Target Philosophy in Degenerative Spinal Disorders: Correlation of Clinical Presentation, Physical Examination, and Response to Interventional Procedures

3 Target Philosophy in Degenerative Spinal Disorders: Correlation of Clinical Presentation, Physical Examination, and Response to Interventional Procedures

Bridget T. Carey, Jaspal Ricky Singh, Neel Mehta, Taylor Wong, Sertac Kirnaz, Michael Sein, and Roger Härtl

The success of MISS in this setting relies upon identifying a clear surgical target, so as to minimize surgical overtreatment and optimize subjective and objective patient outcomes. It is critical to note that not all radiographic evidence of “wear and tear” is necessarily pathological or problematic. This chapter will cover the typical patient presentations for common degenerative spinal conditions, along with the neurologic and musculoskeletal examination maneuvers, electrodiagnostic studies, and diagnostic injections that the minimally invasive spine surgeon must be aware of in order to determine the proper diagnosis.

Keywords: diagnostic injections EMG minimally invasive spine surgery musculoskeletal examination spinal imaging spinal pathologies

3.1 Introduction

Precise diagnosis is of utmost importance for the decision-making process in minimally invasive spine surgery (MISS) for degenerative spine conditions. The success of MISS in this setting relies upon identifying a clear surgical target, so as to minimize surgical overtreatment and optimize subjective and objective patient outcomes.

Several questions are crucial in this context: How can we accurately describe and diagnose pain? How can we use the clinical examination, imaging studies, electrophysiological testing, injections, and other tests to precisely and accurately localize the pain generator? For example, many patients have complex, multilevel spinal pathology on imaging: how can we determine the most appropriate site to target with a successful surgical intervention?

The majority of patients with degenerative disorders who are at the point where surgical intervention is being considered present with pain as a dominant symptom. A careful pain history will allow the surgeon to elucidate the probable predominant pain generator. Pain resulting from degenerative spine disease can be characterized based on its quality, location, radiation, and provoking and palliating factors. The pattern of these pain characteristics often suggests the responsible focal etiology. Therefore, an accurate understanding of the type of pain a patient is experiencing is of great importance in the diagnosis and identification of the underlying pathology that may or may not be surgically treatable.

At our interdisciplinary spine center, we use thorough history and physical examination as the basis of diagnosis, and then, as needed, utilize electrodiagnostic studies, diagnostic injections, and imaging studies to confirm, refute, and/or more precisely localize the site of pathology responsible for the patient’s most problematic pain symptoms. Once a diagnosis has been reached, the surgeon may determine whether this site is amenable to surgical intervention.

In this chapter, we review typical patient presentations for common degenerative spinal conditions, along with the neurologic and musculoskeletal examination maneuvers, electrodiagnostic studies, and diagnostic injections that the minimally invasive spine surgeon must be aware of in order to determine the proper diagnosis. We will also discuss some of the extraspinal musculoskeletal pathology that may masquerade as a spinal condition and confound the diagnostician. Based on clinical experience and literature, we describe the most frequently encountered pain patterns affecting each anatomical spinal segment, and how their recognition can guide in the diagnosis and accurate surgical decision-making.

The goal of MISS in degenerative spinal disorders is to precisely target the pain generator and decompress/stabilize the spinal anatomy if needed, without overtreating the patient.

3.2 Cervical Segment

a)Introduction: In anatomical terms the cervical spine can be divided into three units: the C1 atlas, the C2 axis, and the remaining C3–C7 typical cervical vertebrae. In functional terms these units can be regarded as the cradle, the axis, and the column.1

b)Cervical central canal stenosis:

1.Clinical presentation: Central stenosis of the cervical spine may clinically manifest in a number of ways, depending on the degree and precise location of degenerative change. Neck pain may or may not be a significant presenting symptom. More commonly, the presentation involves neurological signs and symptoms. Gait instability, hand clumsiness, and proximal lower extremity weakness may all be presenting symptoms, along with overt upper extremity weakness.

2.Physical examination:

i)Neurologic examination: The primary neuropathic pathology in central canal stenosis involves the spinal cord. Compression of the cervical spinal cord results in disruption of white matter tracts, the clinical correlate of which is myelopathy. Muscle tone may be increased in the upper and lower extremities. Deep tendon reflexes (DTRs) become abnormally brisk. Weakness of the arms and proximal lower extremities may occur, and there may be impairment of manual dexterity out of proportion to weakness, reflecting compression on the corticospinal tracts. Pathological reflexes may be present, such as positive Babinski’s and Hoffman’s signs.

ii)Provocative maneuvers: Lhermitte’s sign is characterized by the development of paresthesias and/or burning pain down the back and into the extremities upon neck flexion. The absence of this sign does not rule out cervical spinal cord impingement; however, its presence will generally rule it in.

