Absence of coherence effects of carrier energy and velocity in GaAs+-AlGaAs-GaAs- tunnel structures.
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Biomedical subjects
Publications and source records attributed to K Hess.
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The stapedius reflex (StR) was studied in humans by impedance audiometry. Ipsilateral and contralateral reflexes, obtained from 48 multiple sclerosis (MS) patients and 26 controls, were analysed. MS patients showed smaller reflex amplitudes, longer onset latencies and higher contralateral reflex thresholds. Using onset latencies, 33% of all MS patients had at least two abnormal ipsi- and/or contralateral StRs. If the diagnosis was MS of the definite type, this figure was 39%. The StR is therefore a useful tool for detecting a subclinical lesion in the brainstem and can contribute to the early diagnosis of MS.
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A proficient stenographer who had had cerebral metastases suffered from pure alexia for normal print but could still read stenography with ease. It is suggested that especially the visuospatial properties of stenography made possible "alternative" reading, most likely via the right hemisphere.
116 patients from 4 clinics participated in a double blind study to assess the efficacy of (BAY l 5240), a nifedipine-acebutolol fixed combination (10 mg + 100 mg), as compared to nifedipine 20 mg in essential hypertension. During the 10 week study, the mean recumbent blood pressure decreased 1 to 3 h after treatment from 175.5/105.2 to 148.3/88.0 mmHg in the BAY l 5240 group and from 174.3/102.9 to 150.3/86.5 mmHg in the nifedipine group. The results also showed a comparable decrease in the mean systolic (SBP) and diastolic (DBP) blood pressures before treatment (24 h after last tablet) and after physical exertion before and after either drug given for 4 weeks. Doubling of the dose for 4 additional weeks produced a moderate and similar additional decrease in blood pressure. The results show the possibility of treating essential hypertension with a low dose of a beta-adrenergic blocking agent in combination with 10 mg nifedipine. Both regimens were well tolerated. One patient in the BAY l 5240 group and 2 in the nifedipine group, all treated by the same investigator, were withdrawn from the study because of headache during the nifedipine pre-period.
We performed quantitative low and high frequency rotational testing in 17 patients with bilateral peripheral vestibular deficits. A characteristic pattern of decreased gain and increased phase lead at low frequencies of sinusoidal stimulation and decreased time constant to impulsive stimulation was observed in most patients. The results of caloric testing correlated with the results of low frequency rotational testing but not with the results of high frequency testing. Only 2 patients complained of oscillopsia at the time of testing and both of these had decreased vestibulo-ocular reflex gain at low and high frequencies of sinusoidal rotation.
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Quantitative rotational testing was used to study changes in the vestibulo-ocular reflex of patients with unilateral and bilateral peripheral vestibular lesions. Compared with normal subjects, the patients exhibited a characteristic pattern of decreased gain and increased phase lead at low frequencies of sinusoidal stimulation and decreased time constants on impulsive stimulation. By contrast, gain and phase measurements on high-frequency-low-amplitude sinusoidal stimulation were often normal. In the patients with bilateral lesions, the results of caloric testing correlated with the results of low-frequency rotational testing but not with the results of high-frequency testing. There are two main clinical implications of these findings. First, patients with absent response to caloric stimulation (unilateral or bilateral) may have a normal response to high-frequency sinusoidal rotation (i.e., the frequencies that constitute most natural head movements). This probably explains why such patients do not report oscillopsia. Second, low-frequency sinusoidal rotational testing and caloric testing are more sensitive than high-frequency sinusoidal or impulsive rotational testing for detecting early loss of vestibular sensitivity due, for example, to ototoxic drugs.
Electro-oculograms for monitoring eye movements and eye positions were performed in patients having a prolonged episode of acute peripheral vestibulopathy. During the course of such illness counterdrifting eye movements have been observed. Counterdrifting is defined as slow eye movements which develop in the direction opposite to the primary drift (i.e. the slow phase of spontaneous nystagmus), that occur when lateral gaze is attempted in the dark at eye positions on the side ipsilateral to the vestibulopathy. Counterdrifting appears always to be accompanied or followed by some recovery of labyrinthine function on the side of vestibular failure, and in 2 patients it was associated with so-called recovery nystagmus. It has not been observed after vestibular neurectomy. The hypothesis is put forward that counterdrifting could be an oculomotor phenomenon--centripetal drifting--similar to that underlying Alexander's modification of acute vestibular spontaneous nystagmus.
We found a consistent pattern of response to low and high frequency sinusoidal rotational testing in patients with chronic compensated unilateral and bilateral peripheral vestibular lesions. Gain (peak slow phase eye velocity/peak chair velocity) was decreased and phase lead increased at low frequencies but both measurements approached normal at high frequencies. Asymmetries in gain, when present, were approximately the same in the low and high frequency range. These changes can be explained by a simple first order linear model of the vestibulo-ocular reflex if one assumes that the goal of the compensation process is to maintain gain in the high frequency range.
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Two patients with cerebral cysticercosis are described: one with a long-standing infection with multiple intracerebral calcifications, and one who had become infected only recently. Treatment with praziquantel 50 mg/kg body weight daily for 14 days resulted in clinical and radiological improvement in the first patient, although she obviously still harbored a number of viable non-calcified parasites. The second patient was completely cured by the same praziquantel regimen. Both patients needed temporary corticosteroid treatment to suppress development of intracranial hypertension. Computerized tomographic scanning and regular measurement of serum antibody titers against cysticercal and echinococcal antigen seem appropriate methods for follow-up of the effect of chemotherapy.
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In a prospective study, 47 out of 55 patients with benign paroxysmal positional nystagmus (BPN) were reexamined after 3-41/2 years. In a third of these patients head injury was found to be the cause of positional nystagmus. In a few patients BPN was found to be directly connected with non-traumatic labyrinth affection, intermittent vertebro-basilar insufficiency, or anaesthesia. In a quarter of the patients no causative factors were found. In 44% of the patients nystagmus disappeared in an average of 8.6 months. In the follow-up a quarter of the patients (28%) still suffered regularly from positional nystagmus. Finally, in another quarter of the patients (28%), episodic nystagmus occurred over years and averaged 3.6 episodes per patient. The course of BPN is therefore more resistant and less predictable than was previously believed. However, most patients learn to adjust to the symptom and are only mildly handicapped by BPN.
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Fourteen patients with unilateral trigeminal neuropathy of unknown origin were examined 5 to 30 years after onset of the illness. In one patient, sensory loss in the area of the mental nerve was probably due to the pressure of the denture. In another three patients there were signs suggestive of multiple sclerosis. In the remaining ten patients there were no manifestation of any additive progressive disease or polyneuropathy. Unilateral trigeminal neuropathy is a benign disorder. The symptoms can persist, regress or even completely disappear. The significant delay in the reflex response of the blink reflex many years after onset of the disease probably signifies a very extensive involvement in the trigeminal nerve. In this disorder there seems to be no relationship to trigeminal neuralgia. In the examined cases viral etiology of the unilateral trigeminal neuropathy could be postulated. This disorder can extent to all three branches of trigeminal or even facial nerve.