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Distributing Toxin Precisely to the Motor Endplates
Published in Yates Yen-Yu Chao, Optimizing Aesthetic Toxin Results, 2022
The traditional understanding of the nerve-to-muscle interface in the extrafusal muscle fibers of human skeletal muscles is a center-located narrow band of motor endplates (MEP) (Figure 13.1). However, the exact architecture of different muscles and the innervation pattern are much more complex than the assumption of muscle center distribution. In aesthetic practice, botulinum toxin is rarely targeted merely at the center. The forehead myofibers of the frontalis muscle extend from the hairline to the eyebrow, interdigitating with orbicularis oculi muscle. If the MEPs of the frontalis muscle are all distributed about the midline of the muscle as a band, the effect of toxin should vary in intensity according to how many light chains reach that band. However, that seems to conflict with our experience, as we split our dosages into different shots; toxin injection of the forehead is generally reserved for the upper portion to avoid worsening the problem of eyelid or brow ptosis. Forehead toxin injection has even been designed in a V-shaped distribution to augment the pattern of the eyebrow arch. Muscle structures and the MEP distribution should be different from and more complex than what is taught in traditional myology (Figure 13.2).
The Spinal Cord and the Spinal Canal
Published in Bernard J. Dalens, Jean-Pierre Monnet, Yves Harmand, Pediatric Regional Anesthesia, 2019
Bernard J. Dalens, Jean-Pierre Monnet, Yves Harmand
The ventral roots are formed by efferent fibers originating in the ventral horns. The fibers emerge from the spinal cord in two or three irregular rows of rootlets (or filaments), which coalesce to form two bundles near the intervertebral foramen (Figure 1.16). The ventral root reaches the dorsal root just distal to the spinal ganglion, then issues from the dural tube as a mixed spinal nerve. Ventral roots consist only of myelinated fibers: Of these fibers, 65% are large and thick (8 to 18 μm in diameter) myelinated fibers formed by axons of the α motor neurons. They supply motor impulses to extrafusal muscle fibers.Approximately 30% are medium sized (3 to 8 μm in diameter), which correspond to axons from γ motor neurons. They supply motor impulses to intrafusal muscle fibers.The remaining fibers are very thin (diameter smaller than 3 μm and follow sympathetic pathways (B fibers). They are found only in the ventral roots emerging from T1 to L2 spinal segments. They supply visceral motor impulses at a slow rate (3 to 15 m/s) and represent preganglionic visceral efferent fibers. (Some sympathetic fibers are larger and can be up to 10 μm in diameter).
Discussions (D)
Published in Terence R. Anthoney, Neuroanatomy and the Neurologic Exam, 2017
Since publication of the works cited above, attempts to assign differential functional characteristics to nerve fibers in the various categories of the “A, B, C” and “I, II, III, IV” classifications have continued. In some cases, the association between a given functional class of fibers and a certain diameter/conduction rate category has become so strong that the alphanumeric name of the category is commonly used as a synonym for the class. The best-known afferent examples are probably “group la fibers,” defined as those arising from primary endings of muscle spindles, “group lb fibers,” defined as those arising from Golgi tendon organs, and “group II fibers,” defined as those arising from secondary endings of muscle spindles; and the best-known efferent examples are probably “the (α) fibers of α motoneurons,” defined as those innervating extrafusal muscle fibers, and “the (γ) fibers of γ motoneurons,” defined as those innervating intrafusal muscle fibers (e.g., B&K, p. 39 [including Fig. 3–3]; C&S, p. 165–171 |including figures|, 179; W&W, p. 848 [Fig. 7.26A], 857, 859).
An overview of the pharmacotherapeutics for dystonia: advances over the past decade
Published in Expert Opinion on Pharmacotherapy, 2022
O. Abu-hadid, J. Jimenez-Shahed
One of the most interesting hypotheses is that dystonia is a disorder of sensorimotor processing [142]. This concept has gained popularity due to dystonia exacerbation when performing tasks in a ‘particular’ fashion and significant reduction when performing a similar task in a ‘different’ fashion. Further support relates to the frequent presence of certain sensory tricks that can alleviate motor symptoms. Using this concept, pharmacotherapeutics that influence neural plasticity by modulating long-term depression and/or potentiation should be considered. Understanding of the alterations in various sensory modalities that are seen in dystonia has led to evaluating the role of intrafusal muscle spindles, their sensory afferents, and the gamma motor neuron that innervates them. Interestingly, botulinum toxin acts on the neuromuscular junctions of the gamma motor neurons in a similar fashion to how it acts on the alpha motor neurons, implying that botulinum toxin could have a role beyond weakening neuromuscular transmission of extrafusal muscle fibers. Indeed, intramuscular botulinum toxin has been shown in several human studies to alter central sensorimotor processing thereby possibly correcting maladaptive plastic changes [143]. This is postulated to occur either by altering peripheral sensory input to the central nervous system, or from retrograde transport of toxin [142,144].
Regenerative replacement of neural cells for treatment of spinal cord injury
Published in Expert Opinion on Biological Therapy, 2021
William Brett McIntyre, Katarzyna Pieczonka, Mohamad Khazaei, Michael G. Fehlings
Motor neurons (MNs) are detrimentally affected in SCI, where synaptic connections regulating coordinated movement are disrupted. In the healthy cord, functionally and molecularly diverse spinal MN subtypes exhibit distinct profiles of activation and patterns of connectivity. Alpha MNs (α-MNs; Fox3+/Err3-) innervate force-generating extrafusal muscle fibers that control skeletal movement through muscle contractile forces. Gamma MNs (γ-MNs; Fox3-/Err3+) are abundant in the spinal cord, where they connect to intrafusal muscle fibers in muscle spindles. They modulate the sensitivity of muscle spindles to stretch [96], as well as regulate proprioceptive afferent feedback to α-MNs [97]. In several models of degenerative MN diseases, the excitatory afferent feedback present only in α-MNs is implicated in their rapid death following disease onset [97]. Interestingly, this phenomenon is not observed in spinal cord transection, as both α-MNs and γ-MNs exhibit a higher proportion of inhibitory:excitatory inputs, which can be correlated to poor bipedal stepping [98]. This could effectively explain failed attempts to restore α-MN circuitry after spinal transection [99], where it is likely that a diverse group of MN-pools require restoration following spinalization.
Effect of oral baclofen on spasticity poststroke: responders versus non-responders
Published in Topics in Stroke Rehabilitation, 2018
Shiho Mizuno, Kotaro Takeda, Shinichiro Maeshima, Sonoda Shigeru
Clonus and increased muscle tone during fast stretch are both positive signs for an upper motor neuron lesion. The mechanism of increased muscle tone during fast stretch is summarized below. Stretch of the extrafusal muscle fiber is detected by the muscle spindle and transmitted to the central nervous system by Ia afferents that project through the dorsal roots and make connections with the α motor neurons in the spinal cord. The α-motor neurons also receive input from the upper motor neurons. After upper motor neuron lesion, a net loss of inhibition impairs the descending control over the attached α-motor neurons. Additionally, loss of inhibitory control over the interneuronal pathways in the spinal cord also occurs. Thus, increased signals are passed to the α-motor neuron, leading to excessive muscle contraction.22