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Spinal Cord Injuries: Non-Traumatic (FL INITIAL Autonomous Practice -Differential Diagnosis

2 Contact Hours
Only FL APRN's will receive credit for this course.
This course is only applicable for Florida nurse practitioners who need to meet the autonomous practice initial licensure requirement.
This peer reviewed course is applicable for the following professions:
Advanced Practice Registered Nurse (APRN)
This course will be updated or discontinued on or before Sunday, April 7, 2024

Nationally Accredited

CEUFast, Inc. is accredited as a provider of nursing continuing professional development by the American Nurses Credentialing Center's Commission on Accreditation. ANCC Provider number #P0274.


BOC

FPTA Approval: CE22-588747. Accreditation of this course does not necessarily imply the FPTA supports the views of the presenter or the sponsors.
Outcomes

≥ 92% of participants will know how to identify the most common causes of non-traumatic spinal cord injuries.

Objectives

Upon completion of this course, the participant will be able to:

  1. Explain the clinical assessment of a patient with suspected cauda equina.
  2. Compare and contrast the four regions of the spinal cord.
  3. Analyze the cross-sectional anatomy of the spinal cord.
  4. Identify types of vascular malformations of the spinal cord.
  5. Interpret differential diagnoses for various spinal cord dysfunctions.
  6. Determine symptoms of a spinal cord lesion based on location.
CEUFast Inc. and the course planners for this educational activity do not have any relevant financial relationship(s) to disclose with ineligible companies whose primary business is producing, marketing, selling, re-selling, or distributing healthcare products used by or on patients.

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To earn of certificate of completion you have one of two options:
  1. Take test and pass with a score of at least 80%
  2. Reflect on practice impact by completing self-reflection, self-assessment and course evaluation.
    (NOTE: Some approval agencies and organizations require you to take a test and self reflection is NOT an option.)
Author:    Desiree Reinken (MSN, APRN, NP-C)

Introduction

Spinal cord injuries (SCI) are debilitating neurological conditions affecting the quality of life. An estimate of the incidence of spinal cord injuries in the US is approximately 54 cases per one million people, equivalent to about 17,900 new cases of SCI each year (Alizadeh et al., 2019). The average age of SCI is 43 years of age and approximately 78% of cases are in males. Around 30% of individuals with SCI are re-hospitalized one or more times during any given year following injury. Eighteen days is the average length of hospital stay (Alizadeh et al., 2019).

Case Study

Jacob is a 22-year-old male, who had an accident while at the beach with his friends when his head and back hit a sandbank as he was surfing. Jacob hit his head and his back and was floating on the water for approximately 25 seconds. Jacob’s friends were on scene and called for help immediately. Jacob was conscious but had a cough as he ingested water.

When paramedics arrived, Jacob was in a supine position. He reported severe pain in his head, neck, back, and the inability to move his arms or legs. Jacob was oriented and pupils were reactive. Jacob’s vital signs revealed a blood pressure of 142 / 82, heart rate of 110 beats per minute, respirations of 24 per minute. Jacob’s head was immobilized by a c-collar, he was provided oxygen, and he was placed on a stretcher.

Past Medical History:

  • Asthma, broken fibula

Social History:

  • Non-smoker
  • Social drinker
  • No drug use
  • Currently resides in a home with one friend (roommate)

Initial Medical Assessment

Vital Signs:

  • Blood Pressure 142 / 82
  • Heart Rate 110
  • Respiratory Rate 24 with shallow breathing
  • Oral Temperature 37.1 Degrees Celsius
  • Color Pink
  • Skin Cold and Clammy to the touch
  • Oriented

Reflexes:

  • Minimal biceps brachii stretch reflexes, with no wrist or triceps extensor reflexes
  • Stretch reflexes in all extremities absent

Sensation:

  • Not able to localize touch

Strength:

  • Able to elevate his shoulders and isometrically contract his biceps brachii slightly in each arm, but could not raise either arm against gravity
  • Lower extremities were flaccid, despite attempts to move them

Diagnostics:

  • A cervical spine x-ray showed Unstable C6 Compression Fracture or Axial Loading Injury (Burst Fracture)
  • MRI of the spine showed a C6 lesion
  • CT of the brain showed a mild contusion

Treatment:

  • ICU placement for stabilization
  • Intubated to manage respiratory function
  • Spinal Fixation at C4 - C8 with Spinal Decompression on Day 2

Medications given:

  • Steroids
  • Morphine
  • Anesthesia

Life Expectancy

Life expectancy for individuals following an SCI is relatively low, with no improvement since 1980. Depending on the age of injury, life expectancy is drastically different. The most common causes of death for those with an SCI appear to be pneumonia and septicemia. There are increasing mortality rates for endocrine, metabolic, and nutritional diseases, accidents, nervous system diseases, musculoskeletal disorders, and mental disorders in SCI patients.

Complications

Respiratory complications are the most significant cause of morbidity and mortality in SCI patients. The level and amount of respiratory complications depend on the SCI injury level (Berlowitz et al., 2016). SCI often leads to respiratory dysfunction, which includes insufficiency of respiratory muscles, reduction in vital capacity, ineffective cough, decreased lung and chest wall compliance, and excess oxygen cost of breathing. It has been found that SCI patients have a high prevalence of sleep-related respiratory disorders, particularly obstructive sleep apnea syndrome, which can adversely affect the quality of life. Up to 45% of SCI patients have a sleep disorder (Berlowitz et al., 2016); Sezer et al., 2015).

Along with respiratory complications, cardiovascular complications are common as well. Common cardiovascular complications in SCI are orthostatic hypotension, autonomic dysreflexia, impaired cardiovascular reflexes, reduced transmission of cardiac pain, loss of cardiac reflex acceleration, cardiac atrophy with tetraplegia due to loss of left ventricular mass, and pseudo-myocardial infarction (Sezer et al., 2015; Yarar-Fisher et al., 2017).

The loss of genitourinary and gastrointestinal function in SCI is common for patients who have had a chronic injury. SCI is recognized to cause bladder dysfunction, often referred to as the neurogenic bladder (Tate et al., 2016). Incontinence, renal impairment, urinary tract infection, stones, and poor quality of life are complications of neurogenic bladder (Taweel et al., 2015). Many patients with a neurogenic bladder will require management to ensure low-pressure reservoir function of the bladder, complete emptying, and dryness (Taweel et al., 2015; Gater, 2020; Braaf et al., 2017).

Along with neurogenic bladder, neurogenic bowel is also a complication of SCI. Neurogenic bowel occurs when there is a colon dysfunction due to a lack of nervous control (White et al., 2019). Nearly 40% of patients with an SCI will experience neurogenic bowel affecting the quality of life and social activities (White et al., 2019; Emmanuel, 2019).

One of the most common complications of SCI is spasticity. Spasticity is characterized by hypertonus, increased intermittent or sustained involuntary somatic reflexes (hyperreflexia), clonus, and painful muscle spasms (McKay et al., 2018). The pathogenesis of spasticity in SCI patients is not clear but serves as a significant source of burden (Sezer et al., 2015; Abel & Rupp, 2015; Finnerup, 2017).

As imagined, chronic pain is frequently associated with an SCI. At least 80% of patients with an SCI experience some form of pain (Hagen & Rekand, 2015). There are two forms of pain that are most common after an SCI. Neuropathic pain can occur anywhere near the level of injury. Neuropathic pain above the level may arise from complex regional pain syndromes. After SCI, chronic musculoskeletal pain, a type of nociceptive pain, may occur with gait, abnormal posture, and overuse of the arm and shoulder (Hagen & Rekand, 2015).

A significant secondary complication of SCI is pressure ulcers. Pressure ulcers become localized injury to an area of the skin and/or underlying tissue, can be a life-threatening infection (Bhattacharya & Mishra, 2015). Pressure ulcers are usually located in the ischium (31%), trochanters (26%), and sacrum (18%), and occasionally the heel (Sezer et al., 2015).

The last well-known complication of SCI is osteoporosis. Low bone mass with deterioration of the skeletal structure characterizes osteoporosis. Those with an SCI are predisposed to disuse osteopenia from prolonged immobilization and overall decreased mobility and independent functional capabilities. The first 2 weeks after the initial injury or SCI is recognized as the most vulnerable period for decreased bone formation (Soleyman-Jahi et al., 2018).

Spinal Cord Anatomy

The spinal cord, the most important structure between the body and the brain, is a vital link to the rest of the body. The spinal cord lies from the foramen magnum to the lumbar vertebrae. The spinal cord length is 40 to 50 cm long and 1 cm to 1.5 cm in diameter. There are two consecutive rows of nerve roots on each side of the spinal cord. The nerve roots of the spinal cord form 31 pairs of nerves. The spinal cord is a structure of nerve tissue that is composed of white and gray matter and is divided into four different regions: cervical (C), lumbar (L), thoracic (T), and sacral (S). The nerves in the spinal cord contain motor and sensory nerve fibers to and from all body parts (Image 1). Each spinal cord segment innervates a dermatome (Dauleac et al., 2019).

Image 1: Anatomy of the Spinal Cord

graphic showing spinal cord and sections

Longitudinal Organization

The different spinal cord regions can be visually distinguished from one another. Two spinal cord enlargements can be visualized: The cervical enlargement, which extends between C3 to T1, and the lumbar enlargements, extending between L1 to S2 (Samaddar, 2016).

