Pathophysiology of Tethered Cord Syndrome
Tethered cord syndrome (TCS) is a stretch-induced functional disorder of the spinal cord. The mechanical cause of TCS is an inelastic structure anchoring the caudal end of the spinal cord that prevents cephalad movement of the lumbosacral cord. Stretching of the spinal cord occurs in patients either when the spinal column grows faster than the spinal cord or when the spinal cord undergoes forcible flexion and extension.
Research in patients and experimental animals suggests that there is a link between the clinical dysfunctions that characterize TCS and putative pathophysiological changes that accompany this syndrome. Among these changes are depression of electrophysiological activity and shifts in the reduction/oxidation ratio of cytochrome oxidase. The latter suggests that there is impairment of oxidative metabolism. These putative pathophysiological changes in TCS occur mainly within the lumbosacral cord under excessive tension.
The authors discuss the pathophysiology of TCS and examine related symptoms.
The symptomatology of TCS includes lower-limb motor and sensory deficits, incontinence, and musculoskeletal deformities. It is believed that the lesions causing TCS symptoms are located in the lumbosacral cord and that signs and symptoms of TCS can be reversed in many patients. Mechanical causes of cord tethering include a thickening of the terminal filum attached to the elongated spinal cord or any inelastic structures, such as fibrous or fibroadipose filum, tumors, lipoma, epidermoid tumor, myelomeningoceles, lipomyelomeningoceles, or scar formations that are fastened to the caudal spinal cord or osseous or dural septum. These structures lack viscoelasticity, and thus their quality is the determining factor for tight fixation of the spinal cord.
Although the following findings in patients with TCS are recognized by clinicians, their correlation to the TCS pathophysiology may not have been well explained. First, TCS lesions are predominantly restricted to the lumbosacral cord. Second, the associated sensory deficits are often distributed in a patchy pattern. Third, TCS-induced incontinence becomes irreversible earlier than motor and sensory dysfunction. Fourth, scoliosis and exaggerated lumbosacral lordosis are common findings. Fifth, what appear to be adequate untethering procedures in patients with myelomeningoceles are often not followed by neurological improvement, which is different from those with "tethered spinal cord."
Defining the mechanism of cord tethering–induced pathophysiology may provide a key step in addressing these issues and in explaining the patient's clinical signs and symptoms. Such definition may also provide a useful means to formulate a rationale for diagnostic and surgical approaches to this disorder. Insights into the pathophysiology of TCS have been derived from correlations among research data and clinical findings such as symptomatology, diagnosis, and surgery-related outcome. In our research on spinal cord tethering, emphasis has been on oxidative metabolism and electrical activities in spinal cords of humans and of experimental animals, because links are proposed between impairments of these factors and the pathophysiology of TCS. This research has suggested that the pathophysiological effects of spinal cord tethering are analogous to those that occur in animal models of hypoxemia and brain and spinal cord ischemia.
Tethered cord syndrome (TCS) is a stretch-induced functional disorder of the spinal cord. The mechanical cause of TCS is an inelastic structure anchoring the caudal end of the spinal cord that prevents cephalad movement of the lumbosacral cord. Stretching of the spinal cord occurs in patients either when the spinal column grows faster than the spinal cord or when the spinal cord undergoes forcible flexion and extension.
Research in patients and experimental animals suggests that there is a link between the clinical dysfunctions that characterize TCS and putative pathophysiological changes that accompany this syndrome. Among these changes are depression of electrophysiological activity and shifts in the reduction/oxidation ratio of cytochrome oxidase. The latter suggests that there is impairment of oxidative metabolism. These putative pathophysiological changes in TCS occur mainly within the lumbosacral cord under excessive tension.
The authors discuss the pathophysiology of TCS and examine related symptoms.
The symptomatology of TCS includes lower-limb motor and sensory deficits, incontinence, and musculoskeletal deformities. It is believed that the lesions causing TCS symptoms are located in the lumbosacral cord and that signs and symptoms of TCS can be reversed in many patients. Mechanical causes of cord tethering include a thickening of the terminal filum attached to the elongated spinal cord or any inelastic structures, such as fibrous or fibroadipose filum, tumors, lipoma, epidermoid tumor, myelomeningoceles, lipomyelomeningoceles, or scar formations that are fastened to the caudal spinal cord or osseous or dural septum. These structures lack viscoelasticity, and thus their quality is the determining factor for tight fixation of the spinal cord.
Although the following findings in patients with TCS are recognized by clinicians, their correlation to the TCS pathophysiology may not have been well explained. First, TCS lesions are predominantly restricted to the lumbosacral cord. Second, the associated sensory deficits are often distributed in a patchy pattern. Third, TCS-induced incontinence becomes irreversible earlier than motor and sensory dysfunction. Fourth, scoliosis and exaggerated lumbosacral lordosis are common findings. Fifth, what appear to be adequate untethering procedures in patients with myelomeningoceles are often not followed by neurological improvement, which is different from those with "tethered spinal cord."
Defining the mechanism of cord tethering–induced pathophysiology may provide a key step in addressing these issues and in explaining the patient's clinical signs and symptoms. Such definition may also provide a useful means to formulate a rationale for diagnostic and surgical approaches to this disorder. Insights into the pathophysiology of TCS have been derived from correlations among research data and clinical findings such as symptomatology, diagnosis, and surgery-related outcome. In our research on spinal cord tethering, emphasis has been on oxidative metabolism and electrical activities in spinal cords of humans and of experimental animals, because links are proposed between impairments of these factors and the pathophysiology of TCS. This research has suggested that the pathophysiological effects of spinal cord tethering are analogous to those that occur in animal models of hypoxemia and brain and spinal cord ischemia.
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