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026 3-s2 Paraplegia and Spinal Cord Syndromes

Paraplegia and Spinal Cord Syndromes
Bruce H. Dobkin
Spinal Shock
Incomplete Lesions of the Spinal Cord
Foramen Magnum and Upper Cervical Spine
Lower Cervical and Upper Thoracic Spine
Thoracic Levels
Conus Medullaris and Cauda Equina
Pain Syndromes
Local Pain
Projected Pain
Central Neurogenic Pain
Autonomic Dysreflexia
Bowel and Bladder Dysfunction
Paraplegia may result from a variety of systemic and primary
central nervous system medical conditions, as well as trauma
at all segmental levels of the spinal cord (Box 26.1). A
spinal cord syndrome may develop from extramedullary and
intramedullary pathological processes. Initial symptoms may
be gradual in onset and progressive, including pain, dysesthesia, or subtle upper or lower extremity weakness. In other
cases, such as an inflammatory myelitis, acute onset of severe
motor, sensory, and autonomic deficits may develop without
premonitory symptoms. Trauma from a cervical flexion–
extension injury, for example, may produce a central cord
injury of the lower cervical spinal cord with incomplete
quadriparesis, whereas a complete transection injury at the
lower thoracic spinal cord from a fall may result in complete
paraplegia. Thus, both the rostrocaudal segmental level of
disease involvement or trauma and completeness of the
lesion in the transverse plane anticipate the person’s impairments and disability. Details about the relationships between
specific spinal cord segments and sensory dermatomes are
reviewed in Chapter 30, and the segmental innervations of
specific muscle groups are reviewed in Chapters 31 and 32.
The sensorimotor clinical examination allows localization of
the lesion (Fig. 26.1).
When examining a patient who presents with paraparesis
or paraplegia, a careful neurological examination is critical for
planning additional diagnostic workup and care. Identifying
distinct spinal cord syndromes and determining the likely
location of the underlying pathological process will guide
subsequent imaging and electrodiagnostic studies. As in most
upper motor neuron or motor unit diseases, fatigability of
strength occurs with repetitive movements against light resistance. For example, even when the initial manual muscle exam
does not detect iliopsoas weakness, ten leg raises from the
supine position against light downward hand compression
may reveal mild paresis upon immediately retesting hip
flexion. Structural information about the integrity of the spine
may be obtained from radiographic plain films and computed
tomography (CT) for bone pathology. Myelography is indicated when extrinsic cord compression is suspected, especially
when magnetic resonance imaging (MRI) is contraindicated.
MRI with contrast best reveals intrinsic and extrinsic cord
pathology. Spinal angiography identifies vascular pathology.
A review of imaging of the spine is provided in Chapter 39.
Acute and long-term care of patients is influenced by the
clinical presentation, severity of neurological deficits, underlying pathology, and prognosis for gains over time. Patients
presenting with an acute spinal cord syndrome after trauma
show both early (days to 3 months) and late (up to 2 years)
changes in their motor and sensory deficits (Fawcett et al.,
2007). Both neurological improvements and clinical worsening may occur. When some sparing of sensation and movement is present in the first 72 hours after trauma, the prognosis
for walking is rather good. Indeed, up to 90% of patients with
a cervical central cord injury who have any spared sensation
and movement below the level of injury by 4 weeks after
trauma will become functional ambulators (Dobkin et al.,
2006). Thus, serial and careful neurological examinations are
important for monitoring the injury-related deficits, especially
in the first weeks after onset. Rehabilitation of patients with
paraplegia follows after the acute medical needs have been
addressed. The aim is to promote as much functional independence as possible with and without assistive devices,
decrease the risk of complications, and reintegrate the patient
into home and community. Neurological rehabilitation for
paraparesis after spinal cord syndromes is reviewed in
Chapter 57.
The clinical presentation of a spinal cord injury depends on
whether the injury is complete or spares selected fiber tracts.
A number of clinically characterized spinal cord syndromes
may develop as a result of the involvement of different portions of the spinal cord gray and white matter.
Spinal Shock
Spinal shock refers to the period of depressed spinal reflexes
caudal to an acute spinal cord injury; it is followed by emergence of pathological reflexes and return of cutaneous and
muscle stretch reflexes (see Chapter 63). The bulbocavernosus
and cremasteric reflexes commonly return before the ankle
jerk, Babinski sign, and knee jerk.
