Search PubMed⌕ Search

Biomedical subjects

M Vermeulen

Publications and source records attributed to M Vermeulen.

At least 163 records · Page 9Linked to original sources

Effect of fluid intake and antihypertensive treatment on cerebral ischemia after subarachnoid hemorrhage.

We prospectively studied 244 consecutive patients with subarachnoid hemorrhage who were admitted within 72 hours to the same institution between November 1977 and May 1987 and who were not treated with antifibrinolytics. From November 1977 through December 1982 (the first study period), daily fluid intake was 1.5-2.1 and fluid restriction was applied when hyponatremia developed; antihypertensives were administered to all patients with high blood pressure. From January 1983 through April 1987 (the second study period), daily fluid intake was at least 3 l, fluid restriction was not applied, and antihypertensives were administered only when patients were receiving this treatment before admission; calcium antagonists were not administered. Entry variables of the patients admitted during the two study periods were not significantly different, although patients admitted during the second study period were at slightly increased risks of developing cerebral ischemia and of having a poor outcome. Despite this, cerebral ischemia occurred less frequently among patients admitted during the second study period than among those admitted during the first (16 [10%] of 155 patients vs. 19 [21%] of 89 patients; p = 0.030). Overall mortality decreased from 46% to 36% while mortality among patients with cerebral ischemia decreased from 60% to 31% (difference not significant). Rebleeding and acute hydrocephalus occurred with the same frequency among patients admitted during both study periods. We conclude that the combination of increased fluid intake and the avoidance of antihypertensives helps prevent cerebral ischemia after subarachnoid hemorrhage.

Antihypertensive Agents↗

Short-term tranexamic acid treatment in aneurysmal subarachnoid hemorrhage.

Antifibrinolytic treatment for 4 weeks after a subarachnoid hemorrhage has been shown to have no effect on outcome since a reduction in the rate of rebleeding was offset by an increase in ischemic events. To determine if a shorter course (4 days) of antifibrinolytic treatment before the expected onset of ischemic complications might reduce the rate of rebleeding yet avoid ischemic complications, we prospectively studied a series of 119 patients with subarachnoid hemorrhage; 479 patients with subarachnoid hemorrhage from our previous randomized double-blind study (238 treated with placebo, 241 with long-term tranexamic acid) served as historical control groups. At 3 months' follow-up, the outcome of patients treated with short-term tranexamic acid was not different from that of patients treated with long-term tranexamic acid. The rate of rebleeding (24 of 119, 20%) was near that with placebo (56 of 238, 24%). In contrast, the rate of cerebral infarction (33 of 119, 28%) was almost identical to that after long-term tranexamic acid (59 of 241, 24%), although mortality from cerebral infarction was reduced. Compared with historical control groups, treatment with tranexamic acid for 4 days fails to reduce the incidence of rebleeding but still increases the rate of cerebral infarction.

Cerebral Angiography↗

Management problems in acute hydrocephalus after subarachnoid hemorrhage.

In a consecutive series of 473 patients admitted within 72 hours after a subarachnoid hemorrhage, 91 (19%) had hydrocephalus on the initial computed tomogram. Consciousness was unimpaired in 25 of the 91 (28%). In 11 more patients acute hydrocephalus developed within 1 week after subarachnoid hemorrhage. Thirty-eight (8%) of all 473 patients subsequently showed clinical deterioration because of acute hydrocephalus; 11 of these 38 had fluctuations in the level of consciousness. Of the 66 patients with acute hydrocephalus and impaired consciousness on admission, 26 (39%) spontaneously improved within 24 hours. Ventricular drainage was performed in 32 (31%) of the 102 patients with acute hydrocephalus (7% of all 473 patients). Consciousness improved after ventricular drainage in 25 (78%) of the 32 patients. Ventriculitis developed in 12 of the 24 patients with external drainage, mainly after greater than 3 days of drainage, and in none of the eight patients with an internal shunt. Among the 340 patients with aneurysmal subarachnoid hemorrhage and no long-term tranexamic acid treatment, the frequency of rebleeding in patients with ventricular drainage (43% of 23) was significantly higher than in hydrocephalic patients without drainage (15% of 52 patients; chi 2 = 5.009, p = 0.025) and patients without acute hydrocephalus (20% of 265 patients; chi 2 = 5.521, p = 0.019). We conclude that spontaneous improvement occurs in half of the patients with acute hydrocephalus and impaired consciousness on admission, which is usually apparent within 24 hours, and that the outcome of patients who need ventricular drainage will improve if rebleeding and infection after insertion of the ventricular drain can be prevented.

