65
Spinal Cord and Peripheral
Nerve Problems
Kristen J. Costello
http://evolve.elsevier.com/Lewis/medsurg/
CONCEPTUAL FOCUS
Family Dynamics Pain
Functional Ability Sensory Perception
Mobility
LEARNING OUTCOMES
1. Outline the classification of spinal cord injuries and 6. Explain the etiology, clinical manifestations, and
associated clinical manifestations. interprofessional and nursing management of trigeminal
2. Describe the clinical manifestations and interprofessional neuralgia and Bell’s palsy.
and nursing management of neurogenic and spinal shock. 7. Describe the etiology, clinical manifestations, and
3. Relate the clinical manifestations of spinal cord injury to the interprofessional and nursing management of Guillain-
level of disruption and rehabilitation potential. Barré syndrome and inflammatory demyelinating
4. Describe the nursing management of the patient with a polyneuropathy.
spinal cord injury.
5. Explain the types, clinical manifestations, and
interprofessional and nursing management of spinal cord
tumors.
KEY TERMS
autonomic dysreflexia paraplegia
Bell’s palsy spinal cord injury (SCI)
Guillain-Barré syndrome (GBS) spinal shock
neurogenic bladder tetanus
neurogenic bowel tetraplegia
neurogenic (vasogenic) shock trigeminal neuralgia (TN)
This chapter discusses spinal cord and peripheral nerve problems,
including spinal cord injuries, spinal cord tumors, cranial nerve SPINAL CORD PROBLEMS
disorders, and polyneuropathies. We focus on the nursing manage-
ment of the problems encountered by the patient with spinal cord
SPINAL CORD INJURY
injury (SCI). The potential for disruption of individual growth and Spinal cord injury (SCI) is caused by trauma or damage to the
development, altered family dynamics, economic loss from unem- spinal cord. It can result in temporary or permanent alteration
ployment, and the high cost of rehabilitation and long-term health in spinal cord function. About 17,000 Americans have SCIs
care make SCI a major problem. While many people with SCI can each year. Some 282,000 persons in the United States are liv-
care for themselves independently, those with the highest level of ing with SCI. The average life expectancy for persons with SCI
injury need around-the-clock care at home or in a long-term care is shortened and has not improved since the 1980s. In the first
facility. The nurse’s role in providing holistic care can significantly year after injury, mortality rates are high. There is a 30% chance
impact the patient’s general health and well-being. of rehospitalzation.1
1594
, CHAPTER 65 Spinal Cord and Peripheral Nerve Problems 1595
Etiology and Pathophysiology
SCI is usually a result of trauma. The 4 most common causes are
motor vehicle collisions (38%), falls (30.5%), violence (13.5%),
and sports injuries (9%).1
Types of Injury
Neurologic damage caused by SCI occurs in 2 phases: primary
injury (initial physical disruption of the spinal cord) and sec-
ondary injury (from processes such as ischemia, hypoxia, hem-
orrhage, edema).
Primary injury. Primary injury results from direct physical
trauma to the spinal cord due to blunt or penetrating
trauma. Trauma can cause spinal cord compression by bone
displacement, interruption of blood supply, or distraction from
pulling. Penetrating trauma, such as gunshot and stab wounds,
can cause tearing and transection. Scar formation
Secondary injury. Secondary injury refers to the ongoing,
progressive damage that occurs after the primary injury. Fig. 65.1 1 to 2 days after the injury, astrocytes proliferate and surround
Secondary injury causes further permanent damage. It begins the edges of the fibrotic scar. This confines inflammation to the area of
a few minutes after injury and lasts for months. The cascade injury protects and neighboring neural tissue from further damage. This
of events results in edema, ischemia, and inflammation. This process may take 7 to 10 days. (Used with permission from Barrow
causes cell death, disruption of the blood-brain barrier, and Neurological Institute, Phoenix, AZ.)
demyelination. This can extend the level of deficit and worsen
long-term outcomes. Classification of SCI
The edema from the inflammatory response is especially SCI is classified by the (1) mechanism of injury, (2) level of
harmful because of limited space for tissue expansion. Thus, injury, and (3) degree of injury.
compression of the spinal cord occurs. Edema extends above Mechanisms of injury. The major mechanisms of injury
and below the injury, increasing ischemic damage. Within 24 include flexion, flexion-rotation, hyperextension, vertical
hours, permanent damage may occur from edema. compression, extension-rotation, and lateral flexion (Fig. 65.2).