Incomplete Lesions of the Spinal Cord
Unilateral Transverse Lesion
A hemisection lesion of the spinal cord causes a Brown–
Séquard syndrome. A pure hemisection is unusual, but patients
may show features of a unilateral lesion or hemisection. A
Brown–Séquard lesion is characterized by ipsilateral weakness
and loss of both vibration and position sense below the
level of the injury. In addition, there is a loss of temperature
and pain sensation below the level of the lesion on
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PART I Common Neurological Problems
BOX 26.1 Differential Diagnosis of Diseases Affecting
the Spinal Cord
Vertebral body fracture/dislocation
Hyperextension injury
Direct puncture, stab, or missile
Cervical stenosis
Lumbar stenosis
Intervertebral disk herniation
Infectious disorders (e.g., abscess, tuberculosis)
Inflammatory (e.g., rheumatoid arthritis, ankylosing spondylitis,
Epidural hematoma
Congenital disorders
Arachnoid cysts
Paget disease
Epidural metastasis
Intradural extramedullary (e.g., meningioma, neurofibroma,
leptomeningeal metastasis)
Demyelinating (e.g., MS, ADEM)
Hereditary (e.g., spastic paraplegia)
Viral myelitis (e.g., varicella-zoster, AIDS–related myelopathy,
human T-lymphotropic virus type I infection)
Vitamin B12 deficiency and other nutritional deficiencies
Ischemia and hemorrhage from vascular malformations or
Spirochetal diseases (syphilis and Lyme disease)
Toxic myelopathies (e.g., radiation-induced)
Autoimmune diseases (e.g., lupus, Sjögren syndrome)
Neuronal degenerations
Tethered cord at the cauda equina
Acute and subacute transverse myelitis of unknown cause
ADEM, Acute disseminated encephalomyelitis; AIDS, acquired
immunodeficiency syndrome; AVM, arteriovenous malformation; MS,
multiple sclerosis.
the contralateral side. As pain and temperature fibers extend
rostrally a few segments before crossing the midline to enter
the lateral spinothalamic tract, the loss of pain and temperature sensory modalities extends rostrally on the contralateral
side to a segmental level that is a few segments below the level
of the lesion. In addition, at the segmental level of the hemisection injury, a limited patch of ipsilateral loss of pain and
temperature in combination with a lower motor neuron weakness is often detected. A Brown–Séquard syndrome may be
caused by a variety of etiologies but is commonly encountered
after traumatic injuries, including bullet and stab wounds.
Central Cord Syndrome
Traumatic central cord syndrome is commonly characterized
by the triad of (1) motor impairment that is disproportion-
ately more severe in the upper than the lower extremities,
(2) bladder dysfunction that usually includes urinary retention, and (3) sensory dysfunction of varying degrees. An international consensus group suggested that an upper and lower
extremity difference of at least 10 motor score points, based
on the Medical Research Council scale, can be considered as
a quantitative addition to the commonly used qualitative criteria for making the diagnosis (van Middendorp et al., 2010).
An additional clinical feature of the traumatic central cord
syndrome is a dissociated sensory loss for pain and temperature, whereas vibration and position sense remain preserved.
This sensory presentation may be explained by a direct injury
to intramedullary decussating fibers, which normally would
ascend contralaterally as part of the spinothalamic tract. As
a result, a capelike sensory deficit may be encountered in
patients with a cervical level injury, but sensation within more
caudal dermatomes would generally be spared (Fig. 26.2).
A traumatic central cord syndrome is mostly encountered
in elderly patients who have suffered a relatively minor trauma
in the form of a cervical hyperextension injury, commonly in
the setting of an underlying cervical spondylosis. Falls and
motor vehicle injuries are common etiologies. Syringomyelia
or tumors may also produce a central cord syndrome.
Anterior Spinal Artery Syndrome
An anterior cord syndrome involves the anterior two-thirds of
the spinal cord, sparing the posterior columns. The cortico­
spinal and spinothalamic tracts are both affected. The syndrome is clinically characterized by paralysis and sensory
impairments below the level of the lesion, with impaired sensation of pain and temperature; vibration sense and proprioception are preserved. Fiber tracts for autonomic control are
also typically compromised, resulting in bladder, bowel, and
sexual dysfunction. In the acute phase after injury, a spinal
shock phase with decreased muscle tone and areflexia may
present, followed by a gradual return of reflexes and hypertonicity and perhaps spasms.
