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Transient Neurologic Syndrome

A Benign but Confusing Clinical Problem

Harned, Michael E. MD; Dority, Jeremy MD; Hatton, Kevin W. MD

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Advanced Emergency Nursing Journal: July/September 2011 - Volume 33 - Issue 3 - p 232-236
doi: 10.1097/TME.0b013e3182251524
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AN INCREASING NUMBER of the surgical procedures performed today occur in an outpatient setting where the patients are routinely discharged home following recovery in the postanesthesia care unit (Wu, Berenholtz, Pronovost, & Fleisher, 2002). Because these patients are not generally hospitalized following surgery, the emergency department (ED) is the common triage area for postoperative complications that may arise. Emergency department personnel should, therefore, be knowledgeable and experienced with some of the most common postoperative complications, including those issues traditionally managed by surgeons and anesthesiologists.

Transient neurologic syndrome (TNS) is self-limited postoperative pain syndrome occurring in patients after receiving spinal anesthesia for surgery. Although it has a benign clinical course for the patient, its diagnosis and treatment may be confusing to care providers, as it frequently mimics more serious and devastating neurologic complications. For this reason, it is important that ED personnel be familiar with the diagnosis and care of patients with TNS. In this review, we describe the pathophysiology, clinical features, differential diagnosis, and treatment of this benign but clinically confusing postoperative complication.


Spinal anesthesia is a form of “neuraxial anesthesia” where an anesthetic drug (or drug combination) is injected into the subarachnoid space to eliminate intraoperative pain during the surgical procedure and to allow the patient to remain conscious throughout the perioperative period. Drs. August Bier and Hildebrandt first utilized spinal anesthesia in 1898 using cocaine as the anesthetic agent. Currently, spinal anesthesia is used mainly for surgery of the lower extremities, perineum, and some intra-abdominal procedures (Larson, 2010). Despite the popularity of this anesthetic technique with both anesthesiologists and surgeons and its long-standing safety record, case reports describing TNS have caused concern related to the use of spinal anesthesia in patients undergoing certain surgical procedures (Schneider et al., 1993).

To provide spinal anesthesia, a “spinal block” is performed. After the patient is placed into an appropriate position, the skin is cleaned with a sterile solution and a sterile drape is applied to the patient's back. A 20-gauge introducer needle is used to pierce the skin and subcutaneous tissues at the level of the targeted space. A 25-gauge needle is then inserted through the piercing needle and directed through the epidural space and dura mater. The needle tip is ultimately placed into the subarachnoid space, and its correct position is confirmed when cerebral spinal fluid flows freely from the needle hub (Tsai & Greengrass, 2006). Anesthesiologists generally perform this spinal block below the first lumbar vertebra because there is little concern for nerve or spinal cord injury at this level. Injection of local anesthetics or opiates into the subarachnoid space will act directly upon the nerve roots and spinal cord to produce intense anesthesia (both motor and sensory blockade). Although many drugs can be used for spinal anesthesia, lidocaine has long been the drug of choice for most outpatient surgical procedures because of its predictably rapid onset, profound sensory and motor blockade, and short duration of action (Salinas & Liu, 2002).


Although the exact pathophysiologic mechanism of TNS has not yet been fully described, the current hypotheses include stretch-induced ischemia of the spinal cord and cauda equina, direct nerve toxicity from the local anesthetic, and needle trauma to the spinal cord or spinal nerves (Freedman et al., 1998; Horlocker, McGregor, Matsushige, Schroeder, & Besse, 1997; Pollock, Neal, Stephenson, & Wiley, 1996). It is important to note that the rarity of TNS in humans and the lack of an appropriate animal model have limited research into the pathophysiologic causes of this postoperative complication.

The position of the patient during the surgical procedure may be one of the most important factors in the development of TNS. Prospective, observational research studies indicate that both the lithotomy and prone jack-knife positions (compared to the supine position) are associated with an increased incidence of TNS (Hampl et al., 1996; Pollock et al., 1996). In these positions, the hips are flexed relative to the lumbar spine, which lengthens the distance that the lumbar nerves must travel and increases the stretch along the lumbar, sacral, and coccygeal nerves (Pollock, Liu, Neal, & Stephenson, 1999). This nerve stretch may result in periods of ischemia, which would normally be painful to the patient but may go unnoticed because of the spinal anesthetic. This could help to explain the transient nature of the pain associated with TNS. Early postoperative ambulation and morbid obesity may also play a role in stretch-induced nerve ischemia and have been positively associated with the development of TNS (Horlocker et al., 1997). Moreover, researchers have hypothesized that these periods of ischemia may also increase the susceptibility of normally resistant nerves to the direct toxic effects of local anesthetics (Alley & Pollock, 2002; Pollock et al., 1999).

Local anesthetics in elevated concentrations have a direct neurotoxic effect to spinal nerves within the subarachnoid space (Freedman et al., 1998). Because a small needle is used to reduce the risk of postdural puncture headache, local anesthetics injected through the needle spread very little within the subarachnoid space. This can lead to elevated concentrations of local anesthetics, particularly with the placement of microcatheters for continuous local anesthetic delivery. This resultant pooling and maldistribution of local anesthetic may further increase the risk of nerve toxicity (Beardsley et al., 1995).


Transient neurologic syndrome describes a condition characterized by a specific pain distribution typically arising 6–24 hr after the surgical procedure in the absence of focal neurologic findings (Pollock et al., 1996). Observational data suggests that approximately 15% of all patients receiving spinal anesthesia will experience TNS and that back and buttock pain is the predominant complaint (Pollock et al., 1996). Of note, most patients will have attempted to manage their pain symptoms according to the surgeon's instructions prior to seeking advanced medical attention and will usually present with considerable anxiety related to this unexpected complication.

