Flexion (Withdrawal) Reflex
Receptors
The flexion reflex is primarily mediated by pain receptors (nociceptors) consisting of free nerve endings. Noxious stimuli activate these receptors.
Circuitry and Mechanism
A schematic representation of the circuitry involved in the flexion reflex is shown in Figure 9-18. When a noxious stimulus is applied to the skin or deeper structures, free nerve endings are stimulated, and the resulting impulses are conducted through myelinated afferent fibers of small diameter (group III fibers) and unmyelinated afferent fibers (group IV fibers).These fibers synapse with a number of alpha motor neurons located in the spinal cord. These connections are polysynaptic, and at least three to four interneurons are involved. Activation of these polysynaptic pathways in the spinal cord results in contraction of ipsilateral flexor muscles, producing flexion and relaxation of ipsilateral antagonist extensor muscles. The net effect of this reflex is to withdraw the limb in response to a noxious stimulus.
Crossed Extension Reflex
Receptors
Nociceptors are also involved in the crossed extension reflex.
FIGURE 9-18 Flexor (withdrawal) reflex. A noxious stimulus (in this case stepping on a thumbtack) applied to the skin or deeper structures stimulates free nerve endings, and the resulting impulses are conducted through small-diameter myelinated afferent fibers and unmyelinated afferent fibers. These fibers make polysynaptic connections with at least three to four excitatory interneurons. The result is that ipsilateral flexor muscles contract, ipsilateral antagonist extensor muscles relax, and the person withdraws the limb in response to the noxious stimulus.
FIGURE 9-19 Crossed extension reflex. Noxious stimulation (in this case stepping on a thumbtack) activates pain fibers, and the impulses generated are conducted to the spinal cord via afferents that send collaterals through the anterior commissure to alpha motor neurons innervating contralateral flexor and extensor muscles. Activation of these polysynaptic pathways results in relaxation of contralateral flexor muscles, while contralateral extensor muscles are contracted. This neuronal circuitry of the flexion and crossed extension reflexes permits extension of the limb contralat-eral to the site of noxious stimulation and withdrawal (flexion) of the limb ipsilateral to it.
A schematic representation of the circuitry involved in the crossed extension reflex is shown in Figure 9-19. As noted with reference to the flexion reflex, a noxious stimulation activates pain fibers, and the impulses generated are conducted to the spinal cord via afferents, which send collaterals through the anterior commissure of the spinal cord that make multisynaptic connections with alpha motor neurons that innervate contralateral flexor and extensor muscles. Activation of these pathways produce effects opposite to those described for ipsilateral flexor and extensor muscles following activation of the flexor reflex. For example, contralateral flexor muscles are relaxed (note that in the flexion reflex, ipsilateral flexor muscles are contracted), while contralateral extensor muscles are contracted (note that in the flexion reflex, ipsilateral extensor muscles are relaxed). This neuronal circuitry of the flexion and crossed extension reflexes permits extension of the limb contralateral to the site of noxious stimulation and withdrawal (flexion) of the limb ipsilateral to it.
Synchronization of Reflexes of Upper and Lower Limbs
Dorsal root fibers branch after they enter the spinal cord. Some of these collaterals synapse directly on alpha motor neurons. Other collaterals synapse on interneurons; the axons of these interneurons synapse on motor neurons in the same segment, rostral segments, or caudal segments. These ascending and descending axons, crossed or uncrossed, begin and end in the spinal cord and connect many segments. This intersegmental collection of fibers is referred to as fasciculus proprius or spinospinal columns. The reflexes of upper and lower limbs are thus synchronized by the fasciculus proprius system. Therefore, as indicated, the function of this system is to synchronize movements and functions of the upper and lower limbs on each side of the body.
Locomotion
Rhythmic stepping involves coordination of contraction of several muscle groups. The neural circuits that coordinate this rhythmic stepping are located in the spinal cord. However, supraspinal systems are also necessary for normal goal-directed locomotion. Humans with complete spinal cord transections cannot exhibit rhythmic stepping because, corticospinal, rubrospinal, and reticulospinal descending systems are phasically active during locomotion.
Clinical Case
History
Steve is a 37-year-old man who was well until he developed a weakness of his left leg for a few weeks. During this period of time, he gradually began to drag the leg when he walked, and he also noticed that his left leg was numb over the entire leg. He was no longer able to participate in his weekly golf game.
Examination
Steve went to a neurologist. The neurologist examined him and found no problems with Steve’s speech, his cranial nerves, or the sensory or motor function of his arms. His left leg was extremely weak, and the knee-jerk and ankle-jerk reflexes were very brisk. Whereas vibration and position sense were absent on the left leg, pain and temperature sense were absent on the right leg. Pain sensation, when tested with a pinprick was absent on the right aspect of the trunk below the level of the umbilicus, and, at this level, there was also some segmental bilateral loss of pain sensation. When the lateral plantar surface of Steve’s left foot was scratched, the great toe dorsiflexed, and the other toes fanned. When this maneuver was repeated on the opposite side, the toes curled under.
