Absence of donor-type major histocompatibility complex class I antigen-bearing microglia in the rat central nervous system of radiation bone marrow chimeras

Localization of bone marrow-originated cells in the central nervous system (CNS) of the rat was investigated by using bone marrow chimeras. In order to do this, Lewis rats which carry major histocompatibility complex (MHC) class I antigens haplotype 1 (RT1.Al) were reconstituted with (Lew X PVG)F1 (RT1.Al/c) bone marrow cells after lethal irradiation. Transferred bone marrow cells were detected by immunohistochemical staining using a monoclonal antibody, OX27, specific for haplotype c of rat MHC class I antigens (RT1.Ac). The spleen and thymus of chimeric rats were fully reconstituted with transferred F1 cells 4 weeks after bone marrow transplantation. At this stage, mononuclear cells in the subarachnoid space of the CNS expressed OX27 antigen indicating that they were of bone marrow origin. A few OX27-positive blood cells were scattered in the CNS parenchyma 4-12 weeks after reconstitution. Ramified microglia, however, remained OX27-negative. Bone marrow-derived microglia were not observed throughout the period of examination until 24 weeks. In addition, experimental allergic encephalomyelitis (EAE) was induced in chimeric rats in order to augment the expression of MHC class I antigens on microglia. Even under this condition, no OX27-positive microglia were observed. Taken together, ramified microglia might be of neuroectodermal origin and there is little possibility that the microglia are derived from the bone marrow. However, if the ramified microglia are derived from blood cells, the microglia may be expected to have characteristic cell kinetics from the following points: (1) the precursor cells of the microglia may enter the CNS only at the perinatal stage; and (2) even under the condition in which lymphocytes and macrophages enter the CNS as observed in EAE, the precursor cells of the microglia are not supplied from the blood.     

Proliferating resident microglia express the stem cell antigen CD34 in response to acute neural injury

Reactive microgliosis is a highly characteristic response to neural injury and disease, which may influence neurodegenerative processes and neural plasticity. We have investigated the origin and characteristics of reactive microglia in the acute phase of their activation in the dentate gyrus following transection of the entorhino-dentate perforant path projection. To investigate the possible link between microglia and hematopoietic precursors, we analyzed the expression of the stem cell marker CD34 by lesion-reactive microglia in conjunction with the proliferation marker bromodeoxyuridine (BrdU) and the use of radiation bone marrow (BM) chimeric mice. We found that CD34 is upregulated on early-activated resident microglia, rather than by infiltrating bone marrow-derived cells. The number of CD34(+) microglia peaked at day 3 when 67% of the resident CD11b/Mac-1(+) microglia co-expressed CD34, and all CD34(+) cells co-expressed Mac-1, and decreased sharply toward day 5, unlike Mac-1, which was maximally expressed at day 5. Approximately 80% of the CD34(+) cells in the denervated dentate gyrus had incorporated BrdU into their nuclei at day 3. We also showed that CD34 is upregulated on early-activated microglia in the facial motor nucleus following peripheral axotomy. The results suggest lesion-reactive microglia to consist of functionally distinct subpopulations of cells; a major population of activated resident CD34(+)Mac-1(+) microglia with a high capacity for self-renewal, and a subpopulation of CD34(-)Mac-1(+) microglia which has a mixed extrinsic and intrinsic origin and whose proliferative capacity is unknown.     

Organization of glial cells in the adult sea cucumber central nervous system

The nervous system of echinoderms has long been considered too unique to be directly comparable to the nervous system of other Deuterostomia. Using two novel monoclonal antibodies in combination with epifluorescence, confocal, and electron microscopy, we demonstrate here that the central nervous system of the sea cucumber Holothuria glaberrima possesses a major non‐neuronal cell type, which shares striking similarities with the radial glia of chordates. The basic features in common include (a) an elongated shape, (b) long radial processes, (c) short lateral protrusions branching off the main processes and penetrating into the surrounding neuropile, (d) prominent orderly oriented bundles of intermediate filaments, and (e) ability to produce Reissner's substance. Radial glia account for the majority of glia cells in echinoderms and constitutes more than half of the total cell population in the radial nerve cord and about 45% in the circumoral nerve ring. The difference in glia cell number between those regions is significant, suggesting structural specialization within the seemingly simple echinoderm nervous system. Both cell death and proliferation are seen under normal physiological conditions. Although both glia and neurons undergo apoptosis, most of the mitotic cells are identified as radial glia, indicating a key role of this cell type in cell turnover in the nervous system. A hypothesis is proposed that the radial glia could be an ancestral feature of the deuterostome nervous system, and the origin of this cell type might have predated the diversification of the Chordata and Ambulacraria lineages. © 2010 Wiley‐Liss, Inc.     