Apoptosis (programmed cell death) continues for weeks. Flexion-rotation injury is often the most unstable because
It contributes to post-injury demyelination. The inflam- ligaments that stabilize the spine are torn. This injury most often
matory response at the site of the initial injury focuses on contributes to severe neurologic deficits.
clearing up the initial cellular debris without damaging Level of injury. Skeletal level of injury is the vertebral level
normal tissue. This results in a central non-neural core of with the most damage to vertebra and related ligaments.
connective tissue that we refer to as a glial scar (Fig. 65.1). Neurologic level is the lowest segment of the spinal cord with
The glial scar creates a physical barrier. It restricts the cells normal sensory and motor function on both sides of the body.
in the spinal cord from migration and regeneration. This The level of injury may be cervical, thoracic, lumbar, or sacral.
leads to irreversible nerve damage and permanent neuro- Cervical and lumbar injuries are most common because those
logic deficit. areas of the spine are associated with the greatest flexibility and
movement.
Spinal and Neurogenic Shock Injury from C1 to T1 can cause paralysis of all 4 extremi-
Spinal shock may occur shortly after acute SCI. It is charac- ties, resulting in tetraplegia (formerly called quadriplegia). The
terized by loss of deep tendon and sphincter reflexes, loss of degree of impairment in the arms after cervical injury depends
sensation, and flaccid paralysis below the level of injury. This on the level of injury. The lower the level, the more function is
syndrome lasts days to weeks. It often masks post-injury neu- retained in the arms.
rologic function.2 Paraplegia (paralysis and loss of sensation in the legs) can
In contrast to spinal shock, neurogenic (vasogenic) occur in SCI below the level of T2.4 Fig. 65.3 shows affected
shock can occur in cervical or high thoracic injury (T6 or structures and functions at different levels of cord injury.
higher). It occurs from unopposed parasympathetic response Degree of injury. The degree of spinal cord involvement may
due to loss of sympathetic nervous system (SNS) innerva- be complete or incomplete (partial). Complete cord involvement
tion. It causes peripheral vasodilation, venous pooling, and results in total loss of sensory and motor function below the
decreased cardiac output. Manifestations include significant level of injury. Incomplete cord involvement results in a mixed
hypotension (<90 mm Hg), bradycardia, and temperature loss of voluntary motor activity and sensation and leaves some
dysregulation. Neurogenic shock may persist for as long as 5 tracts intact. The degree of sensory and motor loss depends on
weeks after injury.3 Hypotension can result in poor perfusion the level of injury and reflects specific damaged nerve tracts.
and oxygenation to the spinal cord and worsen spinal cord Five major syndromes are associated with incomplete
ischemia.3 injuries: central cord syndrome, anterior cord syndrome,
, 1596 SECTION 12 Problems Related to Movement and Coordination
Ruptured
posterior
Force
ligaments
Forward
dislocation
Damage to
spinal cord
A Flexion injury
Compressed
ligament
Ruptured
Force
anterior
ligament
B Hyperextension injury
Compression
of spinal cord
Force Fractured
vertebrae
C Compression fracture
Force
Displacement
of vertebrae
D Flexion-rotation injury
Fig. 65.2 Examples of mechanisms of spinal cord injury. (A) Flexion injury of the cervical spine ruptures the
posterior ligaments. (B) Hyperextension injury of the cervical spine ruptures the anterior ligaments. (C) Com-
pression fractures crush the vertebrae and force bony fragments into the spinal canal. (D) Flexion-rotation
injury of the cervical spine often results in tearing of ligamentous structures that normally stabilize the spine.
(A–C, From Copstead-Kirkhorn LC, Banasik JL: Pathophysiology, ed 5, St Louis, 2014, Mosby.)
Brown-Séquard syndrome, cauda equina syndrome, and conus We call the sensory regions dermatomes. Each segment of
medullaris syndrome (Table 65.1). the spinal cord innervates a specific area of skin. A dermatome
map is shown in Fig. 60.7. Each dermatome has a recommended
Clinical Manifestations point for testing.
Manifestations of SCI are the result of trauma that causes cord The ASIA Impairment Scale is useful for recording changes
compression, ischemia, edema, and possible cord transection. in neurologic status. It helps us identify rehabilitation goals.
They are related to the level and degree of injury. The patient Movement and rehabilitation potential related to specific loca-
with an incomplete injury may have a mix of manifestations. tions of SCI are described in Table 65.2. In general, sensory
function closely matches motor function at all levels.
Motor and Sensory Effects
The American Spinal Injury Association (ASIA) Impairment Respiratory System
Scale is used to classify the severity of impairment from SCI. Respiratory complications closely correspond to the level
It combines motor and sensory function assessments to deter- of injury. Cervical injuries above C3 present special prob-
mine neurologic level and completeness of injury (Fig. 65.4).5 lems because of the total loss of respiratory muscle function.
