33 research outputs found

    Arahnoidna cista kao uzrok bipolarnog afektivnog poremećaja: prikaz slučaja

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    This report presents the course of diagnostic examinations and treatment of a 20-year-old man with bipolar affective disorder for which an organic basis was demonstrated. Computed tomography of the brain revealed an arachnoid cyst that was surgically treated. The patient underwent both psychiatric and neurosurgical treatment. After two-year follow-up and medicamentous treatment prescribed, the patient was symptom-free requiring no psychopharmacotherapy for the next 5.5 years. His overall life functioning is normal, with no signs of disease.Ovaj prikaz predstavlja tijek dijagnostičkih pregleda i liječenja 20-godiÅ”njeg muÅ”karca koji boluje od bipolarnog afektivnog poremećaja, a za kojega je i prikazana organska podloga same bolesti. Kompjutorska tomografija mozga otkrila je kod bolesnika arahnoidnu cistu koja je kirurÅ”ki liječena. Bolesnik je podvrgnut i psihijatrijskom i neurokirurÅ”kom liječenju. Nakon dvije godine kontinuiranog praćenja stanja bolesnika uz primjenu propisane medikamentne terapije bolesnik viÅ”e nije pokazivao simptome bipolarnog afektivnog poremećaja i nije bila potrebna daljnja primjena psihofarmaka sljedećih 5,5 godina. Njegova ukupna kvaliteta života je zadovoljavajuća, a bolesnik normalno funkcionira u svakodnevnom životu bez ikakvih znakova bolesti