An anterior cord syndrome may be caused by trauma from
central disk compression or a bone fragment, as well as
a myelitis. Vascular occlusive causes are perhaps the most
common etiology. For instance, the anterior cord syndrome
may present as a spinal cord stroke from atherothrombotic or
embolic occlusion of the anterior spinal cord artery. Invasive
vascular and thoraco-abdominal surgical procedures may be
complicated by impaired blood flow to the spinal cord, especially due to obstruction or hypoperfusion of the artery of
Adamkiewicz near the T6 level. This may also follow surgery
at the distal aorta and proximal iliac arteries with the use of
aortic counter pulsation devices and, occasionally, from retroperitoneal hematomas or abscesses. Similarly, survivors of
cardiac arrest and significant hypotensive episodes may demonstrate a mid-thoracic anterior cord ischemic syndrome, as
the vascular supply near the T6 segment is particularly susceptible to distal field ischemia.
Anterior Horn and Pyramidal Tract Syndromes
Paralysis may be encountered in the setting of motor impairments in combination with relative sparing of sensory and
autonomic functions, as seen in motor neuron disease including amyotrophic lateral sclerosis (ALS). Lower motor neuron
weakness with atrophy and loss of reflexes is typically seen in
combination with upper motor neuron weakness, signs of
spasticity, and hyper-reflexia. Different limbs may be affected
to various degrees, but symptoms are progressive over the
course of the disease. However, innervation of the external
anal and urethral sphincters is normally preserved in ALS, with
sparing of bladder and bowel functions.
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Paraplegia and Spinal Cord Syndromes
Loss of vibratory and
position sense
Combined loss
Complete transection
of thoracic cord
(lesion at T10)
Right hemisection
of thoracic cord
(lesion at T3)
Early intra-axial lesion
of thoracic cord at T3 –T6
suspended pattern)
Advanced intra-axial lesion
of thoracic cord at T3 –T6
(sacral sparing)
Anterior spinal
artery syndrome
(lesion at T4)
equina lesion
Right S1
Peripheral neuropathy
(glove stocking
sensory loss)
Fig. 26.1 Characteristic sensory disturbances found in various spinal cord lesions in comparison with peripheral neuropathy.
Combined Posterior and Lateral Column Disease
A clinical syndrome characterized by development of a spastic
ataxic gait pattern may be caused by lesions affecting the posterior and lateral white-matter tracts. Friedreich ataxia represents a genetic etiology, and vitamin B12 deficiency may result
in subacute combined degeneration with spastic paretic gait
and sensory ataxia. Dorsal horn and column injury alone may
result from tabes dorsalis.
Paralysis may be caused by lesions at any segmental level of
the spinal cord from both intramedullary and extramedullary
disease. The characteristic symptoms and signs affecting motor
and sensory functions typically depend on the segmental level
of injury.
Foramen Magnum and Upper Cervical Spine
When structural lesions are located in or adjacent to the
foramen magnum, several different neurological patterns are
possible. For example, brainstem signs may occur together
with symptoms from a spinal cord injury. Involvement of the
lower portion of the brainstem is suggested by speech impairments, including dysarthria and dysphonia, as well as by dysphagia. In addition, facial numbness and nystagmus may be
detected in association with tumors or other structural lesions
in the foramen magnum. When compression of the spinal
cord occurs, long-tract signs may present from injury to the
corticospinal tract with, for instance, a spastic hemiparesis or
quadriparesis. A lower motor neuron injury component may
also be detectable from lesions at the craniocervical junction
and the foramen magnum, with upper extremity weakness,
muscular atrophy, and decreased muscle stretch reflexes.
Several pathological processes and lesions may be present
at the level of the foramen magnum and its immediate vicinity. These conditions include Arnold–Chiari malformations;
traumatic injuries; rheumatoid arthritis; syringomyelia; vascular lesions such as vertebral artery thrombosis, dissection,
or an arteriovenous malformation; and a variety of tumors
including meningiomas. Multiple sclerosis may also cause
intramedullary lesions of the brainstem and the upper cervical
spinal cord and selectively affect long white-matter tracts.
Imaging studies, especially MRI, help determine the nature
and precise anatomical location for pathological processes in
the foramen magnum and upper cervical spine region.
Lesions affecting the uppermost portion of the cervical
spine may be challenging to diagnose owing to a nonlocalizing symptom complex upon initial presentation. Pain is a
common early symptom and may be localized to the neck or
occipital region. At times, the pain may be aggravated by neck
movement. When upper cervical nerve roots are compressed,
a radicular pain may present in the corresponding dermatome.
