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Nerve Injury
418
NERVE INJURY
Cros, D., Gominak, S., Shahani, B. T., et al. (1992). Comparison of electrical and magnetic stimulation in the supraclavicular region. Muscle Nerve 15, 587–590. Gominak, S. C., and Cros, D. (1993). A 66-year-old woman with a 19-year history of progressive weakness of all extremities. N. Engl. J. Med. 329, 1182–1190. Hall, S. M., Hughes, R. A., Atkinson, P. E., et al. (1992). Motor nerve biopsy in severe Guillain–Barre syndrome. Ann. Neurol. 31, 441–444. Kaku, D. A., England, J. D., and Sumner, A. J. (1994). Distal accentuation of conduction slowing in polyneuropathy associated with antibodies to myelin-associated glycoprotein and sulphated glucuronyl paragloboside. Brain 117, 941–947. Kimura, J. (1979). The carpal tunnel syndrome: Localization of conduction abnormalities within the distal segment of the median nerve. Brain 102, 619–635. Lachman, T., Shahani, B. T., and Young, R. R. (1980). Late responses as aids to diagnosis in peripheral neuropathy. J. Neurol. Neurosurg. Psychiatry 43, 156–162. Lewis, R. A., Sumner, A. J., and Shy, M. E. (2000). Electrodiagnostic features of inherited demyelinating neuropathies: A reappraisal in the era of molecular diagnosis. Muscle Nerve 23, 1472–1487. Menkes, D. L., Hood, D. C., Ballesteros, R. A., et al. (1998). Root stimulation improves the detection of acquired demyelinating polyneuropathies. Muscle Nerve 21, 298–308. Rosenbaum, R. B., and Ochoa, J. L. (1993). Acute and chronic mechanical nerve injuries: Pathologic, physiologic and clinical correlations. In Carpal Tunnel Syndrome and Other Disorders of the Median Nerve, pp. 197–232. Butterworth-Heinemann, Boston. Roth, G., and Magistris, M. R. (1987). Detection of conduction block by monopolar percutaneous stimulation of the brachial plexus. Electromyogr. Clin. Neurophysiol. 27, 45–53. Triggs, W. J., Cros, D., Gominak, S. C., et al. (1992). Motor nerve inexcitability in Guillain–Barre syndrome. The spectrum of distal conduction block and axonal degeneration. Brain 115, 1201–1302.
Nerve Fibers see Axons
Nerve Injury Encyclopedia of the Neurological Sciences Copyright 2003, Elsevier Science (USA). All rights reserved.
INJURY can occur at any point along the length of a
peripheral nerve as it courses from the root through the plexus and then to the target organ (Fig. 1). There are a number of mechanisms whereby peripheral nerves may be directly traumatized,
Figure 1 Innervation of a muscle by a myelinated motor nerve. An internode represents a segment of axon surrounded by a myelin sheath. Each one is separated from its neighbor by a node of Ranvier.
including compression, traction, drug injection, and laceration. Furthermore, damage may also occur from toxins, ischemia, infection, and physical agents such as freezing, electrical current, and radiation exposure. In order to understand the pathophysiology of peripheral nerve injury, it is important to be familiar with the anatomical components of a peripheral nerve and its supporting tissues (Fig. 2). One of the principal sites of peripheral nerve injury is the axon, which is composed largely of neurofilaments and microtubules that ferry substances (e.g., organelles) between the nerve cell body and the axon terminal. Injury may also affect specialized neuronal sheath cells called Schwann cells, which are intimately associated with all peripheral nerve axons. In larger (myelinated) nerves, these cells generate concentric layers of myelin around the axon to form a sheath, whereas in smaller (unmyelinated) nerves a single Schwann cell associates with several axons via a single layer of myelin. Trauma can also affect the connective tissue that invests individual axons (endoneurium), nerve fascicles (perineurium), and entire nerve trunks (epineurium), one of the principal functions of which is to protect the underlying nerve from injury by mechanical deformation. A layer of loose areolar tissue, the mesoneurium, extends from the epineurium to surrounding tissue structures and may serve as an endoneurial cushion as well as allowing a degree of mobility in the longitudinal plane. Finally, injury can lead to peripheral nerve ischemia by compromising blood flow through the extensive network of blood vessels that course throughout the connective tissue sheath and the nerve.
