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Biomedical subjects

J van Gijn

Publications and source records attributed to J van Gijn.

At least 307 records · Page 17Linked to original sources
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

Nonsurgical treatment of subdural empyema. Case report.

The nonsurgical treatment of a case of interhemispheric subdural empyema is reported. At the time of diagnosis, the patient had a mild decrease in consciousness and only moderate focal neurological deficits. Computerized tomography (CT) confirmed the limited (interhemispheric) extent of the intracranial infection. After drainage of the nasal sinuses and antibiotic treatment, the patient recovered, although the lesion was initially increased in size on CT scanning.

Adult↗
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

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↗
PubMed1984

Causes of acute deterioration in patients with a ruptured intracranial aneurysm. A prospective study with serial CT scanning.

The authors studied the acute neurological deterioration in 150 patients with aneurysmal hemorrhage. These patients were closely observed for a 4-week period or until death or operation. Forty-six patients suffered a total of 62 episodes of deterioration that developed within 5 minutes after aneurysm rupture; 59 of these episodes consisted of severe impairment of consciousness. Computerized tomography (CT) was performed within a few hours of the event. Serial scans were obtained at least weekly after admission. Rebleeding was diagnosed as the cause of 42 episodes (68%), including six patients who died rapidly without a repeat CT scan. The final diagnosis of the cause in other acute episodes was epilepsy (in six), acute onset of ischemia (in three), and ventricular fibrillation (in one). Ten unexplained events occurred in nine patients. Rebleeding could be excluded with confidence in nine of these events, because the residual clots had disappeared or markedly decreased on CT. It is concluded that a purely clinical diagnosis of rebleeding will be incorrect in about every third patient, even if these patients are under close observation.

Cerebral Hemorrhage↗
PubMed1983

Neostigmine-induced fasciculations--a useful diagnostic test?

Previous studies have concluded that provocation of fasciculations by neostigmine indicates a lesion of lower motor neurones. We performed 20 control experiments in 18 healthy volunteers. Ten subjects received an intramuscular injection of 1.0 mg neostigmine per 60 kg body weight. All showed fasciculations, most profusely after 30-60 minutes, on average in 6-7 muscle groups. Ten other tests with half the dosage provoked fasciculations in eight cases (2-3 muscle groups on average). Neostigmine-induced fasciculations should therefore not be interpreted as a sign of disease.

Adult↗
PubMed1983

Fatal cerebral toxoplasmosis in a bone marrow transplant recipient with leukemia.

Although opportunistic infections after allogeneic bone marrow transplantation are common, cerebral toxoplasmosis has only been reported once. We report a case of lethal cerebral toxoplasmosis in a patient with acute leukemia who had been submitted to intensive cytotoxic therapy and allogeneic marrow rescue. The clinical course was characterized by an unusually sudden neurological onset. It was remarkable that, in this case, toxoplasma serology remained repeatedly negative. The autopsy revealed that the infection also involved the myocardium. Serological data and pathology findings are presented.

Adult↗
PubMed1983

Autosomal recessive spino-olivo-cerebellar degeneration without ataxia.

Five adult siblings from a sibship of ten suffering from an external ophthalmoplegia with a spastic paraplegia are reported. In addition, optic nerve atrophy was present in three of the patients and dementia in two; extrapyramidal signs and cerebellar ataxia were found only in one patient. Contrary to earlier studies of patients with comparable neurological signs the pattern of inheritance was autosomal recessive. Neuropathological investigation of the index case, who had never shown ataxia, nevertheless showed demyelination of the spinocerebellar and the olivocerebellar pathways, and also a severe loss of Purkinje cells, of cells in Clarke's column and in the inferior olives. The dentate nucleus was severely gliotic but showed no cell loss. Earlier neuropathological investigations of this disorder, but with an autosomal dominant heredity, were incomplete. It is concluded that the five siblings of this family have a unique autosomal recessive disorder, which should be considered a distinct entity.

Aged↗
PubMed1983

Ataxic tetraparesis from lacunar infarction in the pons.

A 45-year-old woman with hypertension suffered four episodes of right hemiparesis and two attacks of left hemiparesis, within seven months. On examination she showed weakness and cerebellar ataxia of all four limbs. Computed tomography demonstrated a radiolucent area in the base of the pons, consistent with lacunar infarction.

Cerebellar Ataxia↗
PubMed1983

Spectrophotometric analysis of CSF after subarachnoid hemorrhage: limitations in the diagnosis of rebleeding.

We studied the course of CSF xanthochromia after subarachnoid hemorrhage by serial spectrophotometric analysis of lumbar CSF in 15 patients without clinical or CT evidence of rebleeding. The xanthochromic index rose in some patients up to the seventeenth day, and the proportion of oxyhemoglobin or the absolute concentration of hemoglobin often fluctuated. Therefore, rebleeding can be demonstrated in lumbar CSF only by increased xanthochromia, if previous samples had shown a decrease. These criteria could be applied in only 6 of 17 consecutive patients with rebleeding as demonstrated by CT, and they were met in 5.

Bilirubin↗