The cord is segmentally organized, with 31 segments defined by 31 pairs of nerves exiting the cord. The nerve roots are divided into 12 thoracic, 8 cervical, 5 lumbar, 5 sacral, and 1 coccygeal nerve (Image 2). Ventral and dorsal roots enter and leave the vertebral column through intervertebral foramen at the vertebral segments corresponding to the spinal segment (Samaddar, 2016).

Image 2: Segments of the Spine

graphic showing the structure of the segments of the spine

The C1 through C8 cord segments lie between C1 and C7 vertebral levels. C1 through C7 nerves then emerge above their respective vertebrae. The C8 nerve root occurs between the C7 and T1 vertebral bodies. The remaining nerve roots appear below their respective vertebrae. Between T1 through T8 lie the T1 through T12 cord segments. The five lumbar cord segments are located at T9 through T11 vertebral levels. The S1 through S5 segments are between T12 to L1 (Samaddar, 2016).

Dermatomes

A dermatome is in the skin, and they are supplied by a single spinal nerve to relay information between the rest of the body and the central nervous system (Kondo et al., 2016). Spinal nerves form from the dorsal nerve roots and the ventral nerve roots which branch from the dorsal and ventral horn of the spinal cord, respectively. The spinal nerves exit through the intervertebral foramina or neuroforamina and travel along their respective dermatomal distributions from posterior to anterior, creating the specific, observable dermatomal patterns. In total, there are 31 distinct spinal segments and thus 31 distinct spinal nerves bilaterally.

Spinal Cord Nerves

Cervical nerves: Eight pairs of cervical nerves exist. The nerves are numbered C1 through C8, originating from the neck.

Thoracic nerves: Twelve pairs of thoracic nerves are numbered T1 through T12. They originate in the part of the spine that makes up the torso.

Lumbar nerves: Five pairs of lumbar nerves come from the lower back and are designated L1 through L5.

Sacral nerves: Five pairs of sacral spinal nerves exist. They are associated with the sacrum.

Coccygeal nerves: There is one pair of coccygeal spinal nerves. This pair of nerves originate from the coccyx area or tailbone (Kondo et al., 2016).

The spinal cord and the spinal nerves receive their vascular supply predominantly via the anterior spinal artery and two posterior spinal arteries. The anterior spinal artery supplies the bulk of the spinal cord, the anterior two-thirds, while the two posterior spinal arteries supply the dorsal columns. These spinal arteries branch off the vertebral arteries in the skull and proceed out of the skull and course inferiorly along the spinal cord (Whitman & Adigun, 2021).

Image 3: Dermatomes in the Spine

image showing dermatomes in the spine

Cervical Cord

The atlas and the axis support the head at the atlanto-occiput junction (Seif et al., 2020). The atlanto-axis junction is the interface between the first and second vertebra. The cervical spine (neck region) consists of C1-C7 vertebrae separated from one another by intervertebral discs. The cervical discs allow the spine to move freely (Talekar et al., 2016). Cervical spinal segments run through the skin and muscles of the upper extremity and diaphragm (Image 4):

  • C3 through C5 innervate the diaphragm through the phrenic nerve
  • C4 through C7 innervate the arm and shoulder
  • C6 through C8 innervate the forearm extensors and flexors
  • C8 through T1 innervate the hand muscles (Seif et al., 2020; Talekar et al., 2016).

Image 4: Cervical Spine Roots

image showing the cervical spine roots

Thoracic Cord

The longest region of the spine is the thoracic area, and it is also the most complex (Alizadeh et al., 2019). The thoracic spine runs from the neck down to the abdomen and it connects with the cervical spine above that sits above the lumbar spine. This region is the only one attached to the rib cage (Hachem et al., 2017). It has 12 vertebrae stacked and labeled from T1 down to T12 (Hachem et al., 2017). The foundation of the thoracic region is held by these vertebrae (Image 5).

Image 5: Thoracic Spine

graphic showing thoracic spine from the skeleton posterior

Lumbosacral Cord

The lower back comprises the lumbar spine formed by vertebral bones, intervertebral discs, nerves, muscles, ligaments, and blood vessels. The top of the lumbar spine is where this cord ends. The remaining nerve roots of this cord are called the cauda equina. They descend down the rest of the spinal canal. A single lumbar motion segment is made up of (Toossi et al., 2021):

  • Two consecutive vertebrae are stacked vertically.
  • A tough fibrous covering surrounds an intervertebral disc with a soft inner core between the different vertebrae. The disc allows for flexibility and protects from jarring movements.
  • Two facet joints are located in the lower back and allow bending and twisting movements.
  • Two spinal nerves that branch off from the spinal cord or cauda equina (Toossi et al., 2021). These spinal nerves pass through small holes between consecutive vertebrae and travel down the rear pelvis and legs (Image 6).

Image 6: Lumbar Spine Structure

image of the lumbar spine structure

Cauda Equina

The terminal end of the spinal cord is located in the lower back. The spinal cord and the cauda equina are essential structures (Dias et al., 2017). The spinal canal protects the other structures by providing a robust and bony casing. The cauda equina are nerve roots that travel down from the spinal cord, and the conus medullaris. There are nerve roots from the L2 to the Co1 in the coccygeal area. The cauda equina nerve roots exit from the spinal canal from its respective vertebral (Barraclough, 2020; Dias et al., 2017; Nater & Fehlings, 2015).

Cross-Sectional Anatomy

In the transverse section, the spinal cord is incompletely divided into right and left halves by an anterior (ventral) median fissure and a posterior (dorsal) median sulcus and septum; they are joined by a commissural band of nervous tissue that contains a central canal (van der Burgh et al., 2019). There are both an outer layer and an inner core of the spinal cord; the inner layer is white matter. Grey matter amounts reflect the number of neuronal cell bodies present. It is proportionately most significant in the cervical (C3–T2) and lumbar (L1–S3) enlargements, which contain the neurons that innervate the limbs (de Albuquerque et al., 2017). White matter is most accumulated at cervical levels and decreases at lower levels (Image 7). This is because the descending tracts shed fibers, and ascending tracts accumulate fibers (de Albuquerque et al., 2017; van der Burgh et al., 2019).

Image 7: Cross-Section of the Spinal Cord

graphic showing the cross section of the spinal cord

Dorsal Horn

The dorsal horn contains the first relay for afferent inputs. The superficial dorsal horn contains some neurons that maintain the selectivity for modalities encoded by the primary afferent endings (Jensen & Brownstone, 2019).

In most neurons in the dorsal horn, various combinations of these inputs are integrated to detect features (such as edges, location on the skin, speed of movement, harmful hot objects, etc.). This allows for generating useful motor outputs, such as moving a limb away from a hot object, wiping away an insect crawling on the skin, or scratching a biting insect (Harding et al., 2020).

The dorsal horn neurons are modulated by inputs from higher brain centers. Inputs from other centers can significantly modify the amplitude of signals relayed from primary afferent neurons (Harding et al., 2020; Jensen & Brownstone, 2019).

Ventral Horn

The lower motor neurons cell bodies are located in the ventral horn. The ventral horn has axons that leave via the ventral spinal roots on their way to innervate muscles. The ventral horns are bilateral structures that form the anterior projection of this shape (Huber et al., 2015; Huber et al., 2018).

Two types of lower motor neurons exist:

  • Alpha motor neurons: Innervating extrafusal muscle fibers
  • Gamma motor neurons: Innervating intrafusal muscle fibers

The neurons in the ventral horn are arranged with neurons innervating the axial musculature of the neck and trunk. These neurons tend to be localized more medially. The innervating peripheral muscle fibers are located more laterally (Grabher et al., 2017).

White Matter

White matter containing both myelinated and unmyelinated nerve fibers surrounds the gray matter. Both matters conduce information that goes up (ascending) or down (descending) the cord (Guo et al., 2019). The white matter is divided into two areas, which include the dorsal (or posterior) column (or funiculus), ventral (or anterior) column, and lateral column. The anterior white matter resides in the center of the spinal cord. Crossing nerve fibers are located in this matter and belong to the many tracts of the spinal cord (Image 8). Three nerve fiber types can be distinguished in the white matter of the spinal cord:

  1. Long ascending nerve fibers originally from the column cells
  2. Long descending nerve fibers originating from brainstem nuclei
  3. Shorter nerve fibers that interconnect the fibers responsible for the coordination of reflexes

Ascending tracts are found in the columns of the spinal cord. Descending tracts are located in the lateral and the anterior columns of the spinal cord (Chaddock-Heyman et al., 2018; Grossman & Ruiz, 2021).

Image 8: White Matter

graphic showing afferent sensory information and anterior median fissure

The columns can be divided into tracts which are sometimes called fasciculi. These tracts are named for the structures that they connect with. The spinothalamic tract shows that the fibers carry information from the spinal cord to areas of the brain (Seiler et al., 2018).

Some of the tracts cross over in the spinal cord. When this crossing occurs, it is termed contralateral. Most motor control in the body is contralateral. An example of this is the right arm being controlled by the motor area in the left brain. An ipsilateral relationship is when the origin and destination are on the same side of the body (Seiler et al., 2018).

