Transient Neurologic Symptoms

Description

Transient neurologic symptoms (TNS) present as lower back pain lower extremity dysesthesias radiating to the buttock, thighs, lower limbs after the resolution of a spinal anesthetic.
Symptoms vary from mild to severe often resolve within 5 days.
The pathophysiology remains unclear; neurologic exams, MRI, electrophysiologic testing have failed to demonstrate any abnormalities.
Although typically associated with intrathecal lidocaine, other local anesthetics including bupivacaine, tetracaine, ropivacaine have also been shown to cause TNS.

Epidemiology

Incidence

Transient radicular irritation: 0.4%
TNS after spinal anesthesia: 10–37%
TNS risk is 6–7 times higher with lidocaine than with bupivacaine five-fold higher than with prilocaine
- Lidocaine 2% 5% concentrations: Up to 33% occurrence
- Bupivacaine 1–2%
- Mepivacaine: 7%
- Tetracaine: 1–3%
- Procaine: 1%
- Ropivacaine: 0–1%
- Prilocaine: 0–1%

Morbidity/Mortality

No reported long-term morbidity or mortality with TNS due to the transient nature of symptoms. Patient discomfort is the main adverse effect.

Etiology/Risk Factors

Etiology is not completely understood
Risk factors
- Local anesthetics intrathecally (especially lidocaine)
- Lithotomy position
- Prolonged surgery
- Vasoconstrictor additives to local anesthetic solutions, such as epinephrine
- Outpatient status
- No association with glucose concentration, osmolarity of anesthetic solution injected concentration of lidocaine
- No association with age, height, weight, sex, needle type or size, difficulty of block placement, paresthesias

Physiology/Pathophysiology

Intrathecally administered local anesthetics induce a reversible block of neurotransmission at the spinal cord.
However, all local anesthetics also have the potential for neurotoxic or other adverse effects on the spinal cord, ranging from cauda equina syndrome to TNS.
TNS consist of self-limited lower back pain with radiation to the buttocks, thighs, lower limbs after spinal blockade has resolved. Onset is typically within 12–36 hours of surgery with duration lasting 6 hours to 5 days.
The mechanism remains unclear possibly results from local anesthetic neurotoxicity. The majority of data comes from retrospective studies meta-analyses that help identify associated etiologies describe the clinical course of symptoms.
Theories that have been proposed discarded include spinal cord ischemia, extent of local anesthetic distribution, spinal infection, or hemorrhage.
TNS does not appear to be associated with neurologic pathology. TNS appears to be lacking identifiable pathology. Neurologic exams, radiographic imaging, electromyelography (EMG), nerve conduction studies are usually normal. Specifically, there appears to be an absence of sensory-motor deficits, or muscle-tendon reflex abnormalities that are common with acute radicular irritation.
Local anesthetics
- All local anesthetics have been reported to cause TNS
- Intrathecal lidocaine is attractive for ambulatory surgery due to its intense sensory motor blockade, combined with its short duration of action. Lidocaine, however, has been associated with up to a 30% incidence (even at concentrations as low as 0.5%).
- Intrathecal mepivicaine also has a favorable pharmacokinetic profile in ambulatory surgery, but carries a reasonable incidence of TNS
- Preservative-free 2-chloroprocaine has recently gained popularity for its excellent short-duration of spinal anesthesia with little risk for TNS. It should be noted, however, that in the 1980s, high-dose 2-chloroprocaine was associated with permanent neurological deficits that were believed to be due to the preservatives in the solution.
Position. The lithotomy position has been associated with a higher incidence of TNS. Possible causes include the stretching of the cauda equina reduced perfusion pressure of the vasa nervorum. This combination may increase vulnerability of nerve fibers.
Outcome. TNS is characterized by its self-limited course. Greater than 90% of cases resolve completely within 1 week. This differs from other neurotoxic effects of local anesthetics such as cauda equina syndrome.
- Cauda equina syndrome. Associated with permanent neurologic injury that is characterized by bowel bladder dysfunction, pain paresis of the lower extremities, patchy sensory deficits. It has been associated with continuous spinal microcatheters, lidocaine 5% spinals, 2-chloroprocaine (during the 1980s due to sodium metabisulfate formulations).

