31 research outputs found
The Town of Äabar, Croatia, Familiar Pseudocluster for Multiple Sclerosis ā Descriptive Epidemiological Study
Previous descriptive surveys in the town of ^abar, Croatia carried out by our own epidemiological research group, have established that this area is at high risk for MS. To confirm the above assumption and to update MS frequency in this area we conducted a community-based intensive prevalence and incidence study. On December 31st 2001, the average prevalence was 205.7 per 100,000 with prevailing age-specific prevalence in the group of patients between 30 and 49 years of age. The average incidence (1948.ā2004.) was 5.52/100.000 population per year (95% CI=3.27ā8.72), average mortality in the year was 2.76/100 000 inhabitants (95% CI=1.26ā5.24). Sexual index stood at 1:11, starting time was 10:04Ā±28.53 in the year, and the average duration of the disease to the prevalence 11:11Ā±27.26 years
The Town of Äabar, Croatia, Familiar Pseudocluster for Multiple Sclerosis ā Descriptive Epidemiological Study
Previous descriptive surveys in the town of ^abar, Croatia carried out by our own epidemiological research group, have established that this area is at high risk for MS. To confirm the above assumption and to update MS frequency in this area we conducted a community-based intensive prevalence and incidence study. On December 31st 2001, the average prevalence was 205.7 per 100,000 with prevailing age-specific prevalence in the group of patients between 30 and 49 years of age. The average incidence (1948.ā2004.) was 5.52/100.000 population per year (95% CI=3.27ā8.72), average mortality in the year was 2.76/100 000 inhabitants (95% CI=1.26ā5.24). Sexual index stood at 1:11, starting time was 10:04Ā±28.53 in the year, and the average duration of the disease to the prevalence 11:11Ā±27.26 years
The Town of Äabar, Croatia, a High Risk Area for Multiple Sclerosis ā Analytic Epidemiology of Dietary Factors
Multiple sclerosis (MS) is demyelization disease of central nervous system of unidentified causes. Analytic epidemiological research of 19 patients, clinically approved cases of MS and 25 controls, autochthonic inhabitants of town of ^abar, Croatia, the high-risk zone for the disease, was made. The research plan included case-control investigation ā the Ā»door to doorĀ« questionnaire ā about nutrition habits. An odds ratio (OR) was calculated for all the factors which were more frequently found in the patients than in the controls, and vice versa. The variables that were connected with significant risk for MS in the town of ^abar included: alcohol consumption (p=0.05), animal fats/dried meat products consumption (p=0.007), nitrate salting (p=0.03), strong spices (p=0.007), mixed bread (p=0.002), oat and oat products consumption (p=0.0075). No connection was found with regular consumption of vegetables and fruit (p=0.009), blue fresh fish (p=0.028), other fresh fish (p=0.03), freshwater fish (p=0.002), canned fish (p=0.004), dormouse meat (p=0.007), air-dried meat products (p=0.004) and using the water from water supply (p=0.011). In the town of ^abar nutritional customs, primarily food rich in animal fats, alcohol-abuse, and oat consumption could have an influence on MS pathogenesis in genetically inclined individuals
DijagnostiÄki izazov sindroma anti-GQ1b: diferencijalna dijagnoza izmeÄu Miller-Fischerova sindroma i Bickerstaff ova encefalitisa moždanog debla
