Search PubMed⌕ Search

Biomedical subjects

J Lodder

Publications and source records attributed to J Lodder.

At least 37 records · Page 2Linked to original sources
PubMed1995

Is haemodynamical compromise a specific cause of border zone brain infarcts following cardiac surgery?

We evaluated the hypothesis that if hypotension or hypoperfusion is a major cause of border zone brain infarction, infarcts following cardiac surgery will be likely to be located in the vascular border zone areas, whereas cerebral perfusion would be lower compared with non-border zone infarcts. Ten of 37 patients with brain infarction following cardiac surgery had an infarct in one of the vascular border zones on CT. Haemodynamical characteristics and clinical features did not differ between border zone infarcts and remaining infarct subgroups. We conclude that compared with stroke series brain infarcts following cardiac surgery are more frequently located in one of the vascular border zone areas, but peri-operative haemodynamic compromise alone does not sufficiently explain this difference. Other possible mechanisms, such as showers of (micro-)emboli, should also be considered.

Adult↗
PubMed1994

Infarcts in the anterior choroidal artery territory. Anatomical distribution, clinical syndromes, presumed pathogenesis and early outcome.

From a prospective registry of all consecutive patients with a supratentorial ischaemic stroke, those with a compatible CT lesion were selected to study topographical relationship, clinical syndrome, vascular risk factors, signs of large-vessel disease or cardiogenic embolism, and mortality in cases with an infarct in the anterior choroidal artery (AChA) territory in comparison with other infarct subtypes. First we identified the area supplied by the AChA: in accordance with the consensus in the literature the posterior two-thirds of the posterior leg of the internal capsule was considered as certain AChA territory. After reviewing CT scans, all presumed small deep AChA territory infarcts were displayed in a schematic composite picture of super-imposed areas of infarction in different shades of grey. Infarcts that were located largely outside the generally included territory were presumed to belong to a different vascular territory. Thus, 77 small deep infarcts were considered to be located within, and 83 outside the AChA territory. Twenty-nine AChA infarcts extended from the internal capsule upwards into the posterior paraventricular corona radiata region. Furthermore, the composite representation of 26 infarcts restricted to the posterior part of the paraventricular corona radiata region showed almost complete overlap with the area occupied by AChA infarcts that extended upwards. We therefore concluded that the posterior paraventricular area is most likely supplied by the AChA. The frequency of a clinical lacunar or a cortical syndrome did not differ between small deep AChA and remaining small deep infarcts. Comparison of vascular risk factors by way of multivariate regression analysis only showed that a significant carotid stenosis was more frequent (adjusted odds ratio 8.87; 95% confidence interval 1.44-54.50), and a cardioembolic source was less frequent (odds ratio 0.24; 95% confidence interval 0.07-0.92) in AChA infarcts than in the other small deep infarcts. Carotid stenosis and cardiac embolism were less frequent in AChA infarcts than in superficial infarcts (odds ratio 0.33, 0.23, respectively; 95% confidence interval 0.15-0.74, 0.09-0.52, respectively). One month and one year mortality were lower in small deep infarcts compared with superficial infarcts, but most favourable in the AChA group. However, this was probably related to younger age in the AChA patients. Larger AChA infarcts were infrequent in our series; six of such cases did not differ in any respect from superficial infarcts. We conclude that the posterior paraventricular corona radiata region is most likely supplied by the AChA, and that AChA infarcts do not constitute a separate brain infarct entity.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗
PubMed1994

Isolated hemiataxia after supratentorial brain infarction.

Acute isolated hemiataxia is in most cases due to infratentorial (cerebellar) stroke. It has only twice been described in supratentorial stroke--namely, after thalamic infarction and a capsular haemorrhage. Three patients with isolated hemiataxia after a supratentorial brain infarct are described. These patients were seen in a period of five years during which 899 patients with a first supratentorial brain infarct were registered. Clinically the hemiataxia was of the cerebellar type. In two patients, CT and MRI showed a small, deep (lacunar) infarct restricted to the posterior limb of the internal capsule, a site not previously reported in isolated hemiataxia. The third patient had a small, deep (lacunar) infarct in the thalamus extending into the adjacent posterior limb of the internal capsule. Isolated hemiataxia after a supratentorial brain infarct is a very rare clinical stroke syndrome. The cerebellar type hemiataxia was most likely caused by interruption of the cerebellar pathways at the level of the internal capsule. Our cases confirm prior observations that the cerebellar pathways run through the posterior part of the posterior limb of the internal capsule separately from the motor and sensory pathways.

Acute Disease↗
PubMed1994

What causes false clinical prediction of small deep infarcts?