Image 9: White Matter Tracts

graphic showing the descending and ascending tracks of the spinal column

Ascending Tracts:

The ascending tract's nerve fibers are located in the dorsal root ganglion (DRG). The ascending tracts transmit sensory information to higher levels of the CNS. The ascending gracile and cuneate fasciculi occupy the dorsal column, sometimes called the dorsal funiculus. These fibers carry information related to tactile, two-point discrimination of simultaneously applied pressure, vibration, position, conscious proprioception, and movement sense. In the funiculus, the neospinothalamic tract is located both anteriorly and laterally. It carries temperature, pain, and crude touch information. Both the ventral and dorsal tracts have unconscious or subconscious information from joints and muscles of the lower extremities to the brain. There are four tracts in the ventral column: the paleospinothalamic tract, the spinoolivary tract, the spinoreticular tract, and the spinotectal tract. Intersegmental nerve fibers are located around the gray matter and carry pain information to the brain stem and diencephalon (Seiler et al., 2018).

Descending Tracts:

The descending tracts in the spinal cord originate from cortical areas in the brain stem. The descending pathway carries information associated with maintaining motor activities such as posture, muscle tone, balance, and somatic and visceral activity. These specific tracts carry information that is related to voluntary movement. Other tracts mediate balance and posture. Lissauer's tract lies between the dorsal horn and the spinal surface, carrying the descending fibers that regulate incoming pain sensations (Seiler et al., 2018).

Neurons

The upper and lower motor neurons comprise a two-neuron pathway responsible for various movements. Different neurotransmitters are used to relay signals in the neurons. Upper motor neurons use glutamate, and lower motor neurons use acetylcholine. The lower motor neuron aids in transmitting signals from the upper motor neuron to perform movements (Image 10).

Three types of lower motor neurons exist: Somatic motor neurons, general visceral motor neurons, and special visceral efferent (branchial) motor neurons (Zavvarian et al., 2020).

Image 10: Spinal Cord Neurons

graphic showing spinal cord neurons

A two-neuron circuit is created between both sets of neurons. The upper motor neurons travel down to the brain or the spine. The lower motor neurons start in the spinal cord and innervate various muscles and glands (Diaz & Morales et al., 2016). Understanding the difference between upper and lower motor neurons and their pathway is crucial to diagnosing these neuronal injuries and localizing the lesions efficiently. The upper and lower motor neurons comprise a two-neuron pathway responsible for movement. Upper and lower motor neurons utilize different neurotransmitters to relay their signals. Upper motor neurons use glutamate, while lower motor neurons use acetylcholine (Diaz & Morales et al., 2016; Genc et al., 2019).

Upper motor neurons are located in the cerebral cortex's pre-motor and primary motor region, also called the "motor strip." Typical clinical symptoms of lesions in the upper motor neurons include uncontrolled movement, spasticity, and decreased sensitivity to superficial reflex stimulation (Genc et al., 2019).

The characteristics of lower motor neurons exist in the axonal extension and connection in the CNS. Since lower motor neurons are cholinergic, they receive inputs from upper motor neurons, sensory neurons (SNs), and interneurons (INs). Once damaged, paralysis is a typical clinical symptom of lower motor neuron lesions. This is the only route to convey specific information to the muscles. Lower motor neurons are classified into three groups according to the type of target they innervate (i) branchial, (ii) visceral, and (iii) somatic MNs (Diaz & Morales et al., 2016; Genc et al., 2019).

Blood Supply and Lymphatics

Arterial Supply: The spinal cord blood supply comes from many different sources of the body. A single anterior spinal artery (ASA) and two posterior spinal arteries (PSA) are the primary sources of blood supply. The vertebral arteries form the ASA that originates from the subclavian artery. The vertebral arteries then pass through the transverse foramen and then through the foramen magnum to become the basilar artery (Gofur & Singh, 2021). Before combining to form the basilar artery, the vertebral arteries branch off and become the anterior spinal artery. This artery travels down the spinal cord through the anterior sulcus (Image 11). The posterior spinal arteries branch from the posterior inferior cerebellar artery (PICA). They then travel down the spinal cord through the two posterior sulci. The ASA provides blood to nearly two-thirds of the spinal cord while the PSA delivers blood to the spinal cord's posterior side (Gofur & Singh, 2021; Yuan, 2016; Yuan et al., 2019).

Venous Supply: The spinal cord blood supply drains from the anterior spinal and posterior spinal vein. From here, it drains into the internal vertebral venous plexus, which is located in the epidural space (Yuan, 2016; Yuan et al., 2019). These veins empty into the external vertebral venous plexus from the vertebral veins. Blood drainage depends on the location; for example, the thoracic region of the spinal cord empties into the azygous system. Of note, the Batson venous plexus (which drains many organs in the pelvis region, including bladder, prostate, and rectum) feeds into the internal vertebral plexus, and the Batson plexus does not contain valves (Colman et al., 2015; Gofur & Singh, 2021).

Image 11: Blood Supply to the Spinal Cord

graphic showing blood supply to the spinal cord

Lesions

A lesion is a name given to an abnormal change that occurs to any tissue or organ caused by a disease or injury. The abnormal growths of tissue can occur from some form of trauma, including an accident or spinal cord injury; the different spinal lesions can cause a wide array of dysfunctions — such as motor and sensory deficits (Table 1). There are many lesions and syndromes that affect the spinal cord (Gofur & Singh, 2021).

Table 1 Spinal Cord Syndromes
SyndromeClinical ManifestationsCauses
Segmental (Transection) SyndromeLoss of all sensory modalities, weakness below affected level; bladder dysfunctionTrauma, spinal cord hemorrhage, epidural or intramedullary abscess, transverse myelitis, epidural metastasis
Dorsal (Posterior) Cord SyndromeLoss of proprioception, vibratory sensation, variable weakness; bladder dysfunctionTabes dorsalis, Friedreich ataxia, subacute combined degeneration, AIDS myelopathy, epidural and extramedullary metastases, cervical spondylotic myelopathy, multiple sclerosis, atlantoaxial subluxation
Ventral Cord (Anterior Spinal Artery) SyndromeLoss of pain and temperature sensation, weakness; bladder dysfunctionSpinal cord infarction, intervertebral disc herniation, radiation myelopathy, HTLV-1
Brown Sequard (Hemi-Cord) SyndromeIpsilateral weakness and loss of proprioception; contralateral loss of pain and temperature sensationKnife or bullet injuries, multiple sclerosis, spinal cord tumors, disc herniation, infarction, infection
Central Cord SyndromeSegmental loss of pain and temperature; weakness often more remarkable in the arms than legsSyringomyelia, intramedullary tumor, acute injury in cervical spondylotic myelopathy
Pure Motor SyndromeWeakness without sensory disturbancePoliomyelitis, post-polio syndrome, primary lateral sclerosis, amyotrophic lateral sclerosis, HTLV-1, hereditary spastic paraplegia, lathyrism, progressive muscular atrophy, electric shock-induced myelopathy
Conus Medullaris SyndromeBladder and rectal dysfunction; saddle anesthesiaDisc herniation, spinal fractures, tumors
Cauda Equina SyndromeAsymmetric multiradicular pain, leg weakness, and sensory loss; bladder dysfunctionIntervertebral disc herniation, epidural abscess, epidural tumor, intradural extramedullary tumor, lumbar spine spondylosis, spinal arachnoiditis, chronic inflammatory demyelinating polyneuropathy, sarcoidosis, carcinomatous meningitis, cytomegalovirus, herpes simplex virus, herpes zoster virus, Epstein Barr virus, Lyme disease, mycoplasma, and tuberculosis

Segmental (Transection) Syndrome

The most severe form of SCI is transection syndrome. Spinal cord transection occurs when there is a complete interruption of white matter, gray matter, or ant nerve roots in the spinal cord (Wolpaw, 2018). It compromises normal blood supply and cerebrospinal fluid circulation. Symptoms of spinal cord transection reflect the level at which the spinal cord is affected. The immediate phase of SCI is initiated by the injury itself and lasts as long as 2 h after injury (ALL & Al-Nashash, 2021). Hemorrhage, edema, ischemia, neural tissue disruption, and loss of spinal cord function below the injury characterize the immediate phase. The direct mechanical disorder causes local cell death (Wolpaw, 2018). Disruption of communication between the brainstem and autonomic nervous system is responsible for clinical presentation. Hallmarks of the acute phase of SCIs include hypertension, reflex bradycardia, tachyarrhythmia, and spinal shock. Furthermore, microvascular disturbances lead to ischemia and cell death in spinal cord tissue distant from the actual injury site (ALL & Al-Nashash, 2021).

The hallmarks of the subacute phase (48 h to 14 days after injury) are restoring the blood-brain barrier and resolving edema. The late phase (more than 6 months after injury) is characterized by Wallerian degeneration, axonal terminal and collateral sprouting, neuronal cell body atrophy, mesenchymal cell migration, demyelination, and plasticity of receptive fields, reflex circuits, and motor control systems (ALL & Al-Nashash, 2021; Wolpaw, 2018).

Dorsal (Posterior) Cord Syndrome

Posterior cord syndrome, a rare type of incomplete spinal cord injury, affects the dorsal columns of the spinal cord (Image 12). When only a small portion of the spinal cord is damaged, this is called an incomplete spinal cord syndrome. This syndrome can cause various symptoms that depend on the specific spinal tracts that have been injured. This occurs as a result of damage to the posterior columns. This can be caused by trauma to the spinal cord and damage to the protective myelin sheath (Kunam et al., 2018).

