Background:Various adjuvants are being used with local anesthetics for prolongation of intraoperative and postoperative analgesia. Dexmedetomidine, the highly selective 2 adrenergic agonist is a new neuraxial adjuvant gaining popularity.Settings and Design:The study was conducted in prospective, double blind manner. It included 120 American Society of Anesthesiology (ASA) class I and II patients undergoing lower limb surgery under spinal anesthesia after approval from hospital ethics committee with written and informed consent of patients.Materials and Methods:The patients were randomly allocated into four groups (30 patients each). Group BS received 12.5 mg hyperbaric bupivacaine with normal saline, group BF received 12.5 mg bupivacaine with 25 g fentanyl, group BC received 12.5 mg of bupivacaine supplemented 30 g clonidine, and group BD received 12.5 mg bupivacaine plus 5 g dexmedetomidine. The onset time to reach peak sensory and motor level, the regression time of sensory and motor block, hemodynamic changes, and side effects were recorded.Results:Patients in Group BD had significantly longer sensory and motor block times than patients in Groups BC, BF, and BS with Groups BC and BF having comparable duration of sensory and motor block. The mean time of two segment sensory block regression was 147 ± 21 min in Group BD, 117 ± 22 in Group BC, 119 ± 23 in Group BF, and 102 ± 17 in Group BS (P > 0.0001). The regression time of motor block to reach modified Bromage zero (0) was 275 ± 25, 199 ± 26, 196 ± 27, 161 ± 20 in Group BD, BC, BF, and BS, respectively (P > 0.0001). The onset times to reach T8 dermatome and modified Bromage 3 motor block were not significantly different between the groups. Dexmedetomidine group showed significantly less and delayed requirement of rescue analgesic.Conclusions:Intrathecal dexmedetomidine is associated with prolonged motor and sensory block, hemodynamic stability, and reduced demand of rescue analgesics in 24 h as compared to clonidine, fentanyl, or lone bupivacaine.

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Objective To describe blinking as the only manifestation of seizures from isolated focal and generalized cortical spikes and investigate the relationship between blinks and epileptic discharges. Methods We measured the latency from the onset of spikes to the onset of blinks in two patients using electroencephalogram (EEG) and an electrooculogram (EOG), and calculated the median latency in both cases. We analyzed the latency from spike onset to the onset of additional specific eye movements, seen only in the second case. To determine the frequency of spontaneous blinks (not triggered by spikes), we defined a “control point” at 45 s following a random spike for the first case. We tested for statistically significant associations between latencies of blinks (Case 1) as well as between latencies of blinks and specific eye movements (Case 2). Results A total of 174 generalized spike‐waves followed by a blink were analyzed in the first patient. Approximately 61% of the blinks occurred within 150–450 ms after the onset of the spike. Median latency for blinks following a spike was 294 ms compared to 541 ms for control blinks (p = .02). For the second patient, a total of 160 eye movements following a right occipito‐parietal spike were analyzed. The median spike‐blink latency in the second case was 497 milliseconds. Median latencies of spike onset to contralateral oblique eye movements with blink and left lateral eye movements were 648 and 655 milliseconds, respectively. Conclusions Our study shows that isolated cortical spikes can induce epileptic seizures consisting exclusively of blinks. These findings emphasize the importance of careful EEG and EOG analysis to determine blinking as the only ictal phenomenon. We additionally describe a new technique to prove the temporal relationship between cortical discharges and a specific movement when, in addition to the movements triggered by a spike, the same movement is also spontaneously performed by the patient (in this case, blinking).

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