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Temporal lobe epilepsy (TLE) is the most common form of drug-resistant epilepsy. The main pathological changes primarily involve hippocampal sclerosis (HS). Early resective surgery of the sclerotic hippocampus is typically associated with favorable clinical outcomes. However, not all patients are suitable candidates for resective surgery of mesial temporal lobe structures. Therefore, alternative treatment modalities should be considered. We present the case of a 50-year-old right-handed woman with left HS who underwent unilateral subiculum stimulation for drug-resistant epilepsy (DRE). Since the age of 10, the patient had been experiencing focal to bilateral tonic-clonic seizures (FBTCS). Despite multiple antiseizure medications, she experienced 12 to 17 FBTCS per month in the last two years. Due to concerns about potential memory decline and personal preferences, she refused resective surgery. As an alternative, the patient underwent left unilateral subiculum stimulation. The stimulation resulted in a nearly 67 % reduction in seizure frequency at the last follow-up (20 months after surgery). This case highlights that drug-resistant epilepsy may be effectively treated with subicular stimulation in patients with HS., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2024 The Authors. Published by Elsevier Inc.)

Background: Deep brain stimulation of the anterior nucleus of the thalamus (ANT DBS) is a neuromodulation therapy for patients with refractory focal seizures evolving into bilateral tonic-clonic seizures when pharmacotherapy as well other neuromodulation techniques including vagus nerve stimulation or responsive neurostimulation have failed., Objective: We performed a prospective single-center study investigating the clinical efficacy and exact ANT DBS lead location in patients with DRE., Methods: The primary outcome measure was the proportion of patients with more than 50 % reduction in diary-recorded seizures when compared to three preoperative months (baseline seizure frequency). The close postoperative follow-up was performed every 3 months. The seizure frequency, stimulation settings and adverse events were closely monitored during follow-up visits. We also analyzed the seizure outcome with location of ANT DBS active contacts., Results: Between May 2020 and October 2022, 10 adult patients with a mean age of 38.5 years (range, 30-48 years) underwent bilateral ANT DBS surgery (mean duration of DRE 28.6 years, range 16-41 years). The median seizure count in three months period preceding surgery (baseline seizure count) was 43.2 (range, 4-150). Nine patients achieved more than 50 % seizure reduction at the last follow-up (mean range 3-33 13.6 months, months). ANT DBS caused seizure reduction 3 months after procedure as well as at last follow-up by 60.4 % and 73.3 %, respectively. Due to relatively small number of studying individuals we cannot precisely locate the area within ANT associated with good clinical outcome. Patients with temporal lobe epilepsy had a remarkable reduction of seizure frequency. No patient suffered transient or permanent neurological deficits., Conclusions: Clinical efficacy of ANT DBS may support more widespread utilization of this neuromodulation technique especially for seizures originating from temporal lobes., Competing Interests: Conflict of interest No potential conflict of interest was reported by the authors of this article., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Intracranial collision tumours are rare pathologies in which two distinct neoplasms are found in the same location. We present an unusual case of an intracranial collision tumour composed of meningothelial meningioma (CNS WHO G1) and glioblastoma (IDH-wildtype, CNS WHO G4). This collision tumour was found in a 64-year-old man. This patient was hospitalized urgently due to left-sided hemiparesis. The computed tomography (CT) revealed large multilobar intracranial haemorrhage located in the right hemisphere. The history of hypertension and obesity pointed to the misdiagnosis of a typical haemorrhagic stroke. Despite extensive physiotherapy after initial improvement, the magnetic resonance imaging (MRI) showed signs of a marginal contrast enhancement with a suspicion of a brain tumour. Moreover, the meningioma in the same location was suspected. The neuropathological findings confirmed two neoplasms with fragments of the dura mater infiltrated by malignant glioma cells and small nests of meningothelial cells with psammoma bodies. The presented case is extremely rare showing that more malignant tumour may infiltrate a meningioma. Moreover, this case highlights the clinical observation that glioblastoma may mimic a haemorrhagic stroke. In such cases when pharmacological treatment is not effective, suspicions should be raised about a possible underlying brain tumour.

