PubMed Health⌕ Search

Biomedical subjects

J Fagius

Publications and source records attributed to J Fagius.

At least 55 records · Page 3Linked to original sources

Sympathetic outflow in man after anaesthesia of the glossopharyngeal and vagus nerves.

Bilateral lidocaine blocks of glossopharyngeal and vagus nerves in the neck were made in two healthy subjects to achieve deafferentation of arterial and cardiopulmonary baroreceptors. Microelectrode recordings of muscle nerve sympathetic activity (MSA) were made in one peroneal nerve; in one subject skin sympathetic activity (SSA) was recorded simultaneously in the other peroneal nerve. Following the nerve block in the neck there was a strong increase of MSA accompanied by temporary hypertension and tachycardia. The normal cardiac rhythmicity of MSA disappeared and the outflow appeared as bursts of impulses of variable duration occurring in a slow, irregular rhythm. Thus MSA became similar to SSA, but the activities never became synchronous. During the nerve block arousal stimuli evoked single bursts of MSA, a reflex response which normally occurs in SSA but not in MSA. It is concluded that (1) cardiac rhythmicity of MSA is due to baroreceptor influence; (2) a low level of MSA at rest depends on strong baroreceptor inhibition and not on a weak central drive; (3) central sympathetic outflows to skin and muscle are similar though not identical and the different characteristics normally observed are due to a large extent to different modulatory influences from afferent activity (presumably of baroreceptor origin) in glossopharyngeal and vagus nerves; and (4) baroreceptor deafferentation resulting in resting tachycardia and hypertension may explain sympathetic hyperactivity in the Guillain-Barré syndrome.

Adult↗

Sympathetic outflow to the hand in patients with Raynaud's phenomenon.

Microelectrode recordings of skin nerve sympathetic activity were made in the median nerve supplying the right hand of nine patients with Raynaud's phenomenon and 10 control subjects. With subjects warmed up (finger temperature 33 to 34 degrees C) different manoeuvres were used to evoke strong, single sympathetic bursts, giving rise to vasoconstriction of the same magnitude in patients and control subjects. Immersion of the contralateral hand in ice water for 1 min elicited an increase in sympathetic outflow without any difference between patients and control subjects. It is concluded that neither hypersensitivity of the vessels to strong sympathetic bursts, nor abnormal increase of sympathetic outflow following shortlasting, local cold exposure, was present in the patients. A possible change of the functional relationship between nerve and vessel, the importance of which is uncertain, was observed in the patient group. The study provides direct evidence against a primary sympathetic hyperfunction and indirect support for a local fault mechanism in Raynaud's phenomenon.

Adrenergic Fibers↗

Guillain-Barré syndrome following zimeldine treatment.

Thirteen cases of the Guillain-Barré syndrome are reviewed, all occurring with a similar relationship to recent commencement of treatment with the antidepressive drug zimeldine. The risk of developing Guillain-Barré syndrome was increased about 25-fold among patients receiving zimeldine, as compared with the natural incidence of the disorder. The cases described provide strong evidence that Guillain-Barré syndrome may occur as a specific, probably immunologically mediated, complication of drug therapy.

Aged↗

Peripheral and autonomic nerve function in glucose intolerance.

In 19 middle aged subjects, glucose intolerant according to WHO criteria, obtained from a health survey, peripheral and autonomic nerve function were studied in comparison with 25 control subjects with normal glucose tolerance. Clinically detectable signs of peripheral nerve dysfunction were not more common in glucose intolerant subjects than in the control group. In measurements of sensory thresholds for vibration, nerve conduction velocities and autonomic nerve function, small differences, mainly non-significant, were found in favour of the controls. It is concluded that minor reduction of some peripheral nerve function may be associated with glucose intolerance, but it is not readily demonstrated. Clinically apparent polyneuropathy is not likely to develop.

Autonomic Nervous System↗

Beneficial effects of plasma exchange in acute inflammatory polyradiculoneuropathy.

