Cauda Equina Syndrome

Cauda equina
• Latin for “horse’s tail,”
• Terminal portion of the spinal
cord and roots of the spinal
nerves beginning at the first
lumbar nerve root.
Cauda equina syndrome (CES)

• Compression of some or all of these nerve roots, resulting in

symptoms that include bowel and bladder dysfunction, saddle
anesthesia, and varying degrees of loss of lower extremity sensory
and motor function.
History

• Mixter and Barr1 are credited with the first description in the English-
language literature of CES in 1934.
• Precise definition of CES not well established, most authors believe
that an element of bladder dysfunction is required for the diagnosis.
Epidemiology

• The overall prevalence of CES is unknown.

• Most common cause is a herniated lumbar disk.
 Causes of Cauda Equina Syndrome
• Herniated lumbar disk
•Iatrogenic causes
• Spinal stenosis
•Intradiscal electrothermal
• Tumor
annuloplasty
• Trauma
• Spinal epidural hematoma
•Use of Gelfoam (Pfizer,
• Spinal epidural abscess New York,NY)
•Durotomy
•Spinal surgery
•Epidural fat graft
•Spinal manipulation
•Elective extremity
orthopaedic surgery
Epidural abscess
 Pathophysiology
• In adults, the spinal cord terminates at T12 – L2
vertebrae, most commonly at L1 vertebral body.
• Conus medullaris –
• caudal end of the spinal cord
• is attached to the coccyx by a thin nonneural filament, the
filum terminale.
• Contains the cell bodies and dendrites of L5 to S3 nerve
roots.
• The cauda equina is a collection of peripheral nerves (L1 to
S5) in a common dural sac within the lumbar spinal canal.
During development

• Spinal cord appears to migrate proximally

• Relatively greater growth of the vertebral spinal column.
• L1 nerve roots, actually exit the spinal cord at T10 vertebral level.
• The L2 and L3 nerve roots exit the spinal cord opposite T11 vertebral
body.
Neurophysiologically

• Lower motor neuron lesion.

• May demonstrate
• lower extremity muscle weakness and
• sensory disturbance as well as
• decreased or absent reflexes.
• Neurogenic bladder dysfunction - essential element of CES.
 Innervation of bladder
• Complex
• Components of
• parasympathetic,
• sympathetic and
• somatic nerves.
• The detrusor urinae muscle and internal sphincter of
the bladder are smooth muscles - controlled by the
parasympathetic nervous system via S2-4 sacral nerve
roots and Sympathetic nervous system via the
hypogastric plexus (T11-L3).
• The parasympathetic system promotes emptying of the bladder by
causing contraction of the detrusor urinae muscle and relaxation of the
internal sphincter.
• The reverse is true of the sympathetic system, which promotes storage.
• The external sphincter of the bladder is a striated muscle that is
controlled by the pudendal nerve, which arises from S2-4 sacral nerves.
Bladder dysfunction in CES

• Two broad categories:

• Retention and
• Incontinence.
• CES causes Lower motor neuron lesion interrupts the nerves forming
the reflex arcs.
• Sensory and motor innervation to the bladder is lost.
• Unable to sense the expansion of the bladder as it distends.
• Not able to contract the detrusor urinae muscles and relax the
sphincter muscles to allow emptying.
• Leads to
• urinary retention and
• Eventually overflow incontinence.
Pathophysiology

• Several theories of actual neural injury:

1. Mechanical compression,
2. Ischaemic injury,
3. Nutritional impairment sec to compression and
4. Secondary closed compartment syndrome.
Mechanical compression

• Particularly susceptible to traumatic injury

• Unlike peripheral nerves (epineurium, perineurium, and endoneurium)
• Nerve roots of the cauda equina have only one layer, the endoneurium
(cerebrospinal fluid and the dura sac).
Ischemic injury

• A principal factor in the pathophysiology of CES.

