Glutamate-Related Antibodies and Peripheral Insulin-Like Growth Factor in Bipolar Disorder and Lithium Prophylaxis.

AIMS: The aim of this study was to evaluate serum levels of the antineuronal antibodies anti-N-methyl-D-aspartate receptor (NMDAR) and anti-glutamic acid decarboxylase (GAD), and insulin-like growth factor 1 (IGF-1), in patients with bipolar disorder (BD), during manic and depressive episodes and in remission compared to euthymic patients receiving long-term lithium therapy. METHODS: Serum levels of anti-NMDAR and anti-GAD 450/620 antibodies, as well as IGF-1, were measured using the ELISA method in 19 manic and 17 depressed patients both in an acute episode and in remission after the episode. All of the subjects were under pharmacological treatment. The control group included 18 euthymic BD patients receiving lithium for 9-44 years (mean 22 ± 11) in whom a single measurement was performed. RESULTS: Serum levels of anti-NMDAR antibodies were higher in acute manic episodes than in lithium-treated patients. Serum levels of anti-GAD 450/620 antibodies were higher in acute manic and depressive episodes compared to remission after the respective episode. Their values in both acute manic and depressive episodes were higher than those in lithium-treated patients. Serum levels of IGF-1 were higher in acute manic episodes and in remission after mania than in lithium-treated patients. CONCLUSION: Higher levels of anti-NMDAR and anti-GAD antibodies during episodes may point to an abnormality in the glutamatergic system in BD. Increased levels of IGF-1 during an acute manic episode and in remission after mania may constitute a compensatory mechanism against excitotoxicity. Lower levels of anti-NMDAR, anti-GAD antibodies, and IGF-1 during long-term lithium treatment may reflect normalization of this processes, contributing to mood stabilization.

Increased Serum CD14 Level Is Associated with Depletion of TNF-α in Monocytes in Migraine Patients during Interictal Period.

The aim of the present study was to investigate the levels of circulating CD14 in relation to the expression of tumor necrosis factor alpha (TNF-α) in monocytes, and serum levels of TNF-α and macrophage inflammatory protein-1 (MIP-1) in migraine patients. Numerous studies revealed controversial changes in the components of the immune system during attacks and the interictal period in migraine patients. Our study included 40 migraineurs and 39 controls. The levels of TNF-α, MIP-1 and CD14 were measured in peripheral monocytes and in sera with the Enzyme-Linked Immunosorbent Assay (ELISA) method, and the monocyte expression of TNF-α was also analysed by immunostaining. Serum CD14 concentrations were higher and the expression of TNF-α in monocytes was decreased in migraineurs. The serum MIP-1 level correlated with Verbal Rating Scale (VRS); the MIP-1:CD14 ratio in monocytes correlated with Visual Analogue Scale (VAS); the MIP-1:CD14 ratio correlated with Migraine Severity (MIGSEV)-Pain scores; and serum CD14 concentration correlated with migraine duration in years. Increased serum CD14 and depletion of TNF-α in monocytes can orchestrate other components of the immune system during the interictal period.

The reciprocal links between synaptophysin serum levels and the prevalence of metabolic syndrome according to selected low-grade inflammation indices and age-related androgen serum level changes in men.

UNLABELLED: The correlations between synaptophysin (SYP) plasma levels and the brain neurotransmission activity are still not strictly identified. However, the efficiency of neurotransmission depends, inter alia, on the age, hormonal status, and coexistence of a low-grade systemic inflammation (LGSI) which is regarded as a pathogenic link with obesity and insulin resistance, atherogenesis and aging per se. AIM: The aim of this study was to investigate the associations between synaptophysin serum levels and age, LGSI indices, homocysteine and selected hormonal parameters (dehydroepiandrosterone and its sulfate, free-testosterone, SHBG) and the prevalence of metabolic syndrome (MS) in men over the age of 40. MATERIALS AND METHODS: After randomization, 157 male volunteers aged 40-80 years were included in a retrospective study. MS was diagnosed according to the International Diabetes Federation criteria. For the diagnosis of late-onset hypogonadism (LOH) we adopted the criteria proposed by the European Male Aging Study (EMAS). RESULTS: Synaptophysin plasma concentrations in respondents decreased with age, but only between the ages of 40 to 70 years. There were no differences in SYP plasma concentrations in men suffering from MS compared to healthy subjects (p=0.845). Men suffering from MS demonstrated while higher hs-CRP (high sensitive C - reactive protein) levels than healthy (p=0.019), contrary to the α1-antichymotrypsin and transferrin. A positive monotonic correlation between synaptophysin and hs-CRP was demonstrated (r=0.235; p=0.003). No statistically significant relationships between SYP and homocysteine plasma levels were presented (r=0.047; p=0.562), although in men diagnosed with MS higher homocysteine levels compared to healthy subjects were demonstrated. No correlations between synaptophysin and free testosterone (r=-0.036; p=0.651), DHEA (r=-0.122; p=0.128) and its sulphate (r=-0.024; p=0.764) as well as SHBG (r=-0.088; p=0.288) were demonstrated. CONCLUSIONS: Although the correlations between synaptophysin plasma levels and age as well as strong LGSI indicator (hs-CRP) have been demonstrated, the usefulness of determining SYP serum concentration as a marker of age-related studied diseases (MS, LOH) seems to be significantly limited.

