Tumori mozga i epilepsija

Brain tumors are a common cause of epilepsy. Tumor type and location are determining factors that significantly influence seizure frequency. The aim of this study was to analyze clinical data of patients diagnosed with brain tumors and epilepsy. Data for this study were obtained from patient medical records over a 6-year period (2000-2005). Patient history and findings obtained by diagnostic methods such as electroencephalography, computerized tomography and magnetic resonance were analyzed. Data were analyzed by appropriate statistical methods and the structure, prevalence, mean and standard deviation were calculated. The significance of results was tested by use of t-test and χ2-test. A total of 15 933 patient charts were analyzed. Out of 15 933 patients, 10.8% were diagnosed with epilepsy and 175 (1.09%) patients had brain tumor, 75 (42.86%) of which were significantly associated with epilepsy (P>0.05). Almost forty-three percent (42.86%) of tumors were epileptogenic, with no significant sex difference (confidence level of 95%). Fifty-seven (32.5%) brain tumor patients were aged 51-60. The mean age of all patients with brain tumors was 41.6 years. Focal sensorimotor seizures were dominant in 40 (53.3%) cases. Among epilepsy cases with known etiology, 75 (6.8%) patients had epileptogenic tumors. Types of seizures in patients with epilepsy were different from seizures provoked by brain tumors. The most common tumor site was temporal region (43.4%). There was no significant difference according to epileptogenesis. Focal sensorimotor seizures were common in patients with frontal and parietal region tumors.Tumori mozga su čest uzrok epilepsije. Vrst tumora i lokalizacija su odlučujući čimbenici koji značajno utječu na učestalost konvulzija. Cilj ove studije bio je analizirati kliničke podatke bolesnika s dijagnosticiranim tumorom mozga i epilepsijom. Podaci za studiju prikupljeni su iz medicinske dokumentacije bolesnika kroz 6-godišnje razdoblje, od 2000.do 2005. godine. Analizirani su anamnestički podaci i nalazi dobiveni dijagnostičkim metodama poput elektroencefalografije, kompjutorizirane tomografije i magnetske rezonancije. U analizi su se primijenile odgovarajuće statističke metode, te je izračunata struktura, učestalost te srednja vrijednost i standardna devijacija. Značajnost rezultata ispitana je pomoću t-testa i χ2-testa. Analiza je obuhvatila 15933 bolesničkih kartona. Od 15933 bolesnika epilepsija je bila dijagnosticirana u 10,8%; 175 (1,09%) bolesnika je imalo tumor mozga, od kojih je 75 (42,86%) bilo značajno udruženo s epilepsijom (P>0,05). Gotovo je 43% (točnije, 42,86%) tumora bilo epileptogeno, bez značajne razlike prema spolu, na razini pouzdanosti od 95%. Utvrđeno je 57 (32,5%) slučajeva tumora mozga među bolesnicima u dobi od 51 do 60 godina. Srednja dob svih bolesnika s tumorom mozga bila je 41,6 godina. Žarišni senzomotorni napadaji prevladavali su u 40 (53,3%) bolesnika. Među bolesnicima s epilepsijom poznate etiologije 75 (6,8%) ih je imalo epileptogene tumore. Vrste napadaja u bolesnika s epilepsijom razlikovale su se od napadaja izazvanih tumorom mozga. Najčešće mjesto tumora bilo je temporalno područje (43,4%) i nije bilo značajne razlike u odnosu na epileptogenezu. Žarišni senzomotorni napadaji bili su česti u bolesnika s tumorima frontalnog i parietalnog područja

