Angiogenic T-cells and putative endothelial progenitor cells in hypertension-related cerebral small vessel disease.

BACKGROUND AND PURPOSE: Cerebral small vessel disease (CSVD) may be caused by endothelial dysfunction, whereas endothelial progenitor cells (EPC) may attenuate endothelial dysfunction. Their vitality is lower in CSVD. A subset of lymphocytes, angiogenic T-cells, is capable to stimulate EPC function. The purpose of our study was to explore the relation between CSVD manifestations, angiogenic T-cells, and EPC in hypertensive patients with CSVD. METHODS: We compared 32 essential hypertensive patients with CSVD (white matter lesions, asymptomatic lacunar infarcts, or microbleeds on 1.5-Tesla MRI) to 29 age-matched and sex-matched hypertensive controls. We counted angiogenic T-cells (CD3(+)/CD31(+)/CD184(+)) and putative EPC (CD31(+)/CD34(+)/CD45(-)/KDR(+)) by flow cytometry and determined EPC vitality by in vitro cluster formation. RESULTS: Putative EPC numbers were lower in hypertensive individuals with CSVD than in those without (10±7(.)10(3)/mL versus 13±6(.)10(3)/mL [median±interquartile range]; P=0.011). Angiogenic T-cell numbers were also lower in hypertensive individuals with CSVD than in those without (0.56±0.25(.)10(9)/mL versus 0.78±0.50(.)10(9)/mL; P=0.008). Higher angiogenic T-cell numbers independently related to absence of CSVD (odds ratio, 0.088; 95% confidence interval, 0.012-0.627). CONCLUSIONS: Our data suggest that angiogenic T-cells and putative EPC independently relate to radiological CSVD manifestations in hypertensive patients.

Family history of stroke is an independent risk factor for lacunar stroke subtype with asymptomatic lacunar infarcts at younger ages.

BACKGROUND AND PURPOSE: Results from case-control and case-case studies indicate that a positive family history of stroke (FHstroke) is an independent risk factor for lacunar stroke. Different lacunar stroke phenotypes can be distinguished on the basis of the presence of asymptomatic lacunar infarcts (aLACs), ischemic white-matter lesions, or brain microbleeds. The aim of the present study was to determine whether familial aggregation of stroke was different for lacunar stroke phenotypes. METHODS: In 157 patients with a first-ever lacunar stroke, a complete first-degree FHstroke was obtained by a standardized questionnaire and additional interview. Lacunar stroke patients were categorized successively into groups, depending on the presence of aLACs, ischemic white-matter lesions, and brain microbleeds on magnetic resonance imaging. RESULTS: Fifty-two percent of patients reported a positive FHstroke in at least one of their first-degree relatives. In younger (<65 years) probands, a high frequency of parental FHstroke (59% versus 20%, P<0.01) in those with aLACs compared with probands without aLACs was found. In multivariate analysis, the strongest associations were found for parental FHstroke (odds ratio=6.46; 95% CI=1.96 to 21.33), maternal FHstroke (odds ratio=4.00; 95% CI=1.18 to 13.56), and paternal FHstroke (odds ratio=5.40; 95% CI=1.14 to 25.61). CONCLUSIONS: A family history of stroke might be an independent risk factor for the lacunar stroke phenotype with aLACs at younger ages, suggesting a role for genetic factors in this phenotype caused by diffuse vasculopathy.

Autoantibodies against oxidized low-density lipoprotein in cerebral small vessel disease.