Introduction: The Working Group was established at the initiative of the General Board of the Polish Society of Epileptology (PSE) to develop an expert position on the treatment of convulsive status epilepticus (SE) in adults and children in Poland. Generalized convulsive SE is the most common form and also represents the greatest threat to life, highlighting the importance of the choice of appropriate therapeutic treatment., Aim of Guideline: We present the therapeutic options separately for treatment during the early preclinical (>5-30min), established (30-60min), and refractory (>60min) SE phases. This division is based on time and response to AEDs, and indicates a practical approach based on pathophysiological data., Results: Benzodiazepines (BZD) are the first-line drugs. In cases of ineffective first-line treatment and persistence of the seizure, the use of second-line treatment: phenytoin, valproic acid or phenobarbital is required. SE that persists after the administration of benzodiazepines and phenytoin or another second-line AED at appropriate doses is defined as refractory and drug resistant and requires treatment in the intensive care unit (ICU). EEG monitoring is essential during therapy at this stage. Anesthesia is typically continued for an initial period of 24h followed by a slow reversal and is re-established if seizures recur. Anesthesia is usually administered either to the level of the "burst suppression pattern" or to obtain the "EEG suppression" pattern., Conclusions: Experts agree that close and early cooperation with a neurologist and anesthetist aiming to reduce the risk of pharmacoresistant cases is an extremely important factor in the treatment of patients with SE. This report has educational, practical and organizational aspects, outlining a standard plan for SE management in Poland that will improve therapeutic efficacy., (Copyright © 2018 Polish Neurological Society. Published by Elsevier Sp. z o.o. All rights reserved.)

Background: Perfusion computed tomography (PCT) is part of acute stroke protocol in many hospitals; however, its clinical utility is still being disputed. Beyond its use in core and penumbra estimation, there is also a question about PCT role in stroke mimics diagnosis. Case series or small, retrospective studies showed equivocal results. This is the first published prospective, comparative study on PCT in differentiating stroke and seizure in acute setting., Methods: Patients with acute focal neurologic deficits and without acute ischemic lesions on routine CT underwent PCT and electroencephalography (EEG) within 12 hours after symptom onset. Perfusion parameters were set up as asymmetry indices for corresponding regions of brain hemispheres. EEG findings were assigned to 1 of 5 classes. Neurologic examination was performed using the National Institutes of Health Stroke Scale (NIHSS). Follow-up noncontrast computed tomography was performed on the third day after symptom onset. If no CT changes appeared, magnetic resonance diffusion-weighted imaging was conducted., Results: Final diagnosis was hemispheric ischemic stroke in 17 patients and focal neurologic deficits in the course of seizures (post- and intraictally) in 12 patients. Those groups were significantly different only in one single PCT parameter-time to peak (TTP)-in the lateral part of the middle cerebral artery territory. Analyzed groups were not significantly different in the NIHSS scores and the EEG evaluation., Conclusions: TTP may stay relatively when seizure is a cause of focal neurologic deficits, but not stroke. Further, large, prospective studies are necessary to verify the results., (Copyright © 2017 National Stroke Association. Published by Elsevier Inc. All rights reserved.)

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder that involves the upper and lower motor neurons and leads to the patient's death within 5 years after diagnosis. Approximately 2 per 100,000 people worldwide are affected every year. The only FDA-approved drug available for medical treatment is riluzole. It slows the disease progression and improves limb function and muscle strength for 3-4 months. Thus, looking for new therapeutic agents is a pressing challenge. Valproic acid (VPA) is a short-chain fatty acid, widely used for the treatment of seizures and bipolar mood disorder. The beneficial effect of VPA has been documented in different neurodegenerative experimental models, including amyotrophic lateral sclerosis (ALS). The real mechanisms underlying numerous beneficial effects of VPA are complex, but recently it has been postulated that the neuroprotective properties might be related to direct inhibition of histone deacetylase (HDAC). The aim of this ultrastructural study was to evaluate the beneficial effect of VPA on the spinal cord motor neurons (MNs) in a glutamate (GLU)-induced excitotoxic ALS model in vitro. It had been previously documented that chronic GLU excitotoxicity resulted in various MN injuries, including necrotic, apoptotic and autophagic modes of cell death. The present results demonstrated the neuroprotective properties of VPA associated with inhibition of apoptotic and autophagic changes of spinal MNs in a model of neurodegeneration in vitro.

