Clinical efficacy and safety of anterior thalamic deep brain stimulation for intractable drug resistant epilepsy.

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.

Large haemorrhage within glioblastoma mimicking haemorrhagic stroke and coexistance of meningioma: a case of collision tumours.

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.

Differentiating Stroke and Seizure in Acute Setting-Perfusion Computed Tomography?

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.

Ganglion cell tumours in the sella turcica in close morphological connection with pituitary adenomas.

Ganglion cell tumours in the sellar region are uncommon. They are usually associated with pituitary adenomas, while isolated ganglion cell neoplasms are extremely rare. We report the clinicopathological studies of five cases diagnosed as ganglion cell tumours located in the intrasellar region: four mixed/collision tumours composed of gangliocytoma and pituitary adenoma, and one isolated ganglioglioma unrelated to adenoma. Clinically, two patients presented with acromegaly, while three others were initially diagnosed as non-functioning adenomas. In four cases, the histopathological examination of surgical specimens revealed intermixed lesions composed of pituitary adenoma and ganglion cell elements. The adenomas appeared to secrete growth hormone. Electron microscopy enabled identification of the sparsely granulated somatotroph cells. Neoplastic neuronal lesions were composed of mature ganglion cells, including binucleate or multinucleate cells. In all cases, boundaries between adenomatous and gangliocytic components were not clearly demarcated, and numerous gangliocytic cells were closely intermingled with adenomatous tissue. One case lacked endocrine symptoms, and no pituitary adenoma was identified in the surgically excised material; it was finally diagnosed as low-grade ganglioglioma. The etiopathogenesis of ganglion cell neoplasms in the sellar region is not clearly defined. Our study revealed that if ganglion cell neoplasms were combined with adenoma, both neoplastic components were closely related to each other, and numerous neuronal elements were strictly intermingled with adenoma cells. Such a tissue pattern indicates that these neoplastic changes, including their common respective etiopathogeneses, are closely related. The identification of both components in sellar regions may have some nosological implications.

Protective effect of valproic acid on cultured motor neurons under glutamate excitotoxic conditions. Ultrastructural study.

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.

The coexistence of pleomorphic xanthoastrocytoma and arteriovenous malformation. A case report.

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.

[Difficulties in the diagnosis of the first symptoms of brain tumors prehospital delay diagnosis]. / Trudnosci w rozpoznawaniu pierwszych objawów guzów mózgu--opózniona diagnostyka przedszpitalna.

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.

Amyotrophic lateral sclerosis - looking for pathogenesis and effective therapy.

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterized by loss of motor neurons in the spinal cord, brain stem and motor cortex which dramatically reduces life expectancy. ALS occurs either in familial or, more frequently, in sporadic forms. It finally results in death due to respiratory failure that occurs typically 2-5 years after the disease onset. Although the aetiology of ALS remains largely unclear, its heterogeneity suggests that a combination of various factors, including endogenous and/or environmental ones, may be implicated in progressive motor neuron stress that results in the activation of different cell death pathways. Interactions between genetic, environmental, and age-dependent risk factors have been hypothesized to trigger disease onset. Despite extensive neurobiological, molecular and genetic research, at the beginning of the 21st century ALS still remains one of the most devastating neurodegenerative diseases because of the lack of effective therapeutic strategies. It is a challenge for the clinical and scientific community. Better understanding of the aetiology of amyotrophic lateral sclerosis is necessary to develop effective treatment of this progressive neurodegenerative disease. This review presents the current state of knowledge in ALS research.

Neuroprotective effect of erythropoietin in amyotrophic lateral sclerosis (ALS) model in vitro. Ultrastructural study.

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.

CDP-choline protects motor neurons against apoptotic changes in a model of chronic glutamate excitotoxicity in vitro.

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.

Astroglial alterations in amyotrophic lateral sclerosis (ALS) model of slow glutamate excitotoxicity in vitro.

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.

Apoptotic neuronal changes enhanced by zinc chelator--TPEN in organotypic rat hippocampal cultures exposed to anoxia.

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.

Risk factors for depression in patients with epilepsy.

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.

Hypersexuality in two patients with epilepsy treated with lamotrigine.

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.

[Prevalence of cervical spine inflammatory changes in rheumatoid arthritis patients and the value of neurological examination in their diagnosis]. / Czestosc wystepowania zmian zapalnych w odcinku szyjnym kregoslupa u chorych na reumatoidalne zapalenie stawów i rola badania neurologicznego w ich diagnostyce.

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.

Autophagic degeneration of motor neurons in a model of slow glutamate excitotoxicity in vitro.

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 mode of spinal motor neurons degeneration in a model of slow glutamate excitotoxicity 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.

Expression of apoptosis-related proteins in model of anoxia in vitro.

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.

[Description of mood disorder in patients with epilepsy]. / Charatetyka zaburzen nastruoju u choch na padsczke.

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.