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J Lodder

Publications and source records attributed to J Lodder.

At least 55 records · Page 3Linked to original sources
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↗
PubMed1991

Discrete lesions in the sensorimotor control system. A clinical-topographical study of lacunar infarcts.

In 50 patients with computed tomography-verified small, deep, lacunar, infarcts from a prospective stroke registry, we studied the lesion site in relationship with the clinical syndromes pure motor stroke, sensorimotor stroke and ataxic hemiparesis. Seventy per cent (95% confidence interval: 57-83%) of the lesions were located in the posterior limb of the internal capsule or adjacent paraventricular region, affecting the corticospinal tract in pure motor stroke, as well as the thalamocortical tract in sensorimotor stroke, and the cerebellar (dentato(rubro)thalamocortical and corticopontocerebellar) pathways in ataxic hemiparesis. This most frequently involved area is supplied by the anterior choroidal artery, indicating that this artery is the predominant deep, penetrating artery involved in small vessel disease causing lacunar stroke syndromes.

Aged↗
PubMed1991

Supine and prone head orientation preference in term infants.

Head orientation preference in the supine and prone positions was studied in 62 healthy term born infants at three different times within 24 hours after delivery. Head orientation preference was related to: the foetal position, the initial head position when the newborn was lying prone on the abdomen of the mother, the handedness of the parents and the state of the infant (according to Prechtl). Although for the whole group a head orientation preference for the right side was observed, an individual significant head orientation preference was observed in less than 50% of the infants studied. Neither the occurrence nor the direction of head orientation per individual was constant during the observation period. No relationship was found between an infant's head orientation and foetal position, initial head position, handedness of the parents, or the state of the infant. Our data suggest that persistent head orientation preference to one side in a healthy term born infant within 24 hours after delivery is a sign of abnormality. Head orientation to the right should not be considered as a sign of normality.

Choice Behavior↗
PubMed1991

Lacunar infarcts. Pathogenesis and validity of the clinical syndromes.

BACKGROUND AND PURPOSE: In this study, we investigated the lacunar hypothesis to answer three questions: 1) Is the lacunar syndrome valid for diagnosing lacunar infarction? 2) What is the frequency of potential cardiac versus carotid sources of embolism in patients with lacunar versus cortical infarct? 3) What is the frequency of vascular risk factors in these two groups of patients? METHODS: The study was performed in a well-defined prospective series of 103 patients with a first-ever lacunar infarct and 144 other patients with a first-ever infarct involving the cortex. RESULTS: Sensitivity and specificity of the lacunar syndromes in diagnosing lacunar infarction were 95% and 93%, respectively. Positive and negative predictive values of diagnosing lacunar infarction in patients with lacunar syndromes were 90% and 97%, respectively. Risk factor analysis showed no differences for either group of cerebral infarction. A cardiac source of embolism was significantly less frequent in patients with lacunar infarction (odds ratio = 0.32, 95% confidence interval = 0.17-0.61, p less than 0.001). Significant carotid stenosis (diameter reduction greater than or equal to 50%) was also less frequent in patients with lacunar infarction (odds ratio = 0.35, 95% confidence interval = 0.16-0.76, p less than 0.001). CONCLUSIONS: These findings show that the lacunar syndrome is an excellent clinical test for diagnosing lacunar infarction and that cardiac and carotid embolism are unlikely causes of lacunar infarction, supporting the hypothesis that lacunar infarcts are usually caused by small vessel disease.

Carotid Artery Diseases↗
PubMed1990

How often is non-valvular atrial fibrillation the cause of brain infarction?