    NeurobioloŔke osnove ovisnosti o alkoholu

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    Alcohol addiction is a heterogeneous psychiatric disorder according to both phenotype and etiology. Difference in phenotype characteristics manifests in the manner the addiction arises, history of the alcoholic and history of drinking, comorbid disorders, and the phenomenon of abstinence difficulties. Concerning the etiology of alcoholism, the disease itself is considered to be a consequence of an interactive influence of the environment and genetic factors. Numerous researches conducted in the last decades discovered many aspects of the biochemical, cell and molecular bases of alcohol addiction, leading to a conclusion that alcoholism is, like many other addictions, a brain disease. By recognizing alcoholism as a disease which basically implies changes of the neurobiological mechanisms, as well as a clear genetic basis, it was supposed that the disease, having its basis solely in the symptomatology, is essentially heterogeneous. By trying to solve the problem of a clinically heterogeneous nature of the disease during the last fifty years, various sub-classifications of such patients have been suggested. According to Cloninger, subtypes of alcoholism differ also according to changes in the brain neurotransmission systems, i.e. it is supposed that patients suffering from alcoholism type 1 have a more pronounced dopaminergic transmission deficit, while dopaminergic transmission is not disturbed significantly in patients diagnosed with alcoholism type 2, who, however, have a significant lack of serotonergic transmission. In such a way, Cloninger actually presented the basis of the so-called neurobiological alcoholism model. Since he has connected differences in neurotransmission with differences in personality characteristics, this model is also known as the psychobiological model of alcoholism. The characteristic of alcoholism type 1 is avoiding damage (Harm Avoidance, HA) decreased dopamine transmission and increased serotonin transmission, while the significant characteristic of alcoholism type 2 is seeking for excitement (Novelty Seeking, NS), unchanged dopamine transmission and decreased serotonin transmission. These neurochemical differences among alcoholism subtypes represent the basis for a different therapy approach. Intake of alcohol changes different gene expression in the human brain. The inheritance model of alcoholism is not fully explained, however, it is considered that the disease is connected to a larger gene number included in neurotransmission, cell mechanisms and general metabolic function, with a simultaneous influence of the environment. The contribution of genetic factors is stronger in certain types of alcoholism and thus we have been confronted in the last years of alcoholism research with studies researching the connections of some alcoholism subtypes with the polymorphism phenomenon in the genes coding the synaptic proteins included in the alcoholism etiology. The primary role of monoamine oxidase (MAO) in the brain is catalysis of deamination of the oxidative neurotransmitter amines, i.e. serotonin, adrenaline, noradrenaline and dopamine. Thus, this enzyme is the key factor for maintaining cytoplasmic concentration of various neurotransmitters and for regulation of the neurotransmitting synaptic activity. Taken this MAO function into consideration, MAO is the enzyme included in the etiology and pathogenesis of various neuropsychiatric and neurological disorders. The finding of the decreased platelet MAO activity in various psychiatric disorders has brought us to the assumption that this enzyme may be a constitutional/genetic indicator (trait marker) or an indicator of disease condition (state marker) in biologic psychiatry. There are only a few studies of alcohol addiction researching the connections of the MAO coding gene polymorphism and alcoholism; however, these studies are primarily related to the variable number of tandem repeats (VTNR) polymorphism in the regulatory gene region for MAO-A, considered to influence the transcription activity/functionality of the enzyme.Ovisnost o alkoholu predstavlja heterogeni psihijatrijski poremećaj po svojoj etiologiji i fenotipu. Razlike u fenotipskim karakteristikama se ogledaju u dobi nastanka ovisnosti, alkoholoÅ”koj anamnezi, odnosno povijesti pijenja, komorbidnim poremećajima i nastanku apstinencijskih smetnji. Å to se tiče etiologije alkoholizma, smatra se kako bolest nastaje kao posljedica međusobnog djelovanja okruženja i genetskih čimbenika. Brojnim istraživanjima tijekom posljednjih nekoliko desetljeća upoznati su mnogi aspekti biokemijske, stanične i molekularne podloge ovisnosti o alkoholu, Å”to je dovelo do toga da se alkoholizam kao i druge ovisnosti danas smatra moždanom bolesti. Prepoznavanjem alkoholizma kao bolesti koja u svojoj osnovi ima promjene neurobioloÅ”kih mehanizama, kao i jasnu genetsku podlogu, pretpostavljeno je i da je dijagnoza bazirana samo na simptomatologiji, u osnovi heterogena. Kako bi se pokuÅ”ao rijeÅ”iti problem klinički heterogene prirode ovisnosti tijekom proteklih pedesetak godina predložene su različite subklasifikacije bolesnika. Prema Cloningeru podtipovi alkoholizma razlikuju se i s obzirom na promjene u moždanim neurotransmiterskim sustavima pa tako pretpostavlja da bolesnici tipa 1 alkoholizma imaju jače deficitarnu dopaminergičnu transmisiju, dok kod bolesnika tipa 2 alkoholizma dopaminergična transmisija nije znatnije poremećena, ali je prisutan značajan nedostatak serotonergične transmisije. Time je utemeljio tzv. neurobioloÅ”ki model alkoholizma. Kako razlike u neurotransmisiji povezuje i s razlikama u osobnosti/crtama ličnosti taj model naziva se i psihobioloÅ”ki model alkoholizma. Kod tipa 1 alkoholizma prisutna je izražena osobina izbjegavanja Å”tete (HA), smanjena transmisija dopamina i poviÅ”ena serotoninska transmisija, dok tip 2 alkoholizma ima izraženu osobinu traženja uzbuđenja (NS), nepromijenjenu dopaminsku (DA) transmisiju i smanjenu serotoninsku (5HT) transmisiju. Navedene neurokemijske razlike među podtipovima alkoholizma čine osnovu za drugačiji terapijski pristup bolesnicima. Pijenje alkohola mijenja ekspresiju različitih gena u mozgu čovjeka. Model nasljeđivanja alkoholizma nije jasan, no smatra se da je bolest povezana s većim brojem gena (poligenska) uključenih u neurotransmisiju, stanične mehanizme i opće metaboličke funkcije uz istodobni utjecaj okoliÅ”a. Doprinos genetičkih čimbenika jači kod određenih tipova alkoholizma te se posljednjih godina u istraživanjima alkoholizma susreću studije koje istražuju povezanost pojedinog podtipa alkoholizma s pojavom polimorfizama u genima koji kodiraju sinaptičke proteine uključene u nastanak alkoholizma. Primarna uloga monoaminoksidaze (MAO) u mozgu je katalizacija oksidativne deaminacije neurotransmiterskih amina ā€“ serotonina, adrenalina, noradrenalina, dopamina, i stoga taj enzim predstavlja ključni čimbenik u održavanju citoplazmatske koncentracije različitih neurotransmitera, odnosno u regulaciji neurotransmiterske sinaptičke aktivnosti. Obzirom na svoju funkciju, MAO je enzim koji je uključen u etiologiju i patogenezu različitih neuropsihijatrijskih i neuroloÅ”kih bolesti. Nalaz snižene aktivnosti trombocitne MAO-B u različitim psihijatrijskim bolestima doveo je do pretpostavke da taj enzim može biti konstitucijski/genetički pokazatelj (trait marker) ili pokazatelj stanja bolesti (state marker) u bioloÅ”koj psihijatriji. Vezano uz ovisnost o alkoholu, postoji viÅ”e studija koje su istraživale povezanost polimorfizama u genima koji kodiraju MAO i alkoholizma, no one se prvenstveno odnose na VNTR polimorfizam u regulatornoj regiji gena za MAO-A za koji se smatra da utječe na transkripcijsku aktivnost/funkcionalnost enzima