BACKGROUND AND PURPOSE: Our goal was to identify factors that play a role in false clinical diagnosis of small deep infarcts. METHODS: In 350 prospectively registered patients with a first supratentorial ischemic stroke, we clinically differentiated between lacunar and nonlacunar syndromes. Using computed tomography (CT), we distinguished small deep and territorial infarcts and also recorded leukoaraiosis and asymptomatic infarcts. Degree of initial handicap, potential source of cardioembolic stroke, and hypertension were also noted. RESULTS: One hundred forty-seven patients had a lacunar and 203 a nonlacunar syndrome. Forty-two (12%) had a lesion visualized by CT that was compatible with a recent infarct but was considered inappropriate for the clinical syndrome: nineteen had a nonlacunar syndrome but a small deep infarct, and 23 had a lacunar syndrome but a territorial infarct. Patients with a nonlacunar syndrome but a small deep infarct were more severely disabled (a modified Rankin scale rating of 5) (odds ratio [OR], 4.31; 95% confidence interval [CI], 1.25 to 14.88) and had a cardioembolic source (OR, 4.07; 95% CI, 1.04 to 15.95), leukoaraiosis (OR, 3.79; 95% CI, 1.32 to 10.05), or asymptomatic infarcts visualized by CT (OR, 4.13; 95% CI, 1.45 to 11.71) compared with 124 patients with a correctly diagnosed small deep infarct. Twelve of 19 patients with a nonlacunar syndrome but a small deep infarct had a lesion in the left hemisphere, and 9 of these 12 had "aphasia." Patients with a lacunar syndrome but a territorial infarct more often had a cardioembolic source (OR, 4.02; 95% CI, 1.15 to 14.03) and a pure motor syndrome (OR, 4.52; 95% CI, 1.55 to 13.18) than those with lacunar syndrome but a small deep infarct, although 21 (91%) were in the right hemisphere. Of the first 103 patients with lacunar stroke diagnosed by two of the study neurologists, 5 had an inappropriate lesion compared with 14 of the later 40 diagnosed by colleagues without a specific interest in cerebrovascular diseases (OR, 0.09; 95% CI, 0.03 to 0.26). CONCLUSIONS: (1) Diagnosis of lacunar syndromes should not be influenced by deficit severity or the presence of a potential cardiac source of embolism. (2) Speech disorders should carefully be classified. (3) Routine tests of nondominant higher functions may be inadequate. (4) Doctors interested in cerebrovascular neurology have a lower failure rate in differentiating small deep infarcts from territorial infarcts than those less well-trained or interested in neurology. (5) Among the lacunar syndromes, pure motor syndrome may be the least specific predictor of a small deep infarct.

Aged↗
PubMed1994

Silent brain infarcts in 755 consecutive patients with a first-ever supratentorial ischemic stroke. Relationship with index-stroke subtype, vascular risk factors, and mortality.

BACKGROUND AND PURPOSE: We wanted to establish independent associations of various clinical variables, computed tomographic (CT) scan features, presenting stroke subtypes, and outcome with the presence of silent infarcts on CT. METHODS: We studied 755 consecutive patients in a prospective registration of patients with first-ever supratentorial atherothrombotic, cardioembolic, or lacunar stroke or stroke of undetermined cause by multiple logistic regression analysis. RESULTS: Two hundred six patients (27%) with a first symptomatic territorial or small deep ischemic stroke had one or more silent infarcts on CT. Of all silent lesions, 169 (82%) were small and deep. Silent infarcts were significantly more strongly associated with a lacunar than atherothrombotic (odds ratio [OR], 1.59; 95% confidence interval [CI], 1.02 to 2.47; P = .039) or cardioembolic (OR, 1.89; 95% CI, 1.2 to 2.99; P = .005) index stroke. Silent territorial lesions were more strongly associated with cardioembolic than with lacunar stroke but not with atherothrombotic stroke. In this respect, no differences were found between the atherothrombotic and undetermined-cause group. Advanced age and hypertension were the only risk factors that were significantly associated with silent infarcts (OR, 1.76; 95% CI, 1.14 to 2.71; P = .011; and OR, 1.58; 95% CI, 1.13 to 2.21; P = .007; respectively), mainly because of a strong independent association of these risk factors with silent small deep infarcts (OR, 1.75; 95% CI, 1.10 to 2.79; P = .018; and OR, 1.57; 95% CI, 1.09 to 2.24; P = .014; respectively). A cardioembolic source or atrial fibrillation in specific was not independently associated with any type or number of silent infarcts. Significant carotid stenosis (diameter reduction > 50%) was not significantly associated with any type of silent lesion. Initial severe handicap (Rankin Scale score > 3), 30-day case fatality rate, and 1-year mortality were not affected by the presence of silent infarcts. CONCLUSIONS: The strong association of silent small deep lesions with first symptomatic small deep infarcts suggests a common underlying mechanism (presumably small-vessel vasculopathy), whereas cardiogenic embolism and large-vessel thromboembolism are the most likely causes in both silent and first symptomatic territorial infarcts. Single or multiple silent infarcts do not predict a cardioembolic stroke mechanism in first symptomatic supratentorial brain infarcts. As silent infarcts do not predict the cause of carotid embolic stroke in first symptomatic brain infarcts, their presence should not influence the decision on carotid surgery. Silent infarcts do not affect the degree of initial handicap, 30-day case fatality, or 1-year mortality. The significance of silent infarcts for predicting possible future cognitive decline and risk of recurrent stroke deserves further study.