To calculate how often non-valvular atrial fibrillation should be considered as the cause of ischaemic stroke rather than an incidental finding as in primary cerebral haemorrhage, the frequency of non-valvular atrial fibrillation in 75 consecutive patients with primary intracerebral haemorrhage was compared with that in 63 patients with cortical infarcts and 44 patients with lacunar infarcts who were taken at random from 1487 consecutive patients with cerebral infarcts admitted during the same period. The frequency of non-valvular atrial fibrillation in lacunar infarcts did not differ from that in primary intracerebral haemorrhage (odds ratio: 1.28; 95% confidence interval: 0.32-5.1) (P = 1.0), whereas it was significantly higher in cortical infarcts (odds ratio: 5.57; 95% confidence interval 2.00-15.4) (P = 0.0001). Our findings suggest that non-valvular atrial fibrillation in lacunar infarcts, as in primary intracerebral haemorrhage, is unlikely to be the cause of this type of stroke, whereas perhaps 30% of all cortical infarcts are not caused by non-valvular atrial fibrillation when present. These data are important for the planning and explanatory evaluation of trials on the preventive effect of anticoagulants in stroke patients with non-valvular atrial fibrillation.

Aged↗
PubMed1990

Recovery of uremic neuropathy after renal transplantation.

Two patients are presented with progressive invalidating uremic peripheral neuropathy. The peripheral neuropathy developed despite frequent hemodialysis with a polyacrylonitrile membrane and afterwards in combination with CAPD. The first patient with a long history of progressive peripheral neuropathy before renal transplantation recovered incompletely after renal transplantation, whereas the second patient with a short history of a severe progressive UPN recovered completely after renal transplantation.

Adult↗
PubMed1990

Ataxic hemiparesis following thalamic infarction.

We describe a 73-year-old man with ataxic hemiparesis following infarction of the ventrolateral nucleus of the thalamus demonstrated by computed tomography and magnetic resonance imaging. Cerebellar ataxia was most likely due to interruption of the dentatorubrothalamocortical fibers at the level of the injured ventrolateral nucleus. Hemiparesis was probably caused by local edema compressing the corticospinal tract in the adjacent posterior limb of the internal capsule. We believe this to be the first reported case of classic ataxic hemiparesis following thalamic infarction.

Aged↗
PubMed1990

Are hypertension or cardiac embolism likely causes of lacunar infarction?

We tested the hypothesis that hypertension is more common and cardiac embolism less common in patients with lacunar infarction than in patients with other types of cerebral infarction. We studied risk factor profiles in a series of 102 consecutive patients with a lacunar infarct and 202 consecutive patients with a carotid artery-distribution infarct involving the cortex registered in the Oxfordshire Community Stroke Project, a community-based study of first-ever stroke. The two groups did not differ in the prevalence of prestroke hypertension (defined in a number of ways) or in the prevalence of markers of sustained hypertension. The presence of atrial fibrillation and a history of myocardial infarction, particularly during the 6 weeks before the stroke, were significantly more common in the group with carotid-distribution infarcts involving the cortex. There was no significant difference in the prevalence of other accepted risk factors for ischemic stroke, including previous transient ischemic attack, cervical bruit, diabetes mellitus, peripheral vascular disease, or cigarette smoking. Our results suggest that hypertension is no more important in the development of lacunar infarction than it is in the development of other types of ischemic stroke that are presumed to be due to atherosclerotic thromboembolism in a major cerebral artery. Our data support the autopsy evidence that cardioembolic occlusion is an unusual cause of lacunar infarction.

Aged↗
PubMed1990

Cardiac embolism.

Explore the source record for details and available documents.

Cerebrovascular Disorders↗
PubMed1989

[An unusual sequela of a frequently occurring neurologic disorder: delirium caused by brain infarct].

Six patients are described with delirium after cerebral infarction. Five had a right-sided parietal infarction with involvement of the inferior parietal lobule. One patient presented with a right-sided medial temporo-occipital infarction. The mild neurological signs were dominated by the delirium. The outcome was good in all patients. Delirium after cerebral infarction is probably caused by injury to one of the convergence sites for integration of sensory information with disturbance of the directed attention to relevant stimuli. These sites are localized in the right parietal cortex and the medial temporo-occipital regions. This cause of delirium is probably compatible with the supposition that the right hemisphere is mainly responsible for the distribution of directed attention within extrapersonal space. The importance of an accurate neurological examination in delirious patients is emphasized.