    Impairment of Proprioception After Whiplash Injury

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    Whiplash injury usually occurs in traffic accidents. Persons experienced this injury might have an impairment of proprioception clinically expressed as inability to determine the exact position of their heads. The aim of this study was to examine the loss of proprioception in people who had a whiplash injury. The study included 60 subjects with cervical spine injury, aged 20 to 50 years and 60 healthy volunteers matched by sex and age. The instrument used for cervical spine mobility assessment was the Cervical Measurement System (CMS), which determines the ability of subjects to return their head in the exact position as it was before they turned it 30 degrees left or right. Patients with cervical spine injury showed significant impairment of proprioception in comparison with healthy subjects (P<0.001). The results support the hypothesis that subject with recent cervical spine injury have incorrect perception of their head position. Therefore, their rehabilitation should include the correction of proprioception and head coordination

    Trzajna ozljeda vrata - medicinsko-pravni problem

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    Whiplash injury is the most common injury sustained in traffic accidents. On exposure to different forces, multiple neck injuries may occur. Following the injury, many patients suffer from subjective symptoms that may even persist upon completion of medical treatment. As a result, there are serious problems in the objective evaluation of permanent consequences of the injury. The study included 40 randomly selected whiplash injury victims without previous lesions of cervical spine, and 40 equally selected patients with previously confirmed cervical degenerative changes. They all suffered from permanent whiplash injuries and applied for reimbursement for nonmaterial damage to Zagreb Insurance Company during 2001. Sixty-seven per cent of patients underwent continuous treatment for 5-6 months, however, the sequels of whiplash injury persisted in the form of decreased motility of cervical spine, arm paresthesia, vasospasm of vertebral arteries and permanently narrowed visual field. Pathological findings were verified by objective diagnostic methods: functional x-rays of the cervical part of the spinal cord, electromyoneurographic examination of arms, transcranial Doppler sonography of vertebrobasilar arteries, visual field assessment by Goldman method, and clinical examination by medical censor. The treatment of injured patients with previous degenerative changes of cervical spine took a longer time, with a higher level of head and neck motility reduction. Ultimately, in terms of reimbursement, they were conceded a lesser degree of permanent physical damage than those without previous cervical spine lesions.Trzajna ozljeda vratne kralježnice najčeŔće se događa u prometnim nesrećama. Djelovanjem sila dolazi do ozljeda brojnih struktura vrata. Nakon zavrÅ”enog liječenja zaostaje velik broj subjektivnih simptoma koji se ne mogu objektivno prikazati i stoga predstavljaju velik problem kod ocjene trajnih posljedica. Istraživanje je provedeno u nasumce izabranih 40 ozljeđenika bez prisutnih ranijih oÅ”tećenja vratne kralježnice i 40 isto tako nasumce odabranih ozljeđenika s prisutnim degenerativnim promjenama vratne kralježnice dokazane pomoću RTG. Svi su nakon doživljene prometne nesreće pretrpjeli trzajnu ozljedu vratne kralježnice i podnijeli zahtjev za ostvarivanje nematerijalne Å”tete u OZ Zagreb tijekom 2001. godine. U 67% predmeta ozljeđenici su provodili liječenje tijekom 5-6 mjeseci. Nakon zavrÅ”etka liječenja zaostale su trajne posljedice: ograničena pokretljivost vratne kralježnice, utrnulost ruku, vazospazam vertebralnih arterija, trajno sužena vidna polja; sve prema nalazima objektivne obrade (funkcionalne radioloÅ”ke snimke vratne kralježnice, elektromiĀ¬oneurografije ruku, transkranijske Doppler sonografije vertebrobazilarnog sliva, vidnog polja po Goldmanu te klinički pregled liječnika cenzora). U ozljeđenika s prisutnim degenerativnim promjenama vratne kralježnice liječenje je u proĀ¬sjeku bilo dugotrajnije, nakon zavrÅ”etka liječenja imali su veći stupanj ograničenja pokreta glave i vrata, ali su u konačnici dobili u postotku manji stupanj trajnih posljedica u odnosu na ozljeđenike koji nisu imali izrađene degenerativne promjene vratne kralježnice