BACKGROUND AND PURPOSE: Oxidized low-density lipoprotein (oxLDL) induces endothelial dysfunction and antibody formation. Because endothelial dysfunction is involved in cerebral small vessel disease (CSVD) (dilated Virchow Robin spaces, lacunar infarcts, and white matter lesions), oxLDL antibodies could play a role in CSVD pathogenesis. Therefore, we studied oxLDL antibodies in patients with high prevalence of CSVD: lacunar stroke patients and essential hypertensive patients. METHODS: A total of 158 lacunar stroke patients, 158 hypertensive patients, and 43 healthy controls were included. We determined levels of IgG and IgM against hypochlorite (HOCl) and malondialdehyde (MDA) oxLDL using ELISA (values in optical density). RESULTS: Patients with CSVD had higher levels of IgG-HOCl-oxLDL (0.77 versus 0.70; P<0.01), as well as lower levels of IgM-MDA-oxLDL (0.55 versus 0.65; P<0.05) than patients without such lesions. Higher IgG-HOCl-oxLDL levels were only independently associated with higher numbers of Virchow Robin spaces at the level of the basal ganglia (ß=0.218; P<0.001). CONCLUSIONS: An autoinflammatory process with lower levels of IgM antibodies and higher levels of IgG antibodies against oxLDL may be involved in CSVD.

Endothelial activation in lacunar stroke subtypes.

BACKGROUND AND PURPOSE: Lacunar stroke (LS) can be subtyped according to the absence (isolated lacunar infarct [ILA]) or presence of concomitant white matter lesions (WML) and/or asymptomatic lacunar infarcts. Endothelial activation is thought to play a pivotal role in the subtype with WML and/or asymptomatic lacunar infarcts. The aim of this study was to evaluate whether endothelial activation is associated with WML and/or asymptomatic lacunar infarcts in LS patients. Here, we determined levels of circulating blood markers of endothelial function in LS patients. METHODS: In 149 patients, all of whom had brain-MRI, levels of tissue plasminogen activator (tPA), plasminogen activator inhibitor type 1 (PAI-1), tPA-PAI-1 complex, von Willebrand factor, tissue factor, thrombomodulin, and coagulation factor VIII were determined. Levels of blood markers were related to subtypes of LS and adjusted for age, gender, and vascular risk factors. RESULTS: In subtypes of LS, tPA activity was increased in patients with WML (0.79 IU/mL vs 0.44 IU/mL for ILA; P=0.02) and PAI-1-antigen levels were lowest in patients with WML (27.5 ng/mL vs 44.0 ng/mL for ILA; P=0.02). The association between WML and PAI-1 remained significant after multivariable analysis (OR, 0.99; 95% CI, 0.98-1.00 per ng/mL change of PAI-1; P=0.04). CONCLUSIONS: We found further evidence for the hypothesis of endothelial activation in the subtype of LS caused by a diffuse small vessel vasculopathy, as we found higher levels of tPA in patients with concomitant extensive WML than in those with ILA. Second, low levels of PAI-1 were associated with WML. We postulate that differences in activity of components of the fibrinolytic system might contribute to WML development.

Vasospasm is a significant factor in cyclosporine-induced neurotoxicity: case report.

BACKGROUND: The aetiology of central nervous system lesions observed in cerebral cyclosporine neurotoxicity remains controversial. CASE PRESENTATION: We report a 48-year-old woman with a non-severe aplastic anaemia who presented with stroke-like episodes while on cyclosporine treatment.Transcranial Doppler ultrasound revealed severely elevated flow velocities in several cerebral vessels, consistent with vasospasm. Immediately after reducing the cyclosporine dose, the stroke-like episodes disappeared. Only after cyclosporine withdrawal the transcranial Doppler ultrasound abnormalities fully resolved. CONCLUSIONS: This case demonstrates a significant role of vasospasm in the pathway of cyclosporine-induced neurotoxicity. Transcranial Doppler ultrasound is an effective tool for the diagnosis and follow-up of cyclosporine-induced vasospasm.

The likelihood of decreasing strokes in atrial fibrillation patients by strict application of guidelines.