• The main arterial blood supply to the spinal cord consists of
1. Anterior spinal artery and
2. Paired dorsolateral spinal arteries.
• Arterial blood supply to the nerve roots is less well defined.
 Vascular injection study:
• Parke et al - on 11 perinates:
• Each nerve root - intrinsic blood supply from both
• distal and proximal radicular arteries, which anastomose in
the proximal one third of the nerve root.
• Distal radicular arteries are branches of the ciliary ganglionic
plexus of the spinal artery.
• The ventral proximal radicular arteries branch from the vasa
corona and receive their blood supply from the anterior
spinal artery.
• Dorsal proximal radicular arteries are immediate branches of
the posterior spinal artery.
• U-shaped region of relative hypovascularity
• below the level of the conus
• correlating with areas of vascular anastomoses in the cauda equina.
• an anatomic basis for the suspected
• neuroischemic manifestations of CES
• Nutritional impairment sec to compression:
• by reducing both blood flow and nutrient diffusion from
the surrounding cerebrospinal fluid.
• Secondary closed compartment syndrome:
• By mechanical compression of the nerve roots -
intraneural edema.
• greater than the perfusion pressure of the nerve root.
• damaging effects of venous stasis more pronounced in
two level compression compared with singlelevel.
Postoperative Spine
Patient
• In lumbar diskectomy,
• from direct damage to nerves, especially from excessive retraction of the
dural sac, or
• Postoperatively development of a hematoma.
• Relative spinal stenosis at the involved level in combination with
postoperative tissue edema.
• venous congestion and nerve root ischemia.
• Usually within 24 hrs. – reported upto 7 days.
• Other surgeries:
• lumbar microdiskectomy.
• in situ arthrodesis for grade III or IV spondylolisthesis.
• Delay in diagnosis:
• Post operative pain and
• Routine use of urinary catheters
• HIGH INDEX OF SUSPICION
 Anticoagulation
Following Neuraxial Anesthesia
• In the United States, the current recommendation is to delay
anticoagulation for 2 hours after spinal needle placement or epidural
catheter removal.
• If “bloody tap” or “traumatic tap”, should be delayed longer than the
recommended 2 hours or avoided completely.
• Insertion of a spinal needle – delayed 8 to 12 hours after a prophylactic
dose of low-molecular-weight heparin or heparin.
Anticoagulation in the
Postoperative Spine Patient

• The Seventh American College of Chest Physicians Conference on

Antithrombotic and Thrombolytic Therapy for elective spine surgery
recommends against the routine use of any mechanical or chemical
thromboprophylaxis modality, apart from early and persistent
mobilization.
• Currently, no specific recommendations with regard to resumption of
antithrombotics used for the treatment of medical conditions after
spinal surgery.
• Under proper supervision, antithrombotic therapy usually may be safely
resumed within 48 to 72 hours of spinal surgery.
• Risks weighed.
• Regular medication dose started without the use of a loading dose or
bridging medications.
Clinical Presentation:

• Varying combination of signs and symptoms,

including
• low back pain,
• groin and perineal pain,
• bilateral sciatica,
• lower extremity weakness,
• Hypoflexia or areflexia,
• Sensory deficits,
• Perineal hypoesthesia or saddle anesthesia,
• and loss of bowel or bladder function.
• Bladder dysfunction is a required element.
• Early bladder dysfunction can be subtle and involve
• Difficulty initiating the urinary stream.
• May then progress to urinary retention and eventually
overflow incontinence.
• Prodromal symptoms of
• low back pain and/or unilateral sciatica,
• reflective of uncomplicated lumbar disk herniation or
stenosis.
• Back pain
• characteristically severe, but it may be resolving or even absent in patients
with delayed presentation.
• Bilateral sciatica
• strongly associated with CES, but
• unilateral lower extremity pain is a
• more frequent symptom at the time of initial presentation.
Saddle anesthesia

• Dense sensory loss involving the perineum, buttocks, and

posteromedial thighs,
• Relatively late sign of established CES
• May indicate poor potential for recovery of normal bladder function.
Clinical presentations of CES

• Kostuik et al2 described two distinct clinical presentations of CES:

1. Acute and
2. Insidious.
Acute presentation

• Characterized by
• Sudden onset of severe low back pain, sciatica, urinary retention
requiring catheterization, motor weakness of the lower extremities,
and perineal anesthesia.
• An acute central disk herniation often causes this.
Insidious presentation

• Characterized by
• Recurrent episodes of low back pain occurring over periods of a few
weeks to years,
• Followed by the gradual onset of sciatica, sensorimotor loss, and
bowel and bladder dysfunction.
• Often occurs in the setting of long-standing spinal stenosis
• Relationship between underlying developmental spinal abnormalities
and an increased risk for CES.
• Average time to surgery from the onset of significant bladder
dysfunction was
• 1.1 days in the acute-onset group versus
• 3.3 days in the insidious-onset group.
Kostuik et al
• Extent of sensory deficit in the perineal area—
• partial, complete, unilateral, or bilateral
• Represented the most important prognostic indicator.
Kostuik et al
Patient Evaluation

