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Biomedical subjects

E Rumpl

Publications and source records attributed to E Rumpl.

At least 19 recordsLinked to original sources
PubMed1992

Brain death: timing of apnea testing in primary brain stem lesion.

In a 73-year-old patient complete areflexia of the cerebral and peripheral nerves following the rupture of an aneurysm of the basilar artery was diagnosed. During apnea testing the spectral analysis of electroencephalography (EEG) revealed an irreversible shift of peak from 6 to 3 Hz within the low-frequency bands. These findings suggest that apnea testing in patients with primary lesion of the brain stem should be carried out only after an isoelectric EEG.

Aged↗
PubMed1992

Cerebral sinus thrombosis in a patient with hereditary protein S deficiency: case report and review of the literature.

Hereditary protein S deficiency is an established risk factor for venous thrombosis. The common sites of thrombosis are the deep leg and pelvic veins. We report on a 38-year-old female patient with hereditary protein S deficiency and a previous history of deep leg vein thrombosis, who developed thrombosis of the cerebral straight and superior sagittal sinus while taking oral contraceptives. The diagnosis was established by computerized tomography and carotid angiography. Lysis of the thrombus occurred during heparin treatment. The hereditary nature of protein S deficiency was documented by family studies, since nine additional family members deficient in protein S were identified. Nineteen published cases of cerebral vein thrombosis and a deficiency of either anti-thrombin III, protein C, or protein S were reviewed. Compared with patients without a deficiency state, the clinical features of cerebral vein thrombosis were similar except for an earlier onset and a positive medical history of venous thromboembolic events in a considerable number of patients.

Adult↗
PubMed1991

Endocrine abnormalities in severe traumatic brain injury--a cue to prognosis in severe craniocerebral trauma?

Patients with severe craniocerebral trauma (sCCT) display metabolic and endocrine changes. The question is raised whether hormonal patterns give cues to the prognosis of outcome or not. In 21 patients the function of the adrenocortical, gonadal, thyroid and human growth hormone (hGH)-insulin system was assessed. LH, FSH, TSH, prolactin and hGH were stimulated. 3 groups of patients were formed. Group I: patients in acute phase with a Glasgow Coma Score (GCS) more than 6 (group Ia) and less than 6 (group Ib). Group II: patients in transition to traumatic apallic syndrome (TAS). Group III: patients with full-blown or resolving TAS. The values of group Ia comprised low T3, T4 and testosterone, elevated insulin, normal hGH. Group Ib had hypothyroid T3 and T4 and an attenuated response of LH, TSH, prolactin and hGH to stimulation. Group III: there was seen an endocrine normalisation with elevated T4 and TBG and an altered response of hGH and prolactin to stimulation. Endocrine abnormalities were not helpful in predicting which course, either to better or to worse, a given patient would follow.

Adolescent↗
PubMed1991

Cortical evoked potentials by stimulation of the vesicourethral junction: clinical value and neurophysiological considerations.

In 21 healthy volunteers and 42 patients with either neurogenic bladder dysfunction (24), partial peripheral denervation of the bladder (12) or nonneurogenic bladder dysfunction (6) scalp-derived evoked potentials after stimulation of the vesicourethral junction (cortical evoked potentials) were recorded. In addition, evoked potentials from the posterior tibial nerve (tibial somatosensory evoked potentials) and from the pudendal nerve (pudendal somatosensory evoked potentials) were evaluated. The results obtained in normal subjects were reproducible and comparable to those reported in previous studies. Cortical evoked potentials of vesicourethral junction consisted of a prominent negativity with a mean latency of 95 msec. Tibial and pudendal somatosensory evoked potentials were similar and showed a typical W-shaped complex. In normal subjects stimulation of the vesicourethral junction was described as a stimulus-synchronous pulsation combined with a continuous burning feeling and sometimes with a desire to void. In 4 normal subjects no cortical evoked potentials of the vesicourethral junction could be obtained because of a decreased pain threshold. In regard to clinical value, the results demonstrate that in patients with lesions of the central nervous system (in the group with cauda equina and conus medullaris lesions, and in the group with suprasacral spinal cord lesions) the results of cortical evoked potentials of the vesicourethral junction and pudendal somatosensory evoked potentials widely correlate due to similar afferent nervous pathways within the central nervous system. However, in patients with partial peripheral denervation of the bladder with suspected additional secondary local detrusor damage the results of cortical evoked potentials obtained by stimulation of the vesicourethral junction differ mostly from the results of somatosensory evoked potentials obtained by stimulation of the pudendal nerve. The pattern obtained (increased sensory and pain threshold, normal cortical evoked potentials of the vesicourethral junction with normal latencies and normal or increased amplitude) is indicative of local detrusor damage. In 21 patients the ability to detect cortical evoked potentials of the vesicourethral junction was combined with the sensation of stimulus-synchronous pulsation, whereas in the other 21 patients the absence of this sensation during stimulation was combined with the absence of cortical evoked potentials. On the other hand, no correlation was found between the ability of obtaining cortical evoked potentials of the vesicourethral junction and the stimulus-induced sensation of pain and/or desire to void.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1990

