Search PubMed⌕ Search

Biomedical subjects

J van Gijn

Publications and source records attributed to J van Gijn.

At least 289 records · Page 16Linked to original sources
PubMed1987

Digoxin-like immunoreactive substance in patients with aneurysmal subarachnoid haemorrhage.

Digoxin was measured by radioimmunoassay in the plasma of 25 patients with aneurysmal subarachnoid haemorrhage who had not received digoxin treatment. After heating the plasma an endogenous substance cross reacting with antibodies to digoxin was identified in 18 cases. The presence of this substance was significantly related to the total amount of blood and to the presence of blood in the frontal interhemispheric fissure and could not be explained by hypertension or intake of water and sodium. A negative sodium balance and volume depletion occurred more often in patients who were positive for digoxin, but this relation did not reach statistical significance. It is concluded that a digoxin-like natriuretic factor is released in response to a subarachnoid haemorrhage, probably as a result of hypothalamic damage.

Aged↗
PubMed1987

Effects of low doses of aspirin, 10 mg and 30 mg daily, on bleeding time, thromboxane production and 6-keto-PGF1 alpha excretion in healthy subjects.

To compare the long term effects of two low doses of aspirin taken daily, we performed a placebo-controlled cross-over study in 19 normal subjects. Aspirin 10 mg daily for 3 weeks caused a significant inhibition by 61 +/- 12 percent of platelet thromboxane B2 generation but had no effect on the Simplate bleeding time. Aspirin 30 mg daily for 3 weeks reduced thromboxane B2 production by 94 +/- 5 percent and caused a significant prolongation of the bleeding time, 1.6 times the control value. No cumulative inhibitory effects were observed after the first week of treatment. Both doses did not effect the urinary excretion of 6-keto-PGF1 alpha.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Chronic forms of Borrelia burgdorferi infection of the nervous system.

Three European patients had chronic active forms of Borrelia burgdorferi infection of the nervous system, with high titers of antibodies to this spirochete in serum and CSF. Two patients had meningitis for 3 to 4 years, with remissions in one and slowly progressive symptoms in the other. Both had CT lucencies in the basal ganglia. The third patient had lumbosacral plexus neuropathy for 1 year. All three patients responded to intravenous penicillin treatment.

Borrelia Infections↗
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↗
PubMed1986

Acute disseminated encephalitis documented by magnetic resonance imaging and computed tomography. Report of a case.

A 16-year-old girl developed left hemispheric deficits, which were followed by clouding of consciousness, quadriplegia, and subcortical blindness. Although we could not demonstrate a recent viral infection, the clinical features, laboratory and radiologic findings strongly suggested the diagnosis acute disseminated encephalitis. Cerebrospinal fluid abnormalities incompletely correlated with the clinical course. In contrast, X-ray computed tomography and particularly magnetic resonance imaging of the head closely reflected disease and improvement.

Acute Disease↗
PubMed1986

Hypotonia: an erroneous clinical concept?

Muscle tone, if defined as the resistance felt during passive movement of an extremity, is generally explained by the appearance of stretch reflexes. Consequently, hypotonia would be caused by a decrease or disappearance of these reflexes. This notion has never been challenged by experiments that reproduce the clinical situation. In this study two clinical tests, passive extension and flexion movements at the knee joint and a free fall of the lower leg with gravity, were applied to 72 control legs and 35 'hypotonic' legs. EMG activity was measured in the quadriceps muscle. Despite special care to obtain relaxation in the subjects, the majority of control legs showed voluntary EMG activity on passive movement. During free fall, long-latency reflexes were present in a minority of normal subjects, but the velocity of falling in these legs was within the range obtained in the legs without any EMG spikes. If the fall time was prolonged beyond the upper limit of relaxed legs, this was the result of voluntary activity, confirmed by EMG measurements. Therefore, long-latency stretch reflexes play no role in the clinical assessment of 'normal tone'. This conclusion was further supported by the observation that 'hypotonic' legs did not fall faster than relaxed control legs. If patient's legs feel flaccid this is the result of weakness preventing voluntary activity. Passive movements during the clinical examination are of great value, but only to detect spasticity or rigidity.

Adolescent↗
PubMed1986

Apnoea testing to confirm brain death in clinical practice.

In six patients an apnoea test was carried out to confirm brain death according to a protocol recommended in the USA. After ten minutes' apnoea the pCO2 did not reach the target value of 7.98 kPa (60 mm Hg) in any of these patients. This was caused by the low initial value and the slow increase of the pCO2. Moreover, we could not confirm the belief that the necessary duration of the apnoea test can be predicted by assuming a rise of the pCO2 of 0.33 kPa (2.5 mm Hg) per minute.

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↗