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Biomedical subjects

J R Ostergaard

Publications and source records attributed to J R Ostergaard.

At least 37 records · Page 2Linked to original sources

Epileptic fits or infantile masturbation?

Two infants, one girl, 5 months old, and one boy, 6 months old, presented with rhythmic and sustained motor activities of a stereotyped nature accompanied by moaning and grunting, facial flushing and altered awareness. The episodes occurred frequently and were initially believed to be epileptic. Normal electroencephalograms during the fits, lack of response to antiepileptic medication given to one child and careful reviewing of videotape recordings, enabled us eventually to diagnose the 'seizure-like' episodes as masturbatory activity.

Cerebral Cortex↗

Benign coital headache.

We studied the natural history of patients with a diagnosis of benign coital headache who presented to a private neurological clinic between the years 1978 and 1991. Thirty-two patients (24M, 8F) were invited to participate and 26 patients (83%) responded. The period of follow-up ranged from six months to 14 years (median 6 years). Thirteen patients (50%) had recurrent attacks of coital headache epochs separated by intervals of up to 10 years. Eleven of these patients suffered a concomitant primary headache whereas this was present in only one of those patients without recurrent attacks of coital headache (p < 0.001). In all but one patient, who had a transient blurred vision, the headache was not accompanied by nausea, vomiting, visual disturbances, sensory/motor disturbances, or unconsciousness. We concluded that benign coital headache can be clearly distinguished from headaches due to cerebral aneurysm or arteriovenous malformation rupture. The presence of a concomitant primary headache syndrome is a risk-factor for recurrence of coital headache.

Adult↗

[Infection as the precipitating factor in Schönlein-Henoch purpura].

Shönlein-Henoch's purpura (SHP) is a form of generalized vasculitis. SHP is characterized by a haemorrhagic eruption, colicky abdominal pain, renal involvement with haematuria and proteinuria, arthralgia and cerebral symptoms in the form of headache and seizures. Retrospective investigations have revealed that infection with microorganisms may precipitate SHP. The authors were able to support this observation by means of a prospective investigation. 2/3 of the 26 children in the investigation had symptoms of infection one to two weeks prior to the onset of symptoms of SHP. Ten children had definite positive signs of prior infection. The course of the sedimentation rate and leukocyte counts also support the assumption of previous infection.

Bacterial Infections↗

Headache as a warning symptom of impending aneurysmal subarachnoid haemorrhage.

About half of the aneurysm patients admitted to neurosurgical departments experience warning symptoms in the form of minor bleeding episodes days or even several months before a major haemorrhage occurs. Headache is the most common symptom of this warning leak, occurring in 9 out of 10 patients. The onset of headache is sudden and is unusual in severity and location, being unlike any headache the patient has otherwise experienced. It is frequently accompanied by transient nausea, vomiting, visual disturbances or meningism. Medical advice may be sought by the patient but all too often the diagnostic importance of a warning headache is missed. It is misinterpreted as attacks of migraine, tension headache, the 'flu, sinusitis, or a "sprained neck". A more vigilant attention to the presence of a warning headache probably offers the greatest opportunity for altering the otherwise serious natural history of aneurysmal subarachnoid haemorrhage. If a warning headache is suspected, lumbar puncture is the examination of choice, once CT scanning has ruled out an intracranial mass lesion.

Headache↗

Neurologic manifestations of Schönlein-Henoch purpura.

The presence of a possible cerebral involvement in Schönlein-Henoch Purpura was investigated in a prospective study comprising 26 children. A hampering headache accompanied by behavioural changes was present in 8 patients (31%). No cases of seizures, aphasia, ataxia, pareses or cerebral haemorrhage were found. EEG-abnormalities like slow wave foci, sharp waves, and paroxysms were demonstrated in 12 patients (46%) during the acute phase of the disease. The EEG-changes were transient but persisted in 4 patients during a follow-up period lasting one year. A significant association was found between the presence of headache and an abnormal EEG-tracing.