Pleomorphic xanthoastrocytoma (PXA) is a rare, low-grade astrocytic tumour corresponding to WHO grade II that is usually diagnosed in adolescents and young adults with epileptic seizures. Pleomorphic xanthoastrocytoma typically appears as a superficial, often cystic mass lesion predominantly affecting the temporal lobe. Cases with typical pathology and total tumour excision have a favourable prognosis. Occasionally, the tumour reveals anaplastic features and behaves more aggressively due to local recurrences or subarachnoid spread. The treatment of PXA includes gross total resection followed by neuroradiological monitoring. The association between vascular malformations and cerebral gliomas is rarely encountered, especially if both such lesions occur as separate parts of the same tumour. The vascular pathology of such changes most often refers to arteriovenous malformation (AVM), less frequently - cavernous angioma. The coexistence of PXA and AVM is extremely rare, especially when dealing with two distinct patterns found within the same tumour mass. We present a 36-year-old woman with tumour of parasagittal localization in the right occipital lobe that was composed of two different and clearly demarcated components: PXA and vascular lesion of AVM morphology. The pathogenesis of such coexistence remains still unclear.

Unlabelled: The nervous system tumors pose a current challenge to modern medicine. Diagnosis, established at an early stage of tumor development, increases the chance of the use of radical therapeutic methods, which is associated with better prognosis. The preferred method of treatment of brain tumors is the surgical treatment. Success of this therapy depends on the possibility of the radical removal of neoplastic tissue. The aim of the study was to evaluate the type and duration of clinical symptoms, which were the cause for hospitalization, prehospital diagnostics and possibilities of the use the methods of treatment giving the chance for cure at the time of diagnosis of the neoplastic process within central nervous system., Material and Methods: A retrospective analysis of medical records of 56 patients, hospitalized in 2009-2010 at the Department of Neurology and Epileptology, The Medical Centre of Postgraduate Education in Warsaw. The basis for the diagnosis were the results of two-phase neuroimaging studies. The whole results were analyzed statistically to looking for a correlation between the duration of symptoms prior to hospitalization, their nature and the proposed treatment., Results: Draws attention to the young age of analyzed patients (mean age 67 years). The most common symptoms were disturbances of consciousness or behavioral changes (37% patients), limb weakness and sensory disturbances (37%) and speech disorders (30%). Other, commonly reported nonspecific symptoms were: somnolence, deterioration of everyday functioning, fatigue and malaise. In the group of the 56 patients with confirmed tumor, 14 (25%) were urgently admitted to our Department, 13 (23%) arrived first to the general practitioner practice. Unfortunately, 29 (52%) out of 56 patients did not arrived to the outpatient physician, despite the first discomfort feelings. They got at a later time directly to the hospital emergency room. In most cases the proposed treatment was neurosurgical operation (n = 19, 35%), whereas radiotherapy was suggested to 4 patients (8%), and palliative treatment in the form of radiation therapy to the whole area of the brain (n = 11, 20%) and of the spine (n = 1) to 12 people. We did not find a statistically significant correlation in our study., Conclusions: Nonspecific symptoms that may be the only manifestation of proliferative disease within the central nervous system, should attract particular oncology attention, otherwise the diagnosis may be delayed. Advancement of the disease at the moment of establishment of the diagnosis does not allow for the use of causal treatment.

Erythropoietin (EPO) is a chemokine hormone that is widely distributed throughout the body including nervous system. For last years its role as cytokine involved in many physiological processes out of the bone marrow has been suggested. Moreover, it plays a very important role in CNS as potential neuroprotective agent. There is much evidence that EPO protects neuronal cells in vitro and in vivo models of brain injury, independently of its erythropoietic action. The aim of this study was to determine the potential neuroprotective effects of erythropoietin on the glutamate-mediated injury of motor neurons (MNs) in vitro. The study was performed on organotypic cultures of the rat lumbar spinal cord subjected to glutamate uptake blocker, DL-threo-beta-hydroxyaspartate (THA) and pretreated with EPO. Ultrastructural study evidenced that the spinal cord cultures pretreated with EPO exhibited less severe neuronal injury. The cultures exposed to EPO + THA showed inhibition of early MNs degeneration, including various mode of degenerative changes caused by THA, whereas in the later period the typical postsynaptic necrotic changes of neuronal cells occurred. However, the ultrastructural characteristics of apoptotic MNs changes were not observed during the whole period of observation. The results of this study indicate that, in the model of chronic glutamate excitotoxicity, EPO exhibits the neuroprotective ability mainly through prevention of apoptotic neuronal changes.

