Anatomy of Peripheral Nerves, Neuromuscular Junctions, and Skeletal Muscles

2021 ◽  
pp. 41-59
Author(s):  
Jennifer A. Tracy
Keyword(s):  
Spinal Cord ◽  
Peripheral Nerves ◽  
Dorsal Root ◽  
Neuromuscular Junctions ◽  
Sensory Nerve ◽  
Spinal Nerve ◽  
Sensory Loss ◽  
Nerve Cell Body ◽  
Nerve Roots ◽  
Bipolar Neuron

After exiting the spinal cord, individual nerve roots coalesce into plexi and peripheral nerves that innervate muscle and skin. Clinical localization requires a working knowledge of this anatomy. By evaluating the distribution of muscle weakness, sensory loss, and reflexes, it is often possible to localize lesions and focus a differential diagnosis. The spinal nerve roots consist of dorsal and ventral roots that extend from the spinal cord. The dorsal root ganglion contains a bipolar neuron that is the sensory nerve cell body.

Prostaglandin E2 catabolism in the spinal nerve roots of the cat

1980 ◽  
Vol 58 (2) ◽  
pp. 227-229 ◽  
Author(s):  
I. Bishai ◽  
F. Coceani
Keyword(s):  
Spinal Cord ◽  
Nerve Root ◽  
Peripheral Nerves ◽  
Spinal Nerve ◽  
Spinal Nerve Roots ◽  
Chromatographic Mobility ◽  
Nerve Roots ◽  
Spinal Roots ◽  
Metabolic Degradation ◽  
Rate Limiting

Catabolism of prostaglandin (PG) E2 was studied in homogenates of spinal cord and spinal nerve roots of the cat. Spinal roots enzymatically converted PGE2 to a product (metabolite I) with the chromatographic mobility of 15-keto-PGE2. Little metabolic degradation occurred in the spinal cord; however, incubation of PGE2 with combined spinal cord and nerve root tissue yielded a second metabolite (metabolite II) in addition to metabolite I. Metabolite II was identified as 15-keto-13,14-dihydro-PGE2. These results prove that spinal nerve roots, unlike the spinal cord, contain 15-hydroxyprostaglandin dehydrogenase (15-PGDH) which is the major and rate-limiting enzyme in the inactivation of prostaglandins. The location and functional significance of 15-PGDH in peripheral nerves remain to be elucidated.

scholarly journals Ultrastrutitural Pathology of an Inherited Lower Motor Neuron Disease of Pigs

1994 ◽  
Vol 6 (2) ◽  
pp. 230-237
Author(s):  
Donal O'Toole ◽  
Gerald Wells ◽  
James Ingram ◽  
William Cooley ◽  
Stephan Hawkins
Keyword(s):  
Spinal Cord ◽  
Motor Neuron ◽  
Motor Neuron Disease ◽  
Peripheral Nerves ◽  
Axonal Degeneration ◽  
Clinical Signs ◽  
Spinal Nerve ◽  
Spinal Nerve Roots ◽  
Nerve Roots ◽  
Lumbar Spinal

The ultrastructural features of a recently described inherited lower motor neuron disease were studied in 5 affected pigs. Clinical signs comprised progressive ataxia and paresis of variable severity. Affected pigs, 6, 7, 15, 15, and 19 weeks of age, and 2 unrelated healthy pigs, 9 and 15 weeks of age, were anesthetized and their tissues were fixed by whole body perfusion with mixed aldehydes. From 1 or more affected pigs, samples of cervical and lumbar spinal ventral horn, lateral and ventral spinal columns, dorsal and ventral lumbar spinal nerve roots, 2 peripheral nerves (Nn. phrenicus and fibularis communis), and 2 skeletal muscles (Mm. diaphragma and tibialis cranialis) were examined ultrastructurally. There was widespread degeneration of myelinated axons in peripheral nerves and in lateral and ventral columns of lumbar and cervical segments of spinal cord. Axonal degeneration was present in ventral spinal nerve roots and was absent in dorsal spinal nerve roots sampled at the same lumbar levels. Unmyelinated axons in peripheral nerves and spinal nerve roots were unaffected. In 4 of 5 affected pigs, there were atrophic alpha motor neurons in cervical spinal cord that contained dense, round osmiophilic perikaryal inclusions up to 4 μm in diameter and round swollen mitochondria. Axonal regeneration was present in N. phrenicus of the 19-week-old affected pig that had clinical signs of longest duration (10 weeks). There was no morphologic evidence of axonal degeneration or spinal neuronal atrophy in either control pig. The ultrastructural features of this motor neuron disease distinguish it from other reported progressive spinal neuropathies of pigs.

scholarly journals Spinal Schwannomatosis

2018 ◽  
Vol 21 (1) ◽  
pp. 57-59
Author(s):  
Maurus Marques de Almeida Holanda ◽  
Daniel De Araujo Paz ◽  
Luiz Márcio De Brito Marinho Segundo ◽  
Christian Diniz Ferreira
Keyword(s):  
Spinal Cord ◽  
Peripheral Nerves ◽  
Cranial Nerves ◽  
Spinal Nerve ◽  
Rare Tumor ◽  
Spinal Nerve Roots ◽  
Nerve Roots ◽  
The Central Nervous System ◽  
Multiple Schwannomas ◽  
Strong Contrast