Nummular headache in a patient with ipsilateral occipital neuralgia--a case report.

Nummular headache (NH) is a rarely recognized primary headache, the diagnostic criteria of which are contained in the appendix to the 2nd edition of the International Classification of Headache Disorders (code A13.7.1). We present the case of a 61-year-old female who suffers, regardless of NH, from right-sided occipital neuralgia. The applied treatment - gabapentin and mianserin - had no effect. Injection of bupivacaine twice to the right occipital region resulted in neuralgia resolution up to three months, with no effect on NH. This confirms the independence of two above mentioned head pain conditions.

Heterogeneous phenotypic manifestations of maternally inherited deafness associated with the mitochondrial A3243G mutation. Case report.

The A3243G mutation is one of the most frequent mutations of mitochondrial DNA. The phenotypic expression of the A3243G mutation is variable and causes a wide range of syndromic and non-syndromic clinical disorders. Mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) syndrome is the most frequent syndromic manifestation of the A3243G mutation. Stroke-like episodes seem to be the dominant feature of MELAS. We have investigated the case of a family with A3243G mutation, in which a dominant symptom in three generations was the maternally inherited hearing loss with absence of stroke-like episodes. Besides deafness, we found also other clinical features such as myopathy, neuropathy, migraine, ataxia, short stature, diabetes mellitus, and cardiomyopathy.

Is MS an inflammatory or primary degenerative disease?

Multiple sclerosis (MS) is characterized by multiple areas of inflammation, demyelination and neurodegeneration. Multiple molecular and cellular components mediate neuroinflammation in MS. They involve: adhesion molecules, chemokines, cytokines, matalloproteases and the following cells: CD4+ T cells, CD8+ T cells, B cells, microglia and macrophages. Infiltrating Th1 CD4+ T cells secrete proinflammatory cytokines. They stimulate the release of chemokines, expression of adhesion molecules and can be factors that cause damage to the myelin sheath and axons. Chemokines stimulate integrin activation, mediate leukocyte locomotion on endothelial cells and participate in transendothelial migration. CD8+ cells can directly damage axons. B cells are involved in the production of antibodies which can participate in demyelination. B cells can also function as antigen presenting cells and contribute to T cell activation. Neuroinflammation is not only present in relapsing-remitting MS, but also in the secondary and primary progressive forms of the disease. The association between inflammation consisting of T cells, B cells, plasma cells and macrophages and axonal injury exists in MS patients including the progressive forms of the disease. The above association does not exclude the possibility that neurodegeneration can exist independently from inflammation. Very little inflammation is seen in cortical MS plaques. Anti-inflammatory therapies with different mode of action change the course of MS. Anti-inflammatory and immunomodulatory treatments are beneficial in the early relapsing stage of MS, but these treatments are ineffective in secondary progressive and primary progressive MS. In the stage of progressive MS, inflammation becomes trapped behind a closed or repaired blood-brain barrier. In such a situation current immunomodulatory, immunosuppressive or anti-inflammatory treatments might not reach this inflammatory process to exert a beneficial effect.

The role of neurotrophins in multiple sclerosis-pathological and clinical implications.