Cytidine-5-diphosphocholine (CDP-choline, citicoline) is an endogenous nucleoside involved in generation of phospholipids, membrane formation and its repair. It demonstrates beneficial effects in certain central nervous system injury models, including cerebral ischaemia, neurodegenerative disorders and spinal cord injury. Defective neuronal and/or glial glutamate transport is claimed to contribute to progressive loss of motor neurons (MNs) in amyotrophic lateral sclerosis (ALS). Our previous ultrastructural studies, performed on an organotypic tissue culture model of chronic glutamate excitotoxicity, documented a subset of various modes of MN death including necrotic, apoptotic and autophagocytic cell injury. The aim of this ultrastructural study was to determine the potential neuroprotective effect of CDP-choline on neuronal changes in a glutamate excitotoxic ALS model in vitro. Organotypic cultures of the rat lumbar spinal cord subjected to 100 microM DL-threo-beta-hydroxyaspartate (THA) were pretreated with 100 microM of CDP-choline. The exposure of spinal cord cultures to CDP-choline and THA distinctly reduced the development of typical apoptotic changes, whereas both necrotic and autophagocytic THA-induced MN injury occurred. These results indicate that CDP-choline treatment might exert a neuroprotective effect against neuronal apoptotic changes in a model of chronic excitotoxicity in vitro.

The aim of the study was to evaluate prevalence of cervical spine inflammatory changes, especially atlantoaxial pathology, and their possible relation to subjective and objective neurological symptoms in rheumatoid arthritis patients. 100 patients (88 female and 12 male) aged 23 to 85 (61.4 +/- 12.9), with the mean disease duration of 12.5 +/- 9.5 years were included in the study. According to radiological examination (lateral and antero-posterior X-ray of the cervical spine) supplemented by MR of the cervical spine or CT of the atlanto-axial joint in suspected cases, 26% of patients had only inflammation, next 15% of patients presented with instability of the atlanto-axial joint and 9% developed basilar invagination of the dens of axis. 18% of patients presented subaxial cervical instability. Neurological examitation was performed by independent neurologist in 99 patients, only 14 presented abnormalities suggesting cervical myelopathy. Two of them showed no patology of the cervical spine. Remaining patients presented: C1/C2 inflammation in 4 cases, anterior atlanto-axial subluxation (AAS) in two cases, basilar invagination in 4 cases and instability with medullary compression on lower cervical levels only--in two cases. There were 4 cases of coexisting C1/C2 changes with medullary compression due to discopathy and (in 3 of them) instability on lower cervical levels. In 6 cases surgical stabilisation was proposed (5 patients with basilar invagination and 1 patient with AAS and myelopathy). There was statistically significant correlation between symptoms (like: paraesthesiae, intermittent problems with hearing and seeing), neurological examination and degree of radiological damage of atlanto-axial joint. The authors concluded that careful medical history and neurological examination can be useful in making decision of further radiological diagnostic procedures of the cervical spine in rheumatoid arthritis.

Purpose: Lamotrigine (LTG) is a novel anticonvulsant drug that exerts an antiepileptic effect by decreasing glutamate release through inhibition of voltage-sensitive sodium channels. LTG has no effect on serum levels of most female reproductive hormones, but its effect on male reproductive hormones still remains unclear. Improvement in sexual function after LTG treatment has been reported, and could have been caused by reduction of seizures, inhibition of focal discharges, or an unknown effect of LTG on reproductive hormones and protein levels., Cases: Two male patients exhibited acute hypersexuality while taking lamotrigine as add-on therapy: one patient on carbamazepine and one on oxcarbazepine. Neither prior history of psychiatric illness nor brain damage predisposed them to such a response to treatment, and in both patients, the hypersexuality was not a part of hypomania or a more diffuse psychiatric disturbance. In the first case, sexual hyperactivity resolved after discontinuation of LTG therapy without any concomitant treatment. In the second case, a reduction in the dose of LTG decreased the intensity of the hypersexuality and contributed to the patient's increased satisfaction with his sex life., Conclusions: Lamotrigine may cause drug-related hypersexuality by an unclear underlying mechanism.

