The Patterns of Somatic Sensory Impairments After Spinal Cord Injury
Hoffmann's? Babinski?
Spinal cord injury results in deficits in somatec sensation and in the control of body musculature at the level of, and caudal to, the lesion. Motor deficits that follow such injury are considered in Chapter 10.
Here, somatic sensory deficits are considered. In general, somatic sensory deficits have three major characteristics:
1 The sensory modality that is affected, for example, whether pain or touch is impaired
2 the laterality or side of the body where deficits are observed (ie, ipsilateral versus contralateral)
3 the body regions affected.
Damage to one ohalf of the spinal cord, or hemisection, illustrates all three of these characteristic deficits. Spinal hemisection can occur, for example, when a tumor encroaches on the cord from one side, or when the cord is injured traumatically. The sensory and motor deficits that follow spinal cord hemisection are collectively termed the Brown-Sequard syndrom.
Axons in the dorsal columns are ipsilateral in the spinal cord; hence deficits in touch and limb position sens are present ipsilateral to the spinal cord lesion. In contrast, the axons of the anterolateral system decussate in the spinal cord. Therefore, pain and temperature senses are impared on the side of the body that is contralateral to the lesion.
The spinal cord level at which injury occurs can be determined by comparing the disribution of sensory loss with the sensory innervation patterns of the dorsal roots (ie the dermatomal maps). Because of the differences in the anatomical organization of the two systems mediating somatic sensations, a single level of spinal injyr will result in different levels of sensory impairment for touch and pain. For touch sensation the most rostral dermatome in which sensation is impaired corresponds to the level of injury in the spinal cord. For pain sensation the most rostral dermatome in which sensation is impaired is about two segments lower than the injured spinal cord level. This is because the axons of the anterolateral system decussate over a distance of one to two spinal segments before ascending to the brain stem and diencephalon.
Spinal cord injury results in deficits in somatec sensation and in the control of body musculature at the level of, and caudal to, the lesion. Motor deficits that follow such injury are considered in Chapter 10.
Here, somatic sensory deficits are considered. In general, somatic sensory deficits have three major characteristics:
1 The sensory modality that is affected, for example, whether pain or touch is impaired
2 the laterality or side of the body where deficits are observed (ie, ipsilateral versus contralateral)
3 the body regions affected.
Damage to one ohalf of the spinal cord, or hemisection, illustrates all three of these characteristic deficits. Spinal hemisection can occur, for example, when a tumor encroaches on the cord from one side, or when the cord is injured traumatically. The sensory and motor deficits that follow spinal cord hemisection are collectively termed the Brown-Sequard syndrom.
Axons in the dorsal columns are ipsilateral in the spinal cord; hence deficits in touch and limb position sens are present ipsilateral to the spinal cord lesion. In contrast, the axons of the anterolateral system decussate in the spinal cord. Therefore, pain and temperature senses are impared on the side of the body that is contralateral to the lesion.
The spinal cord level at which injury occurs can be determined by comparing the disribution of sensory loss with the sensory innervation patterns of the dorsal roots (ie the dermatomal maps). Because of the differences in the anatomical organization of the two systems mediating somatic sensations, a single level of spinal injyr will result in different levels of sensory impairment for touch and pain. For touch sensation the most rostral dermatome in which sensation is impaired corresponds to the level of injury in the spinal cord. For pain sensation the most rostral dermatome in which sensation is impaired is about two segments lower than the injured spinal cord level. This is because the axons of the anterolateral system decussate over a distance of one to two spinal segments before ascending to the brain stem and diencephalon.
wo pathological processes can selectively impair the function of the dorsal column-medial lemniscal system and the anterolateral system. First in tabes dorsalis, an advanced stage of neurosyphillis, dorsal root ganglion neurons with large-diameter axons are lost. Thus, patients lose touch and limb position sense. Fortunately, tabes dorsalis is rare today because of antibacterial therapies.
Second, in syringomyelia, (where i can't feelya?) a cavity (or syrinx) forms in the central portion of the spinal cord, damaging selectively the decussating axons of the anterolateral system. This resulsts in a loss of pain and temperature sense and sparing of mechanical sensations. Syringomyelia interrupts decussating axons from both sides of the body; hence, the sensory loss is usally bilaterally symmeetrical. Because the lesion affects the decussating, not the ascending, axons, body regions below the level of injury have normal sensation. By contrast, in spinal cord hemisection, pain and temperature sensations are lost caudal to the lesion because the ascending axons are severed. this is a continuation of Box 5-1 on page 121
Second, in syringomyelia, (where i can't feelya?) a cavity (or syrinx) forms in the central portion of the spinal cord, damaging selectively the decussating axons of the anterolateral system. This resulsts in a loss of pain and temperature sense and sparing of mechanical sensations. Syringomyelia interrupts decussating axons from both sides of the body; hence, the sensory loss is usally bilaterally symmeetrical. Because the lesion affects the decussating, not the ascending, axons, body regions below the level of injury have normal sensation. By contrast, in spinal cord hemisection, pain and temperature sensations are lost caudal to the lesion because the ascending axons are severed. this is a continuation of Box 5-1 on page 121