Multiple sclerosis (MS) is a chronic inflammatory demyelinating and neurodegenerative disease of the central nervous system (CNS) with unknown etiology. It was recently suggested that autoimmunity, which had long been considered to be destructive in MS, might also play a protective role in the CNS of MS patients. Neurotrophins are polypeptides belonging to the neurotrophic factor family. While neurotrophins mediate cell survival and proliferation in the nervous system, they are also expressed within peripheral blood mononuclear cells fraction (PBMCs) of immunological system. In MS additional neurotrophic support from PBMCs might compensate relative neurotrophins deficiency in the damaged CNS tissue that needs to be repaired. Failure to produce the adequate neurotrophins concentrations might result in decreased protection of the CNS, consequently leading to increased atrophy, which is the main determinant of MS patients' end-point disability. There are several lines of evidence, both from clinical research and animal models, suggesting that neurotrophins play a pivotal role in neuroprotective and neuroregenerative processes that are often defective in the course of MS. It seems that neuroprotective strategies might be used as potentially valuable add-on therapies, alongside traditional immunomodulatory treatment in multiple sclerosis.

The alterations of cerebrospinal fluid TNF-alpha and TGF-beta2 levels in early relapsing-remitting multiple sclerosis.

AIM OF THE STUDY: This study aimed to analyze serum and cerebrospinal fluid (CSF) concentrations of proinflammatory and anti-inflammatory cytokines produced by T regulatory (Treg) cells in early RRMS according to the 2017 McDonald criteria. CLINICAL RATIONALE FOR THE STUDY: Multiple sclerosis (MS) is a chronic, inflammatory, demyelinating disease of the central nervous system (CNS) with the cytokine network playing an important role. However, there is a continual lack of data regarding the immunopathogenesis of early RRMS, especially according to the 2017 McDonald criteria. MATERIALS AND METHODS: The study groups included early RRMS patients during relapse (n = 18), remission (n = 14), and the control group. The MS diagnosis was established according to the 2017 McDonald criteria. Patients were studied up to 1 year after diagnosis was made. A quantitative test kit based on ELISA was used for cytokine measurement in the serum and CSF. Comparative and correlation analyses between the levels of TNF-α, TGF-ß2, IgG index, and relapse duration were performed. RESULTS: Significantly higher CSF concentrations of TNF-α in both RRMS-relapse and RRMS-remission groups were found compared to the controls (p < 0.01). The CSF levels of TGF-ß2 in the RRMS-relapse group were significantly lower in comparison to the control group (p = 0.01). CONCLUSIONS AND CLINICAL IMPLICATIONS: An inappropriate inflammatory response seems to occur in early RRMS and includes the production of TNF-α and a decrease in TGF-ß2 release suggesting a significant Treg cells role. Further studies on the topic may contribute to developing new disease-modifying drugs and biochemical markers of the disorder.

CCL5, CXCL10 and CXCL11 chemokines in patients with active and stable relapsing-remitting multiple sclerosis.

OBJECTIVE: Chemokines are involved in the migration of inflammatory cells to the central nervous system in multiple sclerosis (MS). The aim of our study was to estimate the concentrations of CCL5, CXCL10 and CXCL11 in serum and cerebrospinal fluid (CSF) samples of relapsing-remitting MS (RRMS) patients during both relapse and stable disease, and to compare the results with those of controls. We also decided to evaluate the effect of methylprednisolone (MP) therapy on CCL5, CXCL10 and CXCL11 serum concentrations in MS patients with relapse. METHODS: The study groups consisted of 17 RRMS patients during relapse, 30 RRMS patients in remission and 25 patients with tension headache with no symptoms of inflammatory disease as controls. In the group of relapsing MS patients, blood samples were obtained before steroid therapy and after a 5-day treatment with MP at a dose of 1 g i.v. once daily. Chemokine levels were measured by ELISA. RESULTS: CXCL10 levels were significantly higher in the CSF of MS patients both during relapse (mean ± SD, 298.2 ± 143.8 pg/ml) and stable disease (323.7 ± 183 pg/ml) in comparison with the control group (152.4 ± 97.7 pg/ml; p < 0.001). CSF levels of CCL5 were significantly higher in relapsing MS patients (8.74 ± 6.18 pg/ml) in comparison with stable MS patients (4.4 ± 3.9 pg/ml, p = 0.005). CXCL11 levels of MS patients did not significantly differ from control values. There was no effect of MP therapy on serum levels of CCL5, CXCL10 and CXCL11. CONCLUSIONS: These observations suggest involvement of CXCL10 and CCL5 but not CXCL11 in the pathogenesis of MS. CCL5 may induce the recruitment of inflammatory cells in acute-stage MS.

SARS-CoV-2 Infection: Symptoms of the Nervous System and Implications for Therapy in Neurological Disorders.