Bol u multiploj sklerozi

Multiple sclerosis (MS) is a disease of the central nervous system (CNS), beginning most often in late adolescence and early adult life and expressing itself by reccurrent attacks of spinal cord, brainstem, cerebellar, optic nerve and cerebral dysfunction, the result of foci of destrucion of myelinated fibers. Neuropathic pain, such as trigeminal neuralgia might be one of the first symptoms of multiple sclerosis. In this retrospective study we evaluated 290 patients who have been hospitalised at Department of neurology in last three years. According to the results of our study 70% had either an acute or chronic pain syndrome at some time during their disease. Between them 2.7% with acute pain syndroms had episodes of paroxismal pain attacks in distribution of trigeminal nerve. Chronic pain syndromes, occured in 58% of patients and included headache (25%), low back pain (35%) and painful leg spasms in 20% of patients. Our patients were treated with nesteroid antireumatic drugs in case of nociceptive pain, but neuropathic pain was treated with combination of antidepressive and antiepileptic drugs.Multipla skleroza je kronična, demijelinizirajuća bolest koja se najčešće javlja u osoba mlađe životne dobi. Smatra se da je pojava multiple skleroze rezultat međudjelovanja genetskih i čimbenika okoliša. Dugo se smatralo da multipla skleroza nije povezana s pojavom boli, iako su rezultati istraživanja pokazali da neuropatska bol, poput neuralgije trigeminusa može biti jedan od prvih simptoma bolesti. Cilj ovog istraživanja bio je utvrditi prevalenciju i periodu bolnih stanja u bolesnika oboljelih od MS-a, a koji su bili liječeni na Klinici za neurologiju, KB «Sestre milosrdnice». U vremenskom periodu od tri godine obuhvatili smo 290 bolesnika. Od akutnog ili kroničnog bolnog sindroma patilo je 70% pacijenata. Dvanaest pacijenata (2.7%) s akutnim bolnim stanjem imalo je paroksizmalne bolne atake u području trigeminalnog živca. Kronični bolni sindrom dijagnosticiran je u 58% bolesnika i uključivao je razne oblike glavobolje (20%), bol lumbosakralnom dijelu kralježnice (20%) te bolne spazme u 4% bolesnika. Bolesnici su liječni nesteroidnim antireumaticima u slučaju nociceptivne boli. Neuropatska bol je liječena adjuvantnim lijekovima, najčešće kombinacijom antiepileptika i antidepresiva. Na temelju rezultata ove retrospektivne studije vidljivo je da su akutni i kronični bolni sindromi prisutni u velikom broju bolesnika oboljelih od MS-e te da terapija svakog bolesnika mora biti individualizirana

Neuropatska bol

Neuropathic pain refers to pain that originates from pathology of the nervous system. Common causes of neuropathic pain are diabetes mellitus, reactivation of herpes zoster, nerve compression or radiculopathy, alcohol, chemotherapy or abuse of some drugs, and trigeminal neuralgia. Specific symptoms of neuropathic pain are mechanical allodynia and cold hyperalgesia. Drugs to treat neuropathic pain can be divided into adjuvant analgesics (antidepressants and anticonvulsants), opioids and topical agents. The use of multiple drug therapies is common in practice. Despite considerable increase in the number of randomized placebo-controlled trials in neuropathic pain in the last few years, the medical treatment of neuropathic pain is still far from being satisfactory, with less than half of patients achieving significant benefit with any pharmacological drug.Neuropatska bol nastaje kao posljedica disfunkcije perifernog ili središnjeg živčanog sustava. Najčešći uzroci neuropatske boli su dijabetes melitus, reaktivacija infekcije herpes zoster, kompresija živaca ili radikulopatija, pretjerana konzumacija alkohola, kemoterapija ili zlouporaba lijekova te neuralgija trigeminusa. Specifični simptomi neuropatske boli su mehanička alodinija i hladna hiperalgezija. U liječenju neuropatske boli rabi se nekoliko skupina lijekova. U prvu skupinu spadaju adjuvantni lijekovi, a to su antidepresivi i antiepileptici, opioidi i lokalna sredstva. U praksi se najčešće rabi kombinacija dviju ili vise vrsta lijekova. Unatoč brojnim randomiziranim, placebom kontroliranim studijama na području neuropatske boli medikamentno liječenje neuropatske boli jos uvijek nije zadovoljavajuće, te se zadovoljavajuća analgezija postiže u samo 50% bolesnika s neuropatskom boli