• Detailed history
• Detailed examination of the sacral nerve roots.
• Sensations to pin pricks in perianal region – S2 – S4 dermatomes.
• Preserved light touch and pressure
• Rectal examination – decreased tone often an early finding.
• Anal wink test and bulbocavernous reflex.
The bulbocavernosus reflex

• Segmental polysynaptic reflex with crossover in the sacral spinal cord

(S1-3).
• By applying pressure to the glans penis or clitoris and/or traction on
the Foley catheter.
• A normal response
involves contraction
of the anal sphincter.
• Palpation – full bladder
• Post void residual volume
• Urodynamic studies
• Post operative spine patient:
• Increasing back pain followed by unilateral or bilateral leg pain may be potential
signs of developing CES.
• Later may develop classic signs of saddle anesthesia and loss of bowel or bladder
function
Radiographic Evaluation

• MRI
• Myelogram and CT
Treatment

• Surgical exploration and decompression of any compressive lesions.

• Recommended procedures range from
• Simple microdiskectomy to
• Wide laminectomy,diskectomy, and
• Open inspection of the nerve roots within the dural sac.
• No advantage of any one over other.
Timing of Surgery

• Topic of great controversy.

• Traditional practice - preferably within 24 hours.
• Kostuik et al performed a retrospective review of CES and found no
correlation between the timing of surgery and the extent of
neurologic or bladder recovery.
• Conclusion was made that decompression did not have to be
performed within 6 hours,
• But recommendation was that surgery be performed as soon as
possible to prevent further potential progression of neurologic
deficits.
Timing of decompression

• Specifically addressed by a meta-analysis performed by Ahn et al:

• Statistically significant improvement in neurologic outcome in
patients treated within 48 hours versus those treated more than 48
hours after the onset of CES.
• No statistically significant improvement in patients treated within 24
hours of onset and those between 24 and 48 hours.
• Concluded that patients should be treated urgently (within 48 hours)
but that there was no benefit to emergent (within 24 hours) surgical
decompression.
• Not faulted if performed within 24 hrs as exact onset of symptoms
usually not known.
Carpal Tunnel Syndrome
 Median Nerve Anatomy
• Originates from lateral
and medial cords of the
Brachial Plexus
• Contains fibers from
the C6, C7, C8 and T1
nerve roots and
sometimes from C5.

Regional Review Course 1998

 Median Nerve Anatomy Forearm
• Passes between FDS and FDP
• Gives off the palmar cutaneous sensory branch before it
enters the wrist via the carpal tunnel
– Runs radial to the median nerve and ulnar to the FCR tendon to
provide sensation to the radial palm

Regional Review Course 1998

 Median Nerve Anatomy
• Supplies sensation to
– palmar aspect of
thumb, index, long and
radial half of ring
fingers
– dorsal aspect of index,
long and radial half of
ring fingers distal to the
PIP joint

Regional Review Course 1998

 Carpal Tunnel Anatomy
• Contents
– median nerve
– FDP index-small
– FDS index-small
– FPL
• Borders
– transverse carpal ligament
(TCL)
• roof of carpal tunnel
• connects from the pisoform
and hook of the hamate to
the scaphoid tuberosity and
trapezial beak.
• ligament is confluent with
antebrachial fascia of forearm
– carpus forms radial and ulnar
borders and floor
Regional Review Course 1998
 Median Nerve Anatomy
• variations in the take off of the motor branch of the median
nerve
– distal to the ligament (extraligamentous)
– branching proximally and turning around the ligament distally
(subligamentous)
– coursing through the ligament (transligamentous)
– rarely the motor branch comes off the ulnar aspect of the median
nerve.

Lanz U: Anatomical variations of the median Nerve in the Carpal Tunnel J Hand Surg 2A:45;1977
 Median Nerve Anatomy
Muscles Supplied in Hand
• Motor Supply (LOAF)
– Lumbricals
• Index
• Long
– Thenar Muscle
• Opponens Pollicis
• Abductor Pollicis Brevis
• Flexor Pollicis Brevis
(Superficial 1/2)