Spinal Cord and Peripheral
Nerve Problems
Kristen J. Costello
http://evolve.elsevier.com/Lewis/medsurg/
CONCEPTUAL FOCUS
Family Dynamics Pain
Functional Ability Sensory Perception
Mobility
LEARNING OUTCOMES
1. Outline the classification of spinal cord injuries and 6. Explain the etiology, clinical manifestations, and
associated clinical manifestations. interprofessional and nursing management of trigeminal
2. Describe the clinical manifestations and interprofessional neuralgia and Bell’s palsy.
and nursing management of neurogenic and spinal shock. 7. Describe the etiology, clinical manifestations, and
3. Relate the clinical manifestations of spinal cord injury to the interprofessional and nursing management of Guillain-
level of disruption and rehabilitation potential. Barré syndrome and inflammatory demyelinating
4. Describe the nursing management of the patient with a polyneuropathy.
spinal cord injury.
5. Explain the types, clinical manifestations, and
interprofessional and nursing management of spinal cord
tumors.
KEY TERMS
autonomic dysreflexia paraplegia
Bell’s palsy spinal cord injury (SCI)
Guillain-Barré syndrome (GBS) spinal shock
neurogenic bladder tetanus
neurogenic bowel tetraplegia
neurogenic (vasogenic) shock trigeminal neuralgia (TN)
This chapter discusses spinal cord and peripheral nerve problems,
including spinal cord injuries, spinal cord tumors, cranial nerve SPINAL CORD PROBLEMS
disorders, and polyneuropathies. We focus on the nursing manage-
ment of the problems encountered by the patient with spinal cord
SPINAL CORD INJURY
injury (SCI). The potential for disruption of individual growth and Spinal cord injury (SCI) is caused by trauma or damage to the
development, altered family dynamics, economic loss from unem- spinal cord. It can result in temporary or permanent alteration
ployment, and the high cost of rehabilitation and long-term health in spinal cord function. About 17,000 Americans have SCIs
care make SCI a major problem. While many people with SCI can each year. Some 282,000 persons in the United States are liv-
care for themselves independently, those with the highest level of ing with SCI. The average life expectancy for persons with SCI
injury need around-the-clock care at home or in a long-term care is shortened and has not improved since the 1980s. In the first
facility. The nurse’s role in providing holistic care can significantly year after injury, mortality rates are high. There is a 30% chance
impact the patient’s general health and well-being. of rehospitalzation.1
1594
, CHAPTER 65 Spinal Cord and Peripheral Nerve Problems 1595
Etiology and Pathophysiology
SCI is usually a result of trauma. The 4 most common causes are
motor vehicle collisions (38%), falls (30.5%), violence (13.5%),
and sports injuries (9%).1
Types of Injury
Neurologic damage caused by SCI occurs in 2 phases: primary
injury (initial physical disruption of the spinal cord) and sec-
ondary injury (from processes such as ischemia, hypoxia, hem-
orrhage, edema).
Primary injury. Primary injury results from direct physical
trauma to the spinal cord due to blunt or penetrating
trauma. Trauma can cause spinal cord compression by bone
displacement, interruption of blood supply, or distraction from
pulling. Penetrating trauma, such as gunshot and stab wounds,
can cause tearing and transection. Scar formation
Secondary injury. Secondary injury refers to the ongoing,
progressive damage that occurs after the primary injury. Fig. 65.1 1 to 2 days after the injury, astrocytes proliferate and surround
Secondary injury causes further permanent damage. It begins the edges of the fibrotic scar. This confines inflammation to the area of
a few minutes after injury and lasts for months. The cascade injury protects and neighboring neural tissue from further damage. This
of events results in edema, ischemia, and inflammation. This process may take 7 to 10 days. (Used with permission from Barrow
causes cell death, disruption of the blood-brain barrier, and Neurological Institute, Phoenix, AZ.)
demyelination. This can extend the level of deficit and worsen
long-term outcomes. Classification of SCI
The edema from the inflammatory response is especially SCI is classified by the (1) mechanism of injury, (2) level of
harmful because of limited space for tissue expansion. Thus, injury, and (3) degree of injury.
compression of the spinal cord occurs. Edema extends above Mechanisms of injury. The major mechanisms of injury
and below the injury, increasing ischemic damage. Within 24 include flexion, flexion-rotation, hyperextension, vertical
hours, permanent damage may occur from edema. compression, extension-rotation, and lateral flexion (Fig. 65.2).
