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Purves D, Augustine GJ, Fitzpatrick D, et al., editors. Neuroscience. 2nd edition. Sunderland (MA): Sinauer Associates; 2001.

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Neuroscience. 2nd edition.

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Damage to Descending Motor Pathways: The Upper Motor Neuron Syndrome

Injury of upper motor neurons is common because of the large amount of cortex occupied by the motor areas, and because motor pathways extend all the way from the cerebral cortex to the lower end of the spinal cord. Damage to the descending motor pathways anywhere along this trajectory gives rise to a set of symptoms called the upper motor neuron syndrome.

This clinical picture differs markedly from the lower motor neuron syndrome described in Chapter 16 and entails a characteristic set of motor deficits. Damage to the motor cortex or the descending motor axons in the internal capsule causes an immediate flaccidity of the muscles on the contralateral side of the body and face. Given the topographical arrangement of the motor system, identifying the specific parts of the body that are affected helps localize the site of the injury. The acute manifestations tend to be most severe in the arms and legs: If the affected limb is elevated and released, it drops passively, and all reflex activity on the affected side is abolished. In contrast, control of trunk muscles is usually preserved, either by the remaining brainstem pathways or because of the bilateral projections of the corticospinal pathway to local circuits that control midline musculature. This initial period of “hypotonia” after upper motor neuron injury is called spinal shock, and reflects the decreased activity of spinal circuits suddenly deprived of input from the motor cortex and brainstem.

After several days, however, the spinal cord circuits regain much of their function for reasons that are not fully understood. Thereafter, a consistent pattern of motor signs and symptoms emerges, including:


The Babinski sign. The normal response in an adult to stroking the sole of the foot is flexion of the big toe, and often the other toes. Following damage to descending upper motor neuron pathways, however, this stimulus elicits extension of the big toe and a fanning of the other toes (Figure 17.13). A similar response occurs in human infants before the maturation of the corticospinal pathway and presumably indicates incomplete upper motor neuron control of local motor neuron circuitry.


Spasticity. Spasticity is increased muscle tone, hyperactive stretch reflexes, and clonus (an oscillatory motor response to muscle stretching). Extensive upper motor neuron lesions may also be accompanied by rigidity of the extensor muscles of the leg and the flexor muscles of the arm (called decerebrate rigidity; see below). Spasticity is probably caused by the removal of inhibitory influences exerted by the cortex on the postural centers of the vestibular nuclei and reticular formation. In experimental animals, for instance, lesions of the vestibular nuclei ameliorate the spasticity that follows damage to the corticospinal tract. Spasticity is also eliminated by sectioning the dorsal roots, suggesting that it represents an abnormal increase in the gain of the spinal cord reflex due to loss of descending inhibition (see Chapter 16). This increased gain is also thought to explain clonus (Box D).


Hyporeflexia of superficial reflexes. Further signs are the decreased vigor (and increased threshold) of superficial reflexes such as the corneal reflex, superficial abdominal reflex (tensing of abdominal muscles in response to stroking the overlying skin), and the cremasteric reflex in males (elevation of the scrotum in response to stroking the inner aspect of the thigh). The mechanism of this diminishment of superficial reflexes is not well understood.


A loss of the ability to perform fine movements. If the lesion involves the descending pathways that control the lower motor neurons to the upper limbs, the ability to execute fine movements (such as independent movements of the fingers) is lost.

Figure 17.13. The Babinski sign.

Figure 17.13

The Babinski sign. Following damage to descending corticospinal pathways, stroking the sole of the foot causes an abnormal fanning of the toes and the extension of the big toe.

Box Icon

Box D

Muscle Tone. Muscle tone is the resting level of tension in a muscle. In general, maintaining an appropriate level of muscle tone allows a muscle to make an optimal response to voluntary or reflexive commands in a given context. Tone in the extensor muscles (more...)

Although these upper motor neuron signs and symptoms may arise from damage anywhere along the descending pathways, the spasticity that follows damage to descending pathways in the spinal cord is less marked than the spasticity that follows damage to the cortex or internal capsule. For example, the extensor muscles in the legs of a patient with spinal cord damage cannot support the individual's body weight, whereas those of a patient with damage at the cortical level often can. On the other hand, lesions that interrupt the descending pathways in the brainstem above the level of the vestibular nuclei but below the level of the red nucleus cause even greater extensor tone than that which occurs after damage to higher regions. Sherrington, who first described this phenomenon, called the increased tone decerebrate rigidity. In the cat, the extensor tone in all four limbs is so great after lesions that spare the vestibulospinal tracts that the animal can stand without support. Patients with severe brainstem injury at the level of the pons may exhibit similar signs of decerebration, i.e., arms and legs stiffly extended, jaw clenched, and neck retracted. The relatively greater hypertonia following damage to the nervous system above the level of the spinal cord is presumably explained by the remaining activity of the intact descending pathways from the vestibular nuclei and reticular formation, which have a net excitatory influence on these reflexes.

By agreement with the publisher, this book is accessible by the search feature, but cannot be browsed.

Copyright © 2001, Sinauer Associates, Inc.
Bookshelf ID: NBK10898


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