Low-dose gamma-irradiation promotes survival of injured neurons in the central nervous system via homeostasis-driven proliferation of T cells

Protective autoimmunity was only recently recognized as a mechanism for attenuating the progression of neurodegeneration. Using a rat model of optic nerve crush or contusive spinal cord injury, and a mouse model of neurodegenerative conditions caused by injection of a toxic dose of intraocular glutamate, we show that a single low dose of whole-body or lymphoid-organ gamma-irradiation significantly improved the spontaneous recovery. Animals with severe immune deficiency or deprived of mature T cells were unable to benefit from this treatment, suggesting that the irradiation-induced neuroprotection is immune mediated. This suggestion received further support from the findings that irradiation was accompanied by an increased incidence of activated T cells in the lymphoid organs and peripheral blood and an increase in mRNA encoding for the pro-inflammatory cytokines interleukin-12 and interferon-gamma, and that after irradiation, passive transfer of a subpopulation of suppressive T cells (naturally occurring regulatory CD4(+)CD25(+) T cells) wiped out the irradiation-induced protection. These results suggest that homeostasis-driven proliferation of T cells, induced by a single low-dose irradiation, leads to boosting of T cell-mediated neuroprotection and can be utilized clinically to fight off neurodegeneration and the threat of other diseases in which defense against toxic self-compounds is needed.     

Giant cell granulomatous angiitis of the central nervous system

Summary This is a report of five autopsied cases of giant celled granulomatous angiitis of the central nervous system. There were tree males and two females ranging in age from 42 to 71 years, with an acute course in two, death occurring within one and five weeks, and longer duration in three, with recurrent illness of 16 months to 5 years. The clinical features were mental changes associated with hemiparesis or tetraparesis, extrapyramidal signs, visual disorders with optic atrophy, and brainstem syndromes with final coma. Typical CSF findings were mild lymphocytosis with increased protein and gamma globulin levels. General autopsy disclosed generalized giant cell angiitis with aortitis in two cases, in one of which the diagnosis had been made by superficial temporal artery biopsy, while in three patients the inflammatory lesions were confined to the CNS vasculature, affecting all types and sizes of vessels. Although there were no significant differences between the cases with systemic angiitis with CNS involvement and those with vascular lesions limited to the CNS, the latter group showed predominance of the disorder for the small leptomeningeal and intracerebral or spinal vessels without involvement of the large intra- and extracranial brachiocephalic arteries. The latter are more often involved with cranial or systemic giant cell angiitis. The CNS showed disseminated microinfarctions of the brain and spinal cord (2 cases) or larger recent and old infarcts. The similarities in the morphological features and pattern of lesions of the CNS vessels in both isolated and generalized forms of giant cell granulomatous angiitis are in favor of a common basic disorder of hitherto unknown etiology. Granulomatous angiitis of the CNS is, therefore, regarded as a local variant of giant cell vasculitis rather than a separate nosological entity. From recent data, the disease is perhaps best regarded as an immune complex disorder, although viral infection is also considered.

