Shinya Kida

Anatomical pathways for lymphatic drainage of the brain and their pathological significance

Drainage of cerebrospinal and interstitial fluid from the brain into deep cervical lymph nodes has been well documented in a number of mammalian species [l]. Tracer studies have demonstrated that a significant fraction (1447%) of cerebrospinal fluid (CSF) drains into deep cervical lymph nodes within a short time 12, 141. When Indian ink is injected into the cisterna magna, it reaches the deep cervical lymph nodes within 1 min in the rabbit [I 51 and 30 min in the rat [8 ] . However, the anatomical connections from the subarachnoid space to the nasal lymphatics which facilitate such observed high and rapid lymphatic drainage from the brain have until recently remained unclear. In a series of experiments in our laboratory using Indian ink injections into the rat cerebral hemisphere or into the CSF, bulk flow pathways have been identified which correlate well with the physiological findings outlined by Knopf et al. in this symposium. Following the injection of Indian ink into the caudateputamen, carbon particles in the white matter spread diffusely through the extracellular spaces between the nerve fibres into the lateral ventricle. In the grey matter, carbon particles were preferentially distributed along perivascular spaces, not only of small arteries and veins but of large branches of the middle cerebral artery extending towards the surface of the cerebral hemisphere. Following the injection of Indian ink into the CSF in the cisterna magna, the ink accumulated in the basal cisterns and along the main trunks of the middle cerebral arteries and their branches over the surface of the cerebrum. When ink is injected into the subarachnoid space on the surface of the cerebrum, it is seen to drain

Significance of Volume Embolization Ratio as a Predictor of Recanalization on Endovascular Treatment of Cerebral Aneurysms with Guglielmi Detachable Coils

The purposes of this study are, firstly, to define the relationship between volume embolization ratio (VER) and degree of angiographical occlusion in endovascular treatment with Guglielmi detachable coils, and secondly, to examine influences of neck and dome sizes of aneurysms on the VER and the angiographical treatment result, and thirdly, to determine the relationship between the VER and the recanalization of coiled aneurysms. Fifty-two aneurysms in 46 patients were examined. VER ranged 8.1–31.9% (mean 18.5%). The mean VERs of each categories based on angiographical treatment results were 23.1% in complete occlusion, 16.1% in neck remnant and 12.2% in incomplete occlusion, respectively. The VER correlated significantly with both neck and dome size, while the angiographical treatment result was only affected by neck size. Five aneurysms showed aneurysmal recanalization among followed-up 41 aneurysms. All recanalized aneurysms were large, and their VERs were in range of 10.4–17.6%. Measurement of VER is useful to estimate the degree of occlusion objectively and to predict the aneurysmal recanalization. A small aneurysms with a small neck is relatively easy to achieve high VER and angiographical complete occlusion, with the consequence of less recanalization. On the other hand, a large aneurysm is liable to recanalize due to low VER, even if there was little filling of contrast medium in the aneurysmal cavity.

Localization of E-cadherin in peripheral glia after nerve injury and repair

Peripheral nerve injury results in histological and histochemical changes in neurons and glia. We have recently found that Ca2+-dependent cell adhesion molecule E-cadherin plays an important role in the selective fasciculation of a particular subset of unmyelinated sensory fibers. In the present immunohistochemical and immunoblot analyses, the temporal profile of the subcellular expression of this molecule in spinal nerves was examined after crushing, transecting, or ligaturing the sciatic nerve in mice with special attention paid to E-cadherin expression in glial cells. After axotomy of the sciatic nerve, distal axons of the proximal stump and the fibers of the distal stump degenerated, but E-cadherin was still detectable at the outer mesaxons of the myelinated axons as long as they remained morphologically intact. Subsequently, Schwann cells proliferated and migrated to form Schwann cell columns (Büngners bands) as initial responses to denervation, and expressed E-cadherin at their site of contact with each other and later with sprouting axons. At the initial stage of myelin formation, slender processes of a single Schwann cell interdigitated with and enveloped axons, and expressed E-cadherin at the contact site elaborated by a single Schwann cell. Immunoblot analysis on day 7 revealed that E-cadherin was detected in both the proximal nerve segments and the regenerative distal segments, but was negative in the degenerative distal segments. On the basis of present data, it is suggested that E-cadherin might be involved in the stabilization of the peripheral glial network which provides the guidance of sprouting axons and myelination

