Spinal cord injuries (SCI) affect the anatomy and physiology of the spinal cord and result in characteristic changes. Identifying the impairments resulting from SCI is vital for the health care provider. Specifically, this article focuses on neurologic decline after SCI in the subacute to chronic stages. This includes changes in spasticity and its management over time, management of neuropathic pain after SCI, the development of spine complications (posttraumatic syrinx, spinal cord tethering, and so forth), management of dual-diagnosis traumatic brain injury and SCI, and other neurologic complications in chronic SCI management, such as upper-extremity entrapment mononeuropathies.
Key points
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Changes in spasticity and management in SCI overtime.
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Management of neuropathic pain after SCI.
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Development of spine complications in patients with chronic SCI (posttraumatic syrinx, spinal cord tethering, adhesive arachnoiditis, progressive myelopathy, and so forth).
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Subacute to chronic management of dual-diagnosis traumatic brain injury and SCI.
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Additional neurologic complications in chronic SCI management, such as upper-extremity entrapment mononeuropathies.
Background
In the United States, people living with traumatic spinal cord injuries (tSCIs), not including those with nontraumatic spinal cord injury (ntSCI), account for more than 300,000 persons, with about 18,000 new cases occurring annually. Since the model systems’ national SCI database began in 1970, data have shown advances with the average age of injury from 29 to 43 in 2015. However, average life expectancy in persons with tSCI has not improved substantially since the 1980s and remains below the life expectancies of persons without tSCI. In addition, persons with tSCI continue to have a substantial burden of care, including a greater than five million dollars estimated cost of lifetime care, depending on age of injury.
To better understand some of the challenges faced after an SCI, one must have a strong basis in spinal cord anatomy. The spinal cord begins at the caudal end of the medulla as it passes through the foramen magnum into the vertebral canal where it traverses until it terminates between the first and second lumbar vertebrae. There are 31 pairs of spinal nerves that exit through the intervertebral neuroforamina of the vertebra. These spinal nerves then innervate specific myotomes and dermatomes.
The spinal cord in cross-section is organized with a butterfly-shaped central gray matter containing the ventral, lateral, and dorsal horns. The ventral horn represents interneurons and motor neurons affecting skeletal muscle control. The lateral horn primarily contains preganglionic sympathetic neurons in the thoracic and sacral levels that exit with the ventral horn fibers. The dorsal horn contains afferent sensory fibers that synapse on the extraspinal dorsal root ganglion before joining the efferent motor fibers of the ventral horn forming the mixed spinal nerve. These are surrounded by 3 myelinated white matter funiculi (posterior, lateral, and anterior). The posterior funiculus contains myelinated fibers assisting with conscious proprioception, including kinesthesia and discriminative touch. The lateral and anterior funiculi contain specialized myelinated fiber tracts, including the spinocerebellar (cerebellar proprioception), spinothalamic (pain and temperature senses), corticospinal (cortical motor control), rubrospinal (flexor motor activity), vestibulospinal (extensor tone, position, and posture), and reticulospinal tract (voluntary movement and reflex activity). The blood supply to the spinal cord comes from 3 longitudinal arteries (anterior spinal artery and 2 posterior spinal arteries) arising from the vertebral artery, and radicular arteries, including the important artery of Adamkiewicz in the lumbar region.
The spinal cord is subject to various pathologic conditions, including tSCI and ntSCI, such as vascular insult, myelopathies, degenerative or demyelinating disease, infections, and neoplasms. tSCI typically involves mechanical disruption to the spinal cord and can include various mechanisms, such as hyperextension, penetration, transection, or crush injury. In addition to the primary traumatic injury, there are secondary injuries, including edema, diminished vascular perfusion, and myriad biochemical alterations resulting in neurotoxicity. Vascular insults can include infarctions or hemorrhage affecting various levels and anatomic tracts depending on location and cause. Myelopathic insults stem from various pathologic conditions, including disease of the vertebral column, inflammatory disease, toxic/metabolic myelopathies, and other compressive pathologic conditions within the spinal canal. Degenerative or demyelinating disease covers a wide range of pathologic conditions, including genetic conditions, such a Fredrich ataxia, hereditary spastic paraplegia, and spinal muscular atrophy. These degenerative or demyelinating diseases also include pathologic conditions of uncertain genetic components, for instance, amyotrophic lateral sclerosis, primary lateral sclerosis, multiple sclerosis, and neuromyelitis optica spectrum disorder. Infections within the spinal canal cover a broad scope of spinal cord insults and can include spinal abscess (epidural, subdural, or intramedullary), meningomyelitis, viral myelitis, and other microbial infections. Finally, many neoplasms can occur within the spinal cord, but the most common are nerve sheath tumors, meningiomas, ependymomas, astrocytomas, and metastatic tumors.