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Zusammenfassung Es wird über 5 Autopsiefälle von granulomatöser Riesenzell-Angiitis (RZA) des ZNS berichtet. Es handelte sich um 3 Männer und 2 Frauen im Alter von 42–71 Jahren mit akutem Verlauf in zwei Fällen mit letalem Ausgang zwischen 1 und 5 Wochen sowie längerem, rezidivierendem Verlauf bei 3 Patienten mit Dauer zwischen 16 Monaten und 5 Jahren. Das klinische Bild umfaßte psychische Störungen mit Hemi- oder Tetraparese, extrapyramidale Symptome, Sehstörungen mit Optikusatrophie und Hirnstammsyndrome mit terminalem Koma. Typische Liquorbefunde umfaßten leichte lymphozytäre Pleozytose, erhöhte Eiweiß- und Gammaglobulinwerte. Die Autopsie ergab eine generalisierte RZA mit Aortitis in 2 Fällen, wobei einmal die Diagnose bereits durch eine Biopsie der Art. temporalis superficialis gesichert worden war. Bei 3 Patienten waren die entzündlichen Läsionen auf das ZNS-Gefäßsystem beschränkt, wobei alle Gefäßtypen und -kaliber betroffen waren. Obgleich sich zwischen den Fällen mit ZNS-Beteiligung bei systemisierter Angiitis und jenen mit isoliertem ZNS-Gefäßbefall keine wesentlichen Abweichungen ergeben, zeigten die letzteren Formen einen Vorzugsbefall der kleinen meningealen, intrazerebralen und/oder spinalen Gefäße ohne Beteiligung der großen intra- und extrakraniellen brachiocephalen Arterien. Letztere sind häufiger bei der Arteriitis cranialis (temporalis) und systemischen RZA betroffen. Das ZNS bot disseminierte Mikroinfarkte in Hirn und Rückenmark (2 Fälle) oder größere frische und ältere Erweichungen. Die Ähnlichkeiten des morphologischen Bildes und Verteilungsmusters der ZNS-Gefäßläsionen bei isolierten und generalisierten Formen der granulomatösen RZA sprechen für eine gemeinsame nosologische Grundlage bisher ungeklärter Ätiologie. Die granulomatöse RZA des ZNS wird daher eher als Standortvariante der RZ-Vaskulitiden denn als eigene Krankheitseinheit aufgefaßt. Nach neueren Befunden wird die Krankheit als Immunkomplex-Erkrankung aufgefaßt, obwohl auch eine virale Genese diskutiert wird.

     

Glial cell transplanatation and remyelination of the central nervous system

Glial cell transplantation has proved to be a powerful tool in the study of glial cell biology. The extent of myelination achieved by transplanting myelin-producing cells into the CNS of myelin mutants, or into focal demyelinating lesions has raised hope that such a strategy may have therapeutic applications. Oligodendrocytes or Schwann cells could be used for repair. It is likely that the immature stages of the oligodendrocyte lineage have the best phenotypic characteristics for remyelination when transplanted, either as primary cells or as immortalized cells or cell lines. Prior culturing and growth factor treatment provides opportunities to expand cell populations before transplantation as dissociated cell preparations. Cell lines are attractive candidates for transplantation, but the risk of transformation must be monitored. The application of this technique to human myelin disorders may requier proof that migration, division and stable remyelination of axons by the tranplanted cells can occur in the presence of gliosis and inflammation.     

Cyclosporine A-associated fatal central nervous system angiopathy in a bone marrow transplant recipient: an autopsy case

We report here the case of a 32-year-old woman who suffered from a unique angiopathy in the central nervous system (CNS). She died of multiple infarcts in the brain stem and cerebellum during treatment with cyclosporine A after bone marrow transplantation for refractory anemia with excess of blasts. The autopsy findings showed segmental narrowing of the basilar artery, in which circumferential dissection of the internal elastic lamina had occurred. The distal portion of the basilar artery was obstructed by upward dislocation of the dissected intima. Similar angiopathy was also observed at multiple sites along the basilar artery branches. These findings suggest endothelial damage, including vasoconstriction and dissection of the CNS arteries. Received: 22 March 1999 / Revised, accepted: 19 August 1999     

Microglial involvement in experimental autoimmune inflammation of the central and peripheral nervous system

Microglial cells form a network of potential antigen presenting cells throughout the nervous system. Much progress has recently been made towards a better understanding of their immunological properties. This study examines their activation in 2 models of T cell-mediated autoimmune inflammation of the nervous system, experimental autoimmune encephalomyelitis (EAE) and its peripheral counterpart, experimental autoimmune neuritis (EAN), induced by the transfer of antigen-specific T cell lines. In both models microglial activation occurs at early stages of the disease. Activated microglial cells show an increased expression of MHC class I and II antigens. In EAE ultrastructural analysis revealed that MHC antigen expression is pronounced on perivascular microglial cells, suggesting this cell population may be important for antigen presentation at a site close to the blood-brain barrier. In contrast to EAE, the microglial reaction in EAN occurs at sites remote from the inflammatory response in the peripheral nerve, not only in the spinal cord but also in the terminal projection fields of primary sensory neurons in the lower brainstem. This early microglial activation in EAN suggests that a rapid and remote signaling mechanism can operate following peripheral inflammation. Immuno-electron microscopy revealed that activated microglial cells are also involved in the synaptic deafferentation of spinal cord motoneurons during autoimmune reactions. The rapid involvement of microglial cells in experimental autoimmune inflammation of the nervous system further points to their role as the main intrinsic immuneffector cell population of the central nervous system.     

