Termino-lateral neurorrhaphy: The functional axonal anatomy

The goal of this study was to determine the functional axonal anatomy of a termino-lateral neurorrhaphy (TLN). We hypothesize that axons populating a TLN must relinquish functional connections with their original targets prior to establishing new connections via the TLN. Two-month-old F344 rats underwent a TLN between the left peroneal nerve and a nerve graft tunneled to the contralateral hindlimb. Three months postoperatively, an end-to-end neurorrhaphy was performed between the nerve graft and the right peroneal nerve. Four months after the second operation, contractile properties and electromyographic (EMG) signals were measured in the bilateral hindlimbs. Left peroneal nerve stimulation proximal to the TLN site resulted in bilateral extensor digitorum longus (EDL) and tibialis anterior (TA) muscle contractions, with significantly lower forces on the side reinnervated by TLN. Evoked EMGs demonstrated that the right and left hindlimb musculature were electrically discontinuous following TLN. These data support our hypothesis that axons can form functional connections via a TLN, but they must first relinquish functional connections with their original targets. © 2000 Wiley-Liss, Inc. MICROSURGERY 20:6–14 2000Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/34923/1/2_ftp.pd

Chronic pain as well as local pain in neuroma and in other usually painless conditions may be due to compressive paraspinal neural lesion

It has been little discussed why chronic pain (ChP) does not invariably accompany ChP-prone disorders. This question-driven, hypothesis-based narrative review suggests that the reason may be varying occurrence of concomitant compressive proximal (peripheral) neural lesion (cPNL). Nociceptive hypersensitivity induced and/or maintained by cPNL may be responsible for all types of non-organic ChP as well as for pain in isolated tissue conditions that are usually painless, e.g., neuroma, scar, and Dupuytren's fibromatosis. Distal and physiologically silent healed lesions may be insufficient to maintain ChP without accompanying noxious input by cPNL, e.g., by radiculopathy and entrapment plexopathies. Focal neuroinflammation induced by cPNL maintains dorsal root ganglion neuron (DRGn) hyperexcitability (i.e., peripheral sensitization) and thus fuels central sensitization (i.e., hyperexcitability of central nociceptive pathway) and a vicious cycle of ChP. DRGn hyperexcitability and cPNL may reciprocally maintain each other, because cPNL can result from reflexive myospasm-induced myofascial tension and consequent muscle imbalance- and/or pain-provoked compensatory overuse. Sensitization increases nerve vulnerability and thus catalyzes the ChP cycle. Because of these mechanisms and relatively greater number of neurons involved, cPNL, in comparison to distal neural and non-neural lesions, is more likely to maintain DRGn hyperexcitability. Sensitization is accompanied by pressure pain threshold (PPT) decrease, which can cause unusual local pain via natural pressure exerted by space occupying lesions or by their examination. Worsening of local pain is similarly explainable. Neuroma pain may be due to cPNL-induced axonal mechanical sensitivity and hypersensitivity of the nociceptive nervi nervorum of the nerve trunk and its stump

Negative pressure wound therapy: supra-physiological or just physical effects of positive pressure?

This communication provides a new insight into the unexplained physiology of beneficial effects of negative pressure wound therapy (NPWT). Possible mechanisms of beneficial effects of NPWT in failing replantation and free tissue transfer are discussed. Positive pressure generated by NPWT as well as its draining action creates exudate-free tight tissue-to-tissue interface, which may enhance neovascularization

Chronic pain: a unifying theory of mechanism

This article presents a novel practical insight into the continuing debate on the origin and mechanism of chronic pain. The paper hypothesizes that there is a common neuropathic etiology of all types of general chronic pain and that transition of acute to chronic pain involves development (or aggravation) of peripheral compressive proximal neural lesion. Proposed is a cyclic mechanism of dynamic nerve compression. Intermittent nature of proximal neural damage is postulated to be essential in maintaining nociceptive sensitization-driven chronic pain. Hypothesis-based introduction of a vicious cycle of chronic pain and explanation of persistent pain in conditions such as spinal cord injury, neuroma, and overlapping pain should stimulate relevant research. This article encourages diagnostic alertness to compressive proximal neural lesions, which are often misdiagnosed in chronic pain patients

Flap-only technique for hook nail deformity treatment: a bulky palmar flap as an alternative to the “antenna” procedure and to the thenar flap for fingertip coverage.

The hook nail (claw nail or parrot beak) deformity is caused by distal phalangeal tissue loss and volar dislocation of the distal nailbed due to wound contraction or suture. The conventional “antenna” procedure for hook nail deformity involves subungual wire pinning for straightening of the nailbed and cross finger flap or advancement flap for fingertip restoration, which may lead to recurrence due to insufficient padding of the repositioned nailbed and wound contraction. To simplify the treatment, to avoid nail traumatization by K-wiring, and to prevent deformity recurrence this report suggests ample soft tissue cushioning of the repositioned distal nailbed alone. This approach also eliminates inconveniences of the space-occupying hardware removal. A concomitant novelty is application of ulnopalmar pedicled skin flap for restoration of the fingertip. In fingertip reconstruction of the two ulnar digits, the ulnopalmar flap should also serve as a reasonable alternative to the popular thenar flap, which would be cumbersome to use for those fingers and would necessitate thumb immobilization. Pedicled palmar flaps have previously not been reported for hook nail deformity treatment and have been thought to cause interphalangeal joint contractures. In the presented two cases good aesthetic and functional results were achieved

Neurovascular compression-induced intracranial allodynia may be the true nature of migraine headache