Membranous Ultrastructure of Human Arachnoid Cells

The ultrastructure of arachnoid cell membranes was investigated by conventional transmission EM and by freeze-fracture techniques in human arachnoid granulations. Arachnoid cells showed widespread membrane specialization in the granulations including the formation of desmosomes, gap junctions, tight junctions, intermediate junctions, hemidesmosome-likc structures, and micropinocytotic vesicles. However, the extent of the specialization varied from portion to portion; this was clearly shown on freeze-fracture replicas. Numerous extracellular cisterns were separated by cytoplasmic bodies or slender processes, joined by these junctional complexes. Uncoated and coated vesicles were abundant along the surface of extracellular cisterns representing the pathway of CSF. Complexes of branching tight junctions were comprised of 1–50 particle strands, which formed elaborate meshworks accompanied by numerous gap junctions and desmosomes. Micropinocytotic vesicles were often concentrated in the arachnoid cell cluster up to 40 per |xm;, which is equivalent to the concentration in brain capillary endothelial cells. The results of this study clearly suggest that arachnoid cells in arachnoid granulations are not only tightly adherent to form a firm structure for the passage of CSF, but that the arachnoid cells lining the CSF pathway show intense cell-cell communication and pino-cytotic activity. This high transcellular activity probably reflects active transports or secretion of certain molecules by arachnoid cells.

Improved cerebral perfusion and metabolism after stenting for basilar artery stenosis: technical case report.

OBJECTIVERecent advances in stent technology have allowed the introduction of more flexible stents that may be tracked more easily in the intracranial vessels. We present a patient with improved cerebral blood flow and metabolism as assessed by positron emission tomography after stent-assisted angioplasty for symptomatic basilar artery stenosis. CLINICAL PRESENTATION A 62-year-old man, who had undergone left superficial temporal artery to middle cerebral artery bypass surgery for left internal carotid artery occlusion 10 years previously, presented with dizziness, blurred vision, and memory disturbance. Angiography revealed severe stenosis of the proximal basilar artery. Positron emission tomographic scans revealed decreased cerebral blood flow associated with increased oxygen extraction fraction in the entire brain, particularly in the posterior circulation and the left middle cerebral artery territory. Despite medical treatment, the patient experienced worsening visual disturbance and right-sided motor weakness. INTERVENTIONTiclopidine and aspirin were used as antiplatelet agents. In addition, we used argatroban, which is a direct thrombin inhibitor, as an anticoagulant during the procedure. Predilation with a coronary artery balloon was performed, followed by placement of a GFX 3- by 8-mm stent (Arterial Vascular Engineering, Santa Rosa, CA), with excellent angiographic results. The patient made a good neurological recovery, and the postoperative positron emission tomographic scan demonstrated increases in both cerebral blood flow and cerebral metabolic rate of oxygen with a normalization of oxygen extraction fraction. CONCLUSIONStent-assisted angioplasty can provide a favorable clinical course as well as improved cerebral perfusion and metabolism for a patient with basilar artery stenosis. Long-term follow-up data and additional clinical experience are required to assess the durability of this approach.

Basic Fibroblast Growth Factor May Repair Experimental Cerebral Aneurysms in Rats

BACKGROUND AND PURPOSE To determine whether basic fibroblast growth factor (FGF) can induce proliferative response of endothelial cells and/or smooth muscle cells in aneurysmal lesions, we investigated the effect of the intravenous administration of basic FGF on experimental cerebral aneurysms. METHODS Cerebral aneurysms were induced in rats by ligation of the unilateral common carotid artery, producing hypertension. Three months later, basic FGF was intravenously injected in two groups of randomly divided rats on days 1, 3, and 5 at two different doses (low dose: 2 micrograms/100 g body wt per day; high dose: 5 micrograms/100 g body wt per day). In a control group, normal saline was similarly injected. The junctions of the anterior cerebral artery (ACA) and the olfactory artery (OA) were examined with a light microscope. Aneurysmal changes were defined as the lesions with discontinuity of the internal elastic lamina in more than half of the outward dilated wall. Depending on whether the smooth muscle cell layer was present in the whole wall, the lesions were divided into two stages: early aneurysmal lesion (whole area) and saccular aneurysm (not totally preserved). RESULTS The control and the low-dose groups presented no obvious intimal thickening in the intact ACA-OA junctions of both nonligated and ligated sides as well as in the aneurysmal changes. In contrast, in the high-dose group, various degrees of intimal thickening in the wall were detected in 7 of 15 early aneurysmal lesions (P = .019, Fishers exact test). Immunohistochemistry showed the proliferated cells to be smooth muscle cells. CONCLUSIONS These results demonstrate that exogenous basic FGF induces the proliferative response of smooth muscle cells in aneurysmal lesions in rats.