Acute Disease↗

Effect of fludrocortisone acetate in patients with subarachnoid hemorrhage.

In this study with randomized controls, we administered fludrocortisone acetate to 46 of 91 patients with subarachnoid hemorrhage in an attempt to prevent excessive natriuresis and plasma volume depletion. Fludrocortisone significantly reduced the frequency of a negative sodium balance during the first 6 days (from 63% to 38%, p = 0.041). A negative sodium balance was significantly correlated with decreased plasma volume during both the first 6 days (p = 0.014) and during the entire 12-day study period (p = 0.004). Although fludrocortisone treatment tended to diminish the decrease in plasma volume, the difference was not significant (p = 0.188). More patients in the control group developed cerebral ischemia (31% vs. 22%) and, consequently, more control patients were treated with plasma volume expanders (24% vs. 15%), which may have masked the effects of fludrocortisone on plasma volume. Fludrocortisone therefore reduces natriuresis and remains of possible therapeutic benefit in the prevention of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage.

Clinical Trials as Topic↗

Serial electrocardiographic recording in aneurysmal subarachnoid hemorrhage.

We prospectively studied serial electrocardiograms in 61 patients with aneurysmal subarachnoid hemorrhage. Electrocardiographic changes were related to the initial level of consciousness, to subsequent events, and to outcome after 3 months. All 61 patients had at least one abnormal electrocardiogram, but cardiac disease did not contribute directly to morbidity or mortality. Fast rhythm disturbances, ischemic changes, or both on the electrocardiograms were significantly correlated with poor outcome but not with specific outcome events, particularly not with rebleeding or cerebral ischemia. The Glasgow Coma Scale score on admission and the amount of cisternal and (to a lesser extent) intraventricular blood on the initial computed tomogram were also significantly correlated with poor outcome, but these factors only partially confounded the relation between electrocardiographic abnormalities and poor outcome. We conclude that in patients with aneurysmal subarachnoid hemorrhage, electrocardiographic abnormalities do not herald impending cardiac disease but indirectly reflect adverse intracranial factors. Electrocardiographic abnormalities may therefore have some independent value in predicting poor outcome.

Arrhythmias, Cardiac↗

Fatal ischaemic brain oedema after early thrombolysis with tissue plasminogen activator in acute stroke.

Two patients with acute major, disabling cerebral infarction with presumed middle cerebral artery occlusion were treated with the clot specific thrombolytic agent tissue plasminogen activator roughly three and a half hours after the onset of symptoms. Both patients had a normal computed tomography (CT) scan before treatment. No appreciable systemic bleeding complications occurred, apart from bruising. One patient had bleeding into the subarachnoid space from a microscopic angioma, which was found at necropsy. Haematological monitoring of the two patients showed pronounced fibrinogenolysis and alpha 2 antiplasmin consumption in one. One patient showed transient improvement during the infusion. In both cases extensive infarction, partly haemorrhagic in one, with massive concomitant oedema was found on repeated CT. Both patients deteriorated and eventually died as a consequence of transtentorial herniation. In the one patient who came to necropsy a moderate, probably pre-existing smooth stenosis of the ipsilateral carotid artery was found, all cerebral vessels being patent. It is concluded that thrombolytic treatment with a clot specific agent such as tissue plasminogen activator started three to four hours after a major ischaemic stroke may be hazardous, not because of haemorrhagic transformation of the original ischaemia but because early reperfusion may promote massive, potentially fatal cerebral oedema.