3.Electrodiagnostics: If concomitant neural foraminal stenosis is not present, nerve conduction studies (NCS)/electromyography (EMG) will be normal (see Section 3.2c, point 3). In patients with cervical spinal cord compression who have a normal clinical examination, abnormal EMG findings may be helpful in determining whether a decompression should be considered.

4.Diagnostic injections: In patients with cervical spinal stenosis and cord compression, injections are usually not helpful since these patients typically do not present with pain as a dominant symptom. Other symptoms such as numbness or tingling do not respond to injections. In patients with severe spinal cord compression, injections may actually be contraindicated.

c)Cervical radiculopathy and neural foraminal stenosis:

1.Clinical presentation: Patients suffering from cervical radiculopathy most commonly experience a sense of pain radiating from the neck or upper back region into one or both upper extremities. They may complain of pain, numbness, or paresthesias in the sensory distribution of the affected nerve root or roots (Fig. 3.1). Of note, C7 nerve root compression can be associated with pain between the shoulder blades, with or without classic C8 dermatomal pattern pain. Patients may also note arm weakness or muscle atrophy. Typically, the symptoms are unilateral. Root tension signs are typically present. As a consequence, patients with cervical radiculopathy may be noted to place the hand of the affected extremity on top of their head: this reduces tension along the nerve and leads to symptom relief. Flexion typically relieves the pain while extension and/or tilting toward the side of the pain exacerbates it.

2.Physical examination:

i)Neurologic examination: Motor examination includes the visual inspection of muscle for atrophy or fasciculations, which occur in the setting of loss of neural connection between the anterior horn cells and the peripheral motor nerve. Muscle tone should be normal or decreased: if increased, suspicion for myelopathy arises, indicating spinal cord involvement either as an alternative or in addition to root pathology. Muscle strength is assessed with resistance testing of individual muscle groups to include the C5–T1 myotomes, which innervate the musculature of the upper extremities via the brachial plexus (Fig. 3.2). Sensory examination may elicit hypesthesia, hyperesthesia, induced paresthesia, or a combination of sensory derangements in the affected dermatome. If sensory changes are diffuse or bilateral, this argues against radicular etiology. DTRs of the upper extremities should be decreased or absent, specifically the biceps tendon DTR for C5/C6 radiculopathy and the triceps tendon DTR for C7/C8 radiculopathy.
Compression of the C4 nerve at the C3/C4 level is a frequently overlooked diagnosis and can be associated with pain radiating into the tip of the shoulder. The C4 root may in part be assessed by examination of the rhomboid muscle group, which this root innervates along with C5, via the dorsal scapular nerve.
Assessment of the cervical roots superior to C4 (i.e., superior to the brachial plexus) is generally based on symptoms. C2 and/or C3 radiculopathy often presents as posterior lateralized headache, which is actually radicular cephalgia along the dermatomal distribution.

3.Electrodiagnostics: NCS and needle EMG can be useful diagnostic tools in the localization and prognosis of radicular nerve injury. The goal of NCS/EMG for cervical radicular disease is to perform an electrophysiologic interrogation of the cervical nerve roots. Conventional NCS/EMG testing for cervical radiculopathy is easily performed in the outpatient setting and is generally well tolerated by patients. A typical study allows for the thorough assessment of C4–T1 nerve roots through the electrodiagnostic study of the upper extremities, shoulder girdle, and the cervical paraspinal musculature. It is important to note that needle EMG will be normal in patients with low grade compression injury to the nerve root, that is, a demyelinating injury with axonal sparing. Significant axonal dropout must occur prior to the development of electrophysiological evidence of denervation of muscles sharing the affected myotome. Thus, a normal EMG does not rule out radiculopathy. An abnormal study, however, can confirm it. Further, the degree of denervation occurring within a muscle can define the severity of neurological injury, and therefore generally speaking indicate the urgency for surgical intervention.
The sensitivity of needle EMG is dependent on the timing of the study. Spontaneous electrical activity of muscle fibers in the form of positive sharp waves and/or fibrillation potentials begins to be observed 10 to 14 days after interference of axonal innervation to the motor end plates. This finding indicates axonal injury and resultant muscle fiber denervation. In the case of radiculopathy, this finding confirms significant neurological damage to the nerve root. A study performed prior to 14 days following injury may precede the development of this electrophysiologic finding, and therefore appear spuriously normal.
Findings of denervation on needle EMG are concerning because by definition they confirm axonal injury. Prognostication for recovery of neurological function following injury to peripheral nerve is directly related to the degree of injury. An abnormal EMG, therefore, indicates an injury beyond neuropraxia and, hence, a risk of permanent neurological deficit. If little or no findings of reinnervation are observed by 12 weeks after onset of an axonal injury, this indicates a higher lever injury and is a poor prognostic sign.
From the neurological perspective, the identification of axonal injury on the basis of denervation on needle EMG indicates risk of neurological deficit with incomplete recovery. Surgical decompression is indicated to protect neurological function in these cases, with the most favorable prognosis occurring with prompt surgical intervention. The rationale is that compression injury occurs over time, and if left alone, a low-level injury with prognosis for good recovery evolves into a higher level injury with increasingly poorer prognosis for recovery.