Irritation of the second cervical nerve root, for example, may
present with a pain localized within the posterior aspect of the
scalp, whereas an injury to the third and fourth nerve roots
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PART I Common Neurological Problems
disks) that compress individual segmental nerve roots or
spinal nerves. Intramedullary lesions may also present with
pain, but the segmental localization is commonly less precise.
Extramedullary lesions typically first irritate segmental
nerve roots and the spinal nerve, with radicular pain and
sensory deficits typically following the corresponding dermatomal distribution. Similarly, motor deficits involve each
myotome affected by the lesion. Muscle stretch reflexes may
also provide helpful information with regard to the primary
level of injury, as the affected segmental reflex is typically
depressed or absent, and caudal reflexes are hyperactive. For
instance, when a lesion is at the C4–C6 level, a radicular
pattern of pain and sensory symptoms may typically involve
the radial side of the arm, forearm, and hand. Motor deficits
include weakness in elbow flexion. In addition, the biceps and
brachioradialis muscle stretch reflexes may be depressed or
absent, especially when the C5–C6 levels are involved.
In contrast, lesions at the C7–T1 level usually present with
pain and sensory impairments over the ulnar side of the upper
extremity, including the arm, forearm, and hand. Motor deficits related to affected myotomes commonly involve elbow
extension, the intrinsic hand muscles, and the triceps reflex.
Lower and upper motoneuron signs may also be present in
adjacent segments. If segmental nerve roots and the spinal
cord are compressed by a herniated disk or space-occupying
lesion at the C5–C6 level, for example, a decreased brachioradialis reflex may reflect a C6 radiculopathy, whereas a brisk
and hyperactive finger flexor reflex reflects an upper motoneuron syndrome.
Thoracic Levels
Fig. 26.2 Magnetic resonance image of the cervical spine showing
a contrast-enhancing mass. Patient presented with a capelike
sensory loss for pain and temperature. Resection of the mass revealed
a glioma.
may induce pain that is projected to the neck or shoulder. A
lower motoneuron injury presentation with upper extremity
muscular weakness and atrophy may also be part of the clinical presentation. When the spinal cord is compressed by epidural or subdural space-occupying lesions, spastic weakness
of upper and lower extremities typically follows.
An injury or disease process affecting the upper cervical
spinal cord may also compromise breathing. Normal respiration requires functional use of the diaphragm muscle, which
is innervated by the phrenic nerve. Motoneurons contributing
to the phrenic nerve are located within the cervical spinal cord
and contribute efferent axons to the C3–C5 ventral roots.
Therefore, complete injuries affecting the spinal cord above
the C3 segment will compromise the function of the diaphragm, and respiratory failure may follow.
Lower Cervical and Upper Thoracic Spine
Injuries to the lower part of the cervical spine and upper thoracic spine may be caused by extramedullary compression of
nerve roots and the spinal cord or by an intramedullary disease
process. The correlation between presenting symptoms and
localization of the underlying lesion is most precise for the
extramedullary pathological processes (e.g., tumors, herniated
Traumatic spinal cord injury at the thoracic level usually produces a complete lesion. The segmental level of injury is best
determined by a careful sensory examination of dermatomes.
Useful clinical landmarks are the nipple line for the T4 dermatome and the umbilicus for the T10 dermatome. Pain may
follow a radicular pattern around the chest or abdomen, corresponding to the segmental levels of injury. Sensory testing
of pin, temperature, pressure, and light touch appreciation
may determine the most caudal dermatome of normal sensation, as well as a zone of partial preservation. The sensory
testing should include evaluation of dermatomes of the
left and right side of the body, with comparisons of homologous levels. In addition to a combination of at-level pain,
sensory deficits, and muscular weakness, autonomic dysfunction may develop from long-tract involvement and include
urinary retention, bladder–sphincter dyssynergia, and bladder
Conus Medullaris and Cauda Equina
The conus medullaris of the spinal cord terminates approximately at the level of the L1 vertebra, although the precise
location of the tip of the conus may show marked variability
among subjects. This anatomical aspect of the spinal cord is
important because spine trauma commonly takes place at the
thoracolumbar junction, and the extent of such injuries is
highly variable (Kingwell et al., 2008). Traumatic injuries to
the conus medullaris usually result in weakness or paralysis of
the lower extremities, absence of lower extremity reflexes, and
saddle anesthesia (Fig. 26.3). However, some patients with
conus medullaris injuries exhibit a mixed upper and lower
motoneuron syndrome. In contrast, a cauda equina injury that
lesions lumbosacral roots below the level of the conus medullaris is a pure lower motoneuron syndrome. Cauda equina
injuries present with lower extremity weakness, areflexia and
decreased muscle tone, and variable sensory deficits. At least
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Paraplegia and Spinal Cord Syndromes
root distribution often is found immediately after the walk
and resolves within a minute or two.