AIMS: Despite the known increased stroke risk associated with AF and the benefit of oral anticoagulation (OAC) in high-risk patients, still approximately 20% of all ischaemic strokes are atrial fibrillation (AF) related. We aimed to evaluate the frequency of inappropriate anticoagulation in all patients admitted with AF associated ischaemic stroke and calculate the theoretical number of preventable strokes in case of proper guideline adherence and assess secondary stroke prevention at discharge. METHODS AND RESULTS: In this cross-sectional study, all patients with ischaemic strokes admitted to our hospital during May 2003-August 2006 in whom the diagnosis AF was either known or established during hospital stay were identified. We studied if their admission and discharge antithrombotic therapy was in accordance with the published guidelines. Subsequently, we calculated the number of preventable strokes in case AF patients would have received adequate antithrombotic treatment on admission. On admission, in 51% of the OAC eligible known AF patients the drug was withheld. Improved antithrombotic guideline adherence potentially would have prevented 20 out of the 89 (22%) ischaemic strokes. At discharge at least 10% of the patients were still insufficiently protected against recurrent stroke. CONCLUSION: Many known AF patients admitted with ischaemic stroke lack adequate antithrombotic treatment on admission. Antithrombotic guideline adherence in these patients has the potential to prevent a substantial number strokes. Secondary stroke prevention at discharge is also suboptimal.

An unusual cause of transient neurologic deficits: compression of the carotid artery by a thyroid cystic nodule.

We report a case of a 93-year-old man, who presented with limb-shaking transient ischemic attacks (TIAs) after orthostatic position change or turning his head to the left. The limb-shaking TIAs resulted from external compression of the carotid artery. Contrast-enhanced magnetic resonance angiography of the head and neck and Doppler ultrasound examination of the thyroid gland revealed a large cystic nodule in the right thyroid lobe, resulting in compression and posterior displacement of the right common carotid artery. Clinicians should be aware that limb-shaking TIAs can not only result from obstructive extracerebral or intracerebral artery disease, but also from external compression of the carotid artery.

Periventricular white matter lucencies relate to low vitamin B12 levels in patients with small vessel stroke.

BACKGROUND AND PURPOSE: Blood-brain barrier dysfunction may be an early phenomenon in the development of the small vessel disease, which underlies white matter lesions. Because vitamin B12 plays a role in maintaining the integrity of the blood-brain barrier, we studied serum vitamin B12 level in relation to such lesions. METHODS: In 124 patients with first lacunar stroke, we measured serum vitamin B12 level and rated the degree of white matter lesions on MRI. RESULTS: Mean vitamin B12 level was 202 pmol/L (SD, 68.9). Thirty-nine patients (31.5%) had a vitamin B12 level less than the lower reference value of 150 pmol/L. Lower vitamin B12 level was (statistically significant) associated with more severe periventricular white matter lesions (odds ratio/100 pmol/L decrease, 1.773; 95% CI, 1.001-3.003), but not with deep white matter lesions (odds ratio/100 pmol/L decrease, 1.441; 95% CI, 0.881-2.358; ordered multivariate regression analysis). CONCLUSIONS: More severe periventricular white matter lesions in lacunar stroke patients relate to lower vitamin B12 levels. A possible causal relationship should now be studied prospectively.

Brain microbleeds relate to higher ambulatory blood pressure levels in first-ever lacunar stroke patients.

BACKGROUND AND PURPOSE: Hypertension is an important risk factor for brain microbleeds (BMBs) in lacunar stroke patients. However, beyond the qualitative label "hypertension," little is known about the association with ambulatory blood pressure (BP) levels. METHODS: In 123 first-ever lacunar stroke patients we performed 24-hour ambulatory BP monitoring after the acute stroke-phase. We counted BMBs on T2*-weighted gradient-echo MR images. Because a different etiology for BMBs according to location has been suggested, we distinguished between BMBs in deep and lobar location. RESULTS: BMBs were seen in 36 (29.3%) patients. After adjusting for age, sex, number of antihypertensive drugs, asymptomatic lacunar infarcts, and white matter lesions, we found 24-hour, day, and night systolic and diastolic BP levels to be significantly associated with the presence and number of BMBs (odds ratios 1.6 to 2.3 per standard deviation increase in BP). Distinguishing between different locations, various BP characteristics were significantly associated with the presence of deep (or combined deep and lobar) BMBs, but not with purely lobar BMBs. CONCLUSIONS: Our results underline the role of a high 24-hour BP load as an important risk factor for BMBs. The association of BP levels with deep but not purely lobar BMBs is in line with the idea that different vasculopathies might be involved. Deep BMBs may be a particular marker of BP-related small vessel disease, but longitudinal and larger studies are now warranted to substantiate these findings.