[Modifications in the Klagenfurt brain death protocol].

The Klagenfurter Protocol for determining brain death changed in some criteria during a 4 year period of use. The last version contains non-invasive diagnostic measures and includes the so-called isolated brainstem death.

Austria↗
PubMed1990

BRAINDEX: an interactive, knowledge-based system supporting brain death diagnosis.

BRAINDEX (Brain-Death Expert System) is an interactive, knowledge-based expert system offering support to physicians in decision making concerning brain death. The physician is given the possibility of communicating in almost natural language and, therefore, in terms with which he is familiar. This updated version of the system is implemented on an IBM-PC/AT with the expert system shell PC-PLUS and consists of about 430 rules. The determination of brain death is realized with backward chaining and for the optional coma-scaling a forward-chaining mechanism is used.

Brain Death↗
PubMed1988

Short latency somatosensory evoked potentials and brain-stem auditory evoked potentials in coma due to CNS depressant drug poisoning. Preliminary observations.

In patients in coma due to severe CNS depressant drug overdose the central somatosensory conduction time (CCT) after median nerve stimulation is prolonged and N20 is dispersed. Brain-stem auditory evoked potentials demonstrate delayed interpeak latencies (IPLs) I-III, III-V and I-V. This was observed in 4 out of 5 patients investigated after intake of an overdose of amitriptyline (2 cases), barbiturates, meprobamate and nitrazepam (one case each). Toxic levels of drug overdose were related to prolonged CCT and IPLs, whereas normal CCT and IPLs were found at therapeutic drug plasma levels. CCT, IPLs and dispersion of N20 decreased during the course of coma. All patients were successfully treated. It appeared that SSEP and BAEP investigations could make a distinction between a 'toxic' and a 'therapeutic' coma level in severe drug overdose. It further appeared that normalization of CCT and IPLs preceded clinical improvement.

Adult↗
PubMed1988

Central somatosensory conduction time and acoustic brainstem transmission time in post-traumatic coma.

Short-latency evoked potentials (SEPs) of the scalp and neck after median nerve stimulation and acoustic brainstem evoked potentials (BAEPs) were recorded in 85 patients in post-traumatic coma with clinical signs of brainstem impairment between days 2 and 6 after trauma. The central somatosensory conduction time (CCT), the amplitude ratio (AR) N20:N13, the interpeak latencies (IPL) I-III, III-V, I-V, and the ARs between waves I and V (I:V) and between wave I and the wave IV/V complex (I:IV/V) were calculated and related to the outcome of the patients. In cases of coma due to supratentorial lesions, CCT and ARs of SEPs were close to normal in patients with good outcome: CCT increased and ARs decreased with worsening of outcome. In cases of primary brainstem injury, a significant prolongation of CCT was also seen in patients with good recovery, whereas normal CCTs could be found in patients with severe disability and death outcome. In this case, unilateral absent scalp SEPs were frequently found. The IPLs I-III, III-V, I-V, and the ARs of BAEPs increased with worsening of outcome. Significant differences of IPL I-V and III-V (brainstem transmission time) were seen between patients with good recovery or moderate disability outcome and the patients with severe disability or death outcome. There was no difference in BAEPs between patients with primary brainstem lesion and patients with secondary brainstem lesion. Patients with bilateral absent SEPs and bilateral absent BAEPs not related to traumatic or preexisting hearing disorders died or survived severely disabled. Unilateral absence of scalp SEPs and unilateral absence of BAEPs were frequently found in patients who died or who had severe disability. Asymmetries in scalp SEPs appeared to be distributed equally to all outcome categories, but asymmetries in BAEPs increased with worsening of outcome too. In most of the patients who died or survived disabled, both SEPs and BAEPs were abnormal.