In this paper, the neurological aspects of COVID-19 are presented, which may be of significance for physicians. Knowledge about the neurological symptoms of COVID-19 infection should help physicians in diagnoses and in taking appropriate precautions, as some manifestations can appear before typical pulmonary symptoms. Various mechanisms of SARS-CoV-2 neuroinvasion are discussed and symptoms are described, which can be subdivided into manifestations of the central nervous system (CNS) (headache, dizziness, stroke, impaired consciousness, encephalitis, meningitis, seizures) and peripheral nervous system (PNS) (characteristic hyposmia and hypogeusia, Guillain Barré syndrome, myalgia). Additionally, the implications of COVID-19 infection for treatment of patients with common neurological diseases and their management is presented. It can be concluded that neurological symptoms are part of a clinical spectrum of COVID-19 infection, involving the CNS and PNS. COVID-19 may influence decisions regarding the treatment of neurological disorders, especially those with an immune background.

The Comparison of Predictive Value Among Chemerin, IL-18 and Hormonal Parameters in Assessing the Risk of Metabolic Syndrome in Men.

Chemerin (CHEM) is a new proinflammatory adipokine involved in the immune, metabolic and reproductive processes. Low-grade state inflammation (LGSI) is a key element in the pathogenesis of metabolic syndrome (MS). Low SHBG is a good marker of male hypogonadism in MS. This study evaluated the prognostic value of selected adipokine, LGSI, and androgenic parameters in predicting the risk of MS among men. One hundred thirty-two random men aged 40 to 70 years old were enrolled. Measurements of anthropometric indices, blood pressure, and laboratory tests were carried out. A total of 62 men (47%) were diagnosed with MS. Chemerin concentrations were higher in men diagnosed with MS compared to healthy: 89.48 (78.12-112.10) vs. 77.9 (65.12-98.64) ng/mL; p = .002. Men diagnosed with MS presented with lower levels of total testosterone: 5.75 (4.00-6.57) vs. 6.40 (5.50-8.40) ng/mL; p = .0014 and SHBG: 46.58 (35.13-66.28) vs. 71.97 (56.1-92.7) nM/L; p < 0.000001. Elevated LGSI indices were demonstrated in men with MS as opposed to healthy [IL-18: 530.64 (409.12-640.56) vs. 418.85 (348.14-496.44) pg/mL; p = .000033 and hs-CRP: 2.15 (0.97-4.26) vs. 1.01 (0.41-2.68) ng/mL; p = .0057)]. In multivariate regression analysis, the highest negative predictive value in assessing the risk of MS was SHBG serum concentration, while the highest positive predictive values were: IL-18, hypertriglyceridemia, and waist circumference. Decreased SHBG levels, combined with elevated IL-18 concentrations in men showing hypertriglyceridemic waist phenotype, significantly increase the risk of MS.

CCL3 correlates with the number of mood disturbances and personality changes in patients with Alzheimer's disease.

Although Alzheimer's disease (AD) is a primary degenerative disorder, a microglial-mediated inflammatory response, provoked by amyloid beta (Abeta), contributes to the neurodegeneration and subsequently to the cell loss. Since such an inflammatory contribution to neurodegeneration may influence disease progression, a basic question arises concerning the mechanisms of possible clinical signs dependent on inflammatory reactions. In the present study we investigated the levels of CCL3 in the peripheral blood of AD patients and correlated findings with the results of clinical tests such as the Mini-Mental State Examination (MMSE) and the Global Deterioration Scale (GDS), as well as with disturbances of behaviour, mood and personality, thereby extending the spectrum of clinical symptoms to ones not assessed by the MMSE or the GDS. CCL3 levels were lower in patients with AD but correlated positively with such noncognitive symptoms as mood disturbances and personality changes.We found that CCL3 did not correlate with the severity of dementia as assessed by the MMSE or with the degree of disease deterioration as assessed by the GDS. The results from our study on CCL3 levels in AD may, in part, explain the mechanisms of some concomitant, noncognitive clinical features of the disease.

What do we currently know about the clinically isolated syndrome suggestive of multiple sclerosis? An update.