4.Diagnostic injections: Epidural steroid injections are useful for short-term relief from neuropathic symptoms. Diagnostic epidural injection using a local anesthetic alone or with steroid can be used to confirm that radicular pain is due to neural foraminal stenosis at a specific vertebral level. If the patient’s symptoms are temporarily relieved with a targeted injection to the suspected clinically correlated level, this is considered a positive diagnostic test. For this purpose, interlaminar injections can be performed more easily; however, this technique may be less selective. Transforaminal epidural steroid injections with ultrasound or CT guidance can be performed, but caution should be taken to avoid intravascular injection that may be more difficult to see with fluoroscopic guidance.2^,³^,⁴^,⁵^,⁶

d)Cervical facet joint arthropathy:

1.Clinical presentation: The facet joints are true synovial joints. A patient with spinal arthritis will often find that periods of inactivity lead to stiffness and reduced spinal range of motion. Symptoms are typically prominent upon getting out of bed in the morning, or rising from a chair following prolonged sitting. Often times, these symptoms will dissipate following commencement of physical activity or by application of heat to the affected area, only to recur following the next period of inactivity.
In addition, advanced arthropathy of the upper cervical spine may lead to cervicogenic headaches. Irritation of the C2/C3 roots may occur on the basis of neural foraminal stenosis through joint hypertrophy. These roots give rise to the greater and lesser occipital nerves which innervate the head (Fig. 3.3).

2.Physical examination:

i)Neurologic examination: In general, the neurologic examination should be normal in patients with facet mediated symptoms. Neuromuscular examination may reveal decreased cervical range of motion. Paraspinal muscle spasm may be present.

ii)Provocative maneuvers: Facet loading is used to elicit pain in the affected joint. This maneuver is performed by having the patient rotate and extend the cervical spine toward the symptomatic side. Diminished range of motion, audible crepitus, or increased discomfort are suggestive of facet mediated symptoms. A similar maneuver is the Spurling’s maneuver used for the workup of patients with suspected foraminal nerve root compression. However, in these patients radiating radicular pain is elucidated. In patients with facet joint pathology the pain will be more localized and not radiating.

3.Electrodiagnostics: Normal.

4.Diagnostic injections: Diagnostic facet joint blocks may be performed on the clinically suspected symptomatic level. It is important to note that over a third of diagnostic facet joint blocks yield false positive results. Therefore, repeated blocks with two distinct anesthetic agents are recommended to improve diagnostic value.7^,⁸^,⁹

e)Myofascial neck pain or muscle generated pain

1.Clinical presentation: Pain attributed to muscle and its surrounding fascia is termed myofascial pain. The quality of pain is usually described as a dull aching sensation, made worse with aggressive activity and prolonged positioning. Cervical myofascial pain is believed to result from overuse of or trauma to the muscles that support the shoulders and neck. It can also result from compensation for underlying spinal pathology, such as the conditions discussed above. In the cervical spine, the muscles most often implicated in myofascial pain are the trapezius, levator scapulae, rhomboids, and paraspinals (Fig. 3.4). Chapter 5 covers muscular generated pain in detail.

2.Physical examination: The hallmark of myofascial pain is the presence of trigger points: discrete, focal, hyperirritable areas located in a taut band of skeletal muscle. Trigger points produce pain locally and in a referred pattern when palpated:

i)Neurologic examination: Normal

ii)Provocative maneuvers: Trigger point palpation should elicit the patient’s index pain and referred pain patterns. On deep palpation, a muscle twitch response may be seen as well.

3.Electrodiagnostics: Normal.

