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Biomedical subjects

A Hijdra

Publications and source records attributed to A Hijdra.

At least 73 records · Page 4Linked to original sources
PubMed1988

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↗
PubMed1988

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↗
PubMed1987

Mental changes in subcortical arteriosclerotic encephalopathy.

We describe six patients with chronic hypertension, atherosclerotic vascular disease and periventricular leukoencephalopathy (PVL) on CT. PVL was combined with cortical infarcts in one and with lacunar infarcts in five patients. On neuropsychological examination all patients showed the characteristic features of a subcortical type of mental deterioration. Clinico-radiologic correlation suggests a direct association of PVL and subcortical dementia, and it is argued that prominent cortical features in the dementia of patients with vascular disease and PVL suggest the concomitant presence of Alzheimer's disease.

Aphasia↗
PubMed1987

Rerupture of intracranial aneurysms: a clinicoanatomic study.

In a series of 176 prospectively studied patients who survived for at least 24 hours after aneurysmal subarachnoid hemorrhage, 39 had at least one computerized tomography (CT)-proven rebleed within 4 weeks after the first rupture. There were peaks in the incidence of rebleeding at the end of the 2nd and 3rd weeks. Sudden loss of consciousness occurred in 35 patients, preceded in one-third of them by headache. A sudden increase in headache was a symptom of rebleeding in only one patient. Loss of brain-stem reflexes was recorded in 13 patients, respiratory arrest in six, and both symptoms in eight patients. Apnea was temporary in 11 patients. Rebleeding occurred as gross intraventricular hemorrhage in 20 patients, as a space-occupying hematoma in four, as both types of hemorrhage in three, and as a purely subarachnoid hemorrhage in 12. The location of the rebleed could not be inferred from the clinical features. Rebleeding was fatal in 51% of cases (two of 12 patients with a purely subarachnoid hemorrhage, and 18 of the other 27 patients (p less than 0.005)). The risk of rebleeding could not be predicted from the patients' clinical condition on admission or from the amount of subarachnoid blood identified on the initial CT scan. The risk of further rebleeding was significantly increased in survivors of a first rebleed (47%: p less than 0.01). Only seven (18%) of the 39 patients with rebleeding had survived at 3 months after the initial hemorrhage.

Adolescent↗
PubMed1987

Cerebral blood flow imaging with thallium-201 diethyldithiocarbamate SPECT.

Thallium-201 diethyldithiocarbamate ([201TI]DDC) was studied in humans as an agent for cerebral blood flow imaging. Brain uptake proved to be complete 90 sec after injection with no appreciable washout or redistribution for hours. Intracarotid injection suggested an almost 100% extraction during the first passage. Whole-body distribution studies demonstrated a brain uptake of 4.3% of the dose compared with 0.9% for [201TI]chloride. No differences were found in the distribution of [201TI]DDC versus [201TI]chloride in other organs. After the injection of 3 mCi 201TI, good quality single photon emission computed tomographic (SPECT) images of the brain were obtained with both a rotating gamma camera and a multidetector system. In ischemic brain disease, perfusion defects were easily demonstrated. We conclude that [201TI]DDC is a suitable radiopharmaceutical for SPECT studies of cerebral blood flow.

Aged↗
PubMed1986

Functional brain imaging with I123-amphetamine. First experience in the Netherlands.

Single Photon Emission Computed Tomography (SPECT) has been used in the last five years as a method for cerebral bloodflow imaging, especially in cerebral infarction. In this study the first experiences in the Netherlands are presented. In 57.6% of our patients lesions, defined by SPECT were larger than those found by CT. This was not only seen in patients with cerebral infarction but also in hematoma. In 33.3% the size of the lesions were comparable. In 10 out of 14 patients with a solitary lesion in one hemisphere a decreased perfusion was seen in the contralateral cerebellar hemisphere. This phenomenon is called crossed cerebellar diaschisis. One patient with probably Alzheimer disease, showing a specific flow pattern, is discussed.

Aged↗
PubMed1986

Delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage: clinicoanatomic correlations.