Multiple sclerosis (MS) is a chronic, demyelinating, not fully understood disease of the central nervous system. The first demyelinating clinical episode is called clinically isolated syndrome (CIS) suggestive of MS. Although the most common manifestations of CIS are long tracts dysfunction and unilateral optic neuritis, it can also include isolated brainstem syndromes, cerebellar involvement, and polysymptomatic clinical image. Recently, the frequency of CIS diagnosis has decreased due to the more sensitive and less specific 2017 McDonald criteria compared with the revisions from 2010. Not all patients with CIS develop MS. The risk of conversion can be estimated based on many predictive factors including epidemiological, ethnical, clinical, biochemical, radiological, immunogenetic, and other markers. The management of CIS is nowadays widely discussed among clinicians and neuroscientists. To date, interferons, glatiramer acetate, teriflunomide, cladribine, and some other agents have been evaluated in randomized, placebo-controlled, double-blind studies relying on large groups of patients with the first demyelinating event. All of these drugs were shown to have beneficial effects in patients with CIS and might be used routinely in the future. The goal of this article is to explore the most relevant topics regarding CIS as well as to provide the most recent information in the field. The review presents CIS definition, classification, clinical image, predictive factors, and management. What is more, this is one of very few reviews summarizing the topic in the light of the 2017 McDonald criteria.

Phase 2 trial of a DNA vaccine encoding myelin basic protein for multiple sclerosis.

OBJECTIVE: To evaluate the efficacy and safety of BHT-3009 in relapsing-remitting multiple sclerosis (MS) and to confirm that BHT-3009 causes immune tolerance. METHODS: BHT-3009 is a tolerizing DNA vaccine for MS, encoding full-length human myelin basic protein. Relapsing-remitting MS patients were randomized 1:1:1 into three groups: placebo, 0.5 mg BHT-3009, or 1.5 mg BHT-3009, given intramuscularly at weeks 0, 2, 4, and every 4 weeks thereafter until week 44. The primary end point was the 4-week rate of occurrence of new gadolinium-enhancing lesions on brain magnetic resonance images from weeks 28 to 48. Protein microarrays were used to measure levels of anti-myelin autoantibodies. RESULTS: Compared with placebo, in the 267 patient analysis population the median 4-week rate of new enhancing lesions during weeks 28 to 48 was 50% lower with 0.5 mg BHT-3009 (p = 0.07) and during weeks 8 to 48 was 61% lower with 0.5 mg BHT-3009 (p = 0.05). The mean volume of enhancing lesions at week 48 was 51% lower on 0.5 mg BHT-3009 compared with placebo (p = 0.02). No significant improvement in magnetic resonance imaging lesion parameters was observed with 1.5 mg BHT-3009. Dramatic reductions in 23 myelin-specific autoantibodies in the 0.5 mg BHT-3009 arm were observed, but not with placebo or 1.5 mg BHT-3009. CONCLUSIONS: In relapsing-remitting MS patients, treatment with the lower dose (0.5 mg) of BHT-3009 for 44 weeks nearly attained the primary end point for reduction of the rate of new enhancing magnetic resonance imaging lesions (p = 0.07) and achieved several secondary end points including a reduction of the rate of enhancing magnetic resonance imaging lesions from weeks 8 to 48 (p = 0.05). Immunological data in a preselected subgroup of patients also indicated that treatment with 0.5 mg induced antigen-specific immune tolerance. The greater dose was ineffective.

Multiple sclerosis - the remarkable story of a baffling disease.

Multiple sclerosis has always been an enigma to its sufferers, their families, medical investigators, and clinicians. For many centuries, there have been attempts to understand its causes and nature, and to discover treatment methods. In the Middle Ages, the disease was claimed to be sent directly from God. A significant development in exploring multiple sclerosis took place in the 19th century, when Jean-Martin Charcot and his colleagues distinguished the disease, precisely described its symptoms, attempted to explain its pathophysiology, and introduced the first methods of symptomatic treatment. The 20th century was a period of discovery and development of diagnostic techniques, such as cerebrospinal fluid analysis, evoked potentials, and magnetic resonance imaging as well as an era of introducing steroid therapy for acute treatment. Currently, the dynamic development of disease modifying therapy and neuroimaging can be observed. The paper aims to delve into the remarkable history of multiple sclerosis by focusing on the earliest case reports and discovery of the disease and exploring its nature, diagnostic methods, and treatment.

Primary progressive multiple sclerosis and neurofibromatosis type 1.