Prevantative Measures

The avoidance of lidocaine in spinal anesthesia the use of the lowest local anesthetic concentration that is available. If short duration is desired, consider preservative-free 2-chloroprocaine.
Avoidance of vasoconstrictors in spinal anesthetic solution
Precautions to avoid stretch injury during lithotomy positioning or prolonged surgeries.

Symptoms, signs, physical exam
- New onset low back pain after resolution of the sensory motor blockade
- Pain in buttocks radiating to the lower extremities. Thigh pain (especially the back of thighs) is greater than lower limb pain. Usually bilateral, but may be unilateral
- Pain ranges from light to severe
- Dysesthesia
- Hypoesthesia
- Aching
- Hypesthesia
- More commonly pain in thighs (especially back of thighs) rather than lower limbs
Diagnostic procedures studies
- Diagnosis of exclusion
- Laboratory exam. Coagulation studies white blood counts should be normal, which can assist in ruling out epidural hematoma epidural abscess, respectively.
- Consider CT scan or MRI to rule out other neurologic conditions.
- No consistent abnormalities of nerve conduction velocity, EMG or SSEP in acute delayed follow-up of TNS patients.

Differential Diagnosis

Spinal hematoma
Epidural abscess
Permanent neurologic damage
Preexisting lower back pain

NSAIDs
Opioids
Trigger point injections
Pain usually resolves after 2–5 days

Symptoms often disappear spontaneously by Day 5.
EMG, nerve conduction studies, or diagnostic imaging studies are usually not necessary.
Consider neurology consultation if neurologic deficits persist beyond 10 days.

Closed Claims Data

No data, due to transient symptoms

Freedman JM , Li DK , Drasner K , et al. Transient neurologic symptoms after spinal anesthesia. Anesthesiology. 1998;89:633–641.
Liu SS. Current issues in spinal anesthesia. Can J Anesth. 2002;49(6):R1–R5.
Pollock J , Burkhead D , Neal JM , et al. Spinal nerve function in five volunteers experiencing transient neurologic symptoms after lidocaine subarachnoid anesthesia. Anesth Analg. 2000;90:658–665.
Pollock JE , Neal JM , Stephenson CA , et al. Prospective study of the incidence of transient radicular irritation in patients undergoing spinal anesthesia. Anesthesiology. 1996;84:1361–1367.
Zaric D , Christiansen C , Pace NL , et al. Transient neurologic symptoms after spinal anesthesia with lidocaine versus other local anesthetics: A systematic review of romized, controlled trials. Anesth Analg. 2005;100:1811–1816.

See Also (Topic, Algorithm, Electronic Media Element)

Epidural Abscess
Epidural Hematoma

ICD9

724.2 Lumbago
781.99 Other symptoms involving nervous musculoskeletal systems
782.0 Disturbance of skin sensation

ICD10

M54.5 Low back pain
R20.9 Unspecified disturbances of skin sensation
R29.818 Other symptoms signs involving the nervous system

Transient neurologic symptoms are characterized by transient low back pain with radiation to the buttocks thighs. The pathophysiology remains unknown.
Diagnosis of exclusion with normal neurologic exam, radiologic imaging, EMG testing. However, other potentially catastrophic entities such as epidural hematoma epidural abscess should be ruled out.
Risk reduction includes avoiding of lidocaine, high doses of spinal anesthetic medications, vasoconstrictor additives.

Sharon L. Lin , MD

Jane C. Ahn , MD

section name header

Basics ⬇

Incidence

Morbidity/Mortality

Diagnosis ⬆ ⬇

Treatment ⬆ ⬇

Follow-Up ⬆ ⬇

References ⬆ ⬇

Additional Reading ⬆ ⬇

Codes ⬆ ⬇

Clinical Pearls ⬆ ⬇

Author(s) ⬆