Surgical deactivation of migraine trigger sites by extracranial neurovascular decompression has produced encouraging results and challenged previous understanding of primary headaches. However, there is a lack of in-depth discussions on the pathophysiological basis of migraine surgery. This narrative review provides interpretation of relevant literature from the perspective of compressive neuropathic etiology, pathogenesis, and pathophysiology of migraine. Vasodilation, which can be asymptomatic in healthy subjects, may produce compression of cranial nerves in migraineurs at both extracranial and intracranial entrapment-prone sites. This may be predetermined by inherited and acquired anatomical factors and may include double crush-type lesions. Neurovascular compression can lead to sensitization of the trigeminal pathways and resultant cephalic hypersensitivity. While descending (central) trigeminal activation is possible, symptomatic intracranial sensitization can probably only occur in subjects who develop neurovascular entrapment of cranial nerves, which can explain why migraine does not invariably afflict everyone. Nerve compression-induced focal neuroinflammation and sensitization of any cranial nerve may neurogenically spread to other cranial nerves, which can explain the clinical complexity of migraine. Trigger dose-dependent alternating intensity of sensitization and its synchrony with cyclic central neural activities, including asymmetric nasal vasomotor oscillations, may explain the laterality and phasic nature of migraine pain. Intracranial allodynia, i.e., pain sensation upon non-painful stimulation, may better explain migraine pain than merely nociceptive mechanisms, because migraine cannot be associated with considerable intracranial structural changes and consequent painful stimuli. Understanding migraine as an intracranial allodynia could stimulate research aimed at elucidating the possible neuropathic compressive etiology of migraine and other primary headaches

Fetal head-down posture may explain the rapid brain evolution in humans and other primates: an interpretative review

Evolutionary cerebrovascular consequences of upside-down postural verticality of the anthropoid fetus have been largely overlooked in the literature. This working hypothesis-based, narrative review postulates that the rapid evolution of the human brain has been promoted by fetal head-down position due to maternal upright and semi-upright posture. Habitual vertical torso posture is a feature not only of humans, but also of monkeys and non-human apes that spend considerable time in sitting position. Head-down position of the fetus may have caused physiologic craniovascular hypertension that stimulated expansion of the nourishing intracranial vessels and acted as an epigenetic physiological stress, which enhanced neurogenesis and eventually, along with other selective pressures, led to the progressive anthropoid brain enlargement. This article collaterally opens a new insight into the conundrum of high cephalopelvic proportions (i.e., the tight fit between the pelvic birth canal and fetal head) in phylogenetically distant lineages of monkeys, lesser apes, and humans. Low cephalopelvic proportions in non-human great apes could be accounted for by their energetically efficient horizontal nest-sleeping and consequently by their larger body mass compared to monkeys and lesser apes that sleep upright. It can be further hypothesized that brain size varies in anthropoids according to the degree of exposure of the fetus to postural verticality. The supporting evidence for this postulation includes a recent finding that in fossil hominins cerebral blood flow rate increased faster than brain volume. The approaches for testing the hypothesis include experimentation with avian embryo position in vitro, comparative cephalometry of vertex-breech twins, and Doppler assessment of the fetal cerebral circulation in maternal upright and horizontal posture. The current report opens a perspective for further related research on circadian postural behavior, obstetrics, and fetal postural cranial hemodynamics in humans and other primates. It may also be possible to expand the introduced hypothesis into a universal theory of epigenetically enhanced embryonic/fetal cerebral neurogenesis as a driver of evolutionary encephalization

Valdas Macionis' Quick Files

The Quick Files feature was discontinued and it’s files were migrated into this Project on March 11, 2022. The file URL’s will still resolve properly, and the Quick Files logs are available in the Project’s Recent Activity

Chronic pain as well as local pain in neuroma and in other usually painless conditions may be due to compressive paraspinal neural lesion

It has been little discussed why chronic pain (ChP) does not invariably accompany ChP-prone disorders. This question-driven, hypothesis-based narrative review suggests that the reason may be varying occurrence of concomitant compressive proximal (peripheral) neural lesion (cPNL). Nociceptive hypersensitivity induced and/or maintained by cPNL may be responsible for all types of non-organic ChP as well as for pain in isolated tissue conditions that are usually painless, e.g., neuroma, scar, and Dupuytren's fibromatosis. Distal and physiologically silent healed lesions may be insufficient to maintain ChP without accompanying noxious input by cPNL, e.g., by radiculopathy and entrapment plexopathies. Focal neuroinflammation induced by cPNL maintains dorsal root ganglion neuron (DRGn) hyperexcitability (i.e., peripheral sensitization) and thus fuels central sensitization (i.e., hyperexcitability of central nociceptive pathway) and a vicious cycle of ChP. DRGn hyperexcitability and cPNL may reciprocally maintain each other, because cPNL can result from reflexive myospasm-induced myofascial tension and consequent muscle imbalance- and/or pain-provoked compensatory overuse. Sensitization increases nerve vulnerability and thus catalyzes the ChP cycle. Because of these mechanisms and relatively greater number of neurons involved, cPNL, in comparison to distal neural and non-neural lesions, is more likely to maintain DRGn hyperexcitability. Sensitization is accompanied by pressure pain threshold (PPT) decrease, which can cause unusual local pain via natural pressure exerted by space occupying lesions or by their examination. Worsening of local pain is similarly explainable. Neuroma pain may be due to cPNL-induced axonal mechanical sensitivity and hypersensitivity of the nociceptive nervi nervorum of the nerve trunk and its stump