Explanation
The spinal cord syndrome described in Steve’s case is called the Brown-Sequard syndrome, or hemisection of the spinal cord. In this case, the left side of the spinal cord was injured, causing damage to the corticospinal tract and resulting in upper motor neuron weakness on the ipsilateral side. The weakness is ipsilateral because the damage is caudal to the level at which the corticospinal tracts cross in the medullary pyramid. Position and vibratory sense are also lost on the ipsilateral side because the tract in which these fibers travel (fasciculus gracilis) also crosses above the lesion in the medulla. The loss of pain and temperature are on the contralateral side because first-order pain and temperature fibers enter the dorsal root and make synaptic contact with neospinothalamic tract neurons, whose axons cross over to the opposite side. Although the sensory level of diminished function was perceived to be at the umbilicus (approximately T10), the actual lesion was localized toT8 orT9.This is due to the fact that the first-order fibers carrying pain sensation in the zone of Lissauer ascend and descend one to two segments before making synaptic contact with second-order neospinothalamic neurons.The reason for the bilateral segmental loss of pain sensation at the approximate level of the lesion is that hemisection of the cord destroys the crossing neospinothalamic fibers from both sides in the anterior white commissure.
The Brown-Sequard syndrome results from a variety of causes, including tumors and infections of the spinal cord. In Steve’s case, his neurologist ordered a magnetic resonance imaging study of his thoracic spine, which revealed a meningioma, a type of usually benign tumor that was compressing the spinal cord at the level of T8. Several therapies were presented to Steve for relief of his symptoms, including the possible removal of the tumor.
SUMMARY TABLE
Spinal Cord Tracts
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Tract Receptors |
Course and Distribution6 |
Functions |
Effects of Lesions |
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Long Ascending Spinal Tracts |
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Fascicu- Meissner’s lusgra- (touch), Mer-cilis" kel’s (pressure), Pacinian (vibration), and joint receptors (kinesthesia—position and movement) |
Exists at all levels of spinal cord; located medial to fasciculus cuneatus, central processes of first-order neurons ascend ipsilaterally and terminate on second-order neurons located in ipsilateral medullary nucleus gracilis; axons of second-order neurons cross in midline (internal arcuate fibers) to form medial lemniscus and ascend to synapse on third-order neurons located in contralateral thalamic ventral posterolateral nucleus; axons of third-order neurons terminate in medial aspect of sensorimotor cortex |
Carries information about fine touch, pressure, vibration sensation, and conscious proprioception (sense of position and movement) from the lower body and limbs (sacral, lumbar and T6-T12 region) to brainstem |
Loss of sensations of fine touch, pressure, vibration sensation, and conscious proprioception from lower body and limbs ipsilateral to lesion; ataxia due to loss of conscious proprioception from lower limbs |
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Fasciculus Meissner’s cuneatus" (touch), Mer-kel’s (pressure), Pacinian (vibration), and joint receptors (kinesthesia— position and movement) |
Exists atT6 thoracic levels and cervical levels; located lateral to fasciculus gracilis; central processes of first-order neurons ascend ipsilaterally and terminate on second-order neurons located in ipsilateral medullary nucleus cuneatus; axons of second-order neurons project to third-order neurons located in contralateral thalamic ventral posterolateral nucleus; axons of third-order neurons terminate in lateral aspect of sensorimotor cortex |
Carries information about fine touch, pressure, vibration sensation, and conscious proprioception (sense of position and movement) from upper body and limbs to brainstem |
Loss of sensations of fine touch, pressure, vibration sensation, and conscious proprioception from upper body and limbs ipsilateral to lesion |
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Dorsal Muscle spin-(posterior) dies, Golgi spino-cer- tendon ebellar organs in tract lower limbs |
Central processes of first-order neurons project to neurons in nucleus dorsalis of Clarke (C8 to L2); axons of these neurons ascend ipsilaterally, reach inferior cerebellar peduncle in medulla, and terminate ipsilaterally in cerebellar vermis of anterior lobe |
Transmits signals from muscle spindle and Golgi tendon afferents in lower limb to cerebellum, which coordinates non-conscious proprioception |
Likely gait ataxia |
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Ventral Golgi ten-(anterior) don organs spino- in lower cerebellar limbs tract |
Central processes of first-order neurons project to second-order neurons in dorsal horn; axons of most second-order neurons cross to contralateral lateral funiculus and ascend to pons where they join superior cerebellar peduncle, cross again to other side, and terminate in cerebellar vermis of anterior lobe |
Transmits information from Golgi tendon organs located in lower limb to cerebellum |
Unknown |
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Cuneo- Muscle spin-cerebellar dies, Golgi tract tendon organs in upper limbs |