In addition to motor and sensory impairments, pain and dysfunction in the autonomic nervous system can aid localization
of spinal cord syndromes. Pain is frequently associated with
spinal cord injuries, along with autonomic impairments that
may affect blood pressure and heart rate, bladder, bowel,
sexual, and cardiorespiratory functions. The type and severity
of autonomic dysfunction depends on the location of pathology and severity of the spinal cord injury. International spinal
cord injury societies recommend a systematic approach to
document remaining autonomic function after a spinal cord
injury (Alexander et al., 2009).
Fig. 26.3 Magnetic resonance imaging demonstrating the effects of
trauma to the thoracolumbar portion of the spine with a crush injury
of the cauda equina (CE) and conus medullaris (CM) portion of the
spinal cord. Note T12/L1-level spine fracture and dislocation.
Pain Syndromes
Distinct pain syndromes may develop as a result of compression, inflammation, or injury to the vertebral column, ligaments, the dura mater, nerve roots, dorsal horn, and ascending
spinal cord sensory tracts. Neuropathic pain may take the form
of paresthesia (abnormal but not unpleasant sensation that
is either spontaneous or evoked), dysesthesia (an abnormal,
unpleasant sensation that is spontaneous or evoked), allodynia
(pain evoked by ordinary stimuli such as touch or rubbing),
and hyperalgesia (an augmented response to a stimulus that is
usually painful).
Local Pain
a third of these patients suffer considerable central pain.
Affected limb and pelvic floor muscles develop flaccid weakness, and electromyography shows denervation after either a
conus medullaris or cauda equina injury, especially following
anatomically complete lesions.
Both conus medullaris and cauda equina injuries are associated with bladder, bowel, and sexual dysfunction. Urodynamic evaluations typically demonstrate detrusor areflexia,
and a rectal exam identifies a flaccid anal sphincter. In addition, the bulbocavernosus reflex is typically absent or diminished, and reflexogenic erection in males is commonly lost.
Imaging studies (e.g., plain radiographs, CT, MRI) identify
structural pathology. Burst fractures and fracture dislocations
are common injuries to the spinal column that result in neurological deficits, suggesting a conus medullaris or cauda
equina involvement. Following trauma to the thoracolumbar
spine, imaging studies can be used to assess spinal stability
and identify detailed aspects of spine fractures, including the
presence and location of bone fragments, spinal canal
encroachment, epidural hematomas, and herniated disks. A
variety of treatment options exist (e.g., surgical stabilization
of the spine, decompression of the conus medullaris and nerve
A lumbar spinal stenosis due to a congenitally smalldiameter spinal canal or central disk and spondylotic narrowing one or more levels below L1 may present with a subtle
course. Over months to years, lower extremity numbness or
pain, usually in an L3–S1 single or multiradicular pattern,
accompanies standing and walking, often gradually progressing to limit walking distance. Pain is commonly accompanied
by weakness, but patients may not be aware of their deficit.
Clinical insight into this diagnosis and the upper level of
cauda compression is gained by a manual muscle examination
after a few minutes of being supine, followed by having the
subject walk for about 500 feet, and then immediately retesting strength. Transient paresis or greater paresis in the affected
Localized neck or back pain may result from irritation or
injury to innervated spine structures including ligaments, periosteum, and dura. The pain is typically deep and aching, may
vary with a change in position, and often becomes worse from
increased load or weight bearing on affected structures. Percussion or palpation over the spine may in some patients worsen
the local pain. When the injured or diseased spine structures
are irritated, secondary symptoms may develop and include
muscle spasm and a more diffusely located pain. Musculoligamentous sources of pain often persist for more than a week
post spine surgery and develop with compensatory overuse of
joints and muscles. Such pain must be distinguished from
central neurogenic pain, but can amplify it.
Projected Pain
A pathological process involving the facet joints may be experienced as focal or radiating pain in an upper or lower extremity. When a nerve root is irritated or injured, the projected pain
is radicular.