Introduction
Although there are many types of spinal cord insults, the anatomy and physiology of the spinal cord dictate some characteristic changes. These changes include motor deficits, neurogenic bowel and bladder dysfunction, autonomic dysfunction, sensory dysfunction, and others resulting in temporary or permanent disability. Identifying the impairments suffered from an SCI and treating them appropriately is vital for the health care provider. However, comprehensive discussion of these lies outside the scope of this article. This article addresses issues related to neurologic decline after SCI, including the following:
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Changes in spasticity and management over time
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Subacute to chronic management of neuropathic pain (NP) after SCI
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Development of spine complications in patients with chronic SCI (posttraumatic syrinx, spinal cord tethering, adhesive arachnoiditis [AA], cerebrospinal fluid [CSF] fistulas, progressive myelopathy, and so forth)
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Subacute to chronic management of dual-diagnosis TBI and SCI
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Additional neurologic complications in chronic SCI management, such as entrapment mononeuropathies
These complications can worsen disability owing to SCI and negatively affect patient’s quality of life (QOL). Identifying causative insults for worsening neurologic function in persons with subacute to chronic SCI can prevent additional complications and preserve function affecting QOL and performance of activities of daily living.
Discussion
Changes in Spasticity and Management over Time
Spasticity is a motor control disorder characterized by an exaggeration of the stretch reflex resulting in a velocity-dependent increase in tone. The mechanism by which spasticity occurs remains poorly understood but is thought to be an upper motor neuron dysfunction owing to abnormal intraspinal processing of afferent impulses, loss of descending inhibitory regulation, and increased excitability. Positive signs of spasticity include increased deep tendon reflexes, clonus, spasms, and antagonist cocontraction, whereas negative signs include weakness, incoordination, and fatigability. Early and ongoing management of spasticity is important to prevent painful contractures, decreased physical function, difficulty in positioning, and skin breakdown. These complications of spasticity in addition to others limit patient’s self-care and increase caregiver burden. The assessment and quantification of spasticity can be difficult and interrater dependent. Several clinical assessments are commonly used and include tools such as the Modified Ashworth scale (MAS), or Tardieu scale.
Spasticity has long been thought to be an issue of chronic SCI management. However, in a study by Yokota and colleagues, patients with SCI were studied prospectively from 2 weeks through 6 months of injury and were separated into 2 groups. The study found that in the 175 patients studied, the MAS scores of the groups significantly increased over time until 4 months after injury. Spasticity was noted as early as 2 weeks after injury. The study identified that patients with earlier onset of spasticity had higher final overall MAS scores. Surprisingly, there was no correlation found between the American Spinal Injury Association Impairment Scale (AIS) grade and the onset of spasticity. Finally, it was noted that higher spasticity scores were associated with improved AIS A motor scores, indicating that not all spasticity is problematic and may support motor function.