Purpose: Symptoms of depression are present in 40 to 60 percent of patients with epilepsy. Prior research indicated significant correlation between the incidence and frequency of focal seizures and clinical depression, especially in patients with temporal lobe epilepsy. Anticonvulsive drugs and psychosocial factors contribute to the occurrence of depression as well. The aim of the study was to determine the major depression risk factors in patients with epilepsy., Methods: The research was conducted on 203 patients with epilepsy (117 females and 86 males), aged 18 to 50 years, with total time of illness ranging from 60 to 580 months. All subjects underwent the same research protocol, which was applied interictally. Interictal depression was diagnosed according to ICD-10 diagnostic criteria for affective and delusional disorders. The diagnosis was supported by Beck Depression Inventory (BDI), Hamilton Depression Rating Scale (HAM-D) and Montgomery-Asberg Depression Rating Scale (MADRS). Statistical analysis included chi2 test, Fisher's exact test and stepwise logical regression model analysis., Results: In our study 100 patients with epilepsy out of 203 suffered from concurrent depression (49.2%); 76 of them had severe depression (37.4%) and 24 patients had mild depression (11.8%). Complex partial seizures and absence of secondary generalized tonic-clonic seizures were found to be the risk factors for depression. Treatment with clonazepam, frequent hospitalizations (drug-resistancy) and lack of occupational activity were revealed to be additional significant contributing factors., Conclusions: Depression in patients with epilepsy is a serious medical and social problem since it afflicts almost one half of all patients treated in epilepsy referral centers. It seems to be correlated with certain types of epileptic seizures, with high frequency of seizures, sub-optimal pharmacologic treatment and lack of occupational and social activity.

Chronic excitotoxicity mediated through defective glial and/or neuronal glutamate transport may contribute to several neurodegenerative diseases including amyotrophic lateral sclerosis (ALS). This study was performed to determine the ultrastructural characteristics of astroglial changes concomitant with motor neuron (MN) degeneration in a model of slow excitotoxicity in vitro. The study was performed on organotypic cultures of rat lumbar spinal cord subjected to the glutamate uptake blockers threohydroxyaspartate (THA) and L-trans-pyrrolidine-2,4-dicarboxylate (PDC). The chronic inhibition of glutamate transport by THA and PDC resulted in slow degeneration of the rat's MNs accompanied by distinct glial changes predominantly involving protoplasmic astrocytes. The presence of irregular vacuoles and vesicles in the astroglial cells was frequently observed. Occasionally the astrocytes exhibited proliferation and accumulation of abnormal profiles of smooth endoplasmic reticulum. In 3 weeks there were no signs of increased production of glial filaments in the protoplasmic astrocytes. The results evidenced the coexistence of neuronal degeneration and astroglial abnormalities in an ALS model in vitro and suggested an active role of astrocytes contributing to the induction and propagation of MN degeneration.

Both the neurotoxic and neuroprotective effects of zinc have been well established, but the exact mechanism of its dual abilities still remains unclear. It has been shown that zinc deficiency leads to progressive neuronal injury. Therefore a safe zinc concentration levels seem to be necessary in neuronal protection from different noxious factors. This study was undertaken to determine the effect of zinc chelating agent--TPEN on neuronal morphological changes in organotypic hippocampal culture and its effect on post-anoxic changes in this model. The study evidenced that exposition to 15 microM of TPEN induced various stages of apoptotic changes in hippocampal pyramidal neurons and enhanced the anoxia-induced neuronal apoptosis in this model. These results confirmed the hypothesis that manipulations of intracellular pool of zinc by zinc-chelating agents may be a cause of both induction and prevention of apoptotic cell death in various pathological conditions.

