Search PubMed⌕ Search

Biomedical subjects

F Buchthal

Publications and source records attributed to F Buchthal.

At least 37 records · Page 2Linked to original sources
PubMed1977

Peroneal muscular atrophy (PMA) and related disorders. II. Histological findings in sural nerves.

Biopsy of the sural nerves distinguished two groups of patients with peroneal muscular atrophy (Charcot-Marie-Tooth): a hypertrophic type and a neuronal type. In patients with the hypertrophic type (10 nerves), 30-100 per cent of teased fibres of the sural nerve had demyelinated segments, numerous onion-bulb formations and often an increase in endoneurial space. Large and small fibres, with a diameter of more than 7 micron and less than 5 micron were diminished in number. Regeneration was scarce. There were more fibres with 60-120 myelin lamellae than in normal nerve, suggesting an atrophy of the axon. Biopsy of 19 sural nerves of patients with the neuronal type of PMA showed loss of large fibres (more than 7 micron in diameter). The number of small fibres was normal, presumably due to regeneration, since there were many "clusters" of small myelinated fibres. Fibres with demyelinated segments and onion-bulb formations were absent or rare and the endoneurial space was normal or slightly increased. Neither in the hypertrophic nor in the neuronal type did fibre loss occur selectively among the very largest fibres. Nine nerves from patients with hereditary spastic paraplegia and from a family with tremor and spasticity in addition to PMA showed changes similar in type but often milder in degree than nerves of the neuronal type of PMA. The number of unmyelinated fibres was normal in 12 of 21 nerves from patients with PMA; it was increased in 5 and diminished in 3 nerves.

Adolescent↗
PubMed1977

Nerve biopsy and conduction studies in diabetic neuropathy.

Morphological findings in sural nerves were related to nerve conduction in 12 patients with diabetic neuropathy, five with mainly sensory involvement, four with severe, symmetrical sensory-motor polyneuropathy, and three with multiple mononeuropathy. All had loss of large and small myelinated and of unmyelinated fibres, even early in the disease; segmental remyelination was the most prominent myelin alteration in teased fibres, segmental demyelination was found in only a few fibres. Axonal degeneration and Schwann cell damage seem to proceed independently of each other. The relation between recorded conduction velocity and that expected from the diameter of the largest fibres indicated that slowing of 20 to 30% was due to causes other than fibre loss; a grossly diminished conduction velocity was caused mainly by fibre loss. Electrophysiological findings in the sural nerve were largely representative of findings in other nerves, though abnormalities were less marked in the median nerve. In half the endoneurial vessels from diabetic neuropathy the perivascular space was thickened or contained more layers of basal laminae than normal. The same abnormalities were found in one-quarter of the endoneurial vessels from other acquired neuropathies.

Adult↗
PubMed1977

Diagnostic yield of the analysis of the pattern of electrical activity of muscle and of individual motor unit potentials in neurogenic involvement.

The pattern of electrical activity and the properties of individual motor unit potentials were analysed in the flexor muscles of the forearm of 15 patients with motor neurone disease and 15 patients with a lesion of the brachial plexus. The best diagnostic yield from the pattern of electrical activity was obtained when the force was 30% of maximum: The number of spikes (turns/15 s) was diminished in 70% of the patients; none showed the increase in turns characteristic of myopathy. The decrease in the number of turns was often associated with an increased incidence of long time intervals between turns and with an increased amplitude between turns. The mean duration of individual motor unit potentials was prolonged in 78% of the patients; none showed the decrease in mean duration characteristic of myopathy. Prolongation of the mean duration of motor unit potentials produced by cooling of normal muscle, led to a decrease in the number of turns. This suggested that the diminished number of turns in neurogenic involvement was due mainly to the prolonged duration of motor unit potentials.

Adolescent↗
PubMed1977

Post-tetanic mechanical tension and evoked action potentials in McArdle's disease.

The tension produced by the cramp evoked in the adductor pollicis muscle by repetitive stimuli to the nerve (20/s for 50 s) and by full voluntary effort in the brachial biceps was measured in a patient with McArdle's disease. The contracture was 17% of the peaktetanic tension, and was not associated with action potentials. Twitches superimposed on the contracture were at most diminished to half, as were their action potentials. Both slow and fast muscle fibres participated in the contracture. The contraction time of the twitches elicited after the tetanus was prolonged more in the patient than in a normal subject of the same age. There was evidence of delayed firing, first observed 90 seconds after the peak of the contracture. The patient had electromyographic and histological signs of myopathy.