Those with posterior cord syndrome typically present with sensory ataxia, impaired voluntary movement coordination caused by a lack of proprioception (McKinley et al., 2021). This can result in decreased balance, poor coordination, unsteady walking, and frequent falls. These symptoms typically worsen in dark environments or when a person closes their eyes. Some individuals may experience sensory losses, including an impaired sensation of vibration and fine touch, while their sense of pain and temperature is preserved (Kunam et al., 2018; McKinley et al., 2021). In some cases, large spinal cord lesions can also affect surrounding spinal tracts, such as those responsible for motor function and involuntary body functions (e.g. blood pressure, digestion, breathing). Involvement of these tracts can subsequently lead to various clinical manifestations, including muscle weakness and spasticity, decreased tendon reflexes, urinary or bowel incontinence, or low blood pressure, depending on the severity of the lesion.

Posterior cord syndrome can be diagnosed with clinical tests to assess neurological function. Sensory problems can be assessed by asking an individual to identify different sensations (e.g. temperature, pain, vibration) while touching the skin with specific tools (e.g. dull needle, tuning fork, cotton swabs, etc.). Additionally, Romberg’s test can be used to demonstrate sensory ataxia. This test is performed by asking an individual to close their eyes and stand straight with their feet together while the examiner looks for signs of loss of balance. If the individual is not able to stand straight without opening their eyes or swaying to either side, the result is considered to be positive for sensory ataxia (Kunam et al., 2018; McKinley et al., 2021).

Image 12: Location of Lesion in Dorsal Cord Syndrome

graphic showing location of lesion in dorsal cord syndrome

Ventral (Anterior Spinal Artery) Cord Syndrome

Ventral cord syndrome is one of the incomplete cord syndromes and affects the anterior parts of the cord (Image 13). This results in a pattern of neurological dysfunction dominated by motor paralysis and loss of pain, temperature, and autonomic function. The most common cause is anterior spinal artery ischemia (Howard, 2019).

If the anterior half to two-thirds of the spinal cord is involved, this will result in a familiar pattern of neurological impairment that consists of (Klakeel et al., 2015; Vuong et al., 2016):

  • Complete paralysis below the level of the lesion
  • Loss of pain and temperature sensation at and below the level of injury
  • Autonomic dysfunction, including orthostatic hypotension
  • Bladder, bowel, and sexual dysfunction may occur
  • 2-point discrimination, proprioception, and vibratory senses remain intact

Causes of Ventral Cord Syndrome include:

  • Ischemia/infarction (anterior spinal artery syndrome)
    • Atherosclerotic thromboembolism
    • Aortic pathology
      • aortic aneurysm
      • aortic dissection
      • aortic thrombosis
      • aortic surgery/intervention
  • Anterior spinal artery pathology
    • Penetrating trauma (e.g., stabbing)
    • Fibrocartilaginous embolism
    • Arterial dissection (e.g., catheter angiography)
  • External compression or damage to the anterior spinal cord
    • Spinal tumor (e.g., intrathecal extramedullary)
    • Herniated discs
    • Epidural collections (e.g., epidural hematoma and epidural abscess)
    • Kyphoscoliosis
    • Trauma
      • Vertebral body fractures
      • Direct stab injuries (Zhou et al., 2017)

Image 13: Location of Lesion in Ventral Cord Syndrome

graphic showing location of lesion in ventral cord symdrome

Brown-Sequard (Hemi-Cord) Syndrome

Brown-Séquard syndrome occurs when spinal cord hemisection causes a neurologic syndrome. This syndrome produces weakness or paralysis and proprioceptive deficits ipsilateral to the lesion and loss of temperature and pain sensations on the opposite side (Image 14). The presentation and symptoms of Brown-Séquard syndrome vary in severity as it is an incomplete loss (Zeng et al., 2018). Traumatic injuries are far more common causes of this syndrome. Gunshot wounds, motor vehicle accidents, stabbings, blunt trauma, or a fractured vertebra are among the causes. To a lesser extent, Brown-Séquard Syndrome can result from many non-traumatic causes, including vertebral disc herniation, cysts, cervical spondylosis, tumors, multiple sclerosis, and cystic disease radiation, decompression sickness (Meng et al., 2016; Zeng et al., 2018).

With Brown-Sequard syndrome, a clean-cut hemi-section is usually not visible. However, partial hemi-section is evident, and it often includes all the nerve tracts lying along the path in the injured area involved. If the lesion is involved in the cervical region, for example, C5 to T1, that hemi-section would create deficits. A neurological examination should comprise a detailed motor and sensory evaluation, although sometimes it is hard to perform the physical exam in the beginning especially after trauma because patients are in spinal shock. Clinically, there would be an ipsilateral sensory loss of all sensations, pressure, vibration, position and flaccid paralysis at the level of the lesion and spastic paraparesis below the level of the lesion; contralaterally there would be loss of pain and temperature (Shams & Arain, 2021).

Image 14: Location of Lesion in Brown-Sequard Syndrome

graphic showing location of lesion in brown-sequard syndrome

Central Cord Syndrome

The most common cause of paralysis is central cord syndrome. This syndrome is characterized by impairment in the arms, hands, and legs to a lesser extent (Divi et al., 2019). The ability of the brain to send and receive signals below the site of the injury is decreased. Central cord syndrome is characterized by damage to nerve fibers that carry information directly. These nerves are a vital function of the upper extremities. There may be sensory loss below the site of the injury. Loss of bladder control may also occur, and painful sensations such as tinging, burning, or dull ache may occur (Badhiwala et al., 2020; National Institute of Neurological Disorders and Stroke [NINDS], 2019; Smith, 2021).

Most individuals with central cord syndrome will be older patients who have experienced a fall with neck hyperextension. These patients will have more significant upper extremity impairments (NINDS, 2019). There may be sensory deficits below or above the level of injury (Image 15). The feeling of light touch may also be impaired in this syndrome. The most common sensory deficits are in a "cape-like" distribution across their upper back and down their posterior upper extremities. They will often have neck pain at the site of spinal cord impingement. Bladder dysfunction (most commonly urinary retention) and priapism can also be signs of upper motor neuron dysfunction. The sacral sensation is usually preserved, but the clinician should assess the rectal tone to evaluate the severity of the compression (Ameer, 2021).

Image 15: Location of Lesion in Central Cord Syndrome

graphic showing location of lesion in central cord syndrome

Pure Motor Syndrome

Pure motor hemiparesis presents with weakness on one side of the body (face, arm, and leg) without cortical signs and sensory symptoms. The most common cause is intrinsic penetrator disease, but lacunar infarcts can occur secondary to atherosclerosis. These infarcts mainly occur in the basal ganglia and lenticular nucleus. Lacunar infarcts occur in the spinal cord, cerebellum, cerebral gyri.

Conus Medullaris Syndrome

Cauda equina and conus medullaris syndromes are very similar and overlap in anatomy and clinical presentation symptoms. Conus medullaris syndrome (CMS) results when there is compressive damage to the spinal cord from T12-L2. This syndrome is a neurosurgical emergency. This syndrome can present with back pain that radiates, motor and sensory dysfunction of the lower extremities, bladder and/or bowel dysfunction, saddle anesthesia, and sexual dysfunction (Korse et al., 2017). The most common cause of compression in most cases is a herniated lumbar intervertebral disc. Other causes of this syndrome include sepidural abscess, spinal epidural hematoma, diskitis, tumors, trauma, spinal stenosis, and aortic obstruction (Borni et al., 2021; Brouwers et al., 2017).

Cauda Equina Syndrome (CES)

Lumbar and sacral nerve root dysfunction of the cauda equina results in cauda equina syndrome (CES). A herniated disc most commonly causes this in the back's lumbar region. One single injury may cause a disc to herniate, but often there is not an identified cause. The disc herniation in the cauda equina is very extensive. If a patient with a smaller spinal canal due to arthritis, a smaller disc herniation can produce CES (AANA, 2021).

Red flags and findings consistent with CES include bilateral neurogenic sciatica, reduced perineal sensation, altered bladder function leading to painless urinary retention, loss of anal tone, and loss of sexual function. In isolation, history and examination findings demonstrate poor sensitivity.

Urination, defecation, and sexual function are critical components of normal function affected in CES. The bladder's innervation is via the pelvic splanchnic nerves (S2-S4), with sensory input from the hypogastric, pelvic, and pudendal nerves, while the autonomic control is primarily via the parasympathetic system. Stimulation of these nerves causes bladder emptying through stimulation of the detrusor muscle and inhibition of the urethral sphincter. Damage to these nerves results in bladder atony with urinary retention and an absence of voluntary control (AANA, 2021).

Postvoid bladder volume assessments can assist in the evaluation, but the diagnosis typically involves magnetic resonance imaging (MRI) or computed tomography myelography if MRI is not available. Treatment relies upon surgical consultation and operative intervention for decompression (Long et al., 2020).

Image 16: Cauda Equina Syndrome

graphic of cauda equina syndrome (CES)

Lhermitte's Sign

An electric shock-like sensation when flexing the neck is called Lhermitte's sign. This shock-like sensation radiates down the spine and often into the legs and arms.