ABSTRACT ā Miller Fisher syndrome (MFS) may be considered as a rare variant of Guillain-BarrĆ© syndrome (GBS). Together with GBS, Bickerstaff ās brainstem encephalitis and acute ophthalmoparesis without ataxia, MFS is in the group of anti-GQ1b syndrome disorders (anti-GQ1b Sy). Among all GBS variants, MFS is distinctive, presenting with acute symptoms of ophthalmoparesis, ataxia and arefl exia, but without progressive limb weakness as the most characteristic symptom of GBS. MFS is a clinical entity based on typical clinical presentation and defi ned symptoms, and the fi nding of specifi c anti-GQ1b antibodies is not suffi cient for MFS diagnosis. Th e objective of this case report is to demonstrate the diversity of anti-GQ1b Sy clinical presentation. Here we describe a case of a male patient with acute bilateral ophthalmoparesis, mydriasis and unilateral right infranuclear facial nerve palsy, in whom muscle tendon refl exes were preserved and no ataxia was present. Serum antiganglioside antibody test was positive for anti-GQ1b antibody, confi rming the presupposed diagnosis of MFS. Although MFS is rare, it should be considered in patients with acute development of ophthalmoplegia. In rare cases of MFS with uncommon presentation, as it was in our case, positive serum antiganglioside antibody test will lead to the right diagnosisSAŽETAK ā Miller Fisherov sindrom (MFS) može se smatrati rijetkom varijantom Guillain-BarrĆ©ova sindroma (GBS). MFS, zajedno s GBS, Bickerstaff ovim encefalitisom moždanog debla (BBE) i akutnom o ft almoparezom (AO) bez ataksije, pripada skupini poremeÄaja unutar anti-GQ1b sindroma (anti-GQ1b Sy). IzmeÄu svih varijanta GBS, MFS se manifestira na specifi Äan naÄin akutnim razvojem oft almoplegije, ataksije i arefl eksije, no bez progresivne slabosti miÅ”iÄa ekstremiteta kao karakteristiÄnog znaka GBS. MFS je kliniÄki entitet temeljen na tipiÄnoj kliniÄkoj slici i odreÄenim simptomima, no nalaz specifi Änih anti-GQ1b protutijela nije dovoljan za dijagnozu MFS. Cilj je ovoga Älanka prikazati razliÄitosti kliniÄke prezentacije anti-GQ1b sindroma. Opisujemo sluÄaj bolesnika s naglim razvojem obostrane oft almoplegije, midrijaze i unilateralne desnostrane infranuklearne pareze liÄnog živca, bez ataksije te urednih miotatskih refl eksa. S obzirom na kliniÄku sliku i razvoj simptoma postavljena je sumnja na MFS, Å”to je potvrÄeno i pozitivnim nalazom serumskih anti-GQ1b protutijela. U zakljuÄku, premda se rijetko pojavljuje, na MFS treba pomis liti u diferencijalnoj dijagnozi kod bolesnika s naglim razvojem oftalmoplegije. U rijetkim sluÄajevima neuobiÄajene prezentacije MFS-a, kao u naÅ”em sluÄaju, pozitivan nalaz antigangliozidnih protutijela omoguÄava postavljanje toÄne dijagnoz
DijagnostiÄki izazov sindroma anti-GQ1b: diferencijalna dijagnoza izmeÄu Miller-Fischerova sindroma i Bickerstaff ova encefalitisa moždanog debla
ABSTRACT ā Miller Fisher syndrome (MFS) may be considered as a rare variant of Guillain-BarrĆ© syndrome (GBS). Together with GBS, Bickerstaff ās brainstem encephalitis and acute ophthalmoparesis without ataxia, MFS is in the group of anti-GQ1b syndrome disorders (anti-GQ1b Sy). Among all GBS variants, MFS is distinctive, presenting with acute symptoms of ophthalmoparesis, ataxia and arefl exia, but without progressive limb weakness as the most characteristic symptom of GBS. MFS is a clinical entity based on typical clinical presentation and defi ned symptoms, and the fi nding of specifi c anti-GQ1b antibodies is not suffi cient for MFS diagnosis. Th e objective of this case report is to demonstrate the diversity of anti-GQ1b Sy clinical presentation. Here we describe a case of a male patient with acute bilateral ophthalmoparesis, mydriasis and unilateral right infranuclear facial nerve palsy, in whom muscle tendon refl exes were preserved and no ataxia was present. Serum antiganglioside antibody test was positive for anti-GQ1b antibody, confi rming the presupposed diagnosis of MFS. Although MFS is rare, it should be considered in patients with acute development of ophthalmoplegia. In rare cases of MFS with uncommon presentation, as it was in our case, positive serum antiganglioside antibody test will lead to the right diagnosisSAŽETAK ā Miller Fisherov sindrom (MFS) može se smatrati rijetkom varijantom Guillain-BarrĆ©ova sindroma (GBS). MFS, zajedno s