Adult↗
PubMed1993

Brain infarct causes under the age of fifty: a comparison between an east-Asian (Thai) and a western (Dutch) hospital series.

Proportion and causes of brain infarction among young persons may differ between Western world and developing countries, which may require different diagnostic and treatment strategies. We compared a Thai series of 56 hospitalized brain infarct patients younger than 50 years (16% of 357 similar patients from all ages) with a series of 55 Dutch patients (8% of 694 patients). The Thai patients had 12% (95% confidence interval: 3-21) more often a cardioembolic stroke cause, due to a higher frequency of rheumatic heart disease in the Thai series. The percentage of patients with atherothrombotic stroke cause was higher in the Dutch series, whereas the percentage of those with hematologic abnormalities, or those with vasculopathies did not differ. Patients in the Thai series had 17% (95% confidence interval: 7-27) more often an unidentified stroke cause, which was probably related to less extensive ancillary investigations compared with the Dutch series. We conclude that especially centers in developing countries that treat young stroke patients should be supplied with ancillary testing facilities, such as cardiac echo, carotid ultrasound, and some laboratory facilities. Early treatment of infections, especially acute rheumatic fever, could lower the incidence of stroke in the young.

Adolescent↗
PubMed1993

Supratentorial brain infarcts in adult-onset seizures; the Maastricht Epilepsy Case Register.

We studied the frequency of supratentorial brain infarction as the cause of late-onset epilepsy in 680 patients with a first seizure after the age of 20, registered on an epilepsy register: 65 (10%) had seizures following a symptomatic supratentorial brain infarct. Brain infarction as the presumed cause of epilepsy was related to age at first seizure. A first seizure occurred within one year after brain infarction in 62%, and later than two years in 19%. Eight of 14 patients (57%) with an early seizure (< or = 2 weeks), and 28 of 41 patients (68%) with a first seizure later than two weeks post-stroke had seizure recurrences despite anti-epileptic treatment. Of 38 patients who underwent computed tomography head scan (CT), 32 (84%) had a cortical infarct, whereas six (16%) had one or more lacunar infarcts. This may indicate that lacunar infarction may be associated with post-stroke epilepsy. Using a detailed topographic brain atlas to localize the cortical infarcts, no 'specific epileptogenic' gyri could be identified. What factors predict future epilepsy in stroke patients need to be studied in prospective series of well-defined stroke subgroups.

Adult↗
PubMed1993

Two clinically distinct lacunar infarct entities? A hypothesis.

BACKGROUND AND PURPOSE: We investigated the hypothesis that patients with one or more asymptomatic lacunar infarcts and those with only one symptomatic lacunar infarct represent two clinically distinct lacunar infarct entities. METHODS: In a prospective series of 100 lacunar infarct patients, univariate and multivariate logistic regression analysis was performed on clinical features, vascular risk factors, and leukoaraiosis between patients with and without asymptomatic lacunar infarcts. RESULTS: Patients with asymptomatic lacunar infarcts had hypertension significantly more often (71% versus 43%; [crude] odds ratio, 3.31; 95% confidence intervals, 1.16-9.43; p < 0.05) and had leukoaraiosis significantly more often (71% versus 19%; [crude] odds ratio, 10.67; 95% confidence intervals, 3.81-32.10; p < 0.001) than those with only a symptomatic lacunar infarct. After multivariate logistic regression analysis, only leukoaraiosis was significantly associated with the presence of asymptomatic lacunar infarcts. The asymptomatic lacunar infarcts differed in location, involved vascular territory, and volume from the symptomatic infarcts. CONCLUSIONS: Two distinct lacunar infarct entities might be broadly distinguished during life: lacunar infarct patients with a single, symptomatic lacunar infarct, and patients with multiple lacunar infarcts and a high frequency of hypertension and leukoaraiosis, in which the underlying small-vessel vasculopathy might be different.

Aged↗
PubMed1992

[Future numbers of patients with a cerebrovascular accident in The Netherlands].