Adolescent↗
PubMed1986

Secondary cerebral amebiasis due to infection with Entamoeba histolytica. A case report with computer tomographic findings.

The clinical and serological findings and computer tomographic (CT) appearances of a case of secondary cerebral amebiasis due to Entamoeba histolytica are presented. The effect of therapy on the neurological symptoms as well as on the CT findings are described in detail. The multiple intracerebral lesions resolved almost completely and the patient survived without any neurological sequelae.

Amebiasis↗
PubMed1979

Varieties of the locked-in syndrome.

The locked-in syndrome (LiS) was broken down on the basis of neurological symptoms in 12 patients. The criteria of classical LiS are total immobility except for vertical eye movements and blinking. If any other movements are present one should consider the condition as incomplete LiS. Total immobility, including all eye movements, combined with signs of undisturbed cortical function in the EEG led to the concept of total LiS. The anatomical basis for this condition consists of lesions in both cerebral peduncles which interrupt the pyramidal and corticobulbar tracts, the supranuclear fibers for horizontal gaze and the postnuclear oculomotor fibers. As to the course, chronic and transient LiS have been described.

Adult↗
PubMed1979

Recurrent transient global amnesia in a case with cerebrovascular lesions and livedo reticularis (Sneddon Syndrome).

Eight attacks of transient global amnesia were observed in a female patient who suffered from livedo reticularis and a series of other neurological symptoms, which were transient in most stances. The neurological deficits include focal epileptic attacks, unilateral loss of vision, paresis of left arm and/or leg and dysarthria. The first amnestic attack was seen at the age of 19. The episodes lasted from a few to 3 days. The intervals between the amnestic episodes varied between a few days and 11 years. The livedo reticularis became more obvious during each neurological episode and was less pronounced during the time of remission. A benign type of essential hypertension and parproteinemia (gamma-M) was found. The investigations failed to show any evidence of essential thrombocythemia, polyarteriitis nodosa, lupus erythematodes and other immune complex diseases. The underlaying disease remained unclear.

Amnesia↗
PubMed1979

The EEG at different stages of acute secondary traumatic midbrain and bulbar brain syndromes.

One hundred and thirty EEGs were analysed from 113 patients with acute secondary traumatic midbrain and bulbar brain syndromes. The EEG pattern was related to the stage of the midbrain syndrome caused by supratentorial brain shift. A decrease in the number of different EEG patterns was associated with increasing intracranial pressure. Unfavourable prognosis was indicated by the disappearance of sleep or sleep-like activities alternating pattern and loss of reactivity. Lateralization by the EEG proved to be superior to clinical findings in full stages of the midbrain syndrome. EEG abnormalities due to the herniation itself interfered with EEG changes due to secondary circulatory, respiratory and metabolic encephalopathies. In such cases, the above mentioned regularities were blurred.

Adolescent↗
PubMed1979

[Electroencephalographic changes in coma due to hepatic insufficiency with porto-caval shunt (author's transl)].

EEG studies were done in 19 patients comatose due to severe hepatic insufficiency associated with porto-caval shunting. The neurological deficits were graded in 5 stages and related to the abnormal EEG-pattern observed in 38 records. With deepening of coma, alpha-frequencies were gradually replaced by theta- and delta-activities. The frequency of theta- and delta-runs decreased with neurological deterioration. Triphasic waves (typical and/or atypical) were seen in 26% of the records. Typical triphasic waves were found to be limited to stage 3 of coma, whereas atypical forms appeared in earlier and later stages. After infusions of L-Valin, a transient improvement and disappearance of triphasic waves was observed, but no significant effect could be established on the final course of the disease. Sleep-like potentials and the reactivity to external stimuli decreased in deep stages of coma. Severe EEG abnormalities were correlated to low cholinesterase and high lactid acid blood level, but no correlation was found to the level of ammonia.