Fifty-seven of 176 prospectively studied patients with aneurysmal subarachnoid hemorrhage (SAH) developed delayed cerebral ischemia. Clinical features included hemispheric focal signs (13), decrease in level of consciousness (14), or both (30), and mutism (15). Forty-seven patients showed hypodense lesions on CT in one (19) or multiple vascular territories (22), or diffusely in one or both hemispheres (6). Twenty-eight had symmetric decrease in ventricular size. Of 18 autopsied patients, only 1 had a purely univascular lesion. The clinical, CT, and pathologic features suggest that delayed cerebral ischemia after SAH is a multivascular or diffuse process in most patients.

Adult↗
PubMed1985

Hyponatremia and cerebral infarction in patients with ruptured intracranial aneurysms: is fluid restriction harmful?

We studied retrospectively the relationship between hyponatremia and cerebral infarction in 134 consecutive patients with aneurysmal subarachnoid hemorrhage. In 44 patients sodium levels fell below 135 mmol/L on at least two consecutive days between the second and the tenth day after the hemorrhage. Twenty-five of these patients fulfilled the criteria for the syndrome of inappropriate secretion of antidiuretic hormone. Cerebral infarction developed in 27 of the 44 patients with hyponatremia and in 19 of the 90 patients with normal serum sodium levels (p less than 0.001). Cerebral infarctions were more often fatal in patients with hyponatremia (p less than 0.01). Twenty-six of the 44 patients had been treated with fluid restriction to correct the serum sodium levels, and infarctions developed in 21. Fluid restriction to correct hyponatremia appears to be potentially dangerous in patients with aneurysmal subarachnoid hemorrhage.

Cerebral Infarction↗
PubMed1985

Volume depletion and natriuresis in patients with a ruptured intracranial aneurysm.

We studied the sodium balance and changes in plasma volume by an isotope dilution technique in the first week after an aneurysmal subarachnoid hemorrhage in 21 patients. In 11 of the patients, the plasma volume decreased by more than 10%. This was accompanied by a negative sodium balance and hyponatremia in 6 patients, a negative sodium balance without hyponatremia in 4 patients, and a positive sodium balance in 1 patient. Together with a decrease in plasma volume, blood urea nitrogen content increased and body weight decreased. Three patients developed hyponatremia without a decrease in plasma volume. Serum vasopressin was measured in 14 of the 21 patients. The values were elevated on admission and declined in the first week, regardless of the presence of hyponatremia. These findings indicate that natriuresis and hyponatremia in aneurysmal subarachnoid hemorrhage reflect salt wasting and not inappropriate secretion of antidiuretic hormone and that these changes should be corrected by fluid replacement rather than by fluid restriction.

Arginine Vasopressin↗
PubMed1985

Perimesencephalic hemorrhage: a nonaneurysmal and benign form of subarachnoid hemorrhage.

We studied 28 patients with subarachnoid hemorrhage and normal angiograms. On early CT (within 5 days) in 13 cases, blood was seen mainly or only in the cisterns around the midbrain. This pattern of hemorrhage was found in only 1 of 92 patients with a ruptured aneurysm. None of the unexplained perimesencephalic hemorrhages was associated with intracerebral hematoma or intraventricular hemorrhage. The clinical features also differed from those of aneurysmal hemorrhage; loss of consciousness was rare, and after 3 months, all 13 patients had returned to normal life. The cause of this benign disorder remains elusive, but a venous or capillary source seems likely.

Humans↗
PubMed1985

Acute hydrocephalus after aneurysmal subarachnoid hemorrhage.

Hydrocephalus, defined as a bicaudate index above the 95th percentile for age, was found in 34 (20%) of 174 prospectively studied patients with subarachnoid hemorrhage (SAH) who survived the first 24 hours and who underwent computerized tomography (CT) scanning within 72 hours. The occurrence of acute hydrocephalus was related to the presence of intraventricular blood, and not to the extent of cisternal hemorrhage. The level of consciousness was depressed in 30 of the 34 patients. Characteristic clinical features were present in 19 patients, including a gradual obtundation after the initial hemorrhage in 16 patients and small nonreactive pupils in nine patients (all with a Glasgow Coma Scale score of 7 or less). In the remaining 15 patients (44%), the diagnosis could be made only by CT scanning. After 1 month, 20 of the 34 patients had died: six from rebleeding (four after shunting), 11 from cerebral infarction (eight after an initial improvement), and three from other or mixed causes. Only one of nine patients in whom a shunt was placed survived, despite rapid improvement in all immediately after shunting. The mortality rate among patients with acute hydrocephalus was significantly higher than in those without, with the higher incidence caused by cerebral infarction (11 of 34 versus 12 of 140 cases, respectively; p less than 0.001). Death from infarction could not be attributed to the extent of cisternal hemorrhage, the use of antifibrinolytic drugs, or failure to apply surgical drainage, but could often be explained by the development of hyponatremia, probably accompanied by hypovolemia.