Multicentric infantile myofibromatosis in the cranium: case report.

Infantile myofibromatosis is a rare clinical entity characterized by multiple mesenchymal tumors in the neonatal period. We describe a 15-month-old girl with multicentric cranial lesions involving the parietal and occipital bones associated with a single small subcutaneous lesion in the back. Magnetic resonance imaging clearly demonstrated the isointense lesions on T1-, T2-, and proton density-weighted images, which showed marked gadolinium enhancement of the tumors and adjacent dura mater. A histological examination of the resected temporal lesion revealed the myofibroblastic nature of the tumor cells. This is the first description of magnetic resonance features of multicentric infantile myofibromatosis in the cranium, and gadolinium-enhanced magnetic resonance images were useful in showing dural involvement. The importance of recognizing this disorder is emphasized because of its special clinical behavior.

Surgical pathology of spinal schwannomas: a light and electron microscopic analysis of tumor capsules.

OBJECTIVE Although spinal schwannomas are often encountered, the pathology of the tumor capsule has not been reported. In this study, we describe the ultrastructural pathology of the tumor capsule of spinal schwannomas. METHODS In 18 patients who underwent total removal of spinal schwannomas (C2–conus), the tumor capsule was collected and examined by light and electron microscopy. RESULTS The thickness of the tumor capsule ranged from 15 to 800 &mgr;m (mostly 30–100 &mgr;m) and was composed of three layers from the surface to the center: 1) a thinly stretched nerve tissue layer; 2) a fibrous layer of fibrocytes, abundant collagen fibers, and tumor vessels; and 3) a thin transitional layer intermingled with fibrous components and tumor cells. The thickness of each layer varied in different regions of the surface. There was no clear separation between the tumor capsule and the neoplastic tissue, even on the electron microscopic level. A number of nerve fibers ran through the fibrous layer and beneath the capsule as well as in the nerve tissue layer. CONCLUSION Compared with vestibular schwannomas, which have been reported to be covered by an extremely thin layer (3–5 &mgr;m) of connective tissue, spinal schwannomas were well encapsulated. The capsule was composed of three distinct components; however, the cleavage between thin capsule and tumor cells was indistinct, and the thickness of the axon-containing capsule varied from site to site. Therefore, resection of the nerve of tumor origin, rather than enucleation, would be justified to avoid tumor recurrence. Surgeons should be aware of this pathology when performing the procedure.

Morphological Basis for Fluid Transport Through and Around Ependymal, Arachnoidal, and Glial Cells

Cerebrospinal fluid in man is produced by the choroid plexus in the ventricular system at the rate of 500 ml a day; the total cerebrospinal fluid (CSF) is some 150 ml.1 Approximately 20% of the CSF is in the ventricles, but the majority is in the subarachnoid space over the surface of the brain and the spinal cord. There is also interstitial fluid within the extracellular spaces of the gray and white matter of the brain and spinal cord. Such extracellular fluid may be greatly increased in amount when there is cytotoxic and vasogenic cerebral edema associated with trauma, infection, or infarction of the brain or around a tumor.1–3 Extracellular fluid may also be increased in the periventricular white matter in acute hydrocephalus due to the insudation of CSF from the ventricles.4

Infarction in Anterior Inferior Cerebellar Artery Territory Caused by Occlusion of Vertebral Artery

Although the anterior inferior cerebellar artery (AICA) has the smallest territory of all the cerebellar arteries, its exact location and extent varies depending on the calibre and supply of the posterior inferior cerebellar artery (PICA) [1,2]. However, the AICA invariably supplies the middle cerebellar peduncle, inferolateral pons, inner ear, and the anterior surface of the cerebellar hemisphere, including the flocculus [1,3]. Terminal AICA branches usually feature anastomoses with the PICA or superior cerebellar artery [1,4–7]. In cases of occlusion of the PICA or vertebral artery (VA), the clinical signs and territory of the infarction are characterized as “lateral medullary syndrome”, which are clearly distinct from those of occlusion of the AICA [7,8]. We present here a very unusual case with the clinical features of infarction in the territory of the AICA as a result of occlusion of the ipsilateral VA.