Endogenous adult neural stem cells: limits and potential to repair the injured central nervous system

Mitotic activity persists in various regions of the adult mammal CNS. While evidences of neurogenesis appeared, many studies focused on the features of the adult stem cells from germinative areas such as the subventricular zone of the lateral ventricles, the dentate gyrus of the hippocampus, the cortex, the fourth ventricle and the central canal of the spinal cord. In the present paper, we review the potentialities of the adult germinative areas in terms of proliferation, migration and differentiation in non pathological situation and in response to different type of CNS injury. Adult endogenous stem cells are activated in response to various injuries but their capacities to migrate and to undergo either neurogenesis or gliogenesis differ according to the lesion-type and the germinative zone from which they arise. Different works demonstrated that epigenic factors such as growth factors can enhance the repair potential of the adult stem cells. Reactivation and mobilization of endogenous stem cells as well as demonstration of their long-term survival and functionality appear to be interesting strategies to investigate in order to promote endogenous repair of the adult CNS.     

Expression of glial cell line-derived neurotrophic factor mRNA in the human newborn and adult hippocampal formation

Glial cell line-derived neurotrophic factor (GDNF) mRNA-containing neurons were found in normal neonate and adult human hippocampus with a localization pattern consistently similar among different ages. They were numerous in proximal CA1 to CA3 pyramidal layer, granular layer and hilus, and sparse in oriens and molecular layers. The present data provide a map of GDNF-producing neurons in the human archicortex and suggest a role for GDNF in neuronal function throughout life.     

Clinical safety and primary efficacy of bone marrow mesenchymal cell transplantation in subacute spinal cord injured patients

Background

In recent years, some studies were conducted to evaluate the effects of stem cells from different sources on patients with spinal cord injury (SCI). This study was carried out to evaluate the feasibility and therapeutic potential of autologous bone marrow cell (BMC) transplantation in 11 complete spinal cord injured patients at thoracic level.

Methods and materials

This nonrandomized clinical trial compared the results of autologous BMC transplantation into cerebrospinal fluid (CSF) via lumbar puncture (LP) in 11 patients having complete SCI, with 20 patients as control group who received conventional treatment without BMC transplantation. The patients underwent preoperative and follow-up neurological assessments using the American Spinal Injury Association (ASIA) impairment scale. Then, the participants were followed for 12–33 months.

Results

Eleven patients with the mean age of 33.2 ± 8.9 years and 20 patients with the mean age of 33.5 ± 7.2 years were enrolled in the study and in the control group, respectively. None of the patients in the study and control group experienced any adverse reaction and complications, neither after routine treatment nor after cell transplantation. Five patients out of 11 (45.5%) in the study group and three patients in the control group (15%) showed marked recovery, but the result was statistically borderline (P = 0.095).

Conclusion

We conclude that transplantation of autologous BMC via LP is a feasible and safe technique, but at the moment, no clear answer can be given regarding the clinical potential, despite a potential tendency to treat SCI patients, observed through statistics.     

Primary Ki-1 lymphoma in the central nervous system

Large cell anaplastic malignant lymphoma with Ki-1 (CD30) antigen is a new entity among human non-Hodgkin's malignant lymphomas according Updated Kiel Classification and is also a very rare subtype in primary central nervous system (CNS) malignant lymphomas. The precise clinical characteristics and the significance of Ki-1 antigen have yet to be clarified. The authors herein report a case of Ki-1 positive primary T-cell CNS malignant lymphoma. A 49-year-old man presented with multiple mass lesions in the brain on MRI. Immunohistochemical investigations of biopsy specimens from the superior medullary velum revealed a large cell anaplastic T-cell lymphoma positive for Ki-1 antigen. After administering extensive chemo-radiotherapy, the patient has survived for more than 42 months after the onset of symptoms.     

A pericapillary cell in the central nervous system of the human embryo and adult

Summary A cell is described, which appears to be in close attachment to the capillaries of the human central nervous system; and which is seen in the brain as early as the seventh week of embryonic life.

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Zusammenfassung Eine Zellart wird beschrieben, welche in engem Kontakt mit den Capillaren des menschlichen Zentralnervensystems steht und im Gehirn schon in der siebenten Embryonalwoche nachweisbar ist.