Apoptosis (programmed cell death) continues for weeks. Flexion-rotation injury is often the most unstable because
It contributes to post-injury demyelination. The inflam- ligaments that stabilize the spine are torn. This injury most often
matory response at the site of the initial injury focuses on contributes to severe neurologic deficits.
clearing up the initial cellular debris without damaging Level of injury. Skeletal level of injury is the vertebral level
normal tissue. This results in a central non-neural core of with the most damage to vertebra and related ligaments.
connective tissue that we refer to as a glial scar (Fig. 65.1). Neurologic level is the lowest segment of the spinal cord with
The glial scar creates a physical barrier. It restricts the cells normal sensory and motor function on both sides of the body.
in the spinal cord from migration and regeneration. This The level of injury may be cervical, thoracic, lumbar, or sacral.
leads to irreversible nerve damage and permanent neuro- Cervical and lumbar injuries are most common because those
logic deficit. areas of the spine are associated with the greatest flexibility and
movement.
Spinal and Neurogenic Shock Injury from C1 to T1 can cause paralysis of all 4 extremi-
Spinal shock may occur shortly after acute SCI. It is charac- ties, resulting in tetraplegia (formerly called quadriplegia). The
terized by loss of deep tendon and sphincter reflexes, loss of degree of impairment in the arms after cervical injury depends
sensation, and flaccid paralysis below the level of injury. This on the level of injury. The lower the level, the more function is
syndrome lasts days to weeks. It often masks post-injury neu- retained in the arms.
rologic function.2 Paraplegia (paralysis and loss of sensation in the legs) can
In contrast to spinal shock, neurogenic (vasogenic) occur in SCI below the level of T2.4 Fig. 65.3 shows affected
shock can occur in cervical or high thoracic injury (T6 or structures and functions at different levels of cord injury.
higher). It occurs from unopposed parasympathetic response Degree of injury. The degree of spinal cord involvement may
due to loss of sympathetic nervous system (SNS) innerva- be complete or incomplete (partial). Complete cord involvement
tion. It causes peripheral vasodilation, venous pooling, and results in total loss of sensory and motor function below the
decreased cardiac output. Manifestations include significant level of injury. Incomplete cord involvement results in a mixed
hypotension (<90 mm Hg), bradycardia, and temperature loss of voluntary motor activity and sensation and leaves some
dysregulation. Neurogenic shock may persist for as long as 5 tracts intact. The degree of sensory and motor loss depends on
weeks after injury.3 Hypotension can result in poor perfusion the level of injury and reflects specific damaged nerve tracts.
and oxygenation to the spinal cord and worsen spinal cord Five major syndromes are associated with incomplete
ischemia.3 injuries: central cord syndrome, anterior cord syndrome,
, 1596 SECTION 12 Problems Related to Movement and Coordination
Ruptured
posterior
Force
ligaments
Forward
dislocation
Damage to
spinal cord
A Flexion injury
Compressed
ligament
Ruptured
Force
anterior
ligament
B Hyperextension injury
Compression
of spinal cord
Force Fractured
vertebrae
C Compression fracture
Force
Displacement
of vertebrae
D Flexion-rotation injury
Fig. 65.2 Examples of mechanisms of spinal cord injury. (A) Flexion injury of the cervical spine ruptures the
posterior ligaments. (B) Hyperextension injury of the cervical spine ruptures the anterior ligaments. (C) Com-
pression fractures crush the vertebrae and force bony fragments into the spinal canal. (D) Flexion-rotation
injury of the cervical spine often results in tearing of ligamentous structures that normally stabilize the spine.
(A–C, From Copstead-Kirkhorn LC, Banasik JL: Pathophysiology, ed 5, St Louis, 2014, Mosby.)
Brown-Séquard syndrome, cauda equina syndrome, and conus We call the sensory regions dermatomes. Each segment of
medullaris syndrome (Table 65.1). the spinal cord innervates a specific area of skin. A dermatome
map is shown in Fig. 60.7. Each dermatome has a recommended
Clinical Manifestations point for testing.
Manifestations of SCI are the result of trauma that causes cord The ASIA Impairment Scale is useful for recording changes
compression, ischemia, edema, and possible cord transection. in neurologic status. It helps us identify rehabilitation goals.
They are related to the level and degree of injury. The patient Movement and rehabilitation potential related to specific loca-
with an incomplete injury may have a mix of manifestations. tions of SCI are described in Table 65.2. In general, sensory
function closely matches motor function at all levels.
Motor and Sensory Effects
The American Spinal Injury Association (ASIA) Impairment Respiratory System
Scale is used to classify the severity of impairment from SCI. Respiratory complications closely correspond to the level
It combines motor and sensory function assessments to deter- of injury. Cervical injuries above C3 present special prob-
mine neurologic level and completeness of injury (Fig. 65.4).5 lems because of the total loss of respiratory muscle function.