The results of a controlled trial in which 38 patients with severe acute inflammatory polyradiculoneuropathy took part indicate that plasma exchange favourably influenced the course of the disease. Significant benefits were seen in time until onset of improvement, course of muscular weakness, improvement in disability grades over the first 2 months, and working capacity after 1 month. Cost-benefit analysis showed that the exchange treatment resulted in net financial savings. The results suggest that plasma exchange may have a role in the treatment of severe acute inflammatory polyradiculoneuropathy.

Acute Disease↗

Plasma exchange in patients with Guillain-Barré syndrome: clinical improvement in patients with serum IgG antibodies to peripheral nerve tissue.

The mixed hemagglutination technique was used to demonstrate IgG antibodies to peripheral nerve tissue in sera from patients with Guillain-Barré syndrome. The clinical effect and the effect on the antibodies of plasma exchange (PE) were examined in 24 patients, 16 patients with acute form and 8 patients with the chronic form of the disease. Neurological examination with muscle testing and neurophysiological examination of the patients were performed before and immediately after the PE. Before PE antibodies were detected in sera from 15 of the patients. These patients showed clinical improvement during the treatment, however in one of the patients only after a time interval of 2 weeks. After PE, antibodies were detected in sera from only 3 of the patients. The 9 patients without detectable antibodies showed no clinical improvement.

Adolescent↗

Microneurographic evidence of excessive sympathetic outflow in the Guillain-Barré syndrome.

We investigated 3 patients with moderate to severe Guillain-Barré syndrome (GBS) who had transient hypertension and tachycardia during the illness. Microelectrode recordings of muscle nerve sympathetic activity were made in the peroneal nerve once during the acute phase when hypertension and tachycardia were present and twice after recovery from these symptoms. During the acute recording the level of sympathetic activity was considerably higher than after recovery, when the two recordings showed reproducible levels. The normal cardiac rhythmicity was preserved except during brief periods in one patient. Control recordings were made during the acute phase and after recovery in 4 GBS patients without clinical signs of autonomic involvement and twice in 15 healthy subjects. In each control subject the level of sympathetic activity was reproducible, although recordings were made with intervals of two days to four years. The findings show that in the GBS with transient elevations of blood pressure and heart rate there is sympathetic hyperactivity. It is suggested that the increased activity is due to reduced inhibition of the vasomotor centres caused by lesions of the afferent limbs of arterial and perhaps mainly intrathoracic baroreflexes.

Adult↗

Chronic cryptogenic polyneuropathy. The search for a cause.

91 patients with chronic symptoms of polyneuropathy without any previously known underlying disorder underwent extensive clinical and laboratory investigations in an attempt to reveal the cause of the polyneuropathy. A definite or probable origin of polyneuropathy was detected in only 8 patients (9%) and a possible but questionable cause was found in 16 (17%), while the cause in 74% remained undetermined. In only 1 patient could effective treatment be instituted. No evidence was found for an association between polyneuropathy and reduced glucose tolerance without manifest diabetes mellitus. The findings suggest that only a limited investigation is justified in most cases of chronic polyneuropathy without obvious cause.

Adult↗

Acute pandysautonomia and severe sensory deficit with poor recovery. A clinical, neurophysiological and pathological case study.

A patient with acute loss of autonomic functions and virtually all afferent functions of peripheral nerves is described. The course was chronic and the outcome fatal. The clinical course was followed with measurements of sensory thresholds and conduction velocities, autonomic tests and microneurographic recordings. Neuropathological changes were severe and localised in the peripheral nervous system. Previously reported similar cases were reviewed. It was concluded that acute pandysautonomia is a disorder similar to the Guillain-Barré syndrome; the course is often protracted and residual neurological deficit common.

Adult↗

Treatment of the Guillain-Barré syndrome by plasmapheresis.