A miscommunication between demyelinated nerves causes Lhermitte's sign. The pathophysiology of Lhermitte's sign was described as the stretching of the hyperexcitable demyelinated dorsal column of the spinal cord, particularly at the cervical level, thus triggering an electric shock-like sensation. To date, hyperexcitability is considered the primary pathophysiological mechanism for the occurrence of Lhermitte's sign (Chu et al., 2020; Khare & Seth, 2015).

Diagnosis

The differential diagnosis of myelopathy is broad but can be narrowed down by the clinical syndrome (Table 1, above). The examination and patient history also limit the differential diagnoses and aid in tailoring the diagnostic work-up. Clinical presentations of more common causes of myelopathy are detailed in Table 2 (Khare & Seth, 2015).

Table 2 Important Causes of Spinal Cord Dysfunction
AgeCourseClinical FeaturesDiagnosis
Cervical spondylotic myelopathyUsually >60 yearsProgressive or stepwise courseModerate-severe cases demonstrate gait and leg spasticity and amyotrophy of hand or armsMRI cervical spine
Transverse myelitisChildren, young adultsSubacuteSegmental cord syndromeMRI and CSF
Viral myelitisAny ageAcute-subacutePure motor syndrome or Segmental cord syndromeMRI and CSF
Epidural abscessAny ageSubacute; may worsen abruptlySegmental cord syndromeMRI
InfarctionUsually >60 yearsAbrupt onsetAnterior cord syndromeMRI with diffusion-weighted sequences
Vascular malformation>40 years (dural fistula) 20's (intramedullary AVM)Acute and/or stepwiseRadicuomyelopathyMRI, spinal angiography
Subacute combined degenerationAny ageSlowly progressiveDorsal cord syndromeVitamin B12 levels
RadiationAny ageSlowly progressive; beginning 6-12 months after radiation therapySegmental cord syndrome or Ventral cord syndromeMRI, clinical history
SyringomyeliaChildren, young adultsSlowly progressiveCentral cord syndromeMRI
Epidural metastasisUsually >50 yearsSubacute, may worsen abruptlySegmental cord syndromeMRI
Intramedullary tumorYoung adultsSlowly progressiveCentral cord syndromeMRI with gadolinium enhancement
ALSUsually >60 yearsProgressivePure motor syndromeElectromyography

*MRI: magnetic resonance imaging; CSF: cerebrospinal fluid; AVM: arteriovenous malformation; ALS: amyotrophic lateral sclerosis.

Specific Disorders Affecting the Spinal Cord

Inflammatory Diseases

Transverse Myelitis (TM)

A focal inflammation in the spinal cord without compression is known as transverse myelitis. The inflammation present can cause damage to the encapsulating myelin, which can result in neurological dysfunction, including sensory impairments, weakness, and autonomic problems, including the bowel and bladder (Lim, 2020).

Weakness may occur in any or all of the four limbs with varying severity. The level area of the spinal cord usually corresponds to the lesion. However, findings in the lower limb do not preclude a lesion at the cervical level. Sensory complaints may include numbness, hypersensitivity, tingling, coldness, and burning. Pain is a common symptom in one-third to one-half of patients and can have varying characteristics. An increase in bowel movements or constipation can occur. Bladder symptoms include increased frequency, incontinence, and retention (Lim, 2020; Wang & Greenberg, 2019).

Physical Exam: The physical examination should be broadly systemic and include pinprick, vibration, light touch position sense, tone, muscle stretch reflexes, bowel, and bladder functioning, and coordination. Cognitive dysfunction, cranial nerve dysfunction, and visual abnormalities are generally not seen with idiopathic TM (Lim, 2020).

If there is fever, tachypnea, and tachycardia, it may be caused by an infection. Autoimmune diseases and other conditions that cause acute spinal cord inflammation may also start to occur. The rest of the body systems should be examined. The findings from this exam will help determine the level of spinal involvement, guide diagnostic testing, and help rule out other diagnoses.

Diagnostic Studies: The best diagnostic tool when TM is suspected is MRI. MRI allows for visualization of the lesion and rules out other causes, such as a tumor or abscess. Contrast material helps to highlight and identify lesions (Lim, 2020; Wang & Greenberg, 2019).

Table 3 Potential Medical Work-Up for Suspected Acute Transverse Myelitis*
Indicative Signs and SymptomsSuggested Evaluation
Infectious Etiology
FeverCSF Gram stain and bacterial culture
MeningismusCSF PCR: HSV-1, HSV-2, HHV-6, VZV, CMV, EBV, enteroviruses
RashCSF viral culture
Concurrent systemic infectionCSF acid-fast bacilli smear and tuberculous culture
Immunocompromised stateCSF HSV, VZV, and HTLV-1 antibodies
Recurrent genital infectionCSF anti-Borrelia burgdorferi antibodies
Symptoms of zoster radiculopathyCSF VDRL
AdenopathyCSF India ink and fungal culture
Residence in area endemic for parasitic infectionsChest radiograph
LymphadenopathySerology for antibodies to HIV, HSV, VZV, HTLV-1, B.burgdorferi
Serology for hepatitis A, B, C, and Mycoplasma
Consider serology for parasites
Blood cultures
Systemic Inflammatory Disease (Vasculitis, Collagen Vascular Diseases, Mixed Connective Tissue Disease)
RashSerum ACE
Oral or genital ulcersAuto-antibodies: ANA, ds-DNA, Ro/SSA, La/SSB, Sm, RNP
AdenopathyComplement levels
Livedo reticularisUrinalysis with microscopic analysis for hematuria
SerositisLip/salivary gland biopsy
PhotosensitivityChest CT with intravenous contrast
Inflammatory arthritisSchirmer test
Erythema nodosumChest radiograph
XerostomiaGallium scan
KeratitisAntiphospholipid antibodies (anticardiolipin antibodies, Russel viper venom time, partial thromboplastin time)
Conjunctivitis
Contractures or thickening of skin
Anemia/leukopenia/thrombocytopenia
Raynaud phenomenon
History of arterial and venous thrombosis
Multiple Sclerosis
Previous demyelination eventBrain MRI
Incomplete deficit clinically with MRI abnormality =2 spinal segments and <50 percent of cord diameterEvoked potentials
CSF oligoclonal bands and IgG index
Neuromyelitis Optica (Devic's Disease)
Optic neuritisEvoked potentials
Clinical deficit with MRI abnormality =3 spinal segmentsBrain MRI (usually negative)
NMO-IgG testing
Idiopathic Transverse Myelitis
No clinical or paraclinical features suggestive of another diagnostic categoryEvoked potentials
Electromyography/nerve conduction velocity

*ACE: angiotensin-converting enzyme; ANA: anti-nuclear antibodies; CMV: cytomegalovirus; CSF: cerebrospinal fluid; EBV: Epstein-Barr virus; HHV: human herpes virus; HIV: human immunodeficiency virus; HSV: herpes simplex virus; HTLV-1: human T-cell lymphotropic virus 1; IgG: immunoglobulin G; NMO-IgG: neuromyelitis optica IgG autoantibody; VDRL: Venereal Disease Research Laboratory; VZV: varicella-zoster virus.

Modified with permission from: Transverse Myelitis Consortium Working Group. Proposed diagnostic criteria and nosology of acute transverse myelitis. Neurology 2002; 59:499. Copyright © 2002 Lippincott Williams & Wilkins.

Treating TM: First-line therapy to treat transverse myelitis is intravenous glucocorticoids. Treatment should be started as soon as possible, so there is not a delay in treatment while waiting for MRI results. The medication regimen for this would be three to five days. If glucocorticoid therapy fails, plasma exchange may be initiated and tried. Research is being done on immunomodulatory therapy for resistant or chronic TM. Pain management and antivirals should be used as adjunct therapies in TM.

Sarcoidosis

Sarcoidosis is a multisystem disorder affecting any organ in the body. The presence of noncaseating granuloma, mononuclear cells, epithelioid cells, and CD4+ T are typical in this condition. It is possible that genetic predisposition and environmental factors may play a role in the pathogenesis of sarcoidosis, but the etiology is not clearly known (Li et al., 2018; Ungprasert et al., 2019).

Spinal sarcoidosis, referring to involvement of the spine in sarcoidosis, is relatively rare and may mimic other neurological disease affecting the spine. Spinal cord involvement is non-specific, and the diagnosis is often difficult when the spinal involvement is the first clinical presentation especially in the absence of systemic sarcoidosis. The true prevalence of SS is unknown, although it has traditionally been reported in less than 1% of all sarcoidosis patients (Soni et al., 2019).

The symptoms of sarcoidosis vary depending on where in the body it has developed. Clinical and radiologic findings alone cannot diagnose this condition; a biopsy is required. The cornerstone for the treatment of sarcoidosis is the use of glucocorticoids. Since this condition frequently undergoes spontaneous regression, treatment with glucocorticoids is often avoided unless necessary (Jensen & Brownstone, 2019; Ungprasert et al., 2019).

Paraneoplastic Syndromes

There are many paraneoplastic syndromes that involve the spinal cord. These syndromes are caused by an abnormal immune system response to a cancerous tumor.

Motor neuron disease (MND) is characterized by progressive degeneration of motor neurons. One of the most commonly known conditions is amyotrophic lateral sclerosis (ALS). Clinical presentation includes fasciculations, bilateral wasting of the tongues, the "split hand," head drop due to weakness of neck extensors, emotionality, and cognitive or behavioral disorders (Arora et al., 2021).

