axonotmesis


Also found in: Wikipedia.

axonotmesis

 [ak″son-ot-me´sis]
nerve injury characterized by disruption of the axon and myelin sheath but with preservation of the connective tissue fragments, resulting in degeneration of the axon distal to the injury site; regeneration of the axon is spontaneous and of good quality.

ax·on·ot·me·sis

(ak'son-ot-mē'sis),
Interruption of the axons of a nerve that results in degeneration of its distal (peripheral) segment (wallerian degeneration) without appreciable damage to the supporting structures (endoneurium; perineurium; epineurium) of the nerve at the site of the injury.
See also: neurapraxia, neurotmesis.
[axon + G. tmēsis, a cutting]

axonotmesis

/ax·on·ot·me·sis/ (ak″son-ot-me´sis) nerve injury characterized by disruption of the axon and myelin sheath but with preservation of the connective tissue fragments, resulting in degeneration of the axon distal to the injury site; regeneration of the axon is spontaneous and of good quality. Cf. neurapraxia and neurotmesis.

axonotmesis

[ak′sənotmē′sis]
Etymology: Gk, axon + temnein, to cut
an interruption of the axon from nerve injury, with subsequent wallerian degeneration of the distal nerve segment. Connective tissue of the nerve, including the Schwann cell basement membranes, may remain intact.

axonotmesis

Disruption and damage to axons and the myelin sheath with Wallerian degeneration, without disruption of schwann cells, the endoneurium, perineurium or epineurium, which is caused by greater and more prolonged mechanical trauma, and a longer and more profound neurosensory deficit than that seen in neuropraxia.

ax·on·ot·me·sis

(ak'son-ot-mē'sis)
Interruption of the axons of a nerve followed by complete degeneration of the peripheral segment, without severance of the supporting structure of the nerve; such a lesion may result from pinching, crushing, or prolonged pressure.
See also: neurapraxia, neurotmesis
[axon + G. tmēsis, a cutting]

axonotmesis

A severe injury to a peripheral nerve without severance of the sheath, so that, although the nerve fibres may have degenerated, regeneration and ultimate recovery of function is possible. Regeneration, if it occurs, does so at a rate of somewhat less than 1 mm per day.

axonotmesis

nerve injury characterized by disruption of the axon and myelin sheath but with preservation of the connective tissue fragments, resulting in degeneration of the axon distal to the injury site; regeneration of the axon is spontaneous and of good quality.
Mentioned in ?
References in periodicals archive ?
In an attempt to classify the physical and functional state of the damaged nerve trunk, these injuries have also been classified into three broad categories by Seddon (5): neurapraxia, axonotmesis, and neurotmesis [Table 2].
Most of the incomplete injuries in our study were consistent with pure or mixed neuropraxia and partial axonotmesis, while complete injuries represented complete axonotmesis and neurotmesis.
The observations in these studies suggested that axonotmesis occurs in the damaged brain and spinal cord (primary damage) and that even cells of the surrounding area undergo necrosis and apoptosis forming a cavity (secondary injury).
Based on the degrees of damage in the nerve and surrounding connective tissue, peripheral nerve damage may be classified as neurapraxia, axonotmesis, and neurotmesis, with the latter being a severe type of peripheral nerve injury [86].
The results of the study suggested axonotmesis, axon and myelin sheath disruption, of select branches of the left temporal nerve.
Axonotmesis is defined by the severing of axons but variable preservation of connective tissues.
However, the major kinds of experimental lesion to this nerve are axonotmesis by crushing (6) or neurotmesis followed by microsurgical nerve reconstruction (7).
18) reported 27 cases of sciatic neurological damage following THR, which were analysed with EMG (6 were neuropraxis, 20 axonotmesis and 1 neurotmesis): 8 patients recovered fully, the recovery of 7 was fair and 12 patients had considerable permanent disability.
Neurophysiological studies revealed a proximal axonotmesis with a poor prognosis.
Weakness of the extensor hallux longus may have been due to severe swelling of the foot leading to hypoxia and focal tissue necrosis of the deep fibular nerve or axonotmesis directly from the mechanism of injury.
4 There are three types of peripheral nerve injuries; neuropraxia, axonotmesis, and neurotmesis.