Search PubMed⌕ Search

Biomedical subjects

J Egger

Publications and source records attributed to J Egger.

At least 55 records · Page 3Linked to original sources
PubMed1990

[Personality and coping with stress in patients suffering from functional dysphonia].

The examination covers the personality of 20 functional dysphonics, 14 individuals suffering from organic voice disorders and a group of 20 control persons when exposed to stress and its working up. In examining the group of functional dysphonics a significant positive self-assessment regarding their personality with a clear tendency to restraint has become clear. In comparison with the control persons an intensified anxiety state in situations causing stress is the result. Thus the influence of life events has been shown to have an important effect on the etiopathogenesis of functional dysphonia.

Adaptation, Psychological↗
PubMed1989

Oligoantigenic diet treatment of children with epilepsy and migraine.

We studied the role of oligoantigenic diets in 63 children with epilepsy; 45 children had epilepsy with migraine, hyperkinetic behavior, or both, and 18 had epilepsy alone. Of the 45 children who had epilepsy with recurrent headaches, abdominal symptoms, or hyperkinetic behavior, 25 ceased to have seizures and 11 had fewer seizures during diet therapy. Headaches, abdominal pains, and hyperkinetic behavior ceased in all those whose seizures ceased, and in some of those whose seizures did not cease. Foods provoking symptoms were identified by systematic reintroduction of foods, one by one; symptoms recurred with 42 foods, and seizures recurred with 31; most children reacted to several foods. Of 24 children with generalized epilepsy, 18 recovered or improved (including 4 of 7 with myoclonic seizures and all with petit mal), as did 18 of 21 children with partial epilepsy. In double-blind, placebo-controlled provocation studies, symptoms recurred in 15 of 16 children, including seizures in eight; none recurred when placebo was given. Eighteen other children, who had epilepsy alone, were similarly treated with an oligoantigenic diet; none improved.

Adolescent↗
PubMed1989

[Personality and coping with stress in patients with functional dysphonia].

The study was done to prove the etiopathogenetical power of some personality traits, proceeding life events, and strain effects when exposed to an experimental work-stress. 20 functional dysphonics, 14 individuals suffering from organic voice disorders and a group of 20 control persons were examined. The results show that the group of functional dysphonics produced a significant more positive self-evaluation regarding their personality with a clear tendency to restraint. Compared to the control group they showed a higher level of state anxiety in situations causing stress. Furthermore the influence of proceeding life events for the etiopathogenesis of functional dysphonia has become clear.

Adaptation, Psychological↗
PubMed1987

Progressive neuronal degeneration of childhood with liver disease. Computed tomographic features.

The clinical, electrophysiological and neuroradiological features of thirteen patients suffering from progressive neuronal degeneration of childhood with liver failure are presented. The disease commonly presents very early in life with progressive mental retardation, followed by intractable epilepsy, and should be suspected clinically especially if there is a family history of similar disorder in a sibling. On computed tomography there are low density regions, particularly in the occipital and posterior temporal lobes, involving both cortex and white matter, combined with or followed by progressive atrophy. Typical EEG findings may be confirmatory.

Age Factors↗
PubMed1987

Progressive neuronal degeneration of childhood (PNDC) with liver disease.

Thirteen children with progressive neuronal degeneration and liver disease are reported. Clinical features included developmental delay after a normal initial period with later onset of intractable epilepsy. The EEG showed an unusual but characteristic pattern, and visual evoked responses (VER) were abnormal. Rapidly progressive cerebral atrophy was seen on computerized axial tomography (CAT). Inheritance was consistent with an autosomal recessive trait. Pathological findings were neuronal degeneration and spongy change of the cerebral cortex. The calcarine cortex was more severely affected than other areas. Hepatic lesions included severe fatty change and cirrhosis. In six patients liver disease was detected before the onset of epilepsy and exposure to anticonvulsants. Two others were reported to have died from sodium valproate (SV) toxicity, but both had abnormal liver enzymes before treatment with SV, and in both the neuropathological findings were indicative of PNDC. During life, PNDC may be indicated by the characteristic clinical course, abnormal liver function tests, and abnormalities of EEG, VER, and CAT.

Brain↗
PubMed1986

Progressive neuronal degeneration of childhood with liver disease ("Alpers' disease"): characteristic neurophysiological features.