Endothelial dysfunction in lacunar stroke: a systematic review.

BACKGROUND: Endothelial dysfunction is thought to play an important role in the pathogenesis and progression of cerebral small-vessel disease in lacunar stroke patients. METHODS: We systematically searched the literature (MEDLINE, EMBASE) for evidence of endothelial activation and dysfunction in lacunar stroke. The selected papers were assessed by a predefined checklist to estimate methodological and informative quality. The papers were categorized into subheadings concerning the different physiologic functions of the endothelium and a subheading concerning toxins for the endothelium. RESULTS: 29 articles were eligible for further analysis. We found 16 publications on regulation of vascular tone by the endothelium, which showed an impaired function at several time points after the stroke by means of different clinical methods (e.g. flow-mediated vasodilatation and CO2 reactivity). Nine references showed elevated levels of markers of hemostatic function of the vascular endothelium (e.g. von Willebrand factor, thrombomodulin) in acute and subsequent phases. In 4 papers, adhesion molecules (e.g. E- and P-selectin) were elevated only during the acute phase. Homocysteine, a toxin for the endothelium, was elevated in patients in 3 papers. CONCLUSIONS: The current literature suggests that endothelial dysfunction might be involved in the pathogenesis of lacunar stroke, especially in those patients with concomitant silent lacunar infarcts and ischemic white matter lesions. Future research on endothelial function in lacunar stroke should concentrate on long-term clinical as well as radiological follow-up in well-defined cases and combine multiple methods to evaluate endothelial function.

Endothelial progenitor cell research in stroke: a potential shift in pathophysiological and therapeutical concepts.

BACKGROUND AND PURPOSE: Stroke is the leading cause of disability in the Western world; however, few therapies are at hand to decrease this burden. SUMMARY OF REVIEW: Endothelial progenitor cells (EPCs) have been introduced in cardiovascular medicine as factotums. EPCs can repair damaged endothelium and attenuate the development and progression of atherosclerosis. Also, EPCs can form new vessels in ischemic areas and thus promote recovery after ischemic events. In stroke, however, EPC research is limited. In our overview, we provide background information on EPC use as a risk marker and as a potential therapeutic agent. CONCLUSIONS: In our opinion, the lack of EPC studies in stroke should instigate vascular neurologists to participate in EPC research, as EPCs could also change pathophysiological concepts and improve clinical treatments in vascular neurology.

Different classifications of nocturnal blood pressure dipping affect the prevalence of dippers and nondippers and the relation with target-organ damage.

OBJECTIVE: We assessed how different definitions of the awake and asleep periods and use of various blood pressure (BP) indices affect the extent of the nocturnal BP dip, the prevalence of dippers and nondippers, their respective reproducibilities and the relation of nondipping with target-organ damage. METHODS: We performed 24-h ambulatory BP monitoring twice and determined the left ventricular mass index and urinary albumin excretion as indices of target-organ damage in 150 hypertensive patients (off-medication). Awake and asleep periods were assessed using fixed and diary time methods, covering all readings available (wide) or excluding morning and evening transition hours (narrow). Nondipping (BP dip < 10%) was established for systolic BP and diastolic BP, their combinations (and/or), and mean arterial pressure. RESULTS: The different awake-asleep definitions caused significant variation in both the extent of the BP dip and the number of dippers and nondippers in comparison with the wide diary definition (i.e. use of actual awake and sleep periods). The prevalences of dippers and nondippers also varied significantly with the BP index. Reproducibility analyses of the BP dip and the dipping status yielded repeatability coefficients (expressed as percentages of nearly maximal variation) between 42.39 and 48.71%, and kappa values between 0.323 and 0.459, respectively. Some classifications, but not all, discriminated significantly between consistent dippers and nondippers in terms of left ventricular mass index or urinary albumin excretion. CONCLUSIONS: Use of different definitions of awake-asleep and BP indices affects significantly the classification of nocturnal BP dipping and its relation with hypertensive target-organ damage.

