Neurosurgery
Mostafa El Khashab
Constantine J. Pella
Introduction
Neurologists are usually the principal providers for patients with multiple sclerosis (MS). However, there are many reasons when referral to neurosurgery is indicated. Conditions such as surgical removal of benign or malignant brain tumors and repair of aneurysms or arteriovenous malformations require neurosurgical consultation. This chapter will focus on problems seen in the MS patient such as back pain that often prompts referral to neurosurgery.
Low-Back Pain
A 43-year-old female presented to the emergency department complaining of severe acute low-back pain and left-sided sciatic pain. The pain in the left lower extremity corresponded to the distribution of the L5 nerve root. The patient did have sensory impairment in the L5 dermatome and had pain on straight leg raising at 30°. Magnetic resonance imaging (MRI) scans revealed foraminal stenosis at L4/5 with disc bulge at this level. Patient has history of MS. Patient underwent pain management consult and was treated with epidural injections as well as nonsteroidal anti-inflammatory medications and physical therapy for 6 weeks. She continued to be followed up. Conservative treatment was not successful, and the patient elected to have microdiscectomy and laminectomy.
Low-back pain is one of the most common symptoms neurosurgeons encounter in everyday practice. Patients with low-back pain are referred for neurosurgical care for a myriad of reasons, and a thorough clinical examination as well as a thorough workup is needed to pinpoint the diagnosis.
Lumbar spine stenosis is one of the most common causes of low-back pain. It most commonly affects the middle-aged and elderly population and is primarily seen by primary care physicians or orthopedic surgeons.1 The pathogenesis is due to entrapment of the cauda equine roots by hypertrophy of the osseous and soft tissue structures such as the ligamentum flavum which are surrounding the lumbar spinal canal. It is often associated with incapacitating pain in the back and lower extremities, difficulty ambulating, sensory impairment of lower extremities, and weakness and, if severe, may lead to a partial or a full-blown cauda equina syndrome with bowel or bladder disturbances.2
The characteristic syndrome associated with lumbar stenosis is termed neurogenic intermittent claudication, which must be differentiated from true intermittent vascular claudication, which is caused by atherosclerosis of the pelvic and femoral vessels. Although many conditions may be associated with lumbar canal stenosis, most cases are idiopathic and the symptoms are very vague on presentation. Imaging of the lumbar spine performed with computed tomography or MRI often demonstrates narrowing of the lumbar canal with compression of the cauda equina nerve roots by thickened posterior vertebral elements, facet joints, marginal osteophytes, or soft tissue structures such as the ligamentum flavum or herniated discs. Typically, treatment for symptomatic lumbar stenosis is usually surgical decompression with decompressive laminectomies at the level of stenosis with or without instrumented fusion. Surgical treatment would be considered after conservative treatment with medication and physical therapy as well as injections.3,4,5 Examples of injection treatment used by pain management include epidural injections as well as paravertebral blocks. Medical treatment alternatives, such as bed rest, pain management, and physical therapy, should be reserved for use in debilitated patients or patients whose surgical risk is prohibitive as a result of concomitant medical conditions.
Lumbosacral radiculopathy follows a dermatomal distribution and is usually well circumscribed.3 Sensory paresthesias are usually present in the involved root distribution, and MRI often reveals a disc herniation or bulge compromising the exiting nerve root within the spinal canal or at the foramen. Electromyography/nerve conduction testing can be helpful to demonstrate nerve root compression. Patients with lumbar disc disease are usually treated conservatively with medication, physical therapy, and injections. If conservative treatment fails, surgical microdiscetomy with or without foraminotomy is indicated.
Musculoskeletal disorders and back pain can occur as a result of irregular, asymmetric movement patterns and postures. This is typically what is referred to as mechanically induced low-back pain, and as this can be due to muscular weakness, spasticity, or imbalance, the diagnosis of MS must be strongly entertained. Typically, we will order an MRI scan as part of the workup and refer the patient to an MS center or to a neurologist. The aim is to investigate musculoskeletal disorders and risk factors of low-back pain in MS patients.
In the general population, osteoarthritis is a common cause of low-back pain. The prevalence of back pain is in the range of 5% to 22% and significantly limits work and daily activity.6 Osteoarthritis is one of the most common diseases in adults and affects 22.7% of population. Of the patients with osteoarthritis, 25% are restricted in major activities of daily living.