Aged↗
PubMed1989

Accurate noninvasive method to diagnose minor atherosclerotic lesions in carotid artery bulb.

In a prospective study using a multigate pulsed Doppler system, minor (less than 30% diameter reduction) carotid artery lesions were diagnosed by detecting not only abnormalities in the blood flow pattern, but also local changes in artery wall distensibility. For the diagnosis of more severe lesions, additional information was obtained from disturbances in the Doppler audio spectrum. Biplane arteriography was used as a reference. The observed agreement, sensitivity, and specificity were 86.6%, 90.3%, and 88.6%, respectively, for all lesions and 85.7%, 82.1%, and 88.6%, respectively, when only minor lesions were considered. kappa (a chance-corrected measure of agreement) was 81.7%. If only blood flow abnormalities were used to detect minor lesions, 43.5% would be missed. Our results indicate that minor carotid artery lesions can be diagnosed noninvasively more accurately when both local blood flow irregularities and local changes in vessel wall distensibility are taken into account.

Adult↗
PubMed1988

Cooperative study on the value of long term anticoagulation in patients with stroke and non-rheumatic atrial fibrillation.

The benefits of long term anticoagulant treatment of patients with non-rheumatic atrial fibrillation and cerebral infarction were studied by comparing two series of patients with stroke from centres with different policies on anticoagulant treatment. The long term prognosis of 50 patients from the Oxfordshire community stroke project, who did not receive anticoagulants, was compared with that of 70 similar patients from Maastricht, who were treated with anticoagulants. After a mean follow up of 27 months there was no significant difference in either the rate of survival or the rate of recurrent stroke between the two groups. These data suggest that any benefit of anticoagulation is modest. A large randomised trial is planned to establish whether long term anticoagulant treatment is of value and, if so, to what extent.

Aged↗
PubMed1988

Timing of autopsy-confirmed hemorrhagic infarction with reference to cardioembolic stroke.

We studied the temporal profile of hemorrhagic transformation in 34 cases with autopsy-confirmed hemorrhagic infarction who died within 15 days following a supratentorial brain infarct, provided they had undergone computed tomography. It appeared that within 4 days, at least 76% (95% confidence interval 39-100%) of 21 cardioembolic strokes had become hemorrhagic. We conclude that if anticoagulation is considered in cardioembolic stroke, such treatment should not be started sooner than at least 4 days after the onset of stroke, provided that computed tomography at that time shows no hemorrhagic infarction.

Aged↗
PubMed1987

Hemorrhagic infarction on CT in cardioembolic stroke.

CT-scans of 103 patients anticoagulated following cardioembolic stroke were evaluated. Data were taken from a prospective registry on the risk of early anticoagulant treatment in patients with cardioembolic stroke. Ninety-three patients had CT within 24 hours after stroke onset. Sixty-six of 103 CT-scans showed infarction. On initial CT five hemorrhagic infarcts were found (5%). Of 35 follow-up CT-scans randomly performed during anticoagulant treatment, six (= 17%) showed hemorrhagic infarction without clinical worsening. It is argued that a cardioembolic cause of stroke cannot be infered by the presence of HI on CT. In patients with a cardioembolic stroke the value of CT lies in minimizing the risk of early anticoagulant treatment.

Adult↗
PubMed1987

Risk of early anticoagulation in patients with small deep infarcts possibly caused by cardiogenic emboli.

From a prospective registry of 103 stroke patients on early anticoagulation for cardiac embolus we selected 23 patients with a small deep infarct. We studied the incidence of hemorrhagic infarction on CT, and the risk of early anticoagulation. We found no hemorrhagic infarction on CT in any case, and no bleeding complications during the three week observation period. Obviously, early anticoagulation can be started safely in patients with a small deep infarct possibly caused by cardiac embolism.

Aged↗