Child↗

Aetiology of intracranial saccular aneurysms in childhood.

Intracranial saccular aneurysms in childhood are rare neurosurgical lesions, occurring in 1-3% of large epidemiological aneurysm series. Analysis of previous reports indicates several distinct characteristics of this entity. First, there is a predominant male:female ratio approaching 2:1. Second, a disproportionately high number of these aneurysms arise at peripheral locations on the arterial tree. Third, approximately half of them are large or even giant aneurysms. These identifiable characteristics suggest that aneurysms in the younger age group may be a distinct pathophysiological entity from aneurysm in the adult population. In adults, epidemiological evidence indicates that 'acquired' factors such as hypertension, cigarette smoking, alcohol consumption, and oral contraceptive use together with 'intrinsic' or 'vascular' factors are causally related to the formation and rupture of cerebral aneurysms. Inherently, some of the 'acquired' factors must be of minor importance in aneurysm formation and rupture in childhood, whereas the 'intrinsic' factors may have a greater importance.

Age Factors↗

Gamma-aminobutyric acid concentration in lumbar cerebrospinal fluid from patients with febrile convulsions and controls.

The cerebrospinal fluid (CSF) concentration of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) was analysed in 41 children with febrile convulsions (FC), 41 febrile controls of similar age (control group 1), and 59 controls, who had no fever and/or were outside the age range for FC (control group 2). A significant correlation between CSF-GABA and age was demonstrated for controls (1 + 2) (r = 0.63, p less than 0.00001), as well as for patients with FC (r = 0.42, p = 0.003). Patients with FC did not differ significantly from control group 1 in respect to CSF-GABA. Duration of FC was related to both CSF-GABA and age (GABA: r = -0.29, p less than 0.05; age: r = -0.32, p less than 0.05). For 56 controls (1 + 2) greater than 1 year of age, a significant negative correlation between CFC-GABA and body temperature was found (r = -0.34, p = 0.01). The low CSF-GABA in the FC-labile age group, the negative correlation of CSF-GABA to body temperature, and the negative correlation of the duration of FC to both CSF-GABA and age, all indicate that GABA could be of importance in the pathophysiology of FC.

Adolescent↗

Risk factors in intracranial saccular aneurysms. Aspects on the formation and rupture of aneurysms, and development of cerebral vasospasm.

Intracranial saccular aneurysms have been a well-known clinical and pathological entity for over two centuries. The pathophysiological events that lead to aneurysm formation and rupture are, however, poorly understood. Besides an HLA-associated genetic factor, the most widely accepted risk factors are arterial hypertension, female gender, and increasing age. Some aneurysm patients have a deficient formation of Type III collagen. This seems to interfere with the mechanical integrity of the cerebral arterial wall encouraging aneurysm formation. While some of the risk factors may be involved in the process of aneurysm formation, others may be of importance in the actual aneurysm rupture. Medical and surgical developments have only had a slight impact on mortality rates from aneurysm rupture. The principal cause of death and disability is cerebral arterial spasm. Considerable effort has been expended in investigating the etiology of this phenomenon. Previous studies have failed to yield conclusive evidence of the causative agent(s) or the nature of cerebral artery narrowing. The time course of vasospasm after the onset of subarachnoid hemorrhage is consistent with an immune-mediated response, and more recent observations suggest that immunological processes including activation of the complement system may be involved. Missed minor bleeding episodes may thus be a risk factor for aneurysm patients in respect to the development of cerebral vasospasm.

Adolescent↗

Reversible pulmonary arterial hypertension in a 6-year-old girl with extrinsic allergic alveolitis.