Based on future population size estimates, and sex and age specific CVA incidence rates, the yearly number of new cases of CVA in the Netherlands is projected up to 2020. Compared with 1991 the number of patients with a first CVA will increase by at least 4 and at most 6 per cent in 1995, to 41-62 per cent in 2020. Because the prevalence and the number of handicapped patients will probably be much lower, future attention should primarily be directed at support of early phase care facilities.

Aged↗
PubMed1992

Large striatocapsular infarcts: clinical presentation and pathogenesis in comparison with lacunar and cortical infarcts.

In a well-defined prospective series of 247 patients with a first-ever supratentorial brain infarct, 15 patients (6%; 95% confidence interval 3-9%) had a large striatocapsular infarct. Twelve (80%) had signs of cortical dysfunction, whereas risk factor profile, frequency of significant carotid stenosis, and frequency of potential cardioembolic sources did not differ between patients with striatocapsular and those with cortical infarction. However, patients with striatocapsular infarction more frequently had potential cardioembolic source and significant carotid stenosis than patients with lacunar infarction. Our findings show that large striatocapsular infarcts differ from lacunar infarcts with regard to both presenting signs and symptoms, and pathogenesis, whereas they resemble infarcts involving the cortex. Such patients should therefore be managed and treated as patients with cortical infarction.

Aged↗
PubMed1992

TIA, RIND, minor stroke: a continuum, or different subgroups? Dutch TIA Study Group.

The results of CT were studied prospectively in 606 patients with a transient ischaemic attack (TIA), 422 patients with a reversible ischaemic neurological deficit (RIND), and 1054 patients with a minor stroke, were all entered into a multi-centre clinical trial. CT scanning showed a relevant ischaemic lesion in 13% (95% confidence interval 10-16%) of TIAs, 35% (95% confidence interval 30-40%) of RINDs, and 49% (95% confidence interval 46-52%) of minor strokes (p less than 0.000001). Even within the 24 hour margin, relevant infarcts occurred more often with longer attacks, but were still found in some patients with attacks lasting less than a minute. The type and location of the infarcts were similar in the three groups. These findings suggest that the differences between TIAs, RINDs, and minor strokes are quantitative rather than qualitative.

Cerebral Infarction↗
PubMed1992

[Computerized tomography markers of morphologically confirmed hemorrhagic brain infarct].

Radiological differentiation between hemorrhagic infarction and intracerebral hemorrhage is important for patient management. To ascertain CT features of hemorrhagic infarction, we studied the findings in 19 cases with autopsy-proven hemorrhagic infarction. Most cases had multiple, mainly cortically located, small hyperdensities. However, some presented with a single hyperdensity, deeply located, that could be mistaken for primary intracerebral hematoma. Hemorrhagic infarctions usually present as multiple, small hyperdensities within a hypodense area compatible with an arterial territory. The shape can be round, slitlike, curvilinear, or spotted. Most often the hyperdensities are located cortically; however, some larger, deeply located hyperdensities may falsely suggest primary intracerebral hematoma. Some guidelines for a more reliable radiological separation between hemorrhagic infarctions and intracerebral hematomas are suggested.

Aged↗
PubMed1991

Transient ischemic attacks with and without a relevant infarct on computed tomographic scans cannot be distinguished clinically. Dutch Transient Ischemic Attack Study Group.

We prospectively studied clinical and computed tomographic (CT) scan findings in 79 patients with a transient ischemic attack (TIA) and a relevant cerebral infarction on CT, also known as cerebral infarction with transient signs (CITS). We compared the results with those of 527 concurrent patients with TIA and without cerebral infarction and also with 646 patients with persistent neurological symptoms and a relevant infarct on CT. All patients were participating in a multicenter trial. In both groups, most infarcts were of the lacunar type. Compared with TIAs without cerebral infarction, patients with CITS slightly more often had a history of hypertension (52% vs 33%), the attacks lasted longer (greater than 1 hour, 52% vs 34%) and disappeared more slowly (over the course of hours, 39% vs 24%), and the symptoms more frequently involved speech (61% vs 41%). Despite these small differences, the reverse--the prediction of evidence on CT of infarction on the basis of the nature or time course of symptoms--proved impossible, since in each category the majority of patients had a normal CT scan. In comparison with patients with stroke and visible infarction, patients with CITS slightly more often had abnormal speech (61% vs 45%) and had a larger number of attacks (multiple attacks, 46% vs 18%). In conclusion, we found only minor clinical differences between patients with TIA with or without a relevant infarct on CT and equally small differences between patients with CITS and patients with stroke and cerebral infarction. These clinical similarities do not exclude a difference in prognosis.

Cerebral Infarction↗