BACKGROUND: Multiple sclerosis (MS) is a common inflammatory demyelinating disease of the central nervous system. The clinical phenotype is probably modified by interactions from genetic and environmental factors. Neurofibromatosis type 1 (NF1) is an autosomal dominant neurocutaneous disease. NF1 gene mutations lead to clinical manifestation in the peripheral and central nervous system. Coexistence of MS and NF1 is a rare condition. OBJECTIVE: To report the case of the patient with primary progressive MS (PPMS) and NF1. METHODS: A retrospective analysis of a patient who has undergone whole exome sequencing confirmed by Sanger sequencing. RESULTS: We reported a novel de novo c.6817delC deletion and rs1801052 polymorphism in NF1 gene associated with NF1 symptoms, as well as numerous polymorphisms in SPG7, SPG15, SPG39 genes responsible for benign spastic paraplegia. CONCLUSION: Co-occurrence of PPMS and NF1 may be a consequence of genetic changes.

Impact of methylprednisolone treatment on the expression of macrophage inflammatory protein 3alpha and B lymphocyte chemoattractant in serum of multiple sclerosis patients.

In order to extend our studies designed to elucidate the mechanism of action of intravenous methylprednisolone (ivMP) in symptomatic therapy of relapses in multiple sclerosis (MS) victims, we have evaluated the expression of chemokines: macrophage inflammatory protein 3alpha (MIP-3alpha) and B-lymphocyte chemoattractant (CXCL13) before and after treatment. The data from further exploration of the MP mechanism of action in MS relapses may be helpful in establishing the treatment design, that would be specific both for individuals, and for the disease phase. The mean levels of MIP-3alpha in sera of MS patients showed no statistically significant differences compared to control subjects. The comparison of MIP-3alpha level before and after therapy with ivMP gave the same result. The CXCL13 expression in serum was significantly higher in the group of MS patients than in healthy subjects. After therapy with ivMP the estimated level demonstrated an increase as related to the initial values found in MS patients. Such a response was seen also in the responder but not in nonresponder subgroup. The enhancement of CXCL13 expression after iv MP therapy in MS relapses may explain the lack of a long-term effect of MP therapy in MS. The observed difference in CXCL13 expression between responder and non-responder group of patients should be regarded as a step towards elucidation of the therapeutic effect of ivMP in MS relapses.

Cluster Headache in a 76-year-old Woman with Onset at the Age of 74: Case Report.

Cluster headache (CH) is a rare trigeminal autonomic cephalalgia. Although its pathophysiology is not entirely understood, the hypothalamus and trigeminal nociceptive and autonomic pathways seem to play a key role in its pathology. In the majority of cases, CH begins at a young age and affects mainly men. This article presents a case of a 76-year-old woman with CH that developed at the age of 74. This is one of the first documented reports of CH with such atypical features from an epidemiologic point of view. A possibility of symptomatic cluster-like headache (CLH) attributed to cerebrovascular disease in the patient is also discussed.

CXCL11 (Interferon-inducible T-cell alpha chemoattractant) and interleukin-18 in relapsing-remitting multiple sclerosis patients treated with methylprednisolone.

BACKGROUND/AIMS: Chemokines may play a role in the pathogenesis of multiple sclerosis (MS), facilitating the trafficking of immune cells across the blood-brain barrier. Interferon-inducible T-cell alpha-chemoattractant (CXCL11) recruits activated Th1 cells to sites of inflammation. In this study, we wanted to estimate the levels of CXCL11 chemokine and interleukin-18 (IL-18), a proinflammatory cytokine, in sera of relapsing-remitting MS (RRMS) patients, both before and after methylprednisolone (MP) treatment, and to compare the results with those in the control group. MATERIALS AND METHODS: Serum CXCL11 and IL-18 concentrations were measured by the ELISA method in 30 RRMS patients during relapse both before and after MP treatment, and in 20 healthy blood donors. RESULTS: We found significantly increased CXCL11 and IL-18 serum levels in RRMS patients as compared with controls. Additionally, no influence of MP therapy on the serum levels of CXCL11 and IL-18 was observed. CONCLUSION: We suggest that CXCR3 receptor ligand, CXCL11, may be involved in MS pathogenesis.

[Familial Westphal variant of Huntington's disease. Case report]. / Rodzinna postac odmiany Westphala choroby Huntingtona. Opis przypadku.

Huntington's disease (HD) is commonly recognized, and the most common autosomal dominant neurodegenerative disease of the central nervous system. The major clinical symptoms in adults include mood changes, choreic movements and progressive cognitive decline. Juvenile HD known as Westphal variant presents with significantly different signs characterized mainly by rigidity, myoclonus, and therefore causes diagnostic difficulties. In this paper, we present the patient with Westphal variant of HD in the third generation of women.