Differences in long-term survival in two lacunar stroke types: a 15-year follow-up study in 782 cerebral infarct patients.

BACKGROUND: Mortality studies in lacunar (LAC) stroke are scarce and often characterized by short follow-up time, small patient groups and absence of a nonlacunar stroke group for comparison. Besides, there are no separate long-term prognostic data on LAC stroke subtypes. We performed a long-term mortality study in LAC stroke, subtyping two distinct phenotypes and including nonlacunar ischemic stroke for comparison. METHODS: We performed cross-sectional follow-up, determining survival status, after a median of 15.0 years, in 333 first-ever atherothrombotic (AT), 184 cardioembolic (CE) and 265 LAC strokes, distinguishing LAC stroke with (type 2) or without (type 1) asymptomatic LAC lesions on CT. RESULTS: End of follow-up mortality (in 30-day survivors) in LAC stroke (76.2%) was significantly lower than in CE (87.1%; OR 0.48, 95% CI 0.27-0.84), but not AT strokes (79.0%; OR 0.85, 95% CI 0.57-1.26), and was significantly lower in LAC type 1 than type 2 strokes (70.9 vs. 87.5%; OR 0.35, 95% CI 0.17-0.73). Kaplan-Meier analysis showed most favorable survival in LAC type 1 stroke. In the Cox regression analyses, LAC type 1 stroke appeared as an independent predictor of better survival versus LAC type 2, versus AT and versus CE strokes. CONCLUSIONS: LAC stroke in general cannot be considered a 'benign' stroke type: only long-term survival in patients without concomitant asymptomatic LAC lesions is better than in large-vessel stroke. This difference in long-term survival between the two LAC stroke subtypes should be taken into account in prognostic counselling of individual LAC stroke patients.

Incidence of epilepsy and predictive factors of epileptic and non-epileptic seizures.

PURPOSE: To estimate the incidence of unprovoked seizures (US) and epilepsy in a general population from the southern part of the Netherlands, in relation to age, sex, etiology and seizure type, and to identify predictive factors of the epileptic and non-epileptic seizures. METHODS: All patients aged > or =14 years with a first seizure or who had undiagnosed seizures before the study period were included. Patients were identified from different sources and were independently evaluated and classified by a team of neurologists. A predictive profile for the occurrence of epileptic and non-epileptic seizures was obtained by stepwise logistic regression analysis. RESULTS: The overall annual incidence was 55/100,000 and 30/100,000 for US and epilepsy, respectively. The age-specific annual incidence of US and epilepsy increased with age and reached 120/100,000 and 62/100,000 for the > or =65 years of age group, respectively. The incidence of epilepsy and US in males was higher than in females and partial seizures prevailed over generalized seizures (40 versus 9/100,000). In up to 35% of the cases with US or epilepsy, the etiology was mainly cerebrovascular disease and brain tumors. Predictors for epileptic versus non-epileptic seizures of organic origin were an epileptiform EEG pattern (OR=0.06) versus a history of hypertension (OR=2.8) or cardiovascular disease (OR=5.4). Strong predictors for seizures of non-organic origin were female sex (OR=2.2) and head injury (OR=2.4). CONCLUSIONS: The incidence of US and epilepsy (overall, and age-, sex-, seizure-specific) was similar to those reported by other developed countries. The predictive factors found in this study may assist in the early diagnosis of seizures.

Thrombin-induced hyperactivity of platelets of young stroke patients: involvement of thrombin receptors in the subject-dependent variability in Ca2+ signal generation.