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With 5 Figures in the Text     

Giant cell angiitis of the central nervous system with atypical presentation

Giant cell angiitis of the CNS is an uncommon form of vasculitis. Neurological manifestations, both of the peripheral and CNS, are common. The most frequent manifestations are visual loss and stroke. Hemorrhagic onset is uncommon. Most cases have a fatal outcome and a tissue diagnosis is rarely established in life. We describe an unusual case of giant cell angiitis beginning as a hemorrhagic tumoral‐like lesion. The results of the histological and ultrastructural analysis have also been reported. Our case illustrates that giant cell angiitis should be considered as a cause of intracerebral hemorrhage, particularly when associated with a relapsing and remitting disease of the CNS.     

Model of potassium dynamics in the central nervous system

A one-dimensional numerical model of potassium dynamics in the central nervous system is developed. The model incorporates the following physiological processes in computing spatial and temporal changes in extracellular K+ concentration, [K+]o: 1) the release of K+ from K+ sources into extracellular space, 2) diffusion of K+ through extracellular space, 3) active uptake of K+ into cells and blood vessels, 4) passive uptake of K+ into a cellular distribution space, and 5) the transfer of K+ by K+ spatial buffer current flow in glial cells. The following tissue parameters can be specified along the single spatial dimension of the model: 1) the volume fraction and tortuosity of extracellular and glial cell spaces, 2) the volume fraction of the cellular distribution space, 3) rate constants of active uptake and passive uptake processes, and 4) glial cell membrane conductance. The model computes variations in [K+]o and current flow through glial cells for three tissue geometries: 1) planar geometry (the retina and the surface of the brain), 2) cylindrical geometry (tissue surrounding a blood vessel), and 3) spherical geometry (tissue surrounding a point source of K+). For simple sources of K+, the performance of the model matches that predicted from analytical equations. Simulations of previous ion dynamics experiments indicate that the model can accurately predict ion diffusion and K+ current flow in the brain. Simulations of electroretinogram generation and K+ siphoning onto blood vessels suggest that unanticipated K+ dynamics mechanisms may be operating in the central nervous system.     

The role of hypoxia in stem cell regulation of the central nervous system: From embryonic development to adult proliferation

Hypoxia is involved in the regulation of various cell functions in the body, including the regulation of stem cells. The hypoxic microenvironment is indispensable from embryonic development to the regeneration and repair of adult cells. In addition to embryonic stem cells, which need to maintain their self-renewal properties and pluripotency in a hypoxic environment, adult stem cells, including neural stem cells (NSCs), also exist in a hypoxic microenvironment. The subventricular zone (SVZ) and hippocampal dentate gyrus (DG) are the main sites of adult neurogenesis in the brain. Hypoxia can promote the proliferation, migration, and maturation of NSCs in these regions. Also, because most neurons in the brain are non-regenerative, stem cell transplantation is considered as a promising strategy for treating central nervous system (CNS) diseases. Hypoxic treatment also increases the effectiveness of stem cell therapy. In this review, we firstly describe the role of hypoxia in different stem cells, such as embryonic stem cells, NSCs, and induced pluripotent stem cells, and discuss the role of hypoxia-treated stem cells in CNS diseases treatment. Furthermore, we highlight the role and mechanisms of hypoxia in regulating adult neurogenesis in the SVZ and DG and adult proliferation of other cells in the CNS.     

Stroke affects intestinal immune cell trafficking to the central nervous system

Stroke is an acute neurological disease with a strong inflammatory component that can be regulated by the intestinal microbiota and intestinal immune cells. Although stroke has been shown to alter immune cell populations in the gut, the dynamics of cell trafficking have not been elucidated. To study the trafficking of gut-derived immune cells after stroke, we used mice expressing the photoconvertible protein Kikume Green-Red, which turns form green to red when exposed to violet light. Mice underwent laparotomy and the small intestine was exposed to violet laser light. Immune cells were isolated from the small intestine immediately after photoconversion and 2 days later. Percentage of immune cells (CD45⁺KikR⁺) that expressed the red variant of the protein (KikR) was higher immediately after photoconversion than 2 days later, indicating cell egress from the small intestine. To investigate whether intestinal immune cells traffic to the periphery and/or the central nervous system (CNS) after stroke, we analyzed KikR⁺ immune cells (2 days after photoconversion) in peripheral lymphoid organs, meninges and brain, 3 and 14 days after transient occlusion of the middle cerebral artery (tMCAo) or sham-surgery. Although migration was observed in naïve and sham animals, stroke induced a higher mobilization of gut KikR⁺ immune cells, especially at 3 days after stroke, to all the organs analyzed. Notably, we detected a significant migration of CD45^hi immune cells from the gut to the brain and meninges at 3 days after stroke. Comparison of cell trafficking between organs revealed a significant preference of intestinal CD11c⁺ cells to migrate from the small intestine to brain and meninges after stroke. We conclude that stroke increases immune cell trafficking from the small intestine to peripheral lymphoid organs and the CNS where they might contribute to post-stroke inflammation.     