Greater understanding is needed as to what causes musculoskeletal disorders in MS. The most common cause is low-back pain, with a prevalence of 21.4%.6 Asymmetric posture, walking impairment, muscle weakness, sensory dysfunction, and spasticity could cause pain and musculoskeletal disorders. Lumbar disc degeneration as well as herniation is again one of the most common causes of low-back pain and sciatica due to nerve root irritation. Last but not least, vascular malformation of the spine with or without bleeding must be put in the differential diagnosis of low-back pain. It is not uncommon to miss this diagnosis without a thorough workup. MRI as well as CT imaging in addition to neurophysiological examination are important tools for the diagnostic workup.
Spasticity
Spasticity is a common symptom of MS, reported by 80% of patients.7 This symptom could induce abnormal pattern of ambulation, gait impairment, or pain, with a prevalence ranging from 29% to 86%.7 Spasticity is a term that defines a state of continuous increase in muscle tone. This immediately results in stiffness of muscles leading to interference in normal movement, speech, and gait.7 It is expressed in neurosurgical literature as a state of increased resistance to passive muscle stretch. There are other conditions that may be clinically mistaken for spasticity, and it is paramount to differentiate those conditions from spasticity. Common hypertonic movement disorders grouped under the term dystonia are markedly differentiated by the quantification of the amount of abnormal movement.
Spasticity is defined as an isokinetic disorder in which the movement is abnormal, but it is in fact not increased whereby dystonia is a hyperkinetic disorder in which the movement disorder is both increased and abnormal.7,8
Spasticity is clinically manifested by apparent tightness of muscles as well as a sensation of cramping associated with pain. As a result of those feelings, fatigue occurs even from attempted movement. There are variations in the degree and severity of spasticity ranging from mild to extremely disabling. The major components of spasticity are classified into whether they are of spinal origin or cerebral origin and denote damage to the portion of the brain or spinal cord that controls voluntary movement. The consequence of this damage is a disturbance of equilibrium between the central nervous system (CNS) and the muscular system represented in the muscles. This imbalance as we will show at a later stage is both mechanical as well as chemical and involves the release of chemical transmitters. The ultimate result of this imbalance is an increase in muscle activity.
Prevalence and Incidence
Spasticity is not only a common symptom of MS patients but also is condition that affects approximately 12 million people worldwide. Around 320,000 patients with MS have some degree of spasticity in the United States alone.7 However, spasticity can have a high prevalence in people with other disorders, such as traumatic brain injury (TBI) or other neurological diseases. Statistics on precise prevalence rates of spasticity are difficult to obtain due to the varying causes of spasticity (Table 30.1).
It is noteworthy as we explore the incidence of spasticity in MS patients to point out that treating spasticity has a very profound effect on the quality of life in those affected.9 In progressive types of MS, we know that there are neurological deficits that may not be very responsive to medical treatment. The inability to transfer combined with pain on movement and rest does cause great discomfort to the patient and can be an inconvenience to caregivers. In this context, the management of spasticity has proven to be of tremendous benefit in improving patient lives.
Certain factors can worsen symptoms of spasticity in MS patients. Some of those factors are extremes of temperature, infection, humidity, or even tight-fitting clothes.
Certain factors can worsen symptoms of spasticity in MS patients. Some of those factors are extremes of temperature, infection, humidity, or even tight-fitting clothes.
TABLE 30.1 THE MOST COMMON CAUSES OF SPASTICITY | |||||||||
|---|---|---|---|---|---|---|---|---|---|
|
Spasticity in Multiple Sclerosis (MS)
As MS is being increasingly recognized in patients at an earlier stage, more referrals are being made to neurosurgeons from MS neurologists for evaluation of patients with severe spasticity, particularly those patients who fail oral medical treatment regimens. Spasticity in MS is divided into two types of MS-related spasms: flexor and extensor. Flexor spasticity is an involuntary bending of the hips or knees (involving the hamstring muscles on the back of the upper leg). Typically for flexor spasticity, the hips and knees bend up toward the chest. Extensor spasticity is an involuntary straightening of the legs. It involves the quadriceps (muscles on the front of the upper leg) and the adductors (inner thigh muscles).7 The hips and knees typically remain straight, but the legs will be kept very close or even cross. See Figure 30.1 for reference. Spasticity involving the upper extremities is less common but does exist.