Radicular pain commonly has a sharp, stabbing quality or
causes dysesthesia. It may be exacerbated by activities that
stretch the affected nerve root (e.g., straight leg raising or
flexion of the neck). Straining or coughing may also increase
the intensity and severity of radicular pain. Nerve root irritation may also result in sensory and motor deficits following
the same dermatome and myotome distribution as the affected
nerve root. This helps localize the level of spinal cord injury
that is causing paraplegia.
Central Neurogenic Pain
Paresthesia, dysesthesia, allodynia, and hyperalgesia accompany
injury to the spinal cord in at least half of patients, as well as
after thalamocortical stroke. Regardless of segmental level or
completeness of injury, most patients with a traumatic spinal
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PART I Common Neurological Problems
cord injury develop a clinically significant pain syndrome at
some post-lesion time point (Waxman and Hains, 2006).
Neuropathic pain after spinal cord injury may affect different
locations. At-level pain is primarily derived from local cellular
and neuroplastic changes in the dorsal horn and sensory roots
at the segments of injury. Below-level pain is located in body
segments receiving innervation from the spinal cord caudal to
the lesioned segments. Above-level neurogenic pain is less
Pain developing after a spinal cord injury is commonly
described as burning, pricking, or aching in quality. It can be
experienced as deep or superficial. Some patients develop a
severe and excruciating pain syndrome after cord or cauda
trauma that is at-level and below-level even in the absence of
any cutaneous or proprioceptive sensation, which requires
centrally acting medications to control. The most recently
FDA-approved medication for spinal pain is pregabaline. The
mechanisms for such painful phantom phenomena are not
well understood but include structural and molecular dorsal
horn, thalamic, and cortical adaptations to ordinary and
noxious inputs.
Autonomic Dysreflexia
Injuries to the spinal cord that result in paraplegia from a
lesion above T6 may also impair autonomic control and
result in episodes of severe hypertension or hypotension.
Autonomic dysreflexia represents an acute syndrome characterized by excessive and uncontrolled sympathetic output
from the spinal cord. As a result, the blood pressure is suddenly and markedly elevated. Associated symptoms include
headache; malaise; blurring of vision; flushed, sweaty skin
above the level of injury; and pale, cool skin below it. An
episode of autonomic dysreflexia can be triggered by any
noxious stimulation below the segmental level of injury.
Common triggers include bladder distension, constipation,
rectal fissures, joint injury, and urinary tract infection. Autonomic dysreflexia may present soon after the initial injury
but more commonly becomes symptomatic several months
after the spinal cord injury. Prevention is the best approach.
Treatment of acute symptoms targets removal of noxious
stimuli and cautious lowering of the blood pressure (see
Chapter 63).
Bowel and Bladder Dysfunction
Normal bladder and bowel control depend on segmental
reflexes involving both autonomic and somatic motor neurons,
as well as descending and ascending tracts of the spinal cord
(Fowler et al., 2008). As a result, bladder and bowel function
may be impaired after an injury to any segmental level of the
spinal cord. Different clinical syndromes develop depending
on whether the injury or disease process affects the sacral
spinal cord directly or higher segmental levels. Traumatic
spinal cord injuries with paraplegia taking place above the T12
vertebra will interrupt spinal cord long-tract connections
between supraspinal micturition centers in the brainstem and
cerebral cortex and the sacral spinal cord. An upper motoneuron syndrome follows, with detrusor–sphincter dyssynergia
caused by impaired coordination of autonomic and somatic
motor control of the bladder detrusor and external urethral
sphincter, respectively. Incomplete bladder emptying results.
In addition, the upper motoneuron syndrome also includes
detrusor hyper-reflexia with increased pressure within the
bladder. In contrast, injury to the T12 vertebra and below
results in a direct lesion to the sacral spinal cord and associated nerve roots. A direct lesion to preganglionic parasympathetic neurons and somatic motoneurons of the Onuf nucleus
located within the S2–S4 spinal cord segments results in denervation of pelvic targets. Injuries to both the conus medullaris
and cauda equina present as a lower motoneuron syndrome
characterized by weak or flaccid detrusor function. Urinary
retention follows, with risk of overflow incontinence. The goal
for all bladder care is to avoid retrograde urine flow, urinary
tract infections, and renal failure. Management of both upper
and lower motoneuron bladder impairment commonly
includes clean intermittent bladder catheterizations. Chapter
47 discusses evaluation and treatment.
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Paraplegia and Spinal Cord Syndromes
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