GBS, Bickerstaff ovim encefalitisom moždanog debla (BBE) i akutnom o ft almoparezom (AO) bez ataksije, pripada skupini poremeÄaja unutar anti-GQ1b sindroma (anti-GQ1b Sy). IzmeÄu svih varijanta GBS, MFS se manifestira na specifi Äan naÄin akutnim razvojem oft almoplegije, ataksije i arefl eksije, no bez progresivne slabosti miÅ”iÄa ekstremiteta kao karakteristiÄnog znaka GBS. MFS je kliniÄki entitet temeljen na tipiÄnoj kliniÄkoj slici i odreÄenim simptomima, no nalaz specifi Änih anti-GQ1b protutijela nije dovoljan za dijagnozu MFS. Cilj je ovoga Älanka prikazati razliÄitosti kliniÄke prezentacije anti-GQ1b sindroma. Opisujemo sluÄaj bolesnika s naglim razvojem obostrane oft almoplegije, midrijaze i unilateralne desnostrane infranuklearne pareze liÄnog živca, bez ataksije te urednih miotatskih refl eksa. S obzirom na kliniÄku sliku i razvoj simptoma postavljena je sumnja na MFS, Å”to je potvrÄeno i pozitivnim nalazom serumskih anti-GQ1b protutijela. U zakljuÄku, premda se rijetko pojavljuje, na MFS treba pomis liti u diferencijalnoj dijagnozi kod bolesnika s naglim razvojem oftalmoplegije. U rijetkim sluÄajevima neuobiÄajene prezentacije MFS-a, kao u naÅ”em sluÄaju, pozitivan nalaz antigangliozidnih protutijela omoguÄava postavljanje toÄne dijagnoz
Intravenous Thrombolysis for Acute Ischemic Stroke ā Our Experiences
Intravenous (IV) thrombolysis with recombinant tissue plasminogen activator (rt-PA) is the only available pharmacological
therapy to improve the outcome of acute ischemic stroke. We compared 71 patients presenting with ischaemic
stroke and given intravenous rt-PA (0Ā·9 mg/kg total dose) within 3 h with 71 patients who present to the hospital more
than 3 hours after stroke symptom onset. The primary endpoint was the modified Rankin scale (mRS) at 90 days, dichotomised
for favourable and unfavourable (score 2ā6). Outcome measures were symptomatic intracerebral haemorrhage
within 36 h (haemorrhage associated with National Institutes of Health Stroke Scale [NIHSS] 4 points deterioration),
and mortality at 3 months. More patients had favourable outcome with the rt-PA-treated group than with the control
group (64.79% vs. 22.54%; p= 0.0001). The greater proportion of patients left with minimal or no deficit 90 days after
rt-PA treatment, as compared with the control group. In the treated group symptomatic intracranial hemorrhage occurred
in 1 patient who recovered to a level of functional independence, and asymptomatic intracranial hemorrhage was
observed in 2 patients. Our experience of an acute stroke thrombolysis service shows that we are able to provide this treatment
safely and in accordance with established treatment guidelines. We recommend thrombolytic treatment in acute
ischemic stroke for selected population
Systemic thrombolysis for acute ischemic stroke treatment
UnatoÄ Äinjenici da je ishemijski moždani udar zbog visoke smrtnosti i invalidnosti
velik javnozdravstveni problem, do pojave trombolitiÄke terapije nije postojao specifiÄan lijek
za rekanalizaciju okludirane krvne žile. Tromboliza rekombiniranim tkivnim aktivatorom
plazminogena (rt-PA) dokazala je svoju uÄinkovitost u nizu studija i za sada je jedini odobreni
lijek za lijeÄenje ishemijskog moždanog udara. Radi poboljÅ”anja ishoda lijeÄenja potrebno je
lijeÄenje provoditi u specijaliziranim odjelima ā jedinicama za lijeÄenje moždanog udara,
koje uz pravovremeno prepoznavanje moždanog udara i žurno postavljanje dijagnoze predstavljaju
preduvjet za brzo zapoÄinjanje terapije u cilju rane rekanalizacije krvne žile i reperfuzije
moždanog parenhima. Ovakav pristup zbrinjavanju bolesnika s ishemijskim moždanim
udarom omoguÄava ponovno uspostavljanje cirkulacije u ishemijskom podruÄju mozga, dok
je oÅ”teÄenje neurona reverzibilno, Å”to u konaÄnici poboljÅ”ava ishod lijeÄenja.In spite of the fact that ischemic stroke is an important public health problem because
