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The essential features of the peripheral neuromuscular system are motor nerves, sensory nerves, autonomic nerves, the neuromuscular junction (NMJ), and muscle fibers.
Motor neurons originate in the spinal cord and brainstem and innervate skeletal muscle ( Fig. 2.6.1 ). Each motor neuron innervates many muscle fibers, but each muscle fiber is innervated by only one motor neuron. The innervation ratio is the number of muscle fibers innervated by a single motor neuron for a particular muscle; the innervation ratio is lowest for extraocular muscles and greatest for large antigravity muscles. The inset of Fig. 2.6.1 shows a diagrammatic representation of a motor nerve innervating a muscle fiber. With denervation, there is loss of motor axons, so surviving axons sprout processes to innervate the denervated muscle fibers; this process increases the innervation ratio.
Sensory neurons have cell bodies in the dorsal root ganglia or sensory ganglia of the cranial nerves. Most sensory neurons are bipolar, with peripheral projections transducing sensory input into action potentials and central projections conducting action potentials to the spinal cord and brainstem. Fig. 2.6.1 shows sensory nerve endings and their projections through afferent nerve fibers.
Peripheral nerves are surrounded by processes of Schwann cells, which form myelin sheaths around the nerves.
The NMJ transduces action potentials of the motor nerves into muscle fiber action potentials. Acetylcholine (ACh) is released by the presynaptic terminal when it is depolarized. The ACh crosses the synaptic cleft and binds to ACh receptors (AChR); this binding causes channels to open and allows ionic flux in and out of the cell. The preponderance of ionic flux is sodium into the cell, which depolarizes the muscle fiber membrane to the point that it reaches threshold; a muscle fiber action potential is then produced.
The muscle fiber membrane conducts action potentials to the T-tubule system, which triggers release of calcium (Ca + ) from the sarcoplasmic reticulum. Calcium binds to troponin, producing a conformational change in the actin and allowing interaction with myosin, thereby producing muscle shortening.
Normally, each motor neuron action potential produces one action potential in each of its muscle fibers. Many disorders interfere with this one-to-one transmission; these include disorders of the NMJ and of peripheral nerve and muscle. Most disorders cause failure of muscle fiber potential generation, although a few (e.g., myotonia) cause repetitive discharge of muscle fibers innervated by a single axon.
The subsequent discussion in this chapter concerns organization of this peripheral system. Detailed discussion of diagnosis and disorders is presented in Chapter 3.6 . In preparation for that discussion, we present the essentials of clinically relevant anatomy. As with the remainder of this book, this discussion assumes basic knowledge of neuroanatomy and neurophysiology.
The brachial plexus is formed from cervical nerve roots from C4 to T2, although the contributions from C4 and T2 are minor. The output from the brachial plexus is the major nerves radial, median, ulnar, and musculocutaneous and a host of smaller nerves, the most important of which are dorsal scapular, suprascapular, upper and lower subscapular, and lateral pectoral nerves.
We recommend committing to memory the anatomy of the brachial plexus and their formation of the major nerves.
Fig. 2.6.2 shows the anatomy of the brachial plexus. Table 2.6.1 shows the contribution of different portions of the root and plexus system to peripheral nerves. Clinical and diagnostic details of some of the important pathological entities are described in Chapter 5.5 .
Nerve | Plexus | Motor Deficit | Sensory Deficit |
---|---|---|---|
Median | LC, MC; C5–T1 | Finger flexors, | Lateral palmar hand |
Ulnar | LT, MC; C8–T1 | Intrinsic hand muscles, grip | Medial palmar hand |
Radial | LT, MT, PC; C5–T1 | Wrist and finger extension | Posterior-lateral forearm |
Musculocutaneous | UT, LC, C5–6 | Elbow flexion | Lateral forearm |
Axillary | UT, PC, C5–6 | Arm abduction | Lateral shoulder |
Some of the important anatomical details to remember include the following:
Upper plexus lesions produce mainly deltoid and biceps weakness due to damage to C5 and C6 nerve roots.
Lower plexus lesions produce mainly C8 and T1 distribution motor and sensory deficits with prominent weakness of intrinsic muscles of the hand.
Disorders of the brachial plexus and the lumbosacral plexus are discussed in Chapter 5.5 .
The lumbar and sacral plexuses are often referred to as a single entity, the lumbosacral plexus, because they are considered together. The lumbar plexus is formed from nerve roots T12 to L5. The sacral plexus is formed from roots L4 to S5, although most of the portions of the examination that can be performed do not concern roots below S1.
Fig. 2.6.3 shows the lumbosacral plexus anatomy from nerve roots to formation of the proximal nerves.
Table 2.6.2 shows the contribution of different portions of the lumbosacral plexus to peripheral nerves of diagnostic value.
Nerve | Plexus | Motor Deficit | Sensory Deficit |
---|---|---|---|
Peroneal | SP; L5–S1 | Foot drop | Mid and lower calf and top of foot |
Tibial | SP; S1–2 | Foot extension | Lateral heel if sural unaffected |
Femoral | LP; L2–4 | Knee extension | Anterior thigh, medial calf |
Sciatic | LP, SP; L4–S3 | Peroneal and tibial deficits | Peroneal and tibial deficits |
Obturator | LP; L2-4 | Lweg adduction | Medial thigh |
Some important details regarding the lumbosacral plexus include the following:
Most patients with lumbosacral plexus lesions present with posterior pain and motor and sensory symptoms that span distribution of a single nerve.
Plexus lesion is suspected rather than nerve root lesion when more than one nerve root distribution is seen.
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