4.Diagnostic injections: Injection for the treatment of symptomatic trigger points is both therapeutic and diagnostic. Trigger points are diagnosed by examining signs, symptoms, pain patterns, and manual palpation. Using a 25-gauge needle, the muscle is injected either with saline, local anesthetic, or steroid or a combination of the above. Ultrasound guidance can be used for muscle specificity and avoiding lung or nerve injury. Care should be taken to avoid infection, nerve injection, pneumothorax, and intrathecal injection.¹⁰^,¹¹^,¹²^,¹³^,¹⁴^,¹⁵ Also refer to Chapter 5.

f)Primary shoulder pathology

1.Clinical presentation: Overuse injuries of the shoulder are common and can be due to issues involving soft tissue derangements such as rotator cuff tendinopathy, as well as arthropathy of the glenohumeral, sternoclavicular, or acromioclavicular joints. Patients with these conditions may report that pain localizes to the shoulder but may also have referred pain into the neck or upper arm, which can mimic radicular pain. Symptoms tend to be brought on by overhead activities such as reaching to a high shelf or washing one’s hair.

2.Physical examination:

i)Neurologic examination: Normal. However, pain may limit isolated muscle testing of shoulder girdle and/or rotator cuff musculature which may be confounding.

ii) Provocative maneuvers: The two most commonly performed tests for shoulder impingement are the Neer test and the Hawkins test. In the Neer test, the examiner stabilizes the scapula while passively elevating the shoulder, in effect compressing the humeral head into the acromion.

iii)In the Hawkins test, the examiner elevates the arm to 90 degrees of abduction and applies an internal rotation force, sandwiching the tendons of the rotator cuff under the acromion.

iv)Both tests attempt to reduce the acromiohumeral interval to “impinge” the soft tissues in between these bony surfaces.

3.Electrodiagnostics: Normal.

4.Diagnostic injections: Diagnostic intra-articular shoulder injection can assist to rule in or rule out the shoulder joint as the underlying pain source. These can be performed with ultrasound or fluoroscopic guidance for precise placement. Further injections can be considered for isolating the suprascapular nerve using ultrasound, to determine if entrapment is the cause of shoulder versus neck pain.¹⁶^,¹⁷^,¹⁸

g) Brachial plexopathy:

1.Clinical presentation: Brachial plexopathy may occur due to trauma, physiological compression (thoracic outlet syndrome, discussed in Section 3.3b), or due to an idiopathic inflammatory event (Parsonage-Turner syndrome). The typical manifestation of brachial plexopathy is pain, which can occur in the anterior neck region and clavicular region, and radiate distally along affected peripheral nerve courses (Fig. 3.5). Sensory and motor deficits may be present as well, affecting the territory of the regional plexus involvement.
The diagnosis of idiopathic brachial plexopathy, or Parsonage-Turner syndrome, is made on the basis of clinical history, radiographic exclusion of cervical root pathology, and confirmatory electrodiagnostic studies. The classic presentation consists of the development of severe unilateral pain of the neck and shoulder region, which lasts for several days, and then subsequently subsides. The pain is not mechanical, and thus cannot be alleviated by body movement or positioning. Classically, as the pain subsides, weakness develops, with varying degrees of associated sensory deficit.

2.Physical examination: Neurologic examination will identify motor and sensory deficits in a peripheral pattern, which localizes to the plexus as opposed to isolated peripheral nerve or dermatome/myotome pattern. If the upper plexus is involved, the biceps and brachioradialis DTRs will be decreased or absent. If the lower plexus is involved, the triceps DTR will be decreased or absent.

3.Electrodiagnostics: NCS/EMG will reveal abnormal sensory and motor NCS of affected plexus branches.

4.Diagnostic injections: A brachial plexus block of local anesthetic (at the interscalene groove, supraclavicular, or infraclavicular areas) can be considered. Ultrasound guidance or nerve stimulation is strongly suggested for accuracy, and steroid can be added for potentially therapeutic relief.¹⁹ Imaging studies including a brachial plexus MRI can also be helpful.

Fig. 3.1 Dermatomes. (Reproduced from Alignment Examination. In: Vialle L, Vialle L, ed. AOSpine Masters Series, Volume 8: Back Pain. 1st Edition. New York: Thieme; 2016.)

Fig. 3.2 Upper posterior dermatomal distribution of C2–T1. (Reproduced from Motor. In: Albert T, Vaccaro A, ed. Physical Examination of the Spine. 2nd Edition. New York: Thieme; 2016.)