NERVE INJURY
Cros, D., Gominak, S., Shahani, B. T., et al. (1992). Comparison of electrical and magnetic stimulation in the supraclavicular region. Muscle Nerve 15, 587–590. Gominak, S. C., and Cros, D. (1993). A 66-year-old woman with a 19-year history of progressive weakness of all extremities. N. Engl. J. Med. 329, 1182–1190. Hall, S. M., Hughes, R. A., Atkinson, P. E., et al. (1992). Motor nerve biopsy in severe Guillain–Barre syndrome. Ann. Neurol. 31, 441–444. Kaku, D. A., England, J. D., and Sumner, A. J. (1994). Distal accentuation of conduction slowing in polyneuropathy associated with antibodies to myelin-associated glycoprotein and sulphated glucuronyl paragloboside. Brain 117, 941–947. Kimura, J. (1979). The carpal tunnel syndrome: Localization of conduction abnormalities within the distal segment of the median nerve. Brain 102, 619–635. Lachman, T., Shahani, B. T., and Young, R. R. (1980). Late responses as aids to diagnosis in peripheral neuropathy. J. Neurol. Neurosurg. Psychiatry 43, 156–162. Lewis, R. A., Sumner, A. J., and Shy, M. E. (2000). Electrodiagnostic features of inherited demyelinating neuropathies: A reappraisal in the era of molecular diagnosis. Muscle Nerve 23, 1472–1487. Menkes, D. L., Hood, D. C., Ballesteros, R. A., et al. (1998). Root stimulation improves the detection of acquired demyelinating polyneuropathies. Muscle Nerve 21, 298–308. Rosenbaum, R. B., and Ochoa, J. L. (1993). Acute and chronic mechanical nerve injuries: Pathologic, physiologic and clinical correlations. In Carpal Tunnel Syndrome and Other Disorders of the Median Nerve, pp. 197–232. Butterworth-Heinemann, Boston. Roth, G., and Magistris, M. R. (1987). Detection of conduction block by monopolar percutaneous stimulation of the brachial plexus. Electromyogr. Clin. Neurophysiol. 27, 45–53. Triggs, W. J., Cros, D., Gominak, S. C., et al. (1992). Motor nerve inexcitability in Guillain–Barre syndrome. The spectrum of distal conduction block and axonal degeneration. Brain 115, 1201–1302.
Nerve Fibers see Axons
Nerve Injury Encyclopedia of the Neurological Sciences Copyright 2003, Elsevier Science (USA). All rights reserved.
INJURY can occur at any point along the length of a
peripheral nerve as it courses from the root through the plexus and then to the target organ (Fig. 1). There are a number of mechanisms whereby peripheral nerves may be directly traumatized,
Figure 1 Innervation of a muscle by a myelinated motor nerve. An internode represents a segment of axon surrounded by a myelin sheath. Each one is separated from its neighbor by a node of Ranvier.
including compression, traction, drug injection, and laceration. Furthermore, damage may also occur from toxins, ischemia, infection, and physical agents such as freezing, electrical current, and radiation exposure. In order to understand the pathophysiology of peripheral nerve injury, it is important to be familiar with the anatomical components of a peripheral nerve and its supporting tissues (Fig. 2). One of the principal sites of peripheral nerve injury is the axon, which is composed largely of neurofilaments and microtubules that ferry substances (e.g., organelles) between the nerve cell body and the axon terminal. Injury may also affect specialized neuronal sheath cells called Schwann cells, which are intimately associated with all peripheral nerve axons. In larger (myelinated) nerves, these cells generate concentric layers of myelin around the axon to form a sheath, whereas in smaller (unmyelinated) nerves a single Schwann cell associates with several axons via a single layer of myelin. Trauma can also affect the connective tissue that invests individual axons (endoneurium), nerve fascicles (perineurium), and entire nerve trunks (epineurium), one of the principal functions of which is to protect the underlying nerve from injury by mechanical deformation. A layer of loose areolar tissue, the mesoneurium, extends from the epineurium to surrounding tissue structures and may serve as an endoneurial cushion as well as allowing a degree of mobility in the longitudinal plane. Finally, injury can lead to peripheral nerve ischemia by compromising blood flow through the extensive network of blood vessels that course throughout the connective tissue sheath and the nerve.