Acute Disease↗

Association of HLA-DR2 antigen with serum IgG antibodies against Borrelia burgdorferi in Bannwarth's syndrome.

The frequency of the HLA-DR2 antigen in 33 patients with clinical symptoms and signs of Bannwarth's syndrome was 33%, which was not significantly different from the 29% occurrence in 505 control subjects. However, all 11 HLA-DR2-positive patients had elevated serum levels of IgG antibodies against Borrelia burgdorferi, and these were present in 45% of 22 HLA-DR2-negative patients (P = 0.004). In the 21 patients with anti-B. burgdorferi antibodies the frequency of HLA-DR2 was 52%, which is significantly higher than the frequency in the control group (P = 0.04). The diagnosis of Bannwarth's syndrome was serologically confirmed by a positive indirect immunofluorescence assay (IFA). A negative test result does not exclude the diagnosis, as has recently been demonstrated with more sensitive techniques. The association between HLA-DR2 and a positive IFA suggests that the IFA selects a subgroup of patients with Bannwarth's syndrome and a different immune response. We could not demonstrate differences in the clinical spectrum and outcome between the two groups.

Antibodies, Bacterial↗

Cerebellar hemorrhage: diagnosis and treatment.

We have reviewed the records of 22 patients with spontaneous cerebellar hemorrhage. One question that we considered was whether the increased recognition of this disorder, since the introduction of computed tomography (CT) scanning, had brought about a change in the associated signs and symptoms, as compared with previous series. No such change was found. Nine patients died, four after operation (ventricular shunting in one, clot evacuation in one, both procedures in two patients). The five other patients were considered inoperable, because they showed signs of compression of the caudal brainstem. It is improbable that any of these five could have been saved by immediate ventricular drainage, advocated by some as the only treatment. Thirteen patients were treated conservatively and recovered, although four had a hematoma larger than 3 cm. All these patients had a Glasgow coma scale score of 11 points or more. The level of consciousness may be a better guide in management than the size of the clot.

Adult↗

Outcome of aneurysmal subarachnoid hemorrhage in patients 66 years of age and older.

The outcome at three months after aneurysmal SAH in a group of older patients and a group of younger patients is compared. The patients were admitted within 72 hours of their SAH. Of 61 patients 66 years of age and older, comprising 13% of the whole patient group, 52% died, 12% remained dependent and 36% became independent. In the younger group, 55% had an independent outcome (p less than 0.01). In contrast to what we expected in the older patient group, not extracranial, but intracranial events (re-bleeds, infarcts, hydrocephalus) were by far the most frequent cause of deterioration.

Age Factors↗

The effect of fludrocortisone acetate on plasma volume and natriuresis in patients with aneurysmal subarachnoid hemorrhage.

In order to prevent hypovolemia fludrocortisone acetate treatment was started on admission in 39 consecutive patients with CT evidence of subarachnoid hemorrhage. In 28 patients an aneurysm was proven or probable, and in 21 of these the effects of fludrocortisone acetate on sodium balance and on plasma volume could be studied. In the first five days plasma volume decreased more than 10% in four patients, decreased less than 10% in five and increased in 12. The cumulative sodium balance measured over five days was negative in seven of the 21 patients. Plasma renin values were measured in 15 of the 21 patients and also in stored samples of 18 patients who were not treated with fludrocortisone acetate. Plasma renin values were less high in patients treated with fludrocortisone acetate, regardless of the presence of a negative sodium balance. In three of the 39 patients signs of pulmonary edema developed, and low serum potassium values were observed in four of the 21 patients. In comparison with previous studies, these findings suggest that fludrocortisone acetate is an effective method of decreasing the incidence of volume depletion and negative sodium balance.

Blood Volume↗

Patterns of conduction failure in the Guillain-Barré syndrome.

