Transient neurological syndrome: does it really exist?

PURPOSE OF REVIEW Subarachnoid injection of local anesthetics has been related to the appearance of transient neurological symptoms (called transient neurologic syndrome), as reflected by a number of clinical reports showing their incidence in clinical practice. However, the etiology of this syndrome is virtually unknown, as is the number of factors implicated in its development. This review will attempt to clarify this entity and its relationship with spinal anesthesia. RECENT FINDINGS Intrathecal administration of local anesthetics is known to increase glutamate concentration in cerebrospinal fluid and histopathologic changes of motor neurons in the lumbar spinal cord, suggesting damage of dorsal and ventral roots. In-vitro studies of cultured neurons exposed to different concentrations of local anesthetics have shown changes in growth of cones and neurites, which may be related to transient neurologic syndrome. SUMMARY The latest studies show biochemical and anatomopathologic changes that support the structural basis of the existence of transient neurologic syndrome. In the authors' view, transient neurologic syndrome could represent the lower end of a spectrum of local anesthetic toxicity. Recent findings demonstrate that nerve membrane damage induced by highly concentrated local anesthetics such as lidocaine, tetracaine, dibucaine and procaine may generate irreversible neural injury. Still further studies are needed to establish the relationship between morphological changes induced in vitro and the occurrence of clinical symptoms.