Neuropatska bol

Neuropathic pain refers to pain that orginates from pathology of the nervous system. Common causes of neuropathic pain are diabetes mellitus, reactivation of herpes zoster, nerve compression or radiculopathy, alcohol, chemotherapy or abuse of some drugs and trigeminal neuralgia. Specific symptoms of neuropathic pain are mechanical allodynia and cold hyperlgesia. Drugs to treat neuropathic pain can be divided into adjuvent analgesics (antidepressants and anticonvulsants), opioids and topical agents. The use of multiple drug therapies is common in practice. Despite considerable increase in the number of randomized placebo-controlled trials in neuropathic pain over the last few years, the medical treatment of neuropathic pain is still far from being satisfactory, with kless than half of patients achieving signifi- cant benefit with any pharmacological drug.Neuropatska bol nastaje kao posljedica disfunkcije perifernog ili centralnog živčanog sustava. Najčešći uzroci neuropatske boli su diabetes melitus, reaktivacija herpes zoster infekcije, kompresija živaca ili radikulopatija, pretjerana konzumacija alkohola, kemoterapija ili zlouporaba lijekova te neuralgija trigeminusa. Specifični simptomi neuropatske boli su mehanička alodinija i hladna hiperalgezija. U liječenju neuropatske boli koristi se nekoliko skupina lijekova. U prvu skupinu spadaju adjuvantni lijekovi, a to su antidepresivi i antiepileptici, opioidi i topički agensi. U praksi se najčešće koristi kombinacija dvije ili više vrsta lijekova. Unatoč brojnim randomiziranim, placebo-kontroliranim studijama na području neuropatske boli, medikamentozno liječenje neuropatske boli još uvijek nije zadovoljavajuće, te se samo u 50% pacijenata sa neuropatskom boli postiže zadovoljavajuća analgezija

Polymorphic variants of SCN1A and EPHX1 influence plasma carbamazepine concentration, metabolism and pharmacoresistance in a population of Kosovar Albanian epileptic patients

Aim The present study aimed to evaluate the effects of gene variants in key genes influencing pharmacokinetic and pharmacodynamic of carbamazepine (CBZ) on the response in patients with epilepsy. Materials & Methods Five SNPs in two candidate genes influencing CBZ transport and metabolism, namely ABCB1 or EPHX1, and CBZ response SCN1A (sodium channel) were genotyped in 145 epileptic patients treated with CBZ as monotherapy and 100 age and sex matched healthy controls. Plasma concentrations of CBZ, carbamazepine-10,11-epoxide (CBZE) and carbamazepine-10,11-trans dihydrodiol (CBZD) were determined by HPLC-UV-DAD and adjusted for CBZ dosage/kg of body weight. Results The presence of the SCN1A IVS5-91G>A variant allele is associated with increased epilepsy susceptibility. Furthermore, carriers of the SCN1A IVS5-91G>A variant or of EPHX1 c.337T>C variant presented significantly lower levels of plasma CBZ compared to carriers of the common alleles (0.71±0.28 vs 1.11±0.69 μg/mL per mg/Kg for SCN1A IVS5-91 AA vs GG and 0.76±0.16 vs 0.94±0.49 μg/mL per mg/Kg for EPHX1 c.337 CC vs TT; PG showed a reduced microsomal epoxide hydrolase activity as reflected by a significantly decreased ratio of CBZD to CBZ (0.13±0.08 to 0.26±0.17, pT SNP and SCN1A 3148A>G variants were not associated with significant changes in CBZ pharmacokinetic. Patients resistant to CBZ treatment showed increased dosage of CBZ (657±285 vs 489±231 mg/day; P<0.001) but also increased plasma levels of CBZ (9.84±4.37 vs 7.41±3.43 μg/mL; P<0.001) compared to patients responsive to CBZ treatment. CBZ resistance was not related to any of the SNPs investigated. Conclusions The SCN1A IVS5-91G>A SNP is associated with susceptibility to epilepsy. SNPs in EPHX1 gene are influencing CBZ metabolism and disposition. CBZ plasma levels are not an indicator of resistance to the therapy