Subacute Sensory Neuronopathy occurs when there is a degeneration of central and peripheral sensory areas. Loss of deep tendon reflexes, ataxia, and positive sensory symptoms are present (Casseb et al., 2015; Kiernan & Cornblath, 2020).

Encephalomyelitis is characterized by persistent fatigue and a variety of symptoms related to cognitive, endocrinological, immunological, and autonomous dysfunction.

Infections

Epidural Abscess

Spinal epidural abscesses are rare but very serious. These abscesses develop when bacteria access the epidural space in the spinal cord. Hematogenous spread is the most common cause of infection and comes from the skin, urinary, or respiratory tract. The direct spread of infection is also a contributing factor (Shaabi & Moshref, 2021).

Risk factors include:

  • Diabetes mellitus (DM)
  • Alcohol use/abuse
  • IV drug use
  • HIV diagnosis
  • Recent trauma or surgery
  • Degenerative joint disease

Spinal catheters (Sharfman et al., 2020):

Signs and symptoms include back pain. Pain occurs in at least 70% of patients. Fever and tenderness are also common signs and symptoms. Radiculopathy, bowel and bladder dysfunction, and weakness are also reported symptoms (Artenstein et al., 2016).

Symptom analysis is a way to diagnose this. There are other factors that help to diagnose an epidural abscess and include serum C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) to look for leukocytosis. The test of choice for an epidural abscess is Gadolinium-enhanced MRI. Other diagnostic tests not used often include direct tissue via image-guided biopsy and sampling of the infected fluid.

Once infection has been identified, antibiotics should be initiated. The drug of choice is usually vancomycin with either piperacillin-tazobactam or a third- or fourth-generation cephalosporin. Prompt surgery is also indicated in most cases of this form of an abscess (Artenstein et al., 2016).

The mortality rate has declined for this condition, but it varies depending on the length of infection and the patient's past medical history (Bond & Manian, 2016).

Acute Viral Myelitis

The anterior horn becomes invaded by pathogens. There are multiple distinct syndromes associated with this condition. Enteroviruses and Flavivirus are two forms and include conditions such as enterovirus, West Nile Virus, polio, and coxsackievirus.

There is a second form of viral myelitis that is very similar to acute viral or transverse myelitis. Examples of this type of virus include (Bond & Manian, 2016):

  • Cytomegalovirus
  • Hepatitis C
  • Varicella-zoster
  • Epstein Barr Virus
  • Herpes simplex virus

The clinical presentation of all of these viruses vary in nature but does have some common symptoms. Fever and respiratory symptoms such as asthma-like illness can occur. Headache and neurological symptoms such as neck stiffness usually occur.

MRI of the spinal cord is the test of choice for these conditions. In the early phase, lesions are usually ill-defined and affect the grey matter. Marked edema is visually seen on MRI. A lumbar puncture is typically done to evaluate cerebrospinal fluid.

Regarding treatment, acute supportive management is essential. Managing pain, treating bowel and bladder dysfunction, and use of corticosteroids are often used (Murphy et al., 2021).

AIDS Myelopathy

The most common cause of spinal disease in HIV and AIDS is HIV- associated vacuolar myelopathy (HIV-VM). It is usually seen in advanced HIV infections (Leffert et al., 2021).

This condition is usually characterized by progressive spastic paraparesis, autonomic dysfunction, and sensory ataxia (Image 17).

The diagnosis of AIDS myelopathy is usually based on exclusion (Rezaie et al., 2020).

Image 17: Criteria for Clinical Diagnosis

  1. Male or female, over 18 years old, with documented HIV-1 infection
  2. AIDS-associated myelopathy, with or without neuropathy and dementia, defined
    1. Presence of at least two of the following symptoms:
      1. Paresthesias and/or numbness in lower extremities or all four limbs
      2. Weakness of the limbs
      3. Unsteady, stiff, or uncoordinated gait
      4. Sensation of electric shock through the back and legs on neck flexion
      5. Urinary frequency, urgency, incontinence, or retention
      6. Fecal incontinence and retention
      7. Sexual dysfunction with erectile impairment in males
    2. Presence of at least two of the following signs:
      1. Reduction in vibratory and/or position sense
      2. Brisk deep tendon reflexes
      3. Abnormal plantar response
      4. Lhermitte's sign
      5. Spastic, ataxic, or spastic-ataxic gait
  3. Signs and symptoms of AIDS-associated myelopathy for at least 6 weeks
  4. Abnormal Somatosensory evoked potential measurement
  5. No other determinable cause for spinal cord disease by serologic and CSF studies

Image Source: NCBI

MRI helps to support the diagnosis of AIDS myelopathy. Serologic and cerebrospinal fluid studies are performed to help rule out other causes of disease.

Antiretroviral therapy helps to manage symptoms of this condition. Intravenous immunoglobulin has been used to improve neurological deficits. Even though some neurological deficits improve, patients usually experience death within six months of diagnosis (Wuliji et al., 2019).

HTLV-1 Myelopathy

Human T-cell lymphotropic virus type I (HTLV-1) is a neuroinflammatory disease that is progressive in nature. This condition is named HTLV-1- associated myelopathy (HAM) or tropical spastic paraparesis (TSP). This condition is common in areas such as Peru and the Middle East. It is a slow-progressing demyelinating disease that affects the central nervous system.

Clinical presentation of these conditions includes manifestations such as gradual spastic paraparesis, gait disturbances, neurogenic bladder, and many mild sensory signs (Nozuma et al., 2020).

An MRI of the spinal cord is performed to diagnose either of these conditions. An MRI of the brain can be performed to observe white matter lesions. Cerebrospinal fluid is examined via lumbar puncture to examine the amount of lymphocytosis and protein elevation (Sato et al., 2018).

Supportive management is necessary for these conditions. Research on steroids slowing the progression is currently being studied. Even with supportive management, progression is inevitable (Schwalb et al., 2020).

Syphilis

Neurosyphilis (NS) is observed in 4–10% of patients with untreated or insufficiently treated syphilis, which could develop at any stage of the disease. Compared with the intracerebral syphilis, spinal syphilis is relatively rare, mainly including myelitis, myelophthisis, and gumma. Although extremely low in prevalence, spinal syphilitic gumma is a strong inflammatory response in which T. pallidum invades the spinal cord from the meninges and vessels, which may cause severe outcomes.

Syphilitic myelitis, though rare, is a debilitating condition caused by Treponema pallidum. Neurosyphilis is known to affect the brain, brainstem, meninges, spinal cord, nerve roots, and cerebral/spinal vessels.

This condition has clinical presentations of pain and sensory ataxia. Corticosteroids and penicillin can aid in diminishing some of the symptoms experienced (Paulraj et al., 2020).

Cerebrospinal fluid is examined for elevated protein level and lymphocytosis (Yuan et al., 2019).

Tuberculosis

Spinal tuberculosis progresses at a slow rate and is sometimes referred to as Pott's Disease. The severity of the symptoms depends on how long the patient has been infected. A low-grade fever, weakness, and back pain are common presenting symptoms. If the case is complicated, instability, deformity, and neurological manifestations may be present (Fogel, 2015; Rijkers, 2019).

The natural history and presentation are notable for cold abscesses causing mass effect, early or late neurological deficit, and kyphotic deformity of the spine caused by anterior vertebral body destruction. A culture specimen of the infection is obtained to look for Mycobacterium to diagnose spinal tuberculosis. MRI can be used to detect spinal changes in late disease (Rajasekaran et al., 2018).

The cornerstone of medical management is multidrug chemotherapy to minimize relapse and drug resistance and can be curative for spinal tuberculosis with minimal residual kyphosis. Surgical management is reserved for patients presenting with neurological deficits or severe kyphosis. The mainstays of surgical management are debridement, correction of spinal deformity, and stable fusion (Khanna & Sabharwal, 2019).

Parasitic Infections

Schistosoma mansoni and Schistosoma haematobium are common parasitic infections of the spinal cord. Depending on the severity of the infection, there are different clinical presentations (Arndts et al., 2021).

Fever, cough, muscle aches, and chills are common symptoms of both of these infections. Pain, weakness, and urinary retention will develop if the infection or parasite is not controlled.

To diagnose either of these parasitic infections, cerebrospinal fluid examination is done to look at protein elevation. An MRI can also be done to observe the amount of swelling in the spinal cord.

Praziquantel and glucocorticoids can be used to diminish the symptoms and treat parasitic infections (Carpio et al., 2016).

Bacterial meningitis is an inflammation of the meninges, which is located in the spine and spinal cord. When there is swelling, pressure is applied to the spinal cord causing compression.

Vascular Diseases

Spinal Cord Infarction

Spinal cord infarction results in spinal cord cell death due to an ischemic or vascular injury (Qureshi et al., 2017). Though this occurrence is rare, a stroke in the spinal cord is detrimental (Akel, 2017).

Risk factors for this form of stroke include diabetes, hypertension, and high blood glucose levels. Cardioembolism and atherosclerosis have also been known to cause a spinal cord infarction (Ge et al., 2020).

Clinical presentation of a spinal cord infarction includes loss of bowel and bladder function, pain and temperature sensory deficits, paralysis, and back pain (Romi & Naess, 2016).

Diagnostically, there are ways to evaluate for a spinal cord infarction. Laboratory Evaluation is usually performed to evaluate for other potential causes. Lumbar puncture and cerebrospinal fluid analysis are performed to examine white and red blood cell count, protein, and glucose. Neuroimaging is usually performed to review edema and T2-signal change (Costamagna et al., 2020).