Treatment by plasmapheresis was performed in eight adult patients with the Guillain-Barré syndrome. One patient with a chronic relapsing form underwent four separate courses of plasmapheresis and her condition improved rapidly each time. Of seven patients with acute Guillain-Barré syndrome, the condition of three improved markedly, in one partially, and in three it did not improve in association with treatment. There were no apparent differences concerning clinical and neurophysiologic parameters between those whose conditions improved and those whose conditions did not.

Adolescent↗

Microneurographic findings in diabetic polyneuropathy with special reference to sympathetic nerve activity.

Microneurographic recordings of naturally occurring nerve activity in the median or peroneal nerve were made in 25 patients with diabetes mellitus, 17 of whom had signs of polyneuropathy. In patients without polyneuropathy, the electrical findings did not differ from those in healthy subjects. In patients with polyneuropathy, sensory afferent impulses were always normal qualitatively, whereas muscular afferent activity was weak or entirely absent in some patients. Sympathetic activity, if found, showed normal characteristics in muscle and skin fascicles, except that it was difficult to obtain a good signal-to-noise ratio. In 16 of 25 recordings with the electrode positioned intraneurally, sympathetic activity could not be detected in patients with polyneuropathy. The failures correlated with impaired skin sympathetic effector organ responses and reduction of motor nerve conduction velocity. The results suggest that impairment of sympathetic outflow occurs frequently in diabetic polyneuropathy and that sympathetic involvement occurs earlier than in many other types of polyneuropathy.

Diabetic Neuropathies↗

The clinical effect and the effect on serum IgG antibodies to peripheral nerve tissue of plasma exchange in patients wit Guillain-Barré syndrome.

The mixed haemagglutination technique was used to demonstrate IgG antibodies to peripheral nerve tissue in sera from patients with the Guillain-Barré syndrome. The clinical effect and the effect on the antibodies of plasma exchange were examined in 18 patients. Neurological examination with muscle testing and neurophysiological examination of the patients were performed before and immediately after plasma exchange. Before the exchange antibodies were detected in sera from 11 of the patients. These patients showed clinical improvement during the treatment. After plasma exchange, antibodies were detected in sera from only two of the patients. The seven patients without detectable antibodies showed no clinical improvement.

Adolescent↗

Variability of sensory threshold determination in clinical use.

The variability of perception threshold determination for vibration, tactile stimuli and thermal stimuli, with instruments intended for clinical use, was studied in 13 healthy subjects and 27 patients with chronic polyneuropathy. Normal thresholds for tactile and thermal stimuli were determined in 51 healthy subjects. Determinations were made for vibration on hand, lower leg and foot, for touch on pulp of forefinger and great toe and for temperature on hand and foot. Normal thresholds for both tactile and thermal stimuli were age-dependent. Short-term variation, with intervals of some minutes between determinations, remained within 8-18% change from first value. Long-term variation, with intervals of days to some weeks, was pronounced for all types of threshold, with extremes of -90% and +256% change from first determination in 3 or 4 subsequent determinations. Variation was most marked for tactile stimuli and smallest for vibration, but magnitude and pattern of variation was similar for all sensory modalities and for both patients and healthy subjects. Confidence intervals, derived from analysis of variance, showed than as an average a change of less than -60% or greater than +150% from the initial value was needed to ascertain with 95% probability that a subsequent value will reflect a true change of sensory threshold. Basing every threshold value on 2 or more measurements per occasion will reduce the confidence interval. The main cause of variability seems to be central processing mechanisms, i.e. the psychological variability. With proper attention to the variability, sensory threshold determinations should still be a valuable aid in clinical practice and clinical research.

Adult↗

Effects of aldose reductase inhibitor treatment in diabetic polyneuropathy - a clinical and neurophysiological study.