Spasticity can change muscle architecture over time with fatty infiltrations or fibrosis. This can lead to increased echo-intensity on ultrasound imaging. The modified Heckmatt scale was evaluated to grade echo-intensity and was demonstrated via a prospective trial to have moderate to high interrater and intrarater reliability in addition to a high degree of validity compared with a quantitative grayscale measure. The scale is a modified version of the previously validated Heckmatt scale and consists of 4 grades, as shown in Table 1 . Of note, this study was not specifically validated in persons with SCI.
| Grade | Original Heckmatt Scale | Modified Heckmatt Scale |
|---|---|---|
| 1 | Normal | Normal echogenicity in >90% of the muscle that is distinct from bone echo |
| 2 | Increased muscle echo intensity with distinct bone echo | Increased muscle echogenicity in 10%–50% of tissue, but with distinct bone echo and areas of normal muscle echo |
| 3 | Marked increased muscle echo intensity with a reduced bone echo | Marked increase in muscle echogenicity between 50% and 90% of tissue with reduced distinction of bone echo from muscle |
| 4 | Very strong muscle echo and complete loss of bone echo | Very strong muscle echogenicity with near complete loss of distinct bone echo from muscle in >90% of tissue |
There is a paucity of data documenting changes in spasticity over time in SCI. However, clinical observations indicate that spasticity should remain stable, if not progress to contracture. Managed spasticity should also remain stable. If there are appreciable, or reported, changes in spasticity, the causative insult should be identified and treated. This may be as simple as changes in weather, infections such as cystitis, pain, or more insidious dysfunctions. Although myriad, common and uncommon causes should be considered, including pressure injuries, intraabdominal stones, fractures, radiculopathy, or other posttraumatic myelopathies. Posttraumatic myelopathies are discussed in more detail in later discussion. Early identification and attentive management of spasticity are imperative to facilitate optimum outcome and reduce complications. The treatment of spasticity can grossly be classified into regular stretching, pharmacologic management, chemoneurolysis, intrathecal management, and surgical management. Pharmacologic management options include 4 Food and Drug Administration–approved medications: baclofen, diazepam, tizanidine, and dantrolene. The appropriate selection of antispasmodic medications should be based on the anticipated benefit and consideration of their adverse effect profiles.
Additional considerations for spasticity management can include chemoneurolysis and selective neuromuscular blocks. Currently, the most widespread therapies in this modality include the use of botulinum toxin and phenol neurolysis. Each intervention has its own unique advantages and disadvantages. Botulinum toxin chemoneurolysis has the main advantages of relative ease of use, low incidence of side effects, and reversibility. However, it is limited to the maximum dosage, thus limiting the number of targets, and has a relatively prohibitive cost. Phenol neuromuscular blocks have a low cost and long duration of effect but are more technically difficult to perform and have a higher risk profile, including injury to nearby vascular and sensory structures. ,
Baclofen remains one of the most prescribed antispasmodics after SCI. It is a gamma-aminobutyric acid (GABA) B receptor agonist. This mechanism of action results in inhibition of reflexes in the spinal cord, thus reducing spasticity. Despite the widespread adoption of baclofen for spasticity management, it continues to lack high-quality clinical trials to support and clarify its benefits and side effects in SCI. Most data arise from small studies examining treatment across multiple causes. Formulations of both oral and intrathecal baclofen are used to treat SCI-related spasticity with intrathecal use demonstrating improved efficacy and lower rates of toxicity. This is thought to be due to the poor blood-brain barrier penetration of oral baclofen. Patients managed with Intrathecal Baclofen must carefully be monitored for signs of overdose or withdrawal, as shown in Table 2 , as these can require intensive care unit management owing to the high risk for morbidity and mortality.
| System | Baclofen Toxicity | Baclofen Withdrawal |
|---|---|---|
| Systemic | Hypothermia | Pruritus, hyperthermia, and multisystem organ failure |
| Psychiatric | Hallucinations, agitation, mania, or catatonia | Hallucinations, anxiety, paranoia, or delusions |
| Neurologic | Hyporeflexia, tremor, confusion, impaired memory, lethargy, somnolence, seizures, encephalopathy, or coma | Hyperreflexia, tremor, paresthesias, headache, altered mental status, delirium, or seizures |
| Cardiovascular | Conduction abnormalities, prolonged QTc interval, or autonomic dysfunction | Acute cardiomyopathy (reversible), cardiac arrest, or autonomic dysfunction |
| Respiratory | Respiratory failure | Respiratory failure |
| Gastrointestinal | Nausea, vomiting | Nausea, vomiting, or diarrhea |
| Musculoskeletal | Hypotonia | Hypertonia and rhabdomyolysis |
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