    Pregled psihoneuroimunoloÅ”kih spoznaja o etiologiji depresivnih poremećaja

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    The brain is no longer considered an immunoprivileged organ which is completely separated from the circulating immune cells by the blood-brain barrier and which shows a lowered or changed immunoreactivity. It has become clear that there are numerous interactions between the neurological, immune and neuroendocrinologic systems. The psychiatric disorder which is supposed to be connected to changes in the functioning of the immune system is depression. One of the hypotheses suggesting the pathophysiology of depression is the cytokine hypothesis of depression. According to it, the behavior changes in depressed patients are a consequence of changes in cytokines. Physiological and psychological effects of the immune activation during an infection, primarily mediated by central activity of peripherally excreted proinflammatory cytokines, are calledā€œsickness behaviorā€. Depression is connected with the activation of the inflammatory response system. When it comes to the immune characteristics of depressive disorders, it should be stressed that depression is a heterogeneous disorder, so different types of depression can differ not only psychopathologically but also at the immune level. Depression is characterized by disorders in noradrenergic and serotonergic neurotransmission. Proinflammatory cytokines are included in the noradrenergic and serotonergic neurotransmission in the brain areas that are thought to be involved in the pathogenesis of depression. According to this model, depression can be considered a psychoneuroimmune disease in which the peripheral immune activation is responsible (by excreting the inflammatory mediator) for various behavioral, neuroendocrinologic and neurochemical changes connected to the psychiatric condition.Mozak se viÅ”e ne smatra imunoprivilegiranim organom koji je potpuno odvojen od cirkulirajućih imunih stanica krvno moždanom barijerom i koji pokazuje smanjenu ili promijenjenu imunoreaktivnost. Jasno je da postoje brojne interakcije između neuroloÅ”kog, imunog i neuroendokrinog sustava. Psihijatrijski poremećaj za koji se pretpostavlja da je povezan s promjenama u funkcioniranju imunog sustava je depresija. Jedna od hipoteza koja objaÅ”njava patofiziologiju depresije je citokina hipoteza; prema tom shvaćanju promjene ponaÅ”anja u depresivnih bolesnika posljedica su promjena u citokinima. FizioloÅ”ki i psiholoÅ”ki učinci imune aktivacije tijekom infekcije, koji su primarno posredovani srediÅ”njim djelovanjem periferno izlučenih proupalnih citokina, jednim imenom nazivaju se ā€œbolesnim osjećanjemā€. Depresija je povezana s aktiviranjem sustava upalnog odgovora. U svezi s imunoloÅ”kim značajkama depresije treba napomenuti da je depresija heterogeni poremećaj, Å”to znači da različiti tipovi depresije mogu biti ne samo psihopatoloÅ”ki različiti, nego se jedni od drugih mogu razlikovati i na imunoloÅ”koj razini. Depresija je obilježena poremećajima u noradrenergičnoj i serotoninergičnoj neurotransmisiji. Proupalni citokini uključeni su u promjene u noradrenergičnoj i serotoninergičnoj neurotransmisiji u moždanim regijama za koje se misli da su uključene u patogenezu depresije. Prema tom modelu ona se može smatrati psihoneuroimunom boleŔću u kojoj je periferna imuna aktivacija potaknuta lučenjem medijatora upale odgovorna za brojne ponaÅ”ajne, neuroendokrine i neurokemijske promjene koje su povezane s psihijatrijskim stanjem

    Liječenje multiple skleroze

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    Multiple sclerosis is an autoimmune inflammatory demyelinating disease of the central nervous system, characterized by multifocal inflammatory destruction of myelin, axonal damage and loss of oligodendrocytes. The disease is carried through two stages: inflammatory and degenerative. The most common form of disease in approximately 85% of the cases is RRMS (relapsing-remitting form). The treatment of MS is divided into: treatment of the acute phase of illness, prevention of new relapses and disease progression, and symptomatic treatment. Most of the changes in treatment of multiple sclerosis and most of the news in recent years concerning new drugs are used in the treatment of progression of the disease and prevention of disease relapses. Some of these drugs are registrated in most European countries and USA, and others are in various stages of research.Multipla skleroza (MS) je upalna autoimuna demijelinizacijska bolest srediÅ”njega živčanog sustava obilježena multifokalnom upalnom destrukcijom mijelina, oÅ”tećenjem aksona i gubitkom oligodendrocita. Bolest se odvija kroz dvije faze, upalnu i degenerativnu. NajčeŔći oblik bolesti, u otprilike 85% slučajeva je RRMS (relapsno-remitentni oblik). Liječenje MS dijeli se na liječenje akutne faze bolesti, prevenciju novih recidiva i progresije bolesti te simptomatsko liječenje. Posljednjih godina najviÅ”e promjena i novih lijekova u liječenju multiple skleroze rabi se u liječenju odnosno sprječavanju progresije bolesti te prevenciji recidiva bolesti. Neki od tih lijekova su registrirani u većini europskih zemalja i u Americi, a drugi su u različitim fazama istraživanja

