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and by interneurons that mediate reciprocal inhibition during re ex action Gamma-aminobutyric acid (GABA) serves as the inhibitory neurotransmitter of interneurons in the posterior horn L-glutamate and L-aspartate are released by primary afferent terminals and interneurons and act speci cally on excitatory amino acid receptors There are also descending cholinergic, adrenergic, and dopaminergic axons, which play a less well de ned role in re ex functions

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If all or practically all peripheral motor bers supplying a muscle are interrupted, all voluntary, postural, and re ex movements of that muscle are abolished The muscle becomes lax and soft and does not resist passive stretching, a condition known as accidity Muscle tone the slight resistance that normal relaxed muscle offers to passive movement is reduced (hypotonia or atonia) The denervated muscle undergoes extreme atrophy, being reduced to 20 or 30 percent of its original bulk within 3 to 4 months The reaction of the muscle to sudden stretch, as by tapping its tendon, is lost (are exia) Damage restricted to only a portion of the motor bers supplying the muscle results in partial paralysis, or paresis, and a proportionate diminution in the force and speed of contraction The atrophy will be less and the tendon re ex reduced instead of lost The electrodiagnosis of denervation depends upon nding brillations, fasciculations, and other abnormalities on needle electrode examination However, some of these abnormalities do not appear until several days or a week or two after nerve injury (see Chap 45) Lower motor neuron paralysis is the direct result of loss of function or destruction of anterior horn cells or their axons in anterior roots and nerves The signs and symptoms vary according to the location of the lesion In any individual case, the most important clinical question is whether sensory changes coexist The combination of a accid, are exic paralysis and sensory changes usually indicates involvement of mixed motor and sensory nerves or of both anterior and posterior roots If sensory changes are absent, the lesion must be situated in the anterior gray matter of the spinal cord, in the anterior roots, in a purely motor branch of a peripheral nerve, or in motor axons alone (or in the muscle itself) At times it may be impossible to distinguish between nuclear (spinal) and anterior root (radicular) lesions Preserved and often heightened tendon re exes and spasticity in muscles weakened by lesions of the corticospinal systems attest to the integrity of the spinal segments below the level of the lesion However, acute and profound spinal cord lesions and, to a lesser extent, corticospinal lesions in the brainstem and cerebrum may temporarily abolish spinal myotatic re exes ( spinal shock ; see Chap 44) This is due to the interruption of descending tonic excitatory impulses, which normally maintain a suf cient level of excitation in spinal motor neurons to permit the peripheral activation of segmental re exes.

The terms pyramidal, corticospinal, and upper motor neuron are often used interchangeably, although they are not altogether synonymous The pyramidal tract, strictly speaking, designates only

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