Alpha Rhythm↗
PubMed1979

[Electro-neurological correlations in early stages of posttraumatic comatose states. I. The EEG at different stages of acute traumatic secondary midbrain and bulbar brain syndrome (author's transl)].

165 EEG were analysed from 140 patients in posttraumatic coma with secondary traumatic midbrain and bulbar brain syndrome. The EEG-pattern was related to the stage of midbrain or bulbar brain syndrome caused by supratentorial brain shift. There was a close relation between EEG-pattern and the grade of rostro-caudal deterioration. A decrease in the number of different EEG-patterns was associated with increasing intracranial pressure. An unfavourable state of coma was indicated by the disappearance of sleep or sleep-like activities, alternating pattern and loss of reactivity. In deep stages of midbrain syndrome the neurological examination reveals no lateralizing signs at all. The EEG gives the only hint to a local cerebral lesion. EEG abnormalities due to the herniation itself interferred with the EEG-changes due to secondary circulatory, respiratory and metabolic encephalopathies. In such cases the above mentioned regularities were slurred.

Adolescent↗
PubMed1978

Myotonic myopathy with painful muscle contractions and decrease of symptoms by cold.

Myotonic reaction and paresis accompanied by painful muscle contractions limited to the upper limbs, which decrease remarkably in the cold, were observed in a 29 year old man. The histological investigation revealed minimal non-specific signs of myopathy. The biochemical studies of muscular tissue contained a normal amount of myophosphorylase, acid maltase and glycogen. Ischemic work induced normal elevation of venous lactate. The activities of CPK, LDH and SGOT in the blood serum were occasionally increased. The EMG showed typical myotonic bursts and electrical silence during painful muscle contractions. Repetitive high frequency stimulation demonstrated a clear initial increase of the amplitude of action potentials followed by a decrease in the contracted muscle. The father of the patient suffered from dystrophia myotonica. This coincidnece suggests that this myotonic myopathy is a variant of dystrophia myotonica.

Cold Temperature↗
PubMed1978

Plasma lipids, coagulation factors, and fibrin formation after severe multiple trauma, and in adult respiratory distress syndrome.

Following severe multiple trauma, decreases were observed in a) Free cholesterol, b) Cholesteryl esters, c) Total phospholipids, and d) Lysolecithin. Comparatively slight changes in coagulation parameters did not differ regardless of whether pulmonary complications developed. In contrast, increased fibrin lipid complexing was more closely correlated with clinical data, because: a) Plasmatic lipids, particularly triglycerides complexed with fibrins, were elevated severalfold in patients with adult respiratory distress and fat embolism syndromes when compared with multiple trauma patients without pulmonary complications. This was independent of plasma lipid levels. b) Plasmatic triglycerides complexed with fibrins were significantly higher in patients who died than in those who survived. The considerable changes in the plasma lipid pattern following severe trauma suggest the presence of an abnormal lipoprotein with increased affinity to fibrin, thereby inhibiting fibrinolysis. This might well be one pathogenic mechanism in the development of post-traumatic respiratory distress syndrome.

Adult↗
PubMed1978

[Transitory burst-suppression pattern in endogenous-exogenous encephalopathy (author's transl)].

A status epilepticus was observed in a 22 year old female patient during endotoxinshock. The status epilepticus was treated with a high dosage of diazepame. The EEG showed a burst suppression pattern, in our case mixed by anoxia and diazepame. The burst-suppression pattern and the clinical suspicion of delayed degradation of diazepame caused by toxic hepatic failure suggested the therapy of forced diuresis. This therapy was followed by decreasing suppression periods, indicating the dominante influence of the hypnotic drug. This result shows the diagnostic as well as the therapeutic value of forced diuresis in this case.

Adult↗