Prompt surgical treatment is necessary if there is compression or if the aorta is involved. Corticosteroid therapy and antiplatelet therapy aids in decreasing inflammation. Even with treatment, the mortality rate is around 50% (Al-Shaikh & Czervionke, 2021).

Vascular Malformations

There are spinal vascular abnormalities that are debilitating. These malformations are classified based on location and pathology.

Dural arteriovenous fistulas are common vascular abnormalities and make up around 70% of vascular malformations. There are often no origins for these fistulas, but there are risk factors, including male sex and those over 50 years old.

There is a combination of symptoms that can occur with this specific malformation. Headache, seizures, cranial neuropathies, weakness, coordination issues, and increased intracranial hypertension are common symptoms (Al-Shaikh & Czervionke, 2021).

Imaging studies such as computed tomography angiography (CTA) or magnetic resonance angiography (MRA) are often used to evaluate the vessels and arteries in question. The MRA may also reveal dilated pial vessels, early prominent sinus filling, and associated edema from venous hypertension. A six-vessel cerebral digital subtraction angiogram (DSA) can be used to help establish a diagnosis and aid in a treatment plan (Hawkins & Chewning, 2019).

Patient symptoms and the risk of hemorrhage guide the treatment options for patients with this form of a fistula. Conservative treatments are used when there is a low risk of hemorrhage. For those with an increased risk of hemorrhage or other detrimental effects, interventions such as endovascular embolization, open surgery and stereotactic radiosurgery are performed.

Intramedullary spinal arteriovenous malformations (AVMs) are spinal blood vessel defects with vessel engorgement. Though origins are difficult to find, venous hypertension is a contributing risk factor. This congenital malformation usually occurs at the T4 and T3 levels (Clarençon et al., 2021).

Typically, patients present with ischemia and hemorrhage. The gold standard for this malformation is the Spinal digital subtraction angiography (DSA). For initial visualization. MRI is the test of choice due to the risks associated with the DSA. MRA's are supplements to the MRI when necessary.

Surgical resection and endovascular occlusion are commonly used (Patchana et al., 2020).

Spinal Epidural Hematoma

Spinal epidural hematomas are infrequent occurrences. A spinal epidural hematoma means that there is blood within the epidural space. These hematomas can occur with arteriovenous malformations and coagulopathies.

Patients with this typically are in their fourth or fifth decades of life, with men slightly more affected than women. This often presents with an abrupt onset of severe neck or back pain that can radiate into the extremities and commonly is followed by symptoms ranging from nerve root agitation to full neurologic impairment. The symptoms typically are that of a lower motor neuron pathology with hyporeflexia and flaccid paralysis. There can be a delay in the time from the onset of back pain to neurologic decline, and symptom presentation has been documented to range from within hours to several days or even months from the onset of the back pain. Early suspicion and diagnostic imaging are critical, though, as SSEHs can produce devastating, lasting neurologic deficits ranging from persistent paresis to even death.

Back pain, weakness, and motor and sensory deficits are common clinical presentations of patients with spinal epidural hematomas. Depending on the location of the bleeding, symptom presentation will vary. Complete paralysis can occur (Figueroa & DeVine, 2017).

MRI can be performed to observe the ventral epidural space. T1 and T2 signal intensity characteristics will be examined (Image 18). Epidural collections of blood are often seen (Pierce et al., 2018).

When compared to the spinal cord within 24 h from symptom onset, the hematoma typically appears isointense on T1-weighted and hyperintense on T2-weighted MRI imaging. After 24 h, the hematoma often appears hyperintense on both T1- and T2-weighted images. Chronic hematomas become hypointense on both T1- and T2-weighted images. Fat suppression images may be used to distinguish hematoma from epidural fat. Sometimes active bleeding into the hematoma will reveal a central area of enhancement when contrast is used (Figueroa & DeVine, 2017).

Image 18: MRI Appearances of Hemorrhage

MRI Appearances of Hemorrhage
StageAgeT1 Signal IntensityT2 Signal Intensity
Hyperacute<24 hIsointenseMildly hyperintense
Acute1-3 dMildly hypointenseHypointense
Early subacute3-7 dHyperintenseHypointense
Late subacute7-14 dHyperintenseHyperintense
Chronic>14 dMildly hypointenseHypointense

Chart source: RSNA

Hematoma evacuation and decompressive laminectomy are used as surgical management for this condition. To avoid permanent loss, these surgical procedures should be performed as soon as possible (Raasck et al., 2017).

Toxic Metabolic Disorders

Subacute Combined Degeneration

Due to demyelination, the lateral and posterior columns of the spinal cord are affected. This is primarily due to poor absorption of vitamin B12, poor intake of B12, or the use of medications such as proton pump inhibitors or metformin (Goldish & Massagli, 2018).

Sensory ataxia, weakness, bowel and bladder dysfunction, and paranesthesia are presenting symptoms. Patients can also present with paralysis. Hematologically, patients will present with fatigue, pallor and malaise (Cao et al., 2020).

Laboratory analysis including CBC, MCV, B12, and folate levels will be examined. A Complete MRI of the spine will be performed. The MRI may show hyperintense lesions in the spinal cord (Green, 2017).

Supplementation of B12 will aid in diminishing symptoms.

Copper Deficiency Myeloneuropathy

Copper deficiency can present neurological as myelopathy and peripheral neuropathy. It is similar to vitamin B12 deficiency and can co-occur with this syndrome (Grossman & Ruiz, 2021).

Risk factors for this condition include gastrectomy and gastric bypass surgery. A subacute onset is common in copper deficiency and can consist of ataxia and spastic gait symptoms. Hematologic abnormalities can also be present (Al-Tabbaa & Horvath, 2021).

Oral supplementation can prevent progression (Aasim et al., 2020).

Radiation Myelopathy

Radiation therapy of the spinal cord can cause radiation myelopathy. The biggest risk factor is receiving radiation. Fractionated radiation can also be a cause.

Early injury involves nausea, disorientation, and loss of consciousness. Early delayed injury is self-limiting. It usually occurs two to four months after radiation and is characterized by paresthesia of the back and then clinical recovery. Late injury, though irreversible, is characterized by minor to major symptoms.

Radiation therapy is diagnosed based on exclusion. MRI is commonly used to assess and diagnose this version of myelopathy. Focal contrast enhancement, as well as low signals on T1-weighted images and high signals on T2, are often seen on MRI. Positron emission tomography can also be used to view spinal cord segments.

There is no effective treatment for this condition (Wong et al., 2015).

Electrical Injury

Electrical injury with high voltage can cause damage to the spinal cord resulting in neurological conditions.

Classification of symptoms is based on injury. Immediate, secondary, and late effects can be seen.

Immediate side effects include:

  • Severe pain
  • Loss of consciousness
  • Motor Symptoms
  • Vision and hearing loss

Secondary effects include:

  • Temporary paralysis
  • Autoimmune disturbances

Late effects include:

  • Brainstem dysfunction
  • Movement disorders
  • Hemiplegia
  • Cranial Neuropathies (AlQasas et al., 2020)

Early discovery is key so MRI can be performed. Treatment is supportive in nature (Sharma et al., 2018).

Hepatic Myelopathy

Hepatic myelopathy is a rare disorder from chronic liver disease that can cause neurological effects. Portal hypertension is usually involved in hepatic myelopathy.

This condition usually presents as spastic paraparesis that progresses to paraplegia if not treated. Lower extremity deficits are commonly seen.

Laboratory and radiographic examinations are performed. An MRI is essential to rule out other causes or etiologies. T1- and T2- weighted signals are reviewed (Ciarlariello et al., 2019).

To treat hepatic myelopathy, patients ultimately need a liver transplant. However, measures to control ammonia levels will decrease symptoms (Philips et al., 2018).

Decompression Sickness Myelopathy

Decompression sickness occurs as a result of deep-sea diving. It is a rare occurrence but can be reversible. This myelopathy is caused by nitrogen bubbles released from blood and tissue after diving.

Symptoms vary based on whether it is Type 1 or Type 2 decompression.Type 1 symptoms include fatigue, malaise, and muscular or skin symptoms. Type 2 symptoms are more severe and include symptoms of the central nervous system. Depending on the level of injury, paraparesis and paraplegia can occur.

To diagnose this condition, radiologic studies, especially MRI, are used. MRI may demonstrate brain and spinal cord lesions, suggesting edema and ischemia (Akter et al., 2020).

Oxygen therapy followed by recompression therapy is the first-line treatment option. Prognosis is good if treatment is initiated early (Saadi et al., 2019).

Lathyrism and Konzo

Lathyrism occurs from intake disrupts of chickling peas or grass and disrupts the central motor pathway.

Symptoms of lathyrism or neurolathyrism include paraparesis with permanent damages or changes to the knee and surrounding joints. Numbness and bladder impotence are also common symptoms (Banea et al., 2015).

Though treatments have been attempted, success rates are very low. Finding the root cause and preventing this from occurring is the best way to avoid lathyrism (Hussien et al., 2021).

Konzo is a distinct neurological disorder caused by increased exposure to cassava (Manihot esculenta). This disease has a sudden onset that usually occurs with exertion. Initially, patients may tremble, experience weakness and stiffness in the legs (Enefa et al., 2020).