Central processes of first-order neurons ascend ipsilaterally in fasciculus cuneatus and synapse on neurons in accessory cuneate nucleus; neurons in this nucleus give rise to cuneocerebel-lar tract, which terminates ipsilaterally in cerebellar vermis of anterior lobe |
Transmits information about muscle spindle and Golgi tendon afferents in upper limb to cerebellum |
Loss of nonconscious proprioception and coordination of upper limbs ipsilateral to lesion |
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Tract |
Receptors |
Course and Distribution*1 |
Functions |
Effects of Lesions |
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Long Ascending Spinal Tracts |
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Rostral spinocerebellar tract |
Golgi tendon organs in upper limbs |
Same as in ventral spinocerebellar tract except that afferents are from upper limb,tract is uncrossed,and it enters cerebellum via inferior cerebellar peduncle (not known if present in humans) |
Transmits information from Golgi tendon organs located in upper limb to cerebellum |
Unknown |
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Spinothalamic tractc |
Nociceptors: Free nerve endings mediating mechanical, thermal, and polymodal sensations |
Direct: Neospinothalamic Tract: Neurons that give rise to this tract arise mainly from proper sensory nucleus (lamina III and IV); axons of these neurons cross obliquely to enter contralateral white matter, ascend in lateral funiculus, and synapse on third-order neurons located primarily in ventral posterolateral nucleus of thalamus that projects to primary somatosensory cortex in postcentral gyrus |
Mediates discriminative component of pain sensation |
Cervical Lesion: Complete loss of pain, temperature, and simple tactile sensations on contralateral side of body (upper and lower limbs and trunk Lumbar Lesion: Loss of pain, temperature, and simple tactile sensations in contralateral lower limb and trunk |
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Indirect: Paleospinothalamic Tract: Neurons of this pathway are located in dorsal horn and intermediate gray matter; axons of these neurons ascend bilaterally, make several synapses in reticular formation of medulla, pons, and midbrain, and finally project to midline and intralaminar thalamic nuclei, which then project in a diffuse manner to cerebral cortex. Spinoreticular Tract: Neurons of this pathway are also located in dorsal horn and intermediate gray matter; their axons ascend bilaterally and terminate on neurons located in medullary and pontine reticular formation; these neurons activate cerebral cortex through secondary and tertiary projections via midline and intralaminar thalamic nuclei. Spinomesencephalic Tract: Neurons of this pathway are also located in dorsal horn and intermediate gray matter; axons of these neurons ascend to midbrain where they terminate in PAG; activation of neurons in PAG results in inhibition of pain sensation at spinal level via indirect descending projections; sensory information carried by this tract is also transmitted to amygdala via parabrachial nuclei |
Mediate arousal-emotional components of pain sensation |
Lesions of these tracts are believed to cause a lossofarousal-emo-tional components of pain |
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Course and Distribution* |
Functions |
Effects of Lesions |
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Long Descending Spinal Tracts |
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Corticospinal tract |
Cerebral cortex |
Arises from cerebral cortex, passes through medullary pyramids,and terminates in spinal cord; in cortex, cells functionally associated with arm and leg are located in lateral convexity and medial wall of hemisphere, respectively (cortical homunculus); axons arising from cortex converge in corona radiata and descend through internal capsule, crus cerebri in midbrain, pons, and medulla; a majority (about 90%) of fibers cross to contralateral side at juncture of medulla and spinal cord (pyramidal decussation), forming lateral corticospinal tract, which descends to all levels of spinal cord and terminates in spinal gray matter of both dorsal and ventral horns; remaining uncrossed fibers (anterior corticospinal tract) descend through spinal cord and cross over at different segmental levels to synapse with anterior horn cells on contralateral side; pyramidal decussation forms anatomical basis for voluntary motor control of one half of body by contralateral cerebral hemisphere |
Controls voluntary movements of both contralateral upper and lower limbs |
Voluntary control of contralateral upper and lower limbs is lost when corticospinal tract is damaged; symptoms of damage to corticospinal tract (i.e., loss of voluntary movement, spasticity, increased deep tendon reflexes, loss of superficial reflexes, and Babinski sign) comprise an "upper motor neuron paralysis"; symptoms of "lower motor neuron paralysis" include loss of muscle tone, atrophy of muscles, and loss of all reflex and voluntary movement |
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Rubrospinal tract |
Red nucleus (located in the rostral half of the midbrain tegmentum) |
Axons of red nucleus neurons cross midline in ventral midbrain (ventral tegmental decussation) and descend to contralateral spinal cord;fibers in rubrospinal tract are somatotopically arranged; cervical spinal segments receive fibers from dorsal part of red nucleus, which receives inputs from upper limb region of sensorimotor cortex; lumbosacral spinal segments receive fibers from ventral half of red nucleus, which receives inputs from lower limb region of sensorimotor cortex; fibers of rubrospinal tract terminate on interneurons that, in turn, project to dorsal aspect of ventral (motor) horn cells; in humans most of efferent fibers emerging from red nucleus terminate in inferior olive and cervical cord |