Schwannomatosis is a rare tumor syndrome characterized by more than one schwannoma without any evidence of other manifestations of neurofibromatosis (NF). A 32-year-old woman was admitted to our hospital because of weakness in her lower extremities. Neurological examination revealed paraparesis with hypoesthesia below T8 level. Magnetic ressonanceimaging (MRI) showed well-defined masses with strong contrast enhancement at the dorsal and lumbosacral spinal regions. After removal of six tumors compressing the spinal cord, the patient improved rapidly. The histological diagnosis was schwannomas. A detailed clinical examination and MRI scanning of the central nervous system excluded NF2. Not all patients with multiple schwannomas of cranial nerves, spinal nerve roots or peripheral nerves origin have NF-1 or NF-2. Surgery is indicated for symptomatic lesions, while asymptomatic tumors are followed conservatively.

Lumbosacral intersegmental epispinal axons and ectopic ventral nerve rootlets

1987 ◽  
Vol 67 (2) ◽  
pp. 269-277 ◽  
Author(s):  
Wesley W. Parke ◽  
Ryo Watanabe
Keyword(s):  
Nerve Root ◽  
Sensory Nerve ◽  
Conus Medullaris ◽  
Spinal Nerve ◽  
Nerve Fibers ◽  
Ventral Horn ◽  
Spinal Nerve Roots ◽  
Nerve Roots ◽  
Content Type ◽  
Almost All

✓ An epispinal system of motor axons virtually covers the ventral and lateral funiculi of the human conus medullaris between the L-2 and S-2 levels. These nerve fibers apparently arise from motor cells of the ventral horn nuclei and join spinal nerve roots caudal to their level of origin. In all observed spinal cords, many of these axons converged at the cord surface and formed an irregular group of ectopic rootlets that could be visually traced to join conventional spinal nerve roots at one to several segments inferior to their original segmental level; occasional rootlets joined a dorsal nerve root. As almost all previous reports of nerve root interconnections involved only the dorsal roots and have been cited to explain a lack of an absolute segmental sensory nerve distribution, it is believed that these intersegmental motor fibers may similarly explain a more diffuse efferent distribution than has previously been suspected.

scholarly journals Contribution of the Suppressor of Variegation 3-9 Homolog 1 in Dorsal Root Ganglia and Spinal Cord Dorsal Horn to Nerve Injury–induced Nociceptive Hypersensitivity

2016 ◽  
Vol 125 (4) ◽  
pp. 765-778 ◽  
Author(s):  
Jun Zhang ◽  
Lingli Liang ◽  
Xuerong Miao ◽  
Shaogen Wu ◽  
Jing Cao ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Dorsal Horn ◽  
Nerve Injury ◽  
Group Treatment ◽  
Dorsal Root ◽  
Polymerase Chain Reaction Analysis ◽  
Spinal Nerve ◽  
Spinal Cord Dorsal Horn ◽  
Down Regulation ◽  
Neuronal Nuclei

Abstract Background Peripheral nerve injury–induced gene alterations in the dorsal root ganglion (DRG) and spinal cord likely participate in neuropathic pain genesis. Histone methylation gates gene expression. Whether the suppressor of variegation 3-9 homolog 1 (SUV39H1), a histone methyltransferase, contributes to nerve injury–induced nociceptive hypersensitivity is unknown. Methods Quantitative real-time reverse transcription polymerase chain reaction analysis, Western blot analysis, or immunohistochemistry were carried out to examine the expression of SUV39H1 mRNA and protein in rat DRG and dorsal horn and its colocalization with DRG μ-opioid receptor (MOR). The effects of a SUV39H1 inhibitor (chaetocin) or SUV39H1 siRNA on fifth lumbar spinal nerve ligation (SNL)–induced DRG MOR down-regulation and nociceptive hypersensitivity were examined. Results SUV39H1 was detected in neuronal nuclei of the DRG and dorsal horn. It was distributed predominantly in small DRG neurons, in which it coexpressed with MOR. The level of SUV39H1 protein in both injured DRG and ipsilateral fifth lumbar dorsal horn was time dependently increased after SNL. SNL also produced an increase in the amount of SUV39H1 mRNA in the injured DRG (n = 6/time point). Intrathecal chaetocin or SUV39H1 siRNA as well as DRG or intraspinal microinjection of SUV39H1 siRNA impaired SNL-induced allodynia and hyperalgesia (n = 5/group/treatment). DRG microinjection of SUV39H1 siRNA also restored SNL-induced DRG MOR down-regulation (n = 6/group). Conclusions The findings of this study suggest that SUV39H1 contributes to nerve injury–induced allodynia and hyperalgesia through gating MOR expression in the injured DRG. SUV39H1 may be a potential target for the therapeutic treatment of nerve injury–induced nociceptive hypersensitivity.

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