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Discuss Zofran and tremors
- Thread starter Aznfarmerboi
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Huh. That's like the opposite of what I'd expect, if anything.
5ht3 is inhibitory on gaba...so a 5ht3 antagonist...decrease inhibition on gaba=happy sedative times...
5ht3 is inhibitory on gaba...so a 5ht3 antagonist...decrease inhibition on gaba=happy sedative times...
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well, I looked up diphenhydramine in DIH, it did mention adverse effect of: tremor. Must be a pretty rare one.
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But then Zofran supposly does cause EPS symptoms. How?! I think that is the better question.
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Is it 100% selective in its antagonism?
If both the diphenydramine and ondansetron were given, who's to say that it was the ondansetron at all? In fact, if they didn't re-initiate the ondansetron and reproduce the tremor, they can't say that it was EITHER drug that was causing it. It could be something else entirely. BUT... there have been a few documented cases.
From micromedex:
3.3.9.A.2 Extrapyramidal sign
a) Unlike metoclopramide, ondansetron has only very rarely been associated with acute DYSTONIC REACTIONS, AKATHISIA, or other extrapyramidal reactions. Three reports that are consistent with, but not diagnostic for extrapyramidal reactions have been reported (Prod Info Zofran(R), 2001a). Case reports have described extrapyramidal reactions in a few patients receiving ondansetron (Garcia-del-Muro & Ferrer, 1993, Halperin & Murphy, 1992)(Dobrow et al, 1991). The relative lack of extrapyramidal effects with ondansetron confirms the absence of dopamine antagonist activity (Marty et al, 1990c; Marty, 1989c).
b) ACUTE CHOREA lasting 5 days occurred in a 34-year-old woman who received intravenous (IV) ONDANSETRON 4 mg for nausea after a cesarean section. The patient had no relevant medical history; she was not taking any medications and did not use drugs. After the ondansetron injection, she felt a sensation in her feet, which moved up her body. In the recovery room, she started to experience involuntary movements, somewhat similar to intention tremor and shivering. Involuntary movements continued and occurred in her trunk and lower limbs as the motor block wore off. Fifteen episodes lasting 20 to 150 seconds per episode were documented by hospital staff over a 6-hour period. The episodes were characterized by paroxysmal involuntary choreiform movements involving the neck and all 4 limbs (primarily proximal muscles). She was given a loading dose of IV benztropine 2 mg, followed by 1-mg doses orally 3 times a day. As of day 5, the episodes ceased, and the patient experienced full resolution (Duncan et al, 2001).
c) Another case report describes a 71-year-old male who experienced an extrapyramidal reaction (ie, twitching and tremors of the neck, shoulders, and head) following a second 30-milligram dose of ondansetron. After discontinuation of the drug, the symptoms quickly disappeared (Mathews & Tancil, 1996).
From micromedex:
3.3.9.A.2 Extrapyramidal sign
a) Unlike metoclopramide, ondansetron has only very rarely been associated with acute DYSTONIC REACTIONS, AKATHISIA, or other extrapyramidal reactions. Three reports that are consistent with, but not diagnostic for extrapyramidal reactions have been reported (Prod Info Zofran(R), 2001a). Case reports have described extrapyramidal reactions in a few patients receiving ondansetron (Garcia-del-Muro & Ferrer, 1993, Halperin & Murphy, 1992)(Dobrow et al, 1991). The relative lack of extrapyramidal effects with ondansetron confirms the absence of dopamine antagonist activity (Marty et al, 1990c; Marty, 1989c).
b) ACUTE CHOREA lasting 5 days occurred in a 34-year-old woman who received intravenous (IV) ONDANSETRON 4 mg for nausea after a cesarean section. The patient had no relevant medical history; she was not taking any medications and did not use drugs. After the ondansetron injection, she felt a sensation in her feet, which moved up her body. In the recovery room, she started to experience involuntary movements, somewhat similar to intention tremor and shivering. Involuntary movements continued and occurred in her trunk and lower limbs as the motor block wore off. Fifteen episodes lasting 20 to 150 seconds per episode were documented by hospital staff over a 6-hour period. The episodes were characterized by paroxysmal involuntary choreiform movements involving the neck and all 4 limbs (primarily proximal muscles). She was given a loading dose of IV benztropine 2 mg, followed by 1-mg doses orally 3 times a day. As of day 5, the episodes ceased, and the patient experienced full resolution (Duncan et al, 2001).
c) Another case report describes a 71-year-old male who experienced an extrapyramidal reaction (ie, twitching and tremors of the neck, shoulders, and head) following a second 30-milligram dose of ondansetron. After discontinuation of the drug, the symptoms quickly disappeared (Mathews & Tancil, 1996).
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Ugh. Blinding block of text from cut and paste.
It's not surprising that diphenhydramine didn't do jack if the causation of EPS was serotonergic in nature.
Check this badboy out:
M.I. Wilde and A. Markham, Ondansetron. A review of its pharmacology and preliminary clinical findings in novel applications, Drugs 52 (1996), pp. 773794.
Basically suggests a regulatory role of serotonergic innervation on the central dopaminergic receptor motor inhibitory actions in the basal ganglia and related nuclei in the limbic system.
Potentially can inhibit/reduce elevated mesolimbic DA activity and antagonize increased locomotor activity caused by excess DA.
Check some of the case studies that use ondansetron for levodopa-associated psychosis in patients with Parkinsons dz. Pretty wicked. And risky. And expensive. But pertinent.
It's not surprising that diphenhydramine didn't do jack if the causation of EPS was serotonergic in nature.
Check this badboy out:
M.I. Wilde and A. Markham, Ondansetron. A review of its pharmacology and preliminary clinical findings in novel applications, Drugs 52 (1996), pp. 773794.
Basically suggests a regulatory role of serotonergic innervation on the central dopaminergic receptor motor inhibitory actions in the basal ganglia and related nuclei in the limbic system.
Potentially can inhibit/reduce elevated mesolimbic DA activity and antagonize increased locomotor activity caused by excess DA.
Check some of the case studies that use ondansetron for levodopa-associated psychosis in patients with Parkinsons dz. Pretty wicked. And risky. And expensive. But pertinent.
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