Within the limits of the Guillain-Barré syndrome, the pattern of clinical deficit is variable. Motor deficit may begin proximally or distally in the extremities and sensory deficit is sometimes, but not always present. Longitudinal studies were performed in 13 patients, starting during the progressive phase. The severity of the clinical deficit was related to the amplitude of the compound muscle action potentials (CMAPs) and sensory nerve action potentials (SNAPs). Two patterns were detected, but could only be reliably distinguished during the progressive phase of the disease. (1) A length-dependent reduction of the CMAP, i.e., a progressive decrease of the CMAP on moving the stimulating electrode to more proximal stimulation sites. This could often be attributed to conduction block. In this pattern (Group A), the sensory potentials were spared with only 1 exception. These patients had motor involvement without sensory deficit and the myotatic reflexes could be preserved up to MRC grade 3 paresis. (2) A simple reduction of the CMAP, i.e., the amplitude decreased during clinical deterioration, but during a single investigation remained similar for stimulation at all levels of the nerve. In this pattern (Group B), motor and sensory fibres were similarly involved. These patients showed both motor and sensory deficit and early myotatic areflexia. The second pattern might be explained by an immunological mechanism with a predilection for those regions of the peripheral nervous system where the blood-nerve barrier is naturally deficient. In the first pattern the discrepancy between the involvement of motor and sensory fibres raises new questions, the solution of which might be of importance for the understanding of the Guillain-Barré syndrome.

Action Potentials↗

Enlargement of the third ventricle and hyponatraemia in aneurysmal subarachnoid haemorrhage.

Hyponatraemia following aneurysmal subarachnoid haemorrhage is associated with an increased risk of cerebral infarction. Whether the development of hyponatraemia was related to enlargement of the third ventricle on the admission CT scan was investigated in a consecutive series of 133 patients who were seen within 72 hours of aneurysmal haemorrhage. Hyponatraemia occurred significantly more often in patients with enlargement of the third ventricle (with or without dilatation of the lateral ventricles) than in patients with a normal ventricular system (20/41 versus 24/92, p = 0.016). After ventricular drainage, the sodium levels returned to normal in two patients in whom the size of the third ventricle decreased and not in four patients with persistent enlargement of the third ventricle. The significant relationship between enlargement of the third ventricle and hyponatraemia remained after adjustment for the amount of cisternal blood, but not after adjustment for the amount of intraventricular blood. These results suggest that the size of the third ventricle is an important but not the only factor in the relationship between acute hydrocephalus and hyponatraemia in patients with aneurysmal subarachnoid haemorrhage.

Cerebral Angiography↗

Demonstration of hysteresis in refractoriness of canine ventricular myocardium.

The properties and determinants of hysteresis during ventricular effective refractory period (VERP) measurements by an extrastimulus technique were determined in 15 anesthetized open-chest dogs as well as in isolated ventricular muscle (n = 6). VERP was determined both by decreasing the S1-S2 interval and also by increasing S1S2. Hysteresis was then calculated by subtracting the VERP obtained with the decreasing S1S2 from the VERP obtained with the increasing S1S2. The effects of basic cycle length, pulse width, stimulation intensity, and the number of basic drives on VERP and hysteresis were evaluated. VERP was shorter for long pulse width, high stimulation intensities, and shorter basic cycle lengths. These modifications were not associated with significant changes of hysteresis. VERP was shorter during decreasing S1S2 than during increasing S1S2. Hysteresis was greater with 6 basic drive cycles than with 12 (P less than 0.001) in both in vivo and in vitro preparations. The data suggest that 1) hysteresis occurs during VERP measurements; 2) hysteresis is independent of stimulation modality; and 3) hysteresis decreases with the number of basic drive cycles.

Animals↗

Anisotropic conduction and functional dissociation of ischemic tissue during reentrant ventricular tachycardia in canine myocardial infarction.

