Electromyographic Findings in Experimental Botulinum Intoxication

Josefsson, J.‐O.; Thesleff, S.

doi:10.1111/j.1748-1716.1961.tb02124.x

Cited by 53 publications

(17 citation statements)

References 13 publications

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“…In all three muscles, m.e.p.p.s could be recorded in every fibre examined, indicating that no or only very few fibres were denervated. This confirms the findings of others (Josefsson & Thesleff, 1961;Duchen & Stefani, 1971) that fibrillation is associated with muscle supersensitivity (see below), even in the presence of intact nerve.…”

Section: Fibrillationsupporting

confidence: 80%

Control of ACh sensitivity by muscle activity in the rat

Lømo¹,

Rosenthal²

1972

The Journal of Physiology

508

182

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1. Rat soleus and extensor digitorum longus (EDL) muscles were examined following complete blockade of sciatic nerve impulses with anaesthetics or diphtheria toxin for periods up to 14 days. 2. Muscles showed atrophy equivalent to that seen after similar periods of denervation. 3. Nerve blockade appeared to have little or no effect on neuromuscular transmission when tested by stimulation beyond the block. Normal spontaneous miniature end‐plate potentials were present. 4. Nerve impulse blockade caused the entire muscle membrane to become sensitive to iontophoretically applied acetylcholine. 5. The increase in sensitivity in soleus could be prevented by chronic nerve stimulation distal to the region of block. 6. Tenotomy, of 5‐12 days duration, which produced atrophy, had no effect on the sensitivity of soleus to acetylcholine. 7. Chronic direct stimulation of denervated soleus or EDL muscles could prevent the usual denervation supersensitivity, or cause it to decline towards normal once it had appeared. However, the sensitivity of the end‐plate region remained normal.

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Section: Fibrillationsupporting

confidence: 80%

Control of ACh sensitivity by muscle activity in the rat

Lømo¹,

Rosenthal²

1972

The Journal of Physiology

508

182

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“…Common to all procedures by which successful nerve implantation is achieved is the pre-existence of an area of high acetylcholine sensitivity in the muscle membrane. Following denervation (Ginetsinskii & Shamarina, 1942;Axelsson & Thesleff, 1959;Miledi, 1960), the action of botulinum toxin (Thesleff, 1960;Josefsson & Thesleff, 1961), and mechanical injury to the muscle (Katz & Miledi, 1964), the whole muscle membrane becomes chemosensitive. During development the entire membrane of differentiating muscle is similarly chemosensitive S. FEX AND OTHERS before it receives its motor endings (Diamond & Miledi, 1962).…”

Section: Discussionmentioning

confidence: 99%

“…The acetylcholine-sensitive area, normally restricted to the end-plate zone, increases in size until it covers the entire surface of the muscle after about a week. At the same time the fibres become spontaneously active and fibrillation potentials similar to those of denervated muscles can be recorded (Thesleff 1960;Josefsson & Thesleff, 1961).…”

Section: Introductionmentioning

confidence: 99%

Nerve implants in botulinum poisoned mammalian muscle

Fex¹,

Sonesson²,

Thesleff³

et al. 1966

The Journal of Physiology

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SUMMARY1. In albino rats the botulinum poisoned gastrocnemius muscle was supplied with an accessory motor nerve in order to investigate whether muscle fibres with structurally intact but non-transmitting synapses would accept additional innervation. As a control similar operations were made in unpoisoned rats.2. One to three months after nerve implantation the muscles were examined histologically for the presence of a new end-plate zone. In botulinum treated muscles 1662 + 165 (mean + S.D.) of new end-plates were found. In the control animals only a few (90 + 13) were observed in the immediate vicinity of the implanted nerve trunk.3. Following recovery from the paralysing action of botulinum toxin electrical stimulation of both the implanted and the original motor nerve evoked strong mechanical twitches in the gastrocnemius muscle.4. When the nerves were stimulated simultaneously little or no summation of tension occurred, indicating that presumably many of the muscle fibres with new end-plates also had functionally intact junctions from the original nerve. The presence of two end-plates in a muscle fibre was confirmed in a few experiments on single curarized fibres by intracellular recording of end-plate potentials on stimulation of each nerve.

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“…fibrillation and extra-junctional sensitivity to acetylcholine) which are characteristic of denervation. Injection of botulinum toxin causes prolonged inhibition ofthe release of acetylcholine (ACh) without degeneration of the motor nerve terminals, and leads to the development of extra-junctional sensitivity to ACh (Thesleff, 1960), fibrillation (Josefsson & Thesleff, 1961) and axonal sprouting (Duchen & Strich, 1968). Direct electrical stimulation of partially denervated muscles or muscles paralysed by botulinum toxin (Brown, Goodwin & Ironton, 1977) suppresses both the extra-junctional sensitivity to ACh and the nerve sprouting usually seen after use of these experimental procedures.…”

Section: Introductionmentioning

confidence: 99%

Prolonged Paralysis, Caused by the Local Injection of Botulinum Toxin, Fails to Cause Motor Nerve Terminal Sprouting in Skeletal Muscle of the Frog

et al. 1981

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SUMMARYInjection of a sublethal dose of botulinum toxin (type D) into the cutaneus pectoris muscle of the frog caused paralysis for about three months, but in contrast to previous studies in the mammal, did not appear to cause axonal sprouting from motor nerve terminals. In frogs in which the cutaneus pectoris had been denervated by crushing its nerve, reinnervation occurred within 2-3 weeks and axonal sprouts beyond the original end-plates were often observed. When the hypoglossal nerve was implanted into the cutaneus pectoris, crushing the original nerve caused profuse axonal growth from the implanted nerve towards the denervated end-plates within one week, whereas injection of botulinum toxin had little effect. Stimulation of the implanted nerve caused contraction of those cutaneus pectoris muscles whose original nerves had been crushed, but no response to stimulation of the implanted nerve was seen in those muscles in which botulinum toxin had been injected. The failure of botulinum toxin to induce nerve sprouting and acceptance of foreign innervation in the frog may be due to the fact that activity may play a less important role in the neural control of the physiological properties of muscle in this species than in the mammal.

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Electromyographic Findings in Experimental Botulinum Intoxication

Abstract: JOSEFSSON, J.-0. and S. THESLEFF. Electromyographic jindings in experimental botulinum intoxication. Acta physiol. scand. 1961. 51. 163-168. -

Cited by 53 publications

References 13 publications

Control of ACh sensitivity by muscle activity in the rat

Control of ACh sensitivity by muscle activity in the rat

Nerve implants in botulinum poisoned mammalian muscle

Prolonged Paralysis, Caused by the Local Injection of Botulinum Toxin, Fails to Cause Motor Nerve Terminal Sprouting in Skeletal Muscle of the Frog

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