[Anesthesia in Werner syndrome].
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Biomedical subjects
Publications and source records attributed to R Peláez.
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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.
The preparation of new analogues of lignans carrying an imidazole ring has been achieved. Starting from L-histidinol, cis and trans stereoisomers have been obtained. The synthesized products lack the cytotoxicity displayed by related podophyllotoxins and azatoxin.
A 47-year-old woman underwent hysteroscopy and removal of an endometrial polyp because of irregular, acyclic bleeding of 6 months' duration. The procedure was carried out under spinal anesthesia. No adverse events occurred during puncture or surgery, or in the immediate postoperative recovery period. Recovery from the sensory and motor block was normal. Twenty-four hours after surgery gluteal and lower limb pain and paresthesia developed, with no sensory or motor deficit. The symptoms suggested transient neurological syndrome. This syndrome has been defined by pain in the lower limbs, buttocks, thighs and calves after uncomplicated spinal anesthesia and full recovery from the sensorimotor block during the immediate postoperative period (first 24 hours). The condition is self-limiting and does not leave permanent neurological sequelae. Recent studies have demonstrated biochemical and anatomical changes that provide a structural basis for this clinical entity. According to this literature, transient neurological syndrome might be a mild expression of local anesthetic toxicity. Recent findings show that the initial injury to the nerve cell membrane, induced by high concentrations of local anesthetic could lead to permanent neuronal damage.