There is increasing evidence that so-called "autophagic cell death" participates in cell degeneration in certain pathological conditions. Autophagy might be involved in some neurodegenerative processes, including lateral amyotrophic sclerosis (SLA). The exact mechanism leading to progressive motor neuron (MN) loss remains unclear, but glutamate-mediated mechanism is thought to be responsible. Previous ultrastructural studies by the authors performed on a model of SLA in vitro, based on chronic glutamate excitotoxicity, revealed a subset of morphological features characteristic to different modes of neuronal death, including autophagic degeneration. The contribution of this pathway of MNs death is evaluated in organotypic cultures of rat lumbar spinal cord chronically exposed to specific glutamate uptake blockers: DL-threo-beta-hydroxyaspartate (THA) and L-transpyrrolidine-2,4-dicarboxylate (PDC). The study documents the various steps of authophagy in slowly evolving process of MN neurodegeneration. The cells undergoing autophagy usually exhibited sequestration of some parts of cytoplasm with normal and/or degenerated organelles, whereas other parts of cytoplasm as well as neuronal nucleus remained unchanged. The advanced autophagic changes were often associated with other modes of MN death, especially with apoptosis. Numerous MNs revealed apoptotic nuclear features with typical peripheral margination of nuclear chromatin, accompanied by severe autophagic or autophagic-necrotic degeneration of the cytoplasm. These results support the opinion of unclear distinction between different modes of cell death and indicate the involvement of autophagey in MNs neurodegeneration in vitro.

The defective glial and/or neuronal glutamate transport may, in chronic neurotoxicity, contribute to several neurodegenerative diseases including amyotrophic lateral sclerosis (ALS)--a progressive neurodegenerative disorder of lower and upper motor neurons (MNs). To determine the detailed ultrastructural characteristics of excitotoxic motor neurons neurodegeneration we used a model of slow excitotoxicity in vitro based on selective inhibition of glutamate uptake. The study was performed on organotypic cultures of the rat lumbar spinal cord subjected to various concentrations of glutamate uptake blockers: threohydroxyaspartate (THA) and L-trans-pyrrolidine-2, 4-dicarboxylate (PDC). The chronic inhibition of glutamate transport resulted in a dose-dependent slow neurodegeneration of spinal MNs consisting of necrotic, apoptotic and autophagic mode of cell death. There were some MNs that shared certain characteristics of a different type of cell injury. The results showed that a different mode of cell death in excitotoxic MNs degeneration may coexist resulting in apoptosis-necrosis and apoptosis-autophagocytosis continuum.

There has been growing evidence that different modes of cell death exist, among them the apoptosis is thought to be an important mechanism of nerve cell loss implicated in various pathological states. A number of proteins mediated with apoptotic process have been identified, including p53, BAX, BCL-2 and BCL-X. We examined the expression of proteins related to programmed cell death in hippocampal neurons in vitro, exposed to pure anoxia or pretreated with apoptosis modulating agents: zinc and zinc chelator - TPEN. The results evidenced the noticeable differences in the expression of pro- and anti-apoptotic proteins in particular experiments. In the cultures exposed to pure anoxia, a significant increase of p53 and BAX immunoreactivity, associated with the decreased level of BCL-2 and BCL-X immunopositive cells was observed, related to the activation of apoptotic process. Hippocampal cultures pretreated with ZnCl2 before anoxia showed decreased immunoreactivity for p53 and BAX, connected with BCL-2 overexpression, whereas the cultures exposed to zinc chelating agent - TPEN or TPEN connected with anoxia showed significant increase of immunorectivity for p53 and BAX. This strong immunoreactivity of proapototic proteins (p53 and BAX) in hippocampal cultures exposed to anoxia or/and TPEN correlated with previous ultrastructural evidences of anoxia- and TPEN-induced apoptosis, while the overexpression of anti-apoptotic protein (BCL-2 and BCL-X) in zinc-pretreated cultures evidenced the protective ability of this metal against apoptosis in model of anoxia in vitro.

Prevalence of depression among the people with epilepsy is between 40 and 75%, which is higher than in population and among the patients with other chronic illness. Higher percentage of suicides and hospitalizations due to affective disorders make the diagnosis and evaluation of risk factors very important for further treatment. The following study has been performed on the group of one hundred patients with epilepsy lasting more than 5 years, aged 16-55, who were hospitalized or consulted in 2001 year. Depression was diagnosed on the basis of ICD-10 diagnostic scheme using Beck, Hamilton and Montgomery-Asberg Depression Scales. Patients were divided into three groups (with depression, dysthymia and controls). For statistical analysis chi2 (Fisher exact test) and Mann-Whitney test were used. Comparing to controls, the complex partial seizures or simple partial and complex ones were seen more often in patients with depression (p < 0.003) and in patients with dysthymia comparing to controls ones (p < 0.001). All types of epileptic seizures analyzed during one month revealed statistically significant differences between the groups (Mann-Whitney test: controls vs dysthymic ones p < 0.02; controls vs depression ones p < 0.03). Simple partial seizures and (or) complex partial ones and high percentage of complex ones were found to be statistically significant risk factors for depression and dysthymia.