Patients with TNS characteristically experience only mild to moderate pain in their back or buttocks with pain radiating into the proximal portions of both legs. The onset of this pain typically occurs within the first 24 hr after surgery, and although the pain is generally mild, some patients will develop severe, unrelenting pain in this same distribution (Hampl et al., 1996; Pollock et al., 1996; Schneider et al., 1993). Of further interest to researchers, there have been no reports of pain symptoms before the resolution of spinal anesthesia, indicating that there may be a “masking effect” of pain induced by the spinal anesthesia.

In addition to the characteristic history and chief complaint, the lack of significant physical examination findings is also important in the diagnosis of TNS. On examination, patients with TNS will have normal sensory and motor examination findings and the deep tendon reflexes will be intact (assuming they were normal before spinal anesthesia was administered). These findings are important because they suggest that there is no neurologic injury at the level of the spinal cord or nerve roots themselves. Similarly, radiologic testing including x-ray images, computed tomography, and magnetic resonance imaging of the lumber and sacral spinal elements and nerve plexuses will be normal (Boukobza et al., 1994).


Transient neurologic syndrome is largely a diagnosis of exclusion. The differential diagnosis of pain radiating from the back into the lower extremities includes not only TNS but also very serious conditions such as spinal hematoma, spinal infection or abscess formation, and direct spinal cord or spinal nerve damage. The immediate diagnostic goal is to rapidly rule out these medical and surgical emergencies to prevent long-term complications. Research clearly shows that neurologic outcome with these conditions is directly related to the time to surgical decompression (Boukobza et al., 1994).

Spinal hematoma is one of the most dreaded complications arising from spinal block and results from injury to the epidural blood vessels during spinal needle placement. As the blood from these injured vessels accumulates in the spinal canal, an enclosed space, it becomes a space-occupying lesion that presses on the spinal cord and nerves resulting in focal neurologic compromise. This generally causes neurologic findings including the loss of bowel and bladder function, changes in sensation and motor function of the lower extremities, and loss of lower extremity deep tendon reflexes (Boukobza et al., 1994; Horlocker et al., 2010).

Spinal cord infection and abscess are also serious medical conditions that must be aggressively and rapidly investigated. They cause infectious insults to the surrounding nerves and tissues and direct neurologic injury may occur from the effect of an abscess acting as a space-occupying lesion. Fortunately, few patients develop serious infectious complications within the first 24 hr following spinal block and most patients will have concomitant constitutional symptoms including fever and chills, which are easily identified. Focal neurologic findings, including loss of bowel and bladder control, lower extremity weakness, and focal numbness will also usually be present (Wang, Hauerberg, & Schmidt, 1999).

Finally, direct spinal cord or nerve damage is another catastrophic but extremely rare complication from spinal block performed in the lumber spine (Phillips, Ebner, Nelson, & Black, 1969). Because the spinal cord terminates above the level of the lumbar spine, direct injury to the spinal cord is very rare. In with the presence of an acute injury to a spinal nerve, patients typically present with specific neurologic findings including weakness, paresthesias (altered skin sensations) and hypesthesia (atypically decreased sensation) (Phillips et al., 1969). Although patients with spinal cord or nerve injury may have complaints of pain similar to TNS, the focal neurologic findings elicited from the physical examination would be quite different.


Although patients present with very worrisome pain in a pattern consistent with neurologic injury, the symptoms generally resolve within 1–2 days and there are no reports of long-term neurologic complications occurring as a result of TNS. Medications are generally given for symptomatic pain control, and patients are discharged from the ED once their pain is well-controlled.

As has been stated previously, the first and main goal when confronted with the patient who may have TNS is to expeditiously evaluate and exclude the other catastrophic conditions that may have a similar presentation. After these have been excluded, treatment consists of symptomatic pain control and verbal reassurance. On occasion, a neurosurgical consult may be necessary to assist with the diagnosis and to help assuage the patients' fears about their diagnosis.

Although TNS is a transient process, symptomatic pain control is generally necessary. Nonsteroidal anti-inflammatory medications (NSAIDs) appear to be the most beneficial first-line agents (Pollock, 2000). The use of intravenous and oral opiate pain medications such as morphine and hydrocodone are generally reserved for patients who fail or are intolerant of NSAID therapy (Pollock, 2000). Occasionally, TNS pain may be complicated by concomitant muscle spasms and the addition of antispasmodics medications such as tizanidine or cyclobenzaprine to the NSAID or opiate therapy may be helpful. The use of trigger point injections has also been reported as a potential therapy to terminate the muscle spasms (Schneider & Birnbach, 2001).

Following diagnosis, most patients can be discharged home once the patient's pain has been adequately controlled with follow-up only if the pain worsens or does not resolve over the ensuing 48–72 hr.


Although first described more than a 100 years ago, spinal anesthesia remains an excellent choice for lower extremity, perineal, and some intra-abdominal procedures, particularly in the outpatient surgery, because of the short duration of anesthesia and the ability to avoid general anesthesia and its associated complications. Despite this benefit, lidocaine-based spinal anesthesia has been associated with TNS, a benign but painful clinical condition, which closely mimics important medical and surgical emergencies. Once the diagnosis of TNS can be confirmed, reassurance and symptomatic pain treatment are all that are necessary to keep the patient safe and comfortable.


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lidocaine; spinal anesthesia; transient neurologic syndrome

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