of high mortality and disability, until thrombolysis was established as a standard treatment
for ischemic stroke there was no specific therapy for recanalization of occluded blood
vessels. Efficacy of thrombolysis with recombinant tissue plasminogen activator (rt-PA) has
been proven in a number of studies and currently is only approved therapy for acute
ischemic stroke treatment. In order to improve outcome, ischemic stroke patients need to
be treated in specialized units ā stroke units. After early recognitions of stroke symptoms
and urgent diagnosis these units are a prerequisite for an urgent start of therapy with purpose
of early recanalization of blood vessels and reperfusion of brain parenchyma. This approach
in management of ischemic stroke patients makes it possible for circulation to be restored
in the ischemic region of the brain while neurons are still reversible damaged leading
to an improved outcome at the end
Silent brain infarct
Akutni infarkt mozga svojim nastupom i simptomima uzrokuje relativno jasnu i prepoznatljivu
kliniÄku sliku, no postoje kroniÄne pojedinaÄne i/ili difuzne ishemiÄne lezije mozga
koje su kliniÄki asimptomatske i duže vremena se ne prepoznaju. Termin tihi infarkt mozga Äesto
se koristi za opis infarkta mozga koji se sluÄajno utvrdi u osoba koje nikad ranije u svojoj
povijesti bolesti nisu imale kliniÄke simptome tranzitorne ishemijske atake ili moždanog udara.
Može ga se utvrditi obdukcijom ili neuroradioloŔkim pretragama, kompjutoriziranom tomografijom
i magnetskom rezonancijom mozga. Radi se najÄeÅ”Äe o malom infarktu u dubokim subkortikalnim
regijama mozga i morfoloÅ”ki je sliÄan simptomatskom lakunarnom infarktu. Lakunarna
ishemiÄna lezija mozga posljedica je okluzije duboke, penetrantne arterije u Äijoj se
osnovi uglavnom nalazi hipertenzivna moždana mikroangiopatija. Tihom infarktu mozga posljednje
se desetljeÄe pridaje velika pažnja jer su studije pokazale da prisutnost tihog infarkta
mozga dvostruko poveÄava rizik nastanka simptomatskog moždanog udara i demencije. U
ovom preglednom Älanku prikazujemo epidemiologiju, patofizioloÅ”ka obilježja, Äimbenike rizika
i moguÄe posljedice tihog infarkta mozga.With its onset and symptoms the acute brain stroke causes relatively clear and recognizable
clinical features. However, there are chronic, single and/or diffuse ischemic brain lesions
which are clinically asymptomatic and which take longer to recognize. The term āsilent
brain infarctā is frequently used to describe the brain infarct which is determined with the autopsy
by chance or which could be determined with computerized tomography. Such brain infarct
could also be determined using the brain magnetic resonance imaging on people who
never before had clinical symptoms transient ischemic attack or brain stroke in their lives. For
the most of the time this is about small infarct in deep sub-cortical brain regions. It is morphologically
similar to symptomatic lacunar infarct. Lacunar ischemic brain lesion is the consequence
of the deep, perforating artery occlusion. Its base is mainly the hypertensive brain
microangiopathy. The silent brain infarct is given great attention in the last decade because
the studies show the silent brain infarct presence doubles the symptomatic brain stroke and
dementia risk. In this review we show the epidemiology, the pathophysiologic attributes, the
risk factors and possible silent brain infarct consequences
Silent brain infarct
Akutni infarkt mozga svojim nastupom i simptomima uzrokuje relativno jasnu i prepoznatljivu
kliniÄku sliku, no postoje kroniÄne pojedinaÄne i/ili difuzne ishemiÄne lezije mozga
koje su kliniÄki asimptomatske i duže vremena se ne prepoznaju. Termin tihi infarkt mozga Äesto
se koristi za opis infarkta mozga koji se sluÄajno utvrdi u osoba koje nikad ranije u svojoj
povijesti bolesti nisu imale kliniÄke simptome tranzitorne ishemijske atake ili moždanog udara.