We measured the conduction characteristics at the epicardial surface of the left anterior ventricular wall in the in situ canine heart before and 3 to 5 days (n = 9 dogs) after permanent occlusion of the left anterior descending coronary artery (LAD). During ventricular stimulation generating wavefronts conducted along the longitudinal or the transverse fiber direction, 61 unipolar electrograms were recorded with a fine-meshed plaque electrode. Before occlusion, the fastest conduction velocity was consistently found in a direction perpendicular to the nearby LAD segment (longitudinal direction), and the slowest velocity in a direction parallel to the LAD segment (transverse fiber direction). In 3- to 5-day-old infarct preparations, a layer of subepicardial muscle with 1 to 3 mm thickness survived over necrotic tissue. The velocities and directions of fast and of slow conduction measured in ischemic subepicardial muscle were not significantly different from preocclusion values during stimulation at a basic rate, but excitability was found to be depressed in response to premature stimuli. Premature impulses initiated in nonischemic myocardium and conducted into ischemic tissue in the longitudinal or in the transverse directions induced sustained (greater than 100 beats) monomorphic tachycardias during which figure-eight activation patterns were mapped with sock-array electrodes. During these tachycardias, the direction of the common reentrant wavefront of the figure-eight pattern was preferentially oriented along the longitudinal fiber direction, independently of the direction of the initiating impulse. When polymorphic beats were induced, tachycardia terminated spontaneously within 20 beats, or changed to a monomorphic pattern, as described above. In conclusion, the anisotropic organization of surviving subepicardial muscle overlying an infarct provides a spatial constraint that determines a preferential direction of reentrant propagation and may contribute to sustaining monomorphic tachycardia.

Animals↗

Prediction of delayed cerebral ischemia, rebleeding, and outcome after aneurysmal subarachnoid hemorrhage.

Using logistic regression, we analyzed the predictive value of a number of entry variables with respect to the outcome variables delayed cerebral ischemia, rebleeding, and poor outcome (death or severe disability) in patients with aneurysmal subarachnoid hemorrhage. The entry variables were clinical condition on admission (grades on the Glasgow Coma Scale, Hunt and Hess system), the amount of subarachnoid and intraventricular blood and the presence of hydrocephalus on the admission computed tomogram, and antifibrinolytic treatment with tranexamic acid. We used data from a prospectively studied population of 176 patients admitted within 72 hours after subarachnoid hemorrhage. The risk of delayed cerebral ischemia was best predicted by the amount of subarachnoid blood, intraventricular blood, and antifibrinolytic treatment irrespective of clinical condition and hydrocephalus. The site of delayed cerebral ischemia was not related to the location of the subarachnoid hemorrhage. Antifibrinolytic treatment was the only entry variable (negatively) predicting the risk of rebleeding. Death or severe disability after 3 months was best predicted by the amount of subarachnoid blood and the initial clinical condition reflected by the grade on the Glasgow Coma Scale.

Blood↗

Anti-neuroblastoma cell line antibodies in inflammatory demyelinating polyneuropathy: inhibition in vitro and in vivo by IV immunoglobulin.

We tested serum from 48 patients with Guillain-Barré syndrome and 42 with chronic inflammatory demyelinating polyneuropathy (CIDP) against a selected neuroblastoma cell line (NBL 108cc15). Forty-two percent of the patients showed a positive immunofluorescence test against the NBL 108cc15. These antibodies were mainly of the IgM-class; they disappeared in all seven CIDP patients retested after improvement following intravenous IgG treatment (IV-IgG) and were present in only 5% of serum from patients with other disorders. Absorption studies showed a partial homology between the NBL 108cc15 and human sciatic nerve. In vitro studies showed that IgG from pooled normal donors (IV-IgG) inhibits the reaction between serum from a CIDP patient and the NBL cell line. This inhibition may be due to neutralization of autoantibodies against nervous tissue by anti-idiotypic antibodies in IV-IgG.

Antibodies, Neoplasm↗