There is no effective treatment for Konzo, and the effects are permanent (Kashala-Abotnes et al., 2019).

Neoplasms

Benign and malignant tumors can create myelopathy as a result of compression.

Clinical features largely depend on the tumor's location, size, and malignancy status. Back pain is commonly reported. Radicular signs are also common. Weakness and progressive paraplegia are often seen.

Plain radiographs are the first-line diagnostic tool used when there is a suspicion of a spinal tumor. Up to 80% of tumors can be identified by a plain radiograph.

When the spinal cord is involved, MRI is gold standard. With an unknown origin, spinal tumors may need a biopsy to diagnose. To treat neoplasms, surgical treatment may be necessary (Ciftdemir et al., 2016).

Inherited and Degenerative Conditions

Amyotrophic Lateral Sclerosis (ALS)

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder that is progressive in nature. It primarily affects the motor system.

Older age and male sex are risk factors for ALS. Lifestyle risk factors include smoking, dietary factors, body mass index, and level of physical activity (Ingre et al., 2015).

Progressive muscle weakness is the hallmark symptom of ALS. Muscle cramps, weakness, slow movements, and fasciculations are accompanying symptoms. Symptoms are usually focal and spread to adjacent regions of the body. Upper limb involvement usually affects the dominant hand and side of the body (Zhu & Lu, 2020).

Diagnosis of ALS is usually based on clinical symptoms, but an electromyography can be performed to aid in diagnosis.

Prognosis is variable but depends on the patient's state at diagnosis (Masrori & Van Damme, 2020).

There are subtypes of ALS that are difficult to treat. Primary lateral sclerosis (PLS) is a well-known subtype of ALS. Slowing of movements and progressive spasticity are common symptoms, usually in the lower limbs.

The diagnosis of PLS is based on exclusion, and there are no known curative treatments (Statland et al., 2015).

Hereditary Spastic Paraplegias (HSP)

HSP is a large group of neurological disorders that are inherited. There is broad heterogeneity and is characterized by the degeneration of the neuron.

The main symptom of HSP is progressive bilateral spasticity which is a part of pyramidal syndrome. Gait disturbance and urinary dysfunction can be a presenting symptom.

HSP is usually diagnosed based on clinical symptoms, but an MRI can be helpful (Ardolino et al., 2021).

Symptomatic treatment is helpful to patients diagnosed with HSP. Prevention of ataxia complications is necessary. Baclofen is often used as an anti-spastic (Lallemant-Dudek et al., 2021).

Adrenoleukodystrophy

Adrenoleukodystrophy is a fatal and progressive neurodegenerative disorder. It is associated with a mutation associated with the X chromosome (Gordon et al., 2018).

Sensory and sphincter disturbances, as well as spastic paraparesis and mild polyneuropathy, are characteristics of adrenoleukodystrophy.

MRI is used to monitor those with this condition before symptoms become severe. MRI can identify white matter changes early in the diagnosis (Atalar, 2018).

Currently, allogeneic hematopoietic stem cell transplantation is an effective treatment. Many trials are currently being researched for other forms of treatment (Turk et al., 2020).

Friedreich Ataxia

The most frequent type of inherited ataxia is named Friedreich ataxia. This is a slow progressive disorder that presents with gait instability. Scoliosis is also a common symptom.

FRDA is a multisystem disorder, affecting both the central and peripheral nervous systems, the musculoskeletal system, the myocardium and the endocrine pancreas. Whilst the ‘classical’ FRDA phenotype varies substantially, gait and limb ataxia, dysarthria, and loss of lower limb reflexes with deep sensory loss are always detectable. Symptoms tend to present between the ages of 10 and 16, and the mixed ataxia is the result of peripheral sensory neuropathy, spinocerebellar tract degeneration and cerebellar pathology. Gait ataxia develops early, and gait is characteristically unsteady, but not overtly broad-based. Loss of balance and trunk ataxia necessitate progressive degrees of support, with most patients being wheelchair-bound by the third decade. Limb ataxia affects dexterity and coordination such that basic daily activities become increasingly difficult, and nose–finger ataxia, upper limb dysdiadochokinesia and impaired heel–shin slide are all common early signs. Dysarthria consists of slow, slurred speech which progresses from early in the disease towards unintelligibility in the advanced stages. Lower limb reflexes are absent, reflecting the underlying peripheral neuropathy, and early loss of distal vibration sense reflects dorsal root ganglion and dorsal column atrophy.

The later stages of disease are associated with pyramidal weakness, particularly of the lower limbs, and distal wasting, which further exacerbates disability. Spasticity has typically been described in the more advanced stages of the disease, however one study using biomechanical techniques detected lower limb spasticity in ambulant patients, and in those with disease durations of less than 10 years (Cook & Giunti, 2017).

Other symptoms include:

  • Weakness
  • Absent reflexes
  • Areflexia
  • Muscle wasting

Improving clinical symptoms is key to supportive management for Friedreich ataxia (Bürk, 2017).

Others

Syringomyelia

Syringomyelia is a neurologic condition that is caused by a fluid buildup in the central canal of the spinal canal. It is most often associated with Chiari 1 Malformation (CM1). However, it can be associated with post-infective and post-traumatic causes such as spinal cord tumors, post-operative meningitis, and cord compression.

Clinical presentations of syringomyelia are similar to those seen in CM1 and include:

  • Tussive headaches
  • Visual disturbances
  • Coughing
  • Ataxia
  • Gait dysfunction

An MRI is the test of choice to evaluate this disorder. MRI also helps to rule out other etiologies or causes. When MRI cannot be used, myelography with a high-resolution CT scan is often performed.

The goal of treatment is to remove the cause of the problem. For those with CM1, craniocervical decompression is the treatment of choice. Shunts are often used for patients who have this condition from post-infective or post-traumatic causes.

Cervical Spondylotic Myelopathy (CSM)

This is the most common cause of cervical cord dysfunction and is progressive in nature. CSM is caused by direct compression of the cord or the blood vessels near the spine. Spondylosis is the most common reported cause of CSM.

Subtle neurological findings are often the presenting symptom in CSM. Symptoms can present insidiously and include:

  • Urinary urgency and frequency
  • Weakness
  • Stiffness
  • Gait dysfunction
  • Spasticity

MRI is the test of choice for CSM. If an MRI is contraindicated, a CT scan can be performed.

Conservative treatments for CSM include:

  • Lifestyle modifications
  • Neck immobilization
  • Physical modalities
  • Pharmacologic treatments

Surgical interventions are often more favorable, and the surgery of choice is decompression (Bakhsheshian et al., 2017).

Ossification of the Posterior Longitudinal Ligament (OPLL)

This condition is from an abnormal calcification located in the cervical spine. The etiology is poorly understood but often attributed to environmental and genetic factors.

Varying degrees of neurological symptoms are often the first presenting symptom. Radiculopathy and myelopathy are often seen. A CT scan and an MRI are used to identify the ossifications present.

Nonoperative treatment includes:

  • Physical Therapy
  • Oral analgesics

Those with progressive myelopathy and myeloradiculopathy who have not responded to conservative management are subject to surgical treatment. Surgical decompression is the treatment of choice (Abiola et al., 2016).

Surfers' Myelopathy

Given the location of the injury on imaging studies and the anatomical characteristics of the midthoracic region, surfer’s myelopathy is considered an ischemic injury of the thoracic spinal cord, and prolonged prone hyperextension has been suggested as the primary cause. The continuous prone hyperextended posture while paddling can possibly cause avulsion of perforating vessels, vasospasm of the artery of Adamkiewicz, or transient ischemia in areas of borderline perfusion as a result of spinal cord tension due to hyperextension. Prolonged spinal hyperextension has been previously reported as a possible mechanism for spinal cord injury. This condition most commonly results from hyperextension of the back. While it is rare, it is more common in male surfers.

The most common presenting symptoms include:

  • Lower limb weakness
  • Back pain
  • Urinary retention
  • Paraplegia
  • Sensory loss

MRI is an effective diagnostic tool that can identify changes. Spinal angiography should be considered in the acute evaluation and management of surfer’s myelopathy. Spinal angiography can find underlying vascular anomalies or anatomical variations that are vulnerable to ischemic insult or confirm intravascular mechanisms disrupting spinal cord perfusion (Choi et al., 2018).

Preventative measures are necessary to ensure this form of myelopathy does not occur. Treatment is supportive in nature and includes bed rest (Gandhi et al., 2021).

Conclusion

Non-traumatic spinal cord injury (NTSCI) is a neurological emergency associated with a high risk for morbidity and reduced quality of life. It is defined as any damage to the spinal cord resulting from a non-traumatic cause. Etiologies include degenerative, inflammatory, neoplastic, and infectious conditions. Many disorders affect the spinal cord. Various symptoms are produced, depending on the location and extent of the spinal cord injury.

To prevent long-term disability and death, early diagnosis and treatment of patients with NTSCI is critical. There are different modalities of treatment to try to decrease debilitating symptoms. Not all disorders can be treated, and some have dismal prognoses. Nontraumatic etiologies of myelopathy include inflammatory diseases, toxic-metabolic disorders, infections, vascular diseases, neoplasms, inherited-degenerative conditions and many others. The pathogenesis of these conditions will aid in determining the proper treatment modality for the patient (Müller-Jensen et al., 2021).

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