CBF and ICP is not a major cause of neurologic dysfunction. The thalamus seems to be at the core of the pathophysiology of chronic subdural hematomas.

Xanthoma in meckel's cave a case report

A case of xanthoma located within Meckels cave and the semilunar ganglion is described in a patient with a trigeminal nerve deficit. This is the first case of xanthoma in such a location. The distinctive morphological appearance is illustrated and the possible histogenesis is discussed.

Stromal angiogenesis in human glioma: A role of platelet-derived endothelial cell growth factor

BACKGROUND Although several tumor angiogenic factors have been identified previously and characterized, it is not yet fully clear how tumor angiogenic factors induce endothelial cell transformation and proliferation. Platelet-derived endothelial cell growth factor (PD-ECGF) has been recently discovered to be an endothelial cell growth factor initially purified from human platelets. However, there has been no previous report describing the significance of PD-ECGF in the growth of brain tumors by angiogenic stimulation. We report the immunohistochemical localization of PD-ECGF in human gliomas and meningiomas, and discuss whether PD-ECGF could play a role in the modulation of stromal angiogenesis in human glioblastoma multiforme. METHODS Twenty-eight cases of glioma (11 glioblastomas and 17 astrocytomas) derived from the neuroectoderm in embryogenesis and 12 meningiomas from the mesoderm were investigated by both immunohistochemical localization of the PD-ECGF and a semiquantitative assay to determine the degree of stromal angiogenesis. RESULTS Numerous PD-ECGF positive cells were observed within and around the blood vessels of glioblastoma multiforme, especially on the borders of tumor tissue. The PD-ECGF positive cells were negative for anti-von Willebrand factor (vWF) and antiglial fibrillary acidic protein (GFAP) antibodies and were positive for antimacrophage (HAM-56). The expression of PD-ECGF by macrophages closely correlated with the degree of stromal vascularity in glioblastoma multiforme; no such correlation was found in either astrocytoma or meningioma. Proliferating cell nuclear antigen (PCNA) was found to be positive in some endothelial cells of stromal vessels in glioblastoma multiforme. These findings suggest that PD-ECGF expressed by macrophages plays an important role in the growth of glioblastoma multiforme with stromal angiogenesis.

Maffucci's syndrome associated with intracranial chordoma: case report.

This report discusses Maffuccis syndrome associated with intracranial chordoma. Of the 170 reported cases of this syndrome, only 27 have been associated with intracranial lesions and none was involved with intracranial chordoma. Chordomas are occasionally difficult to differentiate from chondroma and chondrosarcoma. An immunohistochemical analysis was able to prove, however, that the chordoma of this case significantly differed from chondroma and chondrosarcoma.

Multiple intracerebral arteriovenous malformations: report of two cases.

We report the cases of two patients, each of whom had two separate angiographically demonstrable intracerebral arteriovenous malformations (AVMs). One patient had an intraventricular hemorrhage with AVMs in the basal ganglia and the insula on the left side, and the other had a pontine hemorrhage with AVMs in the pons and the occipital lobe on the right side. The AVMs in the former patient were removed totally without residual neurological deficit. We discuss the diagnostic problems of multiple intracerebral AVMs and stress the need for thorough neuroradiological evaluation so as not to miss an occult AVM. We also stress the necessity of total excision of all the lesions and point out several problems faced in surgery for AVMs.

Intracerebral cyst associated with meningioma

A 27-year-old male had experienced an episode of severe headache and nausea, sometimes accompanied by an inability to name objects. Magnetic resonance imaging showed a huge cyst within the left temporal lobe and a high degree of brain shift by it. A small round mass, which appeared to be a mural nodule, was located in the tip of left middle fossa. It was highly enhancing together with its attached dura mater, but the cyst wall was not enhanced. Sphenoid ridge meningioma with an associated intracerebral cyst or cystic glioma invading the dura mater was suspected. During surgery the small tumor was found to be arising from the sphenoid ridge and evaginating into the tip of the temporal lobe. The intracerebral cyst had a smooth surface and the tumor was visible outside the cyst through its wall. The tumor was totally removed, but the cyst wall was left without excision. Postoperatively he had no symptoms. Histological examination showed a microcystic meningioma. It is stressed that differentiations of cystic meningiomas from other cystic tumors and, of intratumoral from extratumoral cystic meningiomas using radiological, operative or histological findings are important.

Scalp cavernous angioma presenting as sinus pericranii: diagnostic value of cerebral angiography and magnetic resonance imaging.

Abstract  Objects: Sinus pericranii is only a symptom complex, and it can have a variety of etiologies. Therefore, it is important to differentiate these etiologies preoperatively by means of radiological examinations. A 5-year-old boy was admitted with a soft and fluctuant tumor in the right parietal region near the midline. The tumor appeared when the child was in a recumbent position, distending noticeably with the Valsalva maneuver and disappearing completely when the patient was in the sitting position. Methods: Magnetic resonance imaging showed the lesion with honeycomb-like heterogeneous iso- and low-intensity signals on the T1-weighted image and with heterogeneous high- and iso- intensity signal on the T2-weighted image. Dynamic study with an injection of gadolinium diethylene-triaminopentaacetic acid demonstrated and nodular peripheral enhancement at early phase and subsequent progressive enhancement towards the center of tumor. The internal carotid angiogram was normal. The external carotid angiogram, however, showed a tumor stain fed by the superficial temporal arteries. The stain was retained until the late phase and drained into the scalp veins and into the superior sagittal sinus. Following direct injection of contrast medium into the tumor there was prolonged retention of the medium in the tumor and leakage into scalp veins and the superior sagittal sinus. The mass under the periosteum was totally removed and proved to be a cavernous angioma. Conclusions: Scalp cavernous angioma is one of the etiologies of sinus pericranii and may be diagnosed preoperatively by cerebral angiography or magnetic resonance imaging. Serial dynamic magnetic resonance imaging will be particularly helpful for this diagnosis.