Symptoms
Spasticity is a very diverse phenomenon and may have multiple presentations and symptoms. These symptoms may vary in severity and presentation based on disease progression or the specific disease at hand. There may also be other factors affecting the presentation of symptoms, such as gender or age. Listed below are the most common symptoms of
spasticity. If left untreated, these factors can lead to decreased mobility and fatigue and ultimately can cause severe depressive symptoms and significant interference in family dynamics. Professional and social quality of life can deteriorate as well.7,8,9
spasticity. If left untreated, these factors can lead to decreased mobility and fatigue and ultimately can cause severe depressive symptoms and significant interference in family dynamics. Professional and social quality of life can deteriorate as well.7,8,9
 Figure 30.1. Diagram demonstrating the two types of spasticity commonly seen in multiple sclerosis (MS): flexor spasticity (above) and extensor spasticity (below). Reprinted with permission from Gibson B. Stretching for people with MS. National MS Society; 2016:1-26. Reprinted by permission of National Multiple Sclerosis Society. |
Hypertonicity (increased muscle tone), which often can cause muscle stiffness, rigid joints and bladder dysfunction.
Spontaneous muscle activity in the form of uncontrollable muscle spasms that are either isolated in nature or present as a series of rapid muscle contractions in the form of clonus. These can be extremely painful in nature and cause significant discomfort to the patient. These spasms can also affect the bladder.
Exaggerated tendon reflexes often associated with clonus.
As spasticity worsens, it interferes with all forms of movements, including walking, transfers, and simple muscle movements.
The tone changes associated with the inability of movement ultimately lead to change in posture, as the balance of flexor versus extensors of the trunk and limbs is disturbed.
Classification Criteria for Spasticity
Neurosurgeons tend to classify spasticity according to the anatomical categories, which were first described in cases of cerebral palsy (CP)9 (Table 30.2). These classifications are the most important aspect of spasticity for the practicing neurosurgeon, as the anatomical location (as well as severity) influences treatment strategy.
Pathophysiology
Detailed knowledge is required to understand the neurophysiology of spasticity. It is important to know the mechanisms of the CNS that control
and regulate movement and posture. In normal conditions, there is an equilibrium that exists between the alpha motor neurons being activated by pyramidal tracts and the alpha motor neurons being activated by basal ganglia, cerebellum and reticular activating system via contrary inhibition. This inhibitory influence is exercised by the reticulospinal tracts, which synapse on the motor neurons of the spinal cord. This is the fundamental cornerstone in understanding the baseline normal balance and which is the reason why those opposing influences create a normal muscle tone (Figure 30.2).8,10
and regulate movement and posture. In normal conditions, there is an equilibrium that exists between the alpha motor neurons being activated by pyramidal tracts and the alpha motor neurons being activated by basal ganglia, cerebellum and reticular activating system via contrary inhibition. This inhibitory influence is exercised by the reticulospinal tracts, which synapse on the motor neurons of the spinal cord. This is the fundamental cornerstone in understanding the baseline normal balance and which is the reason why those opposing influences create a normal muscle tone (Figure 30.2).8,10
TABLE 30.2 THE MOST COMMON CAUSES OF SPASTICITY | ||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| ||||||||||||||
Disturbance of this balance is how spasticity originates. The maintenance of posture and normal muscle tone is based on this concept. Spasticity results from any factor that can lead to decreased inhibition or facilitation of hypertonia.8 Spasticity ultimately results in coactivation of agonistic and antagonistic muscle groups at the same time. This immediately leads to an imbalance of excitatory neurotransmitters in the spinal cord (in particular, a lack of the inhibitory substance γ-aminobutyric acid [GABA]). If left untreated, chronic spasticity may lead to denervation, super sensitivity, and ultimately permanent soft tissue contractures requiring some form of surgical release. This is particularly evident in the ankle joint and Achilles tendon.
Diagnosis
A careful history and physical examination is imperative for the precise and accurate diagnosis of both the cause and classification of spasticity. Steps need to be taken to exclude other causes of spasticity as listed in Table 30.1. For MS patients, spasticity is typically heterogeneous in presentation but largely depends on the areas of demyelination. It can often present with leg adductor and extensor imbalance. In physical examination, the hallmark of locating specific muscle groups affected by spasticity is the resistance to passive muscle stretching correlated to the speed of the stretch. This technique allows for better diagnosis of spasticity among the different spasticity-causing neurological diseases. Physicians often use clinical scales to determine the severity of symptoms of spasticity. Two scales that are often used are the Ashworth Scale and Modified Ashworth Scale, as seen in Table 30.3.
Treatment Philosophy of Spasticity
Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