    The Dissections of Craniocervical Arteries

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    Dissection of craniocervical arteries internal carotid artery (ICA), or vertebral artery (VA) is an increasingly recognized entity and infrequent cause of stroke. We investigated 8 patients (4 women and 4 men) with dissections of the craniocervical arteries. Diagnostic procedures for detection of craniocervical dissection included: extracranial ultrasound- color Doppler flow imaging (CDFI) of carotid and vertebral arteries, transcranial Doppler sonography (TCD) and radiological computed tomography (CT) and digital subtractive angiography (DSA) examinations. Ultrasound findings (CDFI of carotid and vertebral arteries) were positive for vessel dissection in seven patients (or 87.5 per cent) and negative in one patient. DSA was consistent with dissection in five patients (or 62.5 per cent), negative in one, while in two patients the examination was not performed due to known allergy to contrast media. Five patients (62.5 per cent) were treated with anticoagulants, one with suppressors of platelet aggregation, and two patients were operated. Six patients (75 per cent) after the treatment showed partial recovery of neurological defects, and an improvement of ultrasound finding of dissected arteries. In one patient, following operation, stroke developed with deterioration of motor deficit, and one patient was readmitted three months later due to a newly developed stroke and soon died. The diagnosis should be suspected in any young or middle-age patient with new onset of otherwise unexplained unremitting headache or neck ache, especially in association with transient or permanent focal neurological deficits

    CLINICAL TRIALS IN DEVELOPING COUNTRIES - ETHICAL CONSIDERATIONS

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    When designing clinical trial or considering decision to take part in particular clinical trial as investigators, even before submission to responsible Central Ethic Committee, we always make certain private assessment about ethical justification of this clinical trial. When making assessment if any clinical trial is ethically justifiable, there should make no difference in which country this clinical trial will be executed. Physicians coming from developing countries must ensure that patient population of developing countries is not misused in any ethically questionable clinical trial. There must be careful assessment of clinical protocols by various independent local advisory committees (e.g. hospital review boards, hospital drug committees, hospital administration and whatever is applicable) to exclude the possibility that only one person or one group of people has concentrated power to make decisions for entire country. Many times physicians/clinical researchers from developing countries are faced with the criticisms that they are not of the same quality as physicians from developed countries and that they can be easily bribed by sponsors, which are based on the prejudice that any clinical trial can be executed in developing countries, no matter of quality or risks for patients. Physicians coming from developing countries must ensure that patient population of developing countries is not misused in any ethically questionable clinical trial

    Korist od liječenja multiple skleroze beta interferonom

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    Over the past twelve years, beta interferons 1a and 1b have been increasingly used as immunomodulatory agents in the treatment of multiple sclerosis as well as for prophylaxis of disease progression. In Croatia, the cost of beta interferons 1a and 1b has been covered by the Croatian Institute of Health Insurance since 1997. Despite numerous doubts about their real benefit, having in mind their price, side effects and occurrence of neutralizing antibodies, numerous clinical trials have confirmed their efficacy. The most efficient are interferon beta 1a (RebifĀ® in a dose of 12 MIU, subcutaneously, three times per week), interferon beta 1b (BetaferonĀ® in a dose of 8 MIU, subcutaneously, every other day) and interferon beta-1a (AvonexĀ® in a dose of 6 MIU weekly intramuscularly).Posljednjih dvanaest godina u svrhu profilakse pogorÅ”avanja bolesti, odnosno u imunomodulacijskom pristupu u liječenju bolesnika oboljelih od multiple skleroze u svijetu se rabe interferoni beta 1a i 1b. U Republici Hrvatskoj se na teret Hrvatskoga zavoda za zdravstveno osiguranje u liječenju multiple skleroze interferoni beta 1a i 1b primjenjuju od 1997. godine. Iako postoje brojne dvojbe o njihovoj stvarnoj koristi s obzirom na cijenu, nuspojave te pojavu neutralizirajućih antitijela, dosad je objavljeno viÅ”e kliničkih studija koje su pokazale njihovu učinkovitost. Najučinkovitiji su interferon beta 1a (RebifĀ® u dozi od 44 mikrograma (mcg) subkutano, tri puta na tjedan), interferon beta 1b (BetaferonĀ® 8 MIU subkutano svaki drugi dan) i interferon beta 1a (AvonexĀ® 6 MIU intramuskularno jedanput na tjedan)
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