Action Potentials↗
PubMed1976

Diagnostic yield of analysis of the pattern of electrical activity and of individual motor unit potentials in myopathy.

The analysis of the pattern of electrical activity and of individual motor unit potentials in the same muscle both identified about 90% of 41 patients as having a myopathy. The pattern of electrical activity was analysed during a force which was a fixed fraction of maximum; individual motor unit potentials were analysed during weak effort. The two methods supplement each other as some of the patients were identified only by one or by the other of the two procedures. The parameter of the pattern of electrical activity which was most often abnormal was the ratio: numbers of turns to mean amplitude between turns.

Action Potentials↗
PubMed1975

Unmyelinated fibres and Schwann cells of sural nerve in neuropathy.

Electron micrographs of 45 sural nerves from patients with acquired (22) or heredodegenerative neuropathy (23) were analysed with respect to the number of unmyelinated nerve fibres, 37 nerves with respect to the number of Schwann cell sub-units and of structures connected with Schwann cells. Findings were compared with those in 6 nerves from control subjects and referred to the total number rather than to the number per mm2 to eliminate error due to increase in the transverse endoneurial area, present in more than half the diseased nerves. Ninety-one per cent of the diseased nerves showed one or several abnormalities in unmyelinated fibres of their Schwann cells. The best indicator of fibre loss was an increase in the number of Schwann cell sub-units devoid of axons, found in more than half the nerves. This was the only abnormality related with decrease in number of myelinated fibres. The increase in number of empty Schwann cell sub-units was due both to loss of unmyelinated nerve fibres and to proliferation of Schwann cells. Proliferation was indicated by the higher incidence of Schwann cell nuclei in cross-sections of diseased nerves than in controls. The earliest sign of involvement was an increase in number of profiles and of small isolated Schwann cell projections, observed in 33 of 37 diseased nerves, as the only abnormality in 7 nerves. The number of unmyelinated nerve fibres by itself was of little value to indicate loss of fibres, since regeneration often replaced or more than replaced degenerated fibres. Regeneration was indicated by an increase in number or incidence of small unmyelinated fibres, present in nearly half of 45 diseased nerves; and by an increased in the total number, present in a third of the nerves. An increase in the number of collagen pockets and of fibres undergoing degeneration (loss of organelles) and a decrease in the number of unmyelinated fibres per Schwann cell sub-units was present in only a quarter to a third of diseased nerves and was not related to other criteria of loss of fibres or of regneration.

Adolescent↗
PubMed1974

Electrophysical study of peroneal palsy.

The diagnostic yield of different electrophysiological criteria was examined to establish whether a peroneal palsy was due to compression of the nerve in the region of the capitulum fibulae. Slowing of sensory conduction along the segment of the nerve across the capitulum fibulae localized the lesion in 64% of 47 consecutive patients with a history indicating or suggesting compression of the nerve in the vicinity of the capitulum fibulae and there were no false positive findings in 18 patients whose peroneal palsy was not due to compression at the capitulum fibulae. In 20% of the patients with slowing along the segment across the capitulum, conduction velocity was normal when measured from the superior retinaculum to the popliteal fossa. Slowing along motor fibres (m. extensor digitorum brevis) localized the site of the lesion in one-third of the patients. Differences in amplitude and in split-up of the sensory responses recorded in the popliteal fossa as compared with those recorded distal to the capitulum fibulae were of limited diagnostic value because of many false positive findings among patients whose peroneal palsy was not due to compression of the nerve at the capitulum fibulae.

Action Potentials↗
PubMed1974

Electrophysiological findings in entrapment of the median nerve at wrist and elbow.

In 117 consecutive patients with carpal tunnel syndrome and 11 patients with a compression syndrome of the median nerve at elbow, motor and sensory conduction along the median and ulnar nerves and quantitative electromyography were compared with findings in 190 normal controls of the same age. In 25% of patients with carpal tunnel syndrome in whom motor conduction and EMG were normal, the lesion was located from abnormalities in sensory conduction. The fact that conduction along the same fibres was moderately slowed from digit to palm, severely slowed across the flexor retinaculum, and normal from wrist to elbow indicates that slowing was due to demyelination at the site of compression. Fifteen per cent of the patients with carpal tunnel syndrome had clinical and electrophysiological signs of ulnar involvement. In the other patients conduction along the ulnar nerve was as in 100 normal controls. Compression at the elbow was located by electromyographical findings rather than by abnormalities in conduction.

Action Potentials↗