Acute Disease↗
PubMed1985

Source of fibrin/fibrinogen degradation products in the CSF after subarachnoid hemorrhage.

In 48 patients with a subarachnoid hemorrhage, levels of fibrin/fibrinogen degradation products (FDP's), total protein, and plasminogen were measured in the cerebrospinal fluid (CSF) between Days 9 and 15 after the bleed. Of these 48 patients, 22 received tranexamic acid. Despite a significant reduction in the incidence of rebleeding in patients taking tranexamic acid, no difference in FDP levels was found between patients receiving tranexamic acid and a control group of patients who were not; nor was any relationship evident between FDP levels and rebleeding. In patients with detectable levels of FDP's, CSF protein and plasminogen values were also increased, and FDP's were found more frequently in the CSF of patients with an impaired level of consciousness or with a neurological deficit. These findings suggest that in the 2nd week after subarachnoid hemorrhage, the presence of FDP's in the CSF reflects a damaged blood-CSF barrier rather than ongoing local fibrinolysis in the subarachnoid space. A finding of FDP's in the CSF is, therefore, an unreliable monitor of antifibrinolytic treatment in subarachnoid hemorrhage and cannot be used for selecting patients at high risk of rebleeding.

Blood Physiological Phenomena↗
PubMed1984

Antifibrinolytic treatment in subarachnoid hemorrhage.

We enrolled 479 patients with subarachnoid hemorrhage in a multicenter, randomized, double-blind, placebo-controlled trial to determine whether treatment with the antifibrinolytic agent tranexamic acid improves outcome by preventing rebleeding. At three months there was no statistical difference between the outcomes in the tranexamic acid group and the control group. Of the 173 patients who died, 84 had received tranexamic acid and 89 placebo (95 per cent confidence interval for the difference in mortality rate, -6 to 11 per cent). Similarly, when analysis was restricted to patients with an angiographically demonstrated aneurysm, there was no significant difference between the groups. This absence of effect was not due to a lack of antifibrinolytic action, since the rate of rebleeding was reduced from 24 per cent in the control group to 9 per cent in the tranexamic acid-treated group (chi-square = 18.07, P less than 0.001), but resulted from a concurrent increase in the incidence of ischemic complications (15 per cent in the control group and 24 per cent in the tranexamic acid group; chi-square = 8.07, P less than 0.01). We conclude that until some method can be found to minimize ischemic complications, tranexamic acid is of no benefit in patients with subarachnoid hemorrhage.

Cerebral Angiography↗
PubMed1984

Balint's syndrome in a man with border-zone infarcts caused by atrial fibrillation.

A 70-year-old man showed Balint's syndrome and other signs of bilateral posterior-hemisphere dysfunction of acute onset without initial unconsciousness. A computerized tomographic scan showed bilateral infarcts in the posterior arterial border-zone areas. Clinical evidence suggests that hypotension at the onset of atrial fibrillation caused these infarcts. There was a marked difference in the time course of recovery between the left and the right infarct which demonstrated that the elements of Balint's syndrome disappeared together with the left-hemisphere symptoms while the right-hemisphere symptoms were still present.

Aged↗
PubMed1984

Respiratory arrest in subarachnoid hemorrhage.

Sudden loss of consciousness and cardiorespiratory disorders occurred in 43 of 254 patients with subarachnoid hemorrhage. Two patients had ventricular fibrillation, 37 had one or more episodes with a disturbance of respiratory rhythm that required assisted ventilation, and 4 died suddenly without recorded vital signs. Sixteen patients recovered after resuscitation. The outcome could not be predicted at an early stage from the anatomic type of hemorrhage on CT, the initial presence or absence of brainstem reflexes, or the type of cardiorespiratory disorder. Spontaneous respiration and responsiveness returned within 1 hour in all patients who recovered.

Arrhythmias, Cardiac↗