Activated platelets are implicated in the development of premature arterial vascular diseases, in particular ischemic stroke. Since elevated cytosolic [Ca(2+)](i) is an integrative marker of platelet activation, we determined the generation of Ca(2+) signal in stimulated platelets from 26 young patients recuperating from stroke, 20 patients with symptomatic peripheral arterial disease, and 56 healthy volunteers. Even in the presence of aspirin, the platelets from various individuals showed highly different thrombin-induced Ca(2+) responses. On average, the thrombin-induced Ca(2+) response was increased for platelets from either patient group in comparison to the controls (P <0.04). Relatively more stroke patients had high-responsive platelets (27%, 7/26) than patients with peripheral arterial disease (10%, 2/20) or healthy subjects (4%, 2/56). The average prothrombinase activities of platelets from patients and controls were similar, but 3 out of 6 patients with increased thrombin-induced Ca(2+) responses also exhibited high prothrombinase activity. In a follow-up study, the subject-dependent thrombin-induced Ca(2+) response was found to correlate strongly with the platelet response to protease-activated receptor 1 (PAR1) agonist (r = 0.91), but was not linked to the Pl(A1/2) polymorphism. It is concluded that a significant part of young patients with stroke have platelets with hyperactivity toward thrombin, which is not normalised by aspirin treatment. Furthermore, the subject-dependent variation in thrombin-induced signalling is likely to involve PAR1-mediated platelet activation.

Stroke subtype and mortality. a follow-up study in 998 patients with a first cerebral infarct.

The aim of this article was to study mortality following a first-ever cerebral infarct, accounting for ischemic stroke subtypes (lacunar, cardioembolic, atherothrombotic) and relevant prognostic variables. This study was done from s a hospital-based prospective registry of all patients with a first cerebral infarct, with a high case ascertainment of first and recurrent stroke by CT. We used a cross-sectional follow-up, using standardized methods. Analyses were performed using crude comparison of mortality data and death causes between stroke subtypes. We analyzed 30-day case fatality and 1-year mortality in 30-day survivors by means of logistic regression analysis, and mortality in 1-year survivors by means of Cox proportional hazard modeling. We also constructed Kaplan-Meier survival curves, and used log-rank testing for differences between stroke subtypes. Thirty-day case fatality was 10%, 1-year mortality 15%, and after 1-year mortality 16%. Mean follow-up was 691, SD 521 days. At the end of follow-up 36% of all patients had died. Mortality was at all three time points lowest in lacunar stroke (2, 12, and 14%, respectively), intermediate in atherothrombotic stroke (10, 16, and 15%, respectively), and highest in cardioembolic stroke (23, 22, and 21%, respectively). Death related to recurrent stroke was similar in all three stroke subtypes (13-16%). Although 30-day case fatality rate was low in lacunar stroke, a quarter of lacunar stroke patients had died at the end of follow-up. Diabetes mellitus, age, stroke subtype, and initial stroke severity were independent predictors of 30-day case fatality, but only diabetes and age were consistent independent predictors for later mortality. Recurrent stroke and heart failure were important death causes. Prognosis for (future) death following a first cerebral infarct differs between stroke subtypes; lacunar stroke patients have the lowest mortality. However, lacunar stroke cannot be regarded as a mild stroke type, as after 2 years more than a quarter of such stroke patients had died. Cardioembolic stroke patients have the grimmest prognosis: more than half of them had died within 1.5 years. Better prognosis for long-term survival following stroke may be achieved by therapies which lower the risk of stroke recurrence, provide better treatment of heart failure, or both.

Validation of the Oxfordshire Community Stroke Project syndrome diagnosis derived from a standard symptom list in acute stroke.