The efficacy of treatment with an aldose reductase inhibitor (1,3-dioxo-1 H-benz-de-isoquinoline-2(3H)-acetic acid, AY-22,284, Alrestatin) on peripheral nerve function in diabetic polyneuropathy was assessed. Thirty patients with long-standing diabetes and slight to moderate neuropathy participated in the double-blind placebo trial. Clinical examination, sensory threshold determinations for vibratory, tactile and thermal stimuli, conduction velocity measurements and studies of automatic function were performed to evaluate the treatment. Significant differences favouring Alrestatin over placebo were found for many of the measured variables, whereas no changes occurred on placebo. The apparent improvement of neuropathy occurred despite persisting hyperglycaemia. The results indicate that aldose reductase inhibitor treatment may be of value in diabetic polyneuropathy, and provide support for the sorbitol pathway hypothesis of diabetic polyneuropathy.

Adult↗

Sympathetic reflex latencies and conduction velocities in normal man.

(1) Micro-electrode recordings were made of multi-unit sympathetic activity in skin or muscle branches of the median nerve at the elbow and the peroneal nerve at the fibular head in 69 healthy subjects. In some recordings changes in skin resistance and pulse plethysmograms were monitored within the receptive field of the impaled fascicles. Conduction velocities in postganglionic sympathetic fibres were measured either directly in double nerve recordings (9 subjects) or indirectly by determining the latency of either of two sympathetic reflexes. For skin nerve sympathetic activity (SSA) the excitatory reflex response to an electrical skin stimulus was used and for muscle nerve sympathetic activity (MSA) the inhibitory baroreflex response to single arterial pulse waves. (2) For MSA, reflex latencies were 0.90--1.13 s in median and 1.22--1.54 s in peroneal nerve recordings. Corresponding latencies for SSA were 0.48--0.66 s and 0.72--0.91 s, respectively. Reflex latency showed a positive correlation with body height and with length of the extremity recorded from. From the correlation with extremity length, average conduction velocities for MSA in median and peroneal nerves were calculated to be 0.74 and 1.11 m/s, respectively. Corresponding figures for SSA were 1.69 and 1.16 m/s. (3) With direct determinations of conduction velocities average values for MSA (comprising mainly vasoconstrictor fibres) in median and peroneal nerves were 0.72 and 1.09 m/s, respectively. With direct SSA determinations, sympathetic bursts containing only vasoconstrictor impulses (giving plethysmographic responses but no changes of skin resistance) had lower conduction velocities than bursts containing only sudomotor impulses (giving electrodermal but no plethysmographic responses) or a mixture of sudomotor and vasoconstrictor impulses. Average values (0.77 and 1.27 m/s, respectively) were similar in median and peroneal recordings. (4) It is concluded that determination of reflex latency is a useful indirect measure of conduction velocity in sympathetic postganglionic fibres.

Adult↗

Sympathetic reflex latencies and conduction velocities in patients with polyneuropathy.

(1) Micro-electrode recordings of multi-unit sympathetic activity were attempted in skin or muscle branches of the peroneal nerve at the fibular head and the median nerve at the elbow in 41 patients with polyneuropathy of different causes. An indirect measure of sympathetic conduction velocity was obtained by determining the latency of either of two sympathetic reflexes. For skin nerve sympathetic activity (SSA) reflex responses to electrical skin stimuli were used and for muscle nerve sympathetic activity (MSA) reflex inhibition caused by the arterial pulse wave. The skin sympathetic function was also evaluated by measuring changes in skin resistance and finger/toe pulse plethysmograms. Motor conduction velocities were measured with surface electrodes. (2) In muscle (but not in skin) nerve fascicles afferent mass activity in myelinated fibres was often weak or absent. (3) There was a significant relationship between symptoms of autonomic impairment and impaired skin resistance and/or plethysmographic responses. There was also a relationship between impairment of these responses and failure to detect SSA. (4) Failure to find sympathetic activity occurred in 60% of diabetic patients but only in 27% of the whole material. When found, sympathetic activity had normal appearance and sympathetic reflex latencies were normal irrespective of degree of slowing of motor conduction velocity. (5) The results suggest that in polyneuropathy conduction velocities of post-ganglionic sympathetic fibres are normal as long as the fibres conduct. Degeneration of sympathetic fibres may be especially common in diabetic neuropathy.

Adult↗