A case is reported of a 6-year-old girl who developed extrinsic allergic alveolitis due to hypersensitivity to her pet budgerigars. Pulmonary artery pressure measurements obtained by a cardiac catheterization demonstrated a significant increase in the pulmonary vascular resistance during the acute stage of the disease. Six months after exclusion of exposure to the budgerigars the hemodynamic of the pulmonary circulation was normalized. The present case thus shows that a reversible increase in the pulmonary vascular resistance in extrinsic allergic alveolitis of childhood may occur without development of an irreversible pulmonary fibrosis.

Alveolitis, Extrinsic Allergic↗

Deficiency of reticular fibers in cerebral arteries. On the etiology of saccular aneurysms in childhood.

A 5-year-old, previous healthy, girl developed a large hematoma of the right cerebral hemisphere and died. An aneurysm was strongly suggested. As previously found in adult aneurysm patients, histological and morphometric investigations showed an abnormality of the reticular fibers of the cerebral arteries. We suggest that arterial deficiency of reticular fibers is of importance in formation and rupture of saccular aneurysm, also in childhood.

Age Factors↗

Histological and morphometric observations on the reticular fibers in the arterial beds of patients with ruptured intracranial saccular aneurysms.

Histological and morphometric studies on the collagenous, reticular, and elastic fibers of the tunica media were performed on the middle cerebral and brachial arteries of patients with ruptured intracranial saccular aneurysms and controls. There was no difference between aneurysm patients and controls in the amount of collagenous and elastic fibers. The amount of reticular fibers was, however, reduced about 35% in aneurysm patients within both the middle cerebral artery (P less than 0.01) and the brachial artery (P less than 0.02). The reticular fibers were irregularly distributed and often appeared shorter and coarser than normally. The observations point to a generalized abnormality of the arterial bed in some patients with rupture of saccular aneurysms.

Adult↗

Immune complexes and complement activation following rupture of intracranial saccular aneurysms.

Circulating immune complexes (CIC) and complement activation (plasma C3d levels) were monitored during a 2-week period in patients with ruptured cerebral aneurysms and also in patients with cerebral hematoma unrelated to saccular aneurysms. Thirteen of 18 aneurysm patients were found to have CIC on admission as compared to three of 21 healthy blood donors (p less than 0.001). The presence of CIC in aneurysm patients was associated with a poor prognosis. Eight of nine patients who developed angiographic vasospasm had CIC on admission compared with one of four without vasospasm. Patients with vasospasm showed a twofold increase in plasma C3d levels at the time when the spasm occurred, whereas no significant changes in the C3d concentration could be demonstrated in aneurysm patients without spasm or in patients with hematoma unrelated to aneurysm rupture. These findings suggest that immunological processes involving complement-activating immune complexes are involved in the pathogenesis of cerebral vasospasm following rupture of saccular aneurysms.

Adult↗

Collagen type III deficiency in patients with rupture of intracranial saccular aneurysms.

Samples of the middle cerebral artery (MCA) and the brachial artery were obtained post mortem from 14 patients who died following rupture of intracranial saccular aneurysms and from a control group of 14 age- and sex-matched patients who died of causes unrelated to aneurysm rupture. The biomechanical properties of ring-shaped arterial specimens were investigated by loading the specimens at a constant deformation rate until rupture. The relative amounts of collagen type I and type III were determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) studies of cyanogen bromide peptides of collagen prepared from the arterial samples. A deficiency of collagen type III was demonstrated in specimens of the MCA in six of 14 patients with a ruptured intracranial saccular aneurysm. This deficiency was not accompanied by alterations in the mechanical arterial strength but resulted in a significant increase in the extensibility at stress values corresponding to blood pressures between 100 and 200 mm Hg. No difference was found between aneurysm patients and the control group in regard to the biomechanical properties of the brachial artery, despite the presence of a significant deficiency of collagen type III. The increase in vascular extensibility of the MCA may represent alterations in the fibrous structure and functional integrity of the cerebral arteries of aneurysm patients with collagen type III deficiency. Together with aggravating hemodynamic stresses, this deficiency may be an important factor in the pathogenesis of saccular aneurysms.

Brachial Artery↗