ASSH Patient Handout Carpal Tunnel Syndrome

Median Nerve Anatomy

Click Picture to Play Video

 Diagnosis of Median Nerve
Compression Syndromes
Diagnosis is founded on:
• A clear history of specific symptoms.
• Clinically apparent signs.
• Clinically measurable sensory and motor
deficits.
• Reproducible provocative diagnostic tests
• And, if needed, electro diagnostic tests.
 Diagnosis of Median Nerve
Compression Syndromes
Diagnosis is founded on:
• A clear history of specific symptoms.
• Clinically apparent signs.
• Clinically measurable sensory and motor
deficits.
• Reproducible provocative diagnostic tests
• And, if needed, electro diagnostic tests.
 Diagnosis of Median Nerve
Compression Syndromes
Diagnosis is founded on:
• A clear history of specific symptoms.
• Clinically apparent signs.
• Clinically measurable sensory and motor
deficits.
• Reproducible provocative diagnostic tests
• And, if needed, electro diagnostic tests.
 Carpal Tunnel Syndrome Definition
• Carpal Tunnel Syndrome is a
disorder caused by pressure
induced dysfunction of the
median nerve in the carpal
tunnel of the wrist.
• The symptoms and signs of
carpal tunnel syndrome are
the symptoms and signs of
distal median nerve
dysfunction in the hand.

ASSH Patient Handout Carpal Tunnel Syndrome

 Carpal Tunnel Syndrome Definition
• Carpal Tunnel Syndrome is a
disorder caused by pressure
induced dysfunction of the
median nerve in the carpal
tunnel of the wrist.
• The symptoms and signs of
carpal tunnel syndrome are
the symptoms and signs of
distal median nerve
dysfunction in the hand.

ASSH Patient Handout Carpal Tunnel Syndrome

 Symptoms Carpal Tunnel Syndrome
• Sensory symptoms include:
• decreased sensation
(numbness),
• tingling in the median nerve
sensory distribution and
• pain radiating both in the
distribution of the median Dorsal Palmar
nerve and more proximally up
the arm.

Regional Review Course 1998

 Epidemiology
• Idiopathic Carpal Tunnel Syndrome
- 3:1 Female : Male
- 4th-5th decade and beyond
- Correlates most with increased Body
mass index (BMI)
• Other Risk Factors
- Diabetes, hypothyroidism, rheumatoid arthritis
and pregnancy
 Motor Symptoms
Motor symptoms
• Of the thenar muscles the
APB is most reliably purely
innervated by the median
nerve with no ulnar
contribution.
•Patients will describe
weakness of grasp or
clumsiness of hand function.

ASSH Patient Handout Carpal Tunnel Syndrome

 Clinical Evaluation
• Observation for thenar atrophy
• Sensory testing
• Motor testing (APB)
• Provocative testing via median nerve
compression
• Electrodiagnostic testing
 Sensory Testing
• Can help determine the
level of the lesion
– No sensory deficits: Pure
motor lesion
• Anterior Interosseous
Nerve Syndrome
– A sensory deficit in
dermatomal pattern
• cervical radiculopathy
(e.g. C6 nerve root
compression)
– Absence of palmar
cutaneous sensation
suggests lesions above
carpal tunnel

Courtesy of Andrew P. Gutow, MD

 Sensory Testing
• Threshold test
– first measurable change in
objective sensory perception
– vibratory threshold and light touch
• Density tests
Semmes Weinstein Monofilament
– test large myelinated fibers Light Touch Testing
• static 2 point discrimination – slow
adapting fibers
• moving 2 point discrimination – fast
adapting fibers
– changes occur later than
threshold tests
Two Point Discrimination Testing
• Subjective comparison
Courtesy of Andrew P. Gutow, MD
 Specific Motor Functions
• Testing of FPL for
anterior interosseous
nerve lesion
• Testing of Index FDP for
anterior interosseous
nerve lesion
• Testing of Abductor
Pollicis Brevis via
palpation of APB with
resisted opposition
Courtesy of Andrew P. Gutow, MD
 Provocative Tests
Provocative diagnostic tests
recreate the patients symptoms
of pain or tingling by putting
increased pressure on the
already sensitive median nerve
at the wrist. The patient should Median nerve Compression Test
report symptoms in the
expected anatomic distribution.

