Factors associated with C5 Palsy

A widely recognized and effective treatment for patients with myelopathy, radiculopathy, or both is cervical decompression, with or without instrumented fusion. Even though cervical decompression can be performed through various approaches, such as anterior, posterior, or combined, to treat myelopathy or radiculopathy, postoperative C5 nerve root palsy (C5P) is a common complication.

Initially referred to as a “dissociated motor loss” caused by nerve root compression, postoperative C5 nerve root palsy (C5P) has been extensively studied with various pathophysiological mechanisms suggested.

Various pathophysiological mechanisms have been proposed to explain postoperative C5 nerve root palsy, including direct injury to the nerve root (caused by mechanical, electrical, or thermal trauma during surgery), nerve root ischemia, reperfusion injury following decompression, spinal cord rotation before or after surgery, nerve root tethering after decompression, and traction injury on the migration of the dorsal spinal cord.

Despite no definitive evidence for any of the theories mentioned, studies and scientific research suggest that nerve root traction or tension following decompression may be a significant contributing factor.

Given that C5P is one of the most frequent and problematic complications of cervical decompression, it is not unexpected that it has been the subject of extensive investigation.

Various risk factors have been identified, including demographic factors such as age, sex, smoking, and diabetes, clinical factors such as preoperative myelopathy, diagnosis, duration of disease, and surgical approach, as well as several radiological factors such as foraminal stenosis, spinal cord MRI signal change, postoperative spinal cord migration, spinal cord rotation, and canal stenosis, among others.

C5P is not a singular clinical entity caused by a single mechanism, but rather a shared clinical outcome resulting from various injuries to the C5 nerve root. C5P is not a singular entity with uniform risk factors across surgical approaches, but rather a spectrum of manifestations with varying characteristics arising from different etiologies and mechanisms.

Different etiologies can result in varying presentations of nerve root insult, including early or delayed onset, painful or painless symptoms, single or multiple root involvement, mild or severe weakness, and the presence of coexisting conditions.

For more than half a century, cervical decompression has been a widely accepted and effective surgical procedure for treating myelopathy and/or radiculopathy with a good safety record. Similarly, C5P as a complication of this surgery has also been acknowledged for the same period. Despite being recognized as a complication of cervical decompression for over 50 years, there has been limited progress in determining a definitive pathophysiological mechanism that can explain its occurrence.

One of the more recent and widely accepted explanations for the occurrence of C5P is the theory of nerve root tethering and traction injury. It is possible that a single mechanism can solely account for the occurrence of C5P.

However, it appears more reasonable to suggest that C5P is merely a clinical representation of any insult or process that impacts the C5 nerve root. This suggests that the diagnosis and cause of C5P will remain complex and involve multiple factors. This concept could account for the diversity of clinical symptoms that patients experience, as C5P has been described as involving sensory sparing or not, as well as other nerve roots.

C5P has been reported with various clinical symptoms, including but not limited to, pain or no pain, immediate or delayed onset (up to 2 weeks), involvement of other nerve roots, and varying rates of recovery. If different etiologies and mechanisms cause different types of damage to the C5 nerve root, it is reasonable to assume that patients may present with similar yet distinct symptoms.

This phenomenon could also elucidate why there are limited independent risk factors that can predict C5P despite numerous studies conducted on the topic. Patients who exhibit similar clinical symptoms, but with different etiologies and mechanisms, are likely to have varying risk factors that contribute to the development of C5P.

Demographic Factors

The association between age and C5P remains ambiguous due to inconsistent findings in various studies. There are conflicting findings across studies regarding the potential link between age and C5P, as some studies have reported an association while others have not.

Older age may be a potential risk factor for C5P due to the higher prevalence and severity of spondylosis, which can exacerbate foraminal stenosis and increase the likelihood of nerve root tethering post-decompression. Other factors, such as patient study heterogeneity and the inclusion or exclusion of other variables, may contribute to the inconsistent identification of age as a risk factor for C5P in studies.

Surgical Factors

One can infer from the available evidence that there is little likelihood of an association between C5 palsy and the number of surgical levels or the use of allograft or autograft.

Despite the assumption that a greater number of decompressed levels would lead to more posterior migration of the spinal cord, no studies in this review found the number of surgical levels to be a risk factor for C5P. The short length of the C5 rootlets and root may explain this finding, as it creates a ceiling effect for the number of compressed and decompressed levels, preventing them from being identified as risk factors for C5P.

Imaging Factors

The following factors are not likely to be associated with C5 palsy:

• Pre- and postoperative C2-7 sagittal angle
• APSAP at C4/5
• Ishihara Index
• Number of compressed segments
• High intensity signal at C3-5
• Hinge angle at C4-6

The evidence is unclear whether C5 palsy is associated with posterior shift C4/5, change in C2-7 angle, laminar opening angle, and preoperative APD at C4/5. The evidence is moderate that C5P is associated with a smaller preoperative FD and preoperative cord malrotation, which supports the hypothesis of nerve root tethering.

Nerve Root Tethering as a Pathophysiological Mechanism for C5P

Researchers have been debating the cause of postoperative C5P. Numerous factors have been put forth to clarify why the C5 nerve root is more susceptible to injury.

Such as having shorter rootlets compared to other nerve roots, a more horizontally positioned course towards the vertebral foramen, and a considerable amount of ligamentous support at the foraminal level that makes C5 more vulnerable to traction injury following decompression due to the lateral root’s tethering within the non-decompressed foramen.

According to the literature, tethering of the nerve root can result in nerve injury similar to neuropraxia, causing impaired nerve action potential conduction. C5P is associated with risk factors such as FD and SC malrotation, and rapid decompression can cause a sudden increase in nerve root strain and traction injury due to SC de-rotation, which can result in a relatively fixed foraminal nerve root and lead to C5P.

Additionally, depending on the extent of the traction injury, in the most severe cases, nerve root ischemia and subsequent infarction may also occur in this region. The findings indicate that in some patients, the occurrence of C5P can be explained by tethering of the nerve root at the foraminal level.

After cervical decompressive surgery, C5P is a frequently occurring complication, with a combined prevalence rate of 6.0%. The pathophysiology of C5P is complex and involves multiple factors, which has resulted in inconsistencies in identifying independent risk factors in previous studies due to variations in study and patient characteristics.

Foraminal stenosis and preoperative SC rotation can be identified as risk factors for C5P, providing evidence in support of the theory that foraminal nerve root tethering may contribute to the development of this complication.

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