The origin of remyelinating cells in the adult central nervous system: the role of the mature oligodendrocyte

The sequence of events by which new oligodendrocytes are generated in the adult mammalian central nervous system has not been clearly defined. Here we review old evidence that remyelinating cells can arise from the division of mature oligodendrocytes. In addition, we report the results of a tissue culture study comparing oligodendrocytes and immature progenitors with regard to their capacity for proliferation, for the generation of new oligodendrocytes and for myelination. Monoclonal antibodies 04 and 01 were used to distinguish oligodendrocytes (04+01+) from progenitors (04+01-). Dissociated cell suspensions from adult rat spinal cord were separated by flow cytometry into 01+ and 01- cell fractions, at greater than 93% purity. The 01+ fraction contained approximately 0.7% 04+01- cells while the 01- fraction contained approximately 4.4% 04+01- cells. Cells from these fractions were plated onto cultures of purified dissociated dorsal root ganglion neurons. The cultures that received 01+ cells developed numerous expanding colonies of cells expressing both 01 and 04, or 04 only, by 8 days and were essentially covered by oligodendrocytes by 16 days. In marked contrast, oligodendrocyte colonies were rare in cultures receiving 01- cells. By 24 days, myelination was extensive in cultures receiving 01+ cells; in contrast, only a few myelin segments were observed in cultures receiving the 01- fraction. Thus, oligodendrocytes (01+ cells) appear more capable than progenitors (04+01-) of generating new myelinating oligodendrocytes in this culture system.     

A reevaluation of the primary diagnosis of hemangiopericytoma and the clinical importance of differential diagnosis from solitary fibrous tumor of the central nervous system

Objectives

Hemangiopericytomas (HPCs) are rare neoplasms with relatively high rates of recurrence and extracranial metastasis. Though the differential diagnoses from angiomatous meningiomas and from solitary fibrous tumors (SFTs) are both important, the latter diagnosis is somewhat more important in light of the benign prognosis of SFTs and the difficulties in distinguishing SFTs from HPCs. Newly developed immunohistochemical methods reveal differences in the specific immunohistochemical features of HPCs and SFTs. To elucidate whether SFTs have been misdiagnosed as HPCs in the past, our group used recent immunohistochemical methods to re-evaluate tissues that had been originally diagnosed as HPCs. We also compared the clinical features of these cases.

Patients and methods

Thirteen sequential cases of HPC diagnosed in Kanazawa University Hospital and Kumamoto University Hospital between 1970 and 2006 were retrospectively analyzed by immunohistochemical staining for CD34, Bcl-2, epithelial membrane antigen (EMA), vimentin, and S100 protein, and by measurement of the MIB-1 labeling index (LI). The cases were then re-evaluated and newly diagnosed based on the results of the immunohistochemical stainings. The clinical course of each case was also evaluated.

Results

Four of the 13 cases were newly diagnosed as SFTs and eight were reconfirmed as HPCs, based on the immunohistochemical studies for CD34, Bcl-2, and reticulin staining. One case was newly diagnosed as meningioma on the basis of a strong EMA positivity. The MIB-1 LI was less than 1% in 12 of the cases. In two cases, one case of HPC and the other of meningioma, the MIB-1 LI was relatively high, 8% and 4% respectively. All eight of the HPCs recurred, and 5 of the HPC patients died of the disease. Only one case of the SFTs recurred.

Conclusion

Our study suggests that a relatively high percentage of the tumors diagnosed as HPCs in the past may have in fact been intracranial SFTs. Immunohistochemical examinations of CD34, Bcl-2, and reticulin stains are keys for the differential diagnosis. Given that SFTs have a considerably better prognosis than HPCs, it is important to carry out meticulous immunohistochemical examinations for the primary diagnosis.