Može ga se utvrditi obdukcijom ili neuroradioloŔkim pretragama, kompjutoriziranom tomografijom
i magnetskom rezonancijom mozga. Radi se najÄeÅ”Äe o malom infarktu u dubokim subkortikalnim
regijama mozga i morfoloÅ”ki je sliÄan simptomatskom lakunarnom infarktu. Lakunarna
ishemiÄna lezija mozga posljedica je okluzije duboke, penetrantne arterije u Äijoj se
osnovi uglavnom nalazi hipertenzivna moždana mikroangiopatija. Tihom infarktu mozga posljednje
se desetljeÄe pridaje velika pažnja jer su studije pokazale da prisutnost tihog infarkta
mozga dvostruko poveÄava rizik nastanka simptomatskog moždanog udara i demencije. U
ovom preglednom Älanku prikazujemo epidemiologiju, patofizioloÅ”ka obilježja, Äimbenike rizika
i moguÄe posljedice tihog infarkta mozga.With its onset and symptoms the acute brain stroke causes relatively clear and recognizable
clinical features. However, there are chronic, single and/or diffuse ischemic brain lesions
which are clinically asymptomatic and which take longer to recognize. The term āsilent
brain infarctā is frequently used to describe the brain infarct which is determined with the autopsy
by chance or which could be determined with computerized tomography. Such brain infarct
could also be determined using the brain magnetic resonance imaging on people who
never before had clinical symptoms transient ischemic attack or brain stroke in their lives. For
the most of the time this is about small infarct in deep sub-cortical brain regions. It is morphologically
similar to symptomatic lacunar infarct. Lacunar ischemic brain lesion is the consequence
of the deep, perforating artery occlusion. Its base is mainly the hypertensive brain
microangiopathy. The silent brain infarct is given great attention in the last decade because
the studies show the silent brain infarct presence doubles the symptomatic brain stroke and
dementia risk. In this review we show the epidemiology, the pathophysiologic attributes, the
risk factors and possible silent brain infarct consequences
Silent brain infarct
Akutni infarkt mozga svojim nastupom i simptomima uzrokuje relativno jasnu i prepoznatljivu
kliniÄku sliku, no postoje kroniÄne pojedinaÄne i/ili difuzne ishemiÄne lezije mozga
koje su kliniÄki asimptomatske i duže vremena se ne prepoznaju. Termin tihi infarkt mozga Äesto
se koristi za opis infarkta mozga koji se sluÄajno utvrdi u osoba koje nikad ranije u svojoj
povijesti bolesti nisu imale kliniÄke simptome tranzitorne ishemijske atake ili moždanog udara.
Može ga se utvrditi obdukcijom ili neuroradioloŔkim pretragama, kompjutoriziranom tomografijom
i magnetskom rezonancijom mozga. Radi se najÄeÅ”Äe o malom infarktu u dubokim subkortikalnim
regijama mozga i morfoloÅ”ki je sliÄan simptomatskom lakunarnom infarktu. Lakunarna
ishemiÄna lezija mozga posljedica je okluzije duboke, penetrantne arterije u Äijoj se
osnovi uglavnom nalazi hipertenzivna moždana mikroangiopatija. Tihom infarktu mozga posljednje
se desetljeÄe pridaje velika pažnja jer su studije pokazale da prisutnost tihog infarkta
mozga dvostruko poveÄava rizik nastanka simptomatskog moždanog udara i demencije. U
ovom preglednom Älanku prikazujemo epidemiologiju, patofizioloÅ”ka obilježja, Äimbenike rizika
i moguÄe posljedice tihog infarkta mozga.With its onset and symptoms the acute brain stroke causes relatively clear and recognizable
clinical features. However, there are chronic, single and/or diffuse ischemic brain lesions
which are clinically asymptomatic and which take longer to recognize. The term āsilent
brain infarctā is frequently used to describe the brain infarct which is determined with the autopsy
by chance or which could be determined with computerized tomography. Such brain infarct
could also be determined using the brain magnetic resonance imaging on people who
never before had clinical symptoms transient ischemic attack or brain stroke in their lives. For
the most of the time this is about small infarct in deep sub-cortical brain regions. It is morphologically
similar to symptomatic lacunar infarct. Lacunar ischemic brain lesion is the consequence
of the deep, perforating artery occlusion. Its base is mainly the hypertensive brain
microangiopathy. The silent brain infarct is given great attention in the last decade because
the studies show the silent brain infarct presence doubles the symptomatic brain stroke and
dementia risk. In this review we show the epidemiology, the pathophysiologic attributes, the
risk factors and possible silent brain infarct consequences