A clinico-pathological entity of progressive neuronal degeneration of childhood with liver disease has now been recognised. Onset is in early childhood with intractable fits and progressive dementia. EEG/ERG/VEP studies have been carried out in 12 children with this condition. In most patients the EEG showed strikingly similar and unusual abnormal patterns (high amplitude slow activity together with smaller polyspikes). The flash VEP was usually abnormal and often asymmetrical. In the appropriate clinical setting the neurophysiological features are sufficiently characteristic to aid the clinician in early diagnosis of this autosomal recessive disorder.

Atrophy↗
PubMed1986

Progressive neuronal degeneration of childhood with liver disease. A pathological study.

A clinicopathological study of 10 cases of progressive neuronal degeneration of childhood is reported. In the typical clinical course early developmental delay is followed by intractable epilepsy leading rapidly to death, in some cases in liver failure. Diagnostically useful investigations include characteristic EEG changes, evidence of progressive atrophy (particularly occipital) on CT scan, absent or reduced visual evoked responses, and biochemical evidence of abnormal liver function in many cases before commencement of anticonvulsant therapy. Siblings of 4 of the reported cases suffered a similar clinical disorder. Macroscopic appearances of the brain varied from virtual normality to severe atrophy. The cortical ribbon showed patchy lesions, but the calcarine cortex was characteristically involved, narrowed, granular and discoloured. Histological damage to the cerebral cortex was widespread but patchily accentuated. In milder lesions status spongiosus, astrocytosis and neuronal loss occurred only in the superficial cortex, in moderately affected areas deeper laminae were involved, and in the most severe lesions the entire cortex was reduced to a thin densely gliotic remnant. There was a pronounced tendency for the striate cortex to be the worst affected area. Of subcortical structures the thalamus, hippocampus and cerebellum were particularly severely involved. There was usually accompanying liver disease, particularly a subacute hepatitis comprising massive fatty degeneration, hepatocyte loss, bile duct proliferation and fibrous scarring, with or without cirrhosis. These pathological features are distinct from other combined degenerations of liver and brain and the cortical lesions differ significantly from the neuropathological sequelae of birth injury or severe epilepsy. Hepatic pathology is distinctive and does not appear to be related to drug therapy. It is concluded that these 10 cases of progressive neuronal degeneration of childhood with concomitant liver disease, together with a small number of previously reported cases, are a nosological entity which may result from an autosomal recessive inherited metabolic defect, the nature of which is at present obscure.

Brain Diseases↗
PubMed1986

[Myocardial infarct promoting type A behavior--an attempt to modify stress-inducing behavior].

To change some crucial elements of coronary-prone behaviour in cardiac patients is considered an important task of behaviour medicine, to reduce physico-chemical and, in particular, psychosocial "risk factors". The experimental study presented had examined whether the type A behaviour pattern, defined as the essential element of coronary-prone behaviour for its latent provocation of stress reactions, can be positively modified through behaviour therapy-focussed treatment within a clinical setting. A total of 91 persons, i.e. 49 recent-MI patients from an inpatient rehabilitation programme and 42 clients of a smoker counselling centre, were examined to identify type A or type B behaviour patterns (Rosenman u. Friedman, 1964). Of 39 type A post-MI patients, 13 (randomly selected) subjects were included in the "trial group" (VG), and participated, within a 4-8 week inpatient rehabilitation programme, in psychological training of stress management, relaxation, and self-control techniques; 3 patients denied participation; the remaining 23 type A post-MI patients, and the 20 type A smoker counselling clients, served as control group KG (A) and KG (B), who did not receive psychological training. Psychological and physiological parameters were assessed at the beginning (t1), the end (t2), as well as 3 and 6 months (t3 and t4) following completion of the psychological training. The results obtained confirm that the MI group includes significantly more type A persons (80 percent) than the cardiologically inconspicious control group of smokers (48 percent). Analysis of the data obtained at the various measurement points show that, as opposed to KG (A) and KG (B), significant improvements have in fact occurred in the trial group, such as reduced mental and psychovegetative stress reactions, which persisted even 3 months after programme completion.(ABSTRACT TRUNCATED AT 250 WORDS)

Arousal↗
PubMed1985

Controlled trial of oligoantigenic treatment in the hyperkinetic syndrome.

76 selected overactive children were treated with an oligoantigenic diet, 62 improved, and a normal range of behaviour was achieved in 21 of these. Other symptoms, such as headaches, abdominal pain, and fits, also often improved. 28 of the children who improved completed a double-blind, crossover, placebo-controlled trial in which foods thought to provoke symptoms were reintroduced. Symptoms returned or were exacerbated much more often when patients were on active material than on placebo. 48 foods were incriminated. Artificial colorants and preservatives were the commonest provoking substances, but no child was sensitive to these alone.

Adolescent↗