BACKGROUND: The Oxfordshire Community Stroke Project (OCSP) classification allows distinction of stroke subtypes with different prognosis. OCSP classification inferred from clinical signs filled out on patient entry forms has been used to facilitate subgroup analysis in clinical trials. However, such procedure has not been validated against clinical diagnosis. In preparation for an acute stroke trial, we set out to perform such a validation. METHODS: An OCSP syndrome diagnosis of 194 acute stroke patients in four hospitals was made within 24 h using a standard list with neurological signs, to be filled out by a stroke physician or neurological resident on duty. This was compared with OCSP diagnosis within 2 days of stroke onset by a (blinded) stroke neurologist ("gold standard"). RESULTS: The proportion of the OCSP syndromes was quite similar between standard list and clinical judgement. Sensitivity, specificity, positive and negative predictive values were respectively: LACS: 0.76, 0.88, 0.72, 0.90; TACS: 0.63, 0.93, 0.62, 0.88; PACS: 0.62, 0.76, 0.63, 0.75; POCS: 0.50, 0.98, 0.60, 0.97. Kappa for agreement was 0.63 (LACS), 0.37 (PACS), 0.50 (TACS). Neuro-imaging falsified stroke subtype diagnosis in 40 cases (20.6%) diagnosed using the standard list, and 42 (21.6%) diagnosed by stroke neurologists. CONCLUSION: A standard list-derived stroke syndrome diagnosis may be used as a clinical test to make an OCSP syndrome diagnosis in acute stroke. The use of such list in acute stroke trials may facilitate uniformity in early stroke subtype diagnosis. However, to increase such uniformity, ancillary methods such as acute MRI should be evaluated.

The diagnosis of epileptic and non-epileptic seizures.

The aim of this prospective population-based study was to systematically define a cluster of diagnostic items which can assist in the early identification and classification of epileptic and non-epileptic seizures. A cohort of patients aged > or =14 years, suspected with a first epileptic seizure, were included in this study. A team of neurologists evaluated and classified all cases. Diagnostic items for epileptic and non-epileptic seizures were identified using logistic regression analysis. Three hundred and fifty cases entered this study. Distinctive features for epileptic seizures were postictal confusion (OR 0.09), an epileptiform EEG pattern (OR 0.02), and abnormal neuroimaging findings (OR 0.07), whereas for non-epileptic seizures of organic origin there was a history of hypertension (OR 7.5), and provoking factors (OR 13.4) such as exercise and warmth. Diagnostic items for seizures of non-organic origin were a history of febrile seizures (OR 5.8), treatment by a psychologist or psychiatrist (OR 9.1), and presentiment of the seizure (OR 3.7) such as a feeling of choking and palpitations. A separate analysis for the patients who were systematically investigated provided some additional diagnostic items for the different subgroups of patients. For instance, back arching during the seizure for the patients with seizures of non-organic origin and female sex for the patients with non-epileptic seizures of organic origin.

Predicting the cost of hospital stay for stroke patients: the use of diagnosis related groups.

In order to provide tailor-made care, governments are considering the implementation of output-pricing based on hospital case-mix measures, such as diagnosis related groups (DRG). The question is whether the current DRG classification system can provide a satisfactory prediction of the variance of costs in stroke patients and if not, in what way other variables may enhance this prediction. In this study, data from 731 stroke patients hospitalized at University Hospital Maastricht during 1996-1998 are used in the cost analysis. The DRG classification for this group uses information--in addition to the DRG classification operation or no operation--on the patient's age combined with discharge status. The results of regression analysis show that using DRGs, the variance explained in the costs amounts to 34%. Adding other variables to the DRGs, the variance explained increases to about 61%. Additional factors highly correlating with inpatient costs are the level of functioning after stroke, comorbidity, complications, and 'days of stay for non-medical reasons'. Costs decreased for stroke patients discharged during the latter part of the years studied, and if stroke patients happened to die during their hospital stay. The results do suggest that future implementation of output-pricing based on the DRG case-mix measures is feasible for stroke patients only if it is enhanced with information on complications and the level of functioning.

Bilateral thalamic infarction may result from venous rather than arterial obstruction.

Two patients are presented with bilateral thalamic infarcts, in whom magnetic resonance venography (MRV) revealed venous occlusion. These cases stress the notion that bilateral thalamic infarcts may result from venous rather than arterial obstruction, which requires different evaluation and eventual treatment.