Function of this tract is to facilitate flexor motor neurons and inhibit extensor motor neurons |
Although effects of lesions restricted to red nucleus are not known in humans, lesions of midbrain tegmentum including red nucleus are reported to elicit contralateral motor disturbances (tremor, ataxia, and choreiform activity), possibly because of involvement of axons arising from basal ganglia or cerebellum |
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Tectospinal tract |
Superior col-liculus |
Axons of neurons in superior colliculus terminate in upper cervical segments |
May direct head movements in response to visual and auditory stimuli |
Not established |
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Tract |
Origin |
Course and Distribution” |
Functions |
Effects of Lesions |
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Long Descending Spinal Tracts |
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Lateral vestibulospinal tract |
Lateral vestibular nucleus (border of the pons and medulla) |
Fibers in this tract are uncrossed, descend entire length of spinal cord, and terminate on interneurons that activate motor neurons innervating extensor muscles of trunk and ipsilateral limb |
Facilitates ipsilateral extensor alpha-motor neurons and associated gamma motor neurons; main function is to control muscles that maintain upright posture and balance |
Disturbances in maintaining posture and balance; effects of lesions limited to lateral vestibulospinal tract have not been described in humans |
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Medial vestibulospinal tract |
Ipsilateral and contralateral medial vestibular nuclei |
Descends in ventral funiculus of cervical spinal cord,and terminates in ipsilateral ventral horn |
Main function of this tract is to adjust position of head in response to changes in posture (such as keeping head stable while walking) |
Possible disturbances in positioning of head when position of body is affected |
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Reticulospinal tracts |
Medulla: Nucleus reticularis giganto-cel- lularis |
Projects bilaterally to all levels of spinal cord; this tract is called medullary (lateral) reticulospinal tract |
Inhibits extensor spinal reflex |
Believed to contribute to spasticity in upper motor neuron paralysis |
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Pons: Nucleus reticularis pontis cau- dalisand oralis |
Projects ipsilaterally to entire spinal cord; this tract is called pontine (medial) reticulospinal tract |
Facilitates extensor spinal reflexes |
Not established; possible loss of muscle tone of extensor muscles |
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Ventrolateral medulla |
Projects to IML of thoracolumbar cord |
Excites sympathetic preganglionic neurons in IML, which provide sympathetic innervation to visceral organs |
Not established; presumed to contribute to Horner’s syndrome |
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PAG |
Enkephalinergic neurons located in midbrain PAG project to serotonergic neurons located in nucleus raphe magnus of medulla (first limb); second limb of pathway consists of projections from serotonergic raphe magnus neurons to enkephalinergic interneurons in dorsal horn of spinal cord, which, in turn, synapse upon primary afferent pain fibers |
Modulates activity of pain impulses that ascend in spinothalamic system |
Not established; possible disturbance of pain sensation |
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Course and Distribution6 |
Functions |
Effects of Lesions |
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Long Descending Spinal Tracts |
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MLF |
Medial vestibular nucleus, reticular formation, and superior colliculus (tectospinal fibers) |
Descending fibers in MLF project primarily to ipsilateral upper cervical spinal cord segments |
Descending MLF fibers monosynap-tically inhibit motor neurons located in upper cervical spinal segments and control position of head in response to excitation by labyrinth of vestibular apparatus |
Although damage to descending fibers of MLF is presumed to disrupt control of position of head in response to inputs from labyrinth and vestibular apparatus, these symptoms have not been clinically established; damage to ascending fibers in MLF at the level of brainstem produces internuclear ophthalmoplegias; lesions of MLF are common in patients with multiple sclerosis in which symptoms include nystagmus and occasionally diplopia in ipsilateral eye; these symptoms may be due to damage to projections from lateral, superior, and medial vestibular nuclei to oculomotor, abducens, and trochlear cranial nerve nuclei |
IML = intermediolateral cell column; MLF = medial longitu dinal fasciculus; PAG = periaqueductal midbrain gray. "Fasciculi gracilis and cuneatus together form the dorsal column of the spinal cord. ‘First-order neuron of all ascending tracts are located in the dorsal root ganglia.
‘Direct (neospinothalamic) and indirect (paleospinothalamic, spinoreticular, and spinomesencephalic) tracts comprising the spinothalamic tract are collectively known as the anterolateral system of ascending tracts.