Symptoms should be in
Median Sensory Area
Top right: Courtesy of Andrew P. Gutow, MD;
Bottom right: ASSH Patient Handout Carpal Tunnel Syndrome
 Phalen’s Test
Phalen’s test of wrist flexion is
positive if it recreates the
symptoms of numbness or
tingling within 60 seconds.
Helpful to reconfirm diagnosis
with clinical history (sensitivity
0.75) but has high incidence of
fall positive (specificity 0.47).
The test is gravity assisted without
extreme flexion of the elbow, which
can cause ulnar nerve symptoms
from stretching of the ulnar nerve in
Courtesy of Andrew P. Gutow, MD
the cubital tunnel in the elbow.
 Tinel’s (Sign) Test
Direct tapping of a irritated
nerve can recreate tingling in the
sensory distribution of the nerve.
For the median nerve tapping at
the proximal aspect of the carpal
tunnel over the median nerve is
confirmatory (sensitivity 0.60)
but not absolute (specificity
0.67). The median nerve enters the
carpal tunnel just radial to the
palmaris longus at the ulnar
side of the thenar eminence.
Courtesy of Andrew P. Gutow, MD
 Compression Test (Durkan’s)
Median nerve compression test is the most sensitive
(0.87) and specific ( 0.90) provocative test for carpal tunnel
syndrome. Direct pressure is placed over the median nerve
at the carpal tunnel.
A positive test recreates within
30 seconds the patient’s sense
of tingling or numbness in the
median nerve distribution.

Courtesy of Andrew P. Gutow, MD

Diagnostic Imaging Radiographs
• Radiographic imaging not always required in
diagnosis of carpal tunnel syndrome
• May be helpful in cases of
– higher level lesions
• Radiographs of the distal humerus can identify a
supracondylar process in cases of pronator syndrome
– patients with past history of trauma
• Radiographs of the wrist can identify old fractures of the
distal radius, carpal instabilities, and wrist arthritis which
may contribute to carpal tunnel syndrome.
– patients with inflamatory arthropathy
– older patients.
 Diagnostic Imaging
Cross Sectional Imaging
• MRI
– generally not used as a diagnostic tool for
primary median nerve compression
– may identify causes of compression such as
tumors or ganglions when clinically
indicated
– may be used to assess recurrent carpal
tunnel syndrome
 Electro diagnostic Testing
• Electrodiagnostic testing of nerves consists of Nerve
Conduction Velocity (NCV) and Electromyography
(EMG).
• These studies can help confirm the diagnosis of carpal
tunnel syndrome, but do not in themselves give a
diagnosis which requires treatment without co occurring
symptoms.
• NCV/EMG can be helpful in confirming the anatomic
level of compression of a nerve and in looking for more
proximal lesions or generalized neuropathies.
 Electro diagnostic Testing
• NCV testing measures both conduction velocity as well
as the amplitude of action potentials.
• NCV can show slowing of conduction latencies (distal
latency) across the carpal tunnel and decreased
action potential amplitude.
• Sensory conduction latencies (distal sensory latency)
increase first in mild cases before motor conduction
latencies increase.
• Decreased amplitude of the compound motor action
potential (CMAP) is a finding in more severe disease.
 Electromyogram (EMG)
• The needle electromyogram study requires direct
recording from a muscle and is used to assess for
denervation of specific muscles or to measure severity of
the nerve dysfunction.
• Denervated muscles show increased insertional activity,
abnormal fibrillation potentials at rest and poor
recruitment of motor units.
• EMG can be helpful in separating proximal from distal
nerve compression if muscles proximal to the carpal
tunnel are tested and also show evidence of
denervation.
 Prevention
• Control of contributing diseases
– Control sugar in DM
– Medically control tenosynovitis in RA
– Correct Hypothyroidism
• No strong evidence of prevention from work
modification.
– Some suggestion of benefit to avoidance of continual
strenuous grasping and extreme wrist positions
 Treatment
• Treatment is based on decreasing the pressure in the
carpal tunnel and thereby improving the blood flow and
nourishment to the median nerve.

• Non operative treatment can decrease the volume of

structures in the carpal tunnel by treating tendon
enlargement or improve median nerve nourishment by
using night time neutral
wrist splinting to provide
a daily period of
improved blood flow.

Courtesy of Andrew P. Gutow, MD

 Cortisone Injection
Injection of corticosteroid
into the carpal tunnel has
been shown to improve
symptoms, although at one
year follow up only 50% of
patients injected were
symptom free. Risks of
injection include infection Injection is performed starting just
and iatrogenic injury to the proximal to the wrist crease and
just ulnar to the palmaris longus
median nerve during aiming to enter the carpal tunnel
injection. radial to the hook of the hamate
and ulnar to the median nerve.
Regional Review Course 1998
 Surgical Treatment
• Increases space available for the median nerve by
sectioning transverse carpal ligament opening up the
volar aspect of the carpal tunnel.
• Surgical options including open release, endoscopic
directed release and minimal incision release
• Earlier return to work / activity seen with endoscopic /
minimal incision techniques.
• Slight increase risk of nerve or tendon injury with
minimal incision methods, with long term outcome and
complication similar for all techniques with > 90%
success and patient satisfaction rates.