Malignant peripheral nerve sheath tumours (MPNSTs) are rare soft tissue neoplasms arising from elements of the nerve sheath that often occur in the context of neurofibromatosis (NF) type 1. Their poor prognosis results from high local recurrence rate and distant dissemination. Nevertheless, the brain metastases are exceptional. We are presenting an unusual case of intrathoracic MPNST in a 33-year-old man with a five-year clinical course characterised by multiple times local recurrences of primary tumour and multiple remote metastases into the brain structures, thyroid and suprarenal gland. Moreover, the cerebellar metastasis regrew in spite of its total excision. Histologically, brain metastatic tumours were composed of spindle cells closely arranged in interlacing and woven fascicles. This highly cellular nerve tissue exhibited an advanced nuclear hyperchromasia and a high mitotic activity. The tumour exhibited rich delicate reticulin network. The schwannian nature of brain metastases has been confirmed by immunohistochemical findings showing S-100 protein and GFAP expression and ultrastructural evidences of the pericellular basal lamina.

An exceptional case of a recurrent intracranial ependymoma of myxopapillary type arising from the lateral ventricle is reported in a 37-year-old man. This distinctive morphological variant of ependymoma is virtually restricted to the region of cauda equina and filum terminale or occasionally to pre- or post-sacral soft tissue. The intracranial cases of myxopapillary ependymoma are extremely rare and are generally associated with the primary ependymal tumour at the typical lumbosacral site. This case of intraventricular myxopapillary ependymoma did not demonstrate any MRI evidence of a primary spinal cord tumour. Moreover, the initial diagnosis of this histologically benign tumour was followed by two tumour recurrences during the three-year follow-up period. To our knowledge, this is the third documented case of a primary intraventricular myxopapillary ependymoma and the first one of intracranial localisation associated with local recurrences.

Pleomorphic xanthoastrocytoma (PXA) is a rare variant of a superficial cerebral astrocytoma characterised by distinct clinical and histological features. Its derivation from subpial astrocytes has been proposed, although the capacity of neoplastic cells for expression of different immunohistochemical markers is still under debate. These immunohistochemical studies were performed on eight cases of PXA in order to evaluate the expression and co-expression of glial and macrophage/histiocytic markers in various tumour cell populations. The expression of antigens was examined with the use of single- and double-immunolabelling methods for GFAP, vimentin, LCA, CD68, HLA-class II and MAC 387. All the cases of PXA showed variable immunoreactivity to GFAP, both in spindle-shaped and pleomorphic lipidised tumour cells. A subset of neoplastic cells was stained strongly with HLA-class II monoclonal antibody and with antibody to CD68. The reactivity to LCA and MAC 387 was absent in neoplastic cells, while it was easily evidenced in the non-neoplastic infiltrative component. The immunohistochemical double staining demonstrated the co-expression of GFAP and HLA-class II or CD68 antigens in the cytoplasm of individual neoplastic cells, including large pleomorphic, lipid-laden ones. It seems that tumour cells in PXAs derived from subpial astrocytes reveal monocyte/macrophage immunophenotype and demonstrate the capability of functional behaviour as mesenchymal cells with phagocytic activities. The variability in expression of antigens related to glial and monocytic/macrophage differentiation stressed the immunophenotypic heterogeneity of tumour cells in PXAs.

Zinc is one of the trace elements playing an important role in many fundamental biological processes. However, it is also one of the possible etiological agents involved in nerve cell damage in certain human neurodegenerative disorders. The precise mechanism of neuroprotective ability of Zn against neurotoxicity evidenced in various pathological conditions remains unclear, especially concerning the intrinsic potential toxicity of this metal. This ultrastructural study was undertaken to determine the effect of zinc on the evolution of anoxia-induced neuronal injury in the organotypic cultures of rat hippocampus. The in vitro model of oxygen deprivation was produced by maintaining the cultures in a pure nitrogen atmosphere in flask adapted for permanent gas flow for 20 min. The selected cultures were pretreated with micromolar concentration of ZnCl2 (25-500 microM) at 30 min prior anoxia. The ultrastructural findings documented that Zn exhibited dose-dependent ability to reduce anoxia-induced neuronal changes in hippocampal neurons in vitro. Zn at a concentration of 100 microM was able to significantly protect the hippocampal formation against the development of late apoptotic changes, whereas the early necrotic anoxia-induced neuronal injury was not so efficiently reduced.

Five cases of anaplastic oligodendrogliomas containing numerous GFAP-positive cells have been analysed by electron microscopy to establish the fine structural characteristics of neoplastic cells. Ultrastructurally, all tumours have revealed monotonous appearance typical of oligodendrogliomas, however some structural variability, particularly with reference to astrocytic differentiation, has been observed. The majority of neoplastic cells have shown the fine structural features of oligodendrocytes, accompanied by various numbers of intermediate cytoplasmic filaments. These filaments have been usually distributed in the perinuclear, less often in the peripheral, parts of the cytoplasm. The cells exhibiting features common to both oligodendroglial and astroglial cells might be regarded as an intermediate morphological form between these two cell types. True neoplastic astrocytes could be encountered only sporadically. The present electron microscopic studysupports the opinion that GFAP-positive oligodendroglial tumours contain heterogeneous neoplastic cell populations with the transitional cell types between oligodendroglial and astroglial lineage.

Increasing evidence suggests that two distinct modes of cell death, known as apoptosis and necrosis, are involved in many different pathological states. The morphological pattern of postanoxic changes has been widely studied in various experimental models, however the exact mechanism of neuronal cell death induced by ischaemic/anoxic insult is still not fully understood. The aim of this study was to determine the detailed ultrastructural criteria of postanoxic neuronal changes in in vitro model of anoxia. The electron-microscopic examination of organotypic cultures of rat hippocampus, exposed to 10- and 20-minute anoxic insult, revealed the morphological features typical for both necrotic and apoptotic neuronal cell death. Numerous neurones revealed a typical picture of passive necrotic lysis, such as advanced swelling of intracellular organelles associated with cell membrane disruption, whereas others clearly reflected an active apoptotic form of cell injury, consisting of condensation of nuclear chromatin with early preservation of cell membranes. However, there was also a subset of damaged cells sharing several features typical for both necrosis and apoptosis. These results add additional evidence to the previous studies suggesting not only that neurones injured by anoxic insult can die in a pure necrotic or apoptotic way but also that a continuum might exist between apoptosis and necrosis in certain pathological conditions.

The subject of this study is a case of anaplastic ependymoma originally arising from the central canal of the lower spinal cord followed by the 13 years history of events of upper spinal dissemination and retrograde intracranial spread. The specimens from four subsequent surgeries generally displayed the same microscopic features of neoplastic tissue and were consistent with the diagnosis of anaplastic ependymoma. The histological diagnosis was based upon the high cellularity, considerable nuclear atypia and pleomorphism, brisk mitotic activity, focally exhibited vascular endothelial proliferation and extensive necrosis. Apart from the typical pattern of ependymoma, the tumors contained areas composed almost entirely of large, uniform clear cells or pseudogemistocytes indicating the morphological heterogeneity of neoplastic cells population. The surgical specimens from four surgical resections shared light microscopic similarities suggesting spinal and intracranial dissemination from the primary spinal tumor. Since the retrograde spread via the cerebrospinal fluid (CSF) pathway is extremely rare, the authors of this study discuss the mechanism of such way of tumor metastases.

An unusual case of a giant intraspinal schwannoma in a 45-year-old woman with 14-year history of preoperative symptoms was presented. MRI of the spine revealed an intradural, extramedullary tumor extending from the intervertebral space C4/C5 to T4 vertebral body level (2 x 1.2 x 12 cm) and filling almost the entire spinal canal. Microscopical examination showed a typical neurinoma pattern with two distinct zones of Antoni A and Antoni B tissue. Some areas exhibited nuclear atypia and hyperchromasia reflecting the degenerative changes in this slowly growing nerve sheath tumor. A rich pericellular reticulin network was seen in the areas composed of Antoni A tissue. Immunohistochemically, the tumor cells were strongly positive for S-100 protein. The diagnostic difficulties in the presented case of longstanding schwannoma resulted in the late surgical treatment. The importance of the early diagnosis of spinal nerve sheath tumors for the patient's quick recovery is stressed.