Posted by ed_uk on July 30, 2005, at 4:02:03
In reply to Re: Propranolol (Inderal) for PTSD, posted by med_empowered on July 29, 2005, at 21:13:26
Hi Med :-)
>But...propranolol can cause depression and has all kinds of cardiovascular side effects for some people. It is cheap, though.
I don't like it. It makes me really fatigued and my eyes get dry and sore :-( It doesn't help my anxiety. I don't have PTSD though.
Have a read........
Disruption of reconsolidation but not consolidation of auditory fear conditioning by noradrenergic blockade in the amygdala.
Debiec J, Ledoux JE.
W. M. Keck Foundation, Laboratory of Neurobiology, Center for Neural Science, New York University, 4 Washington Place, Room 809, New York, NY 10003, USA. email@example.com
Consolidation is a process through which labile memories are made persistent [Science 287 (2000) 248]; [Annu Rev Psychol 55 (2004) 51]. When retrieved, a consolidated memory is rendered labile again and undergoes reconsolidation [Learn Mem 7 (2000) 73]; [Trends Neurosci 26 (2003) 65]). Reconsolidation thus offers the opportunity to manipulate memory after it is formed, and may therefore provide a means of treating intrusive memories associated with post-traumatic stress disorder (PTSD). Reconsolidation is most usually studied using protein synthesis inhibitors, which is not practical in humans. However, the beta adrenergic receptor antagonist propranolol impairs consolidation of declarative memory in humans [Science 287 (2000) 248]; [Nature 371 (1994) 702] and consolidation and reconsolidation of inhibitory avoidance learning in rats [Brain Res 368 (1986) 125]; [J Neurosci 19 (1999) 6623]. Here, we show that systemic or intra-amygdala infused propranolol blocks reconsolidation but not consolidation. If the effects on reconsolidation are verified in humans, the results would suggest the possibility that propranolol after memory retrieval might be an effective way of treatment of intrusive memories in PTSD. That the systemic effects of propranolol on reconsolidation are achieved via an action in the amygdala is especially important in light of the fact that PTSD involves alterations in the amygdala [Arch Gen Psychiatry 53 (1996) 380].
CNS Spectr. 2005 Feb;10(2):99-106.
Conceptually driven pharmacologic approaches to acute trauma.
Pitman RK, Delahanty DL.
Massachusetts General Hospital, Charlestown, MA 02129, USA. firstname.lastname@example.org
Secondary prevention of posttraumatic stress disorder (PTSD) entails intervening in the aftermath of a traumatic event to forestall the development of PTSD. There has been little psychopharmacologic research in this area. This is surprising, given that PTSD is the mental disorder with the most clearly identified cause and onset. In a translational model of PTSD's pathogenesis presented herein: A traumatic event (unconditioned stimulus) overstimulates endogenous stress hormones (unconditioned response); these mediate an overconsolidation of the event's memory trace; recall of the event in response to reminders (conditioned stimulus); releases further stress hormones (conditioned response); these cause further overconsolidation; and the overconsolidated memory generates PTSD symptoms. Noradrenergic hyperactivity in the basolateral amygdala is hypothesized to mediate this cycle. Preventing pre-synaptic norepinephrine release with alpha2-adrenergic agonists or opioids, or blocking post-synaptic norepinephrine receptors with beta-adrenergic antagonists such as propranolol, reduces hormonally enhanced memories and fear conditioning. Two controlled studies of trauma victims presenting to emergency rooms suggest that posttrauma propranolol reduces subsequent PTSD, as does one naturalistic clinical study of morphine treatment of burned children. Cortisol both enhances memory consolidation and reduces memory retrieval, leading to mixed predictions. Two controlled studies of intensive care unit patients found that cortisol reduced PTSD. One study did not find benzodiazepines effective in preventing PTSD. Selective serotonin reuptake inhibitors, antiepileptics, and alpha2-adrenergic agonists have yet to be tried.
Biol Psychiatry. 2003 Nov 1;54(9):947-9.
Immediate treatment with propranolol decreases posttraumatic stress disorder two months after trauma.
Vaiva G, Ducrocq F, Jezequel K, Averland B, Lestavel P, Brunet A, Marmar CR.
Clinical School of Psychiatry, University of Lille II, Lille, France.
BACKGROUND: This study investigated the efficacy of propranolol prescribed shortly after trauma exposure in the prevention of posttraumatic stress disorder (PTSD) symptoms and diagnosis. METHODS: Eleven patients received 40 mg of propranolol 3 times daily for 7 days, followed by a taper period of 8-12 days. They were compared with eight patients who refused propranolol but agreed to participate in the study. Though nonrandomized, the two groups did not differ on demographics, exposure characteristics, physical injury severity, or peritraumatic emotional responses. RESULTS: Posttraumatic stress disorder rates were higher in the group who refused propranolol (3/8) compared with those who received the medication (1/11), as were the levels of PTSD symptoms (U = 85, p =.037). CONCLUSIONS: Our results are consistent with earlier findings and suggest that propranolol may be useful for mitigating PTSD symptoms or perhaps even preventing the development of PTSD.
J Trauma Stress. 2002 Oct;15(5):433-7.
Propranolol for reemergent posttraumatic stress disorder following an event of retraumatization: a case study.
Taylor F, Cahill L.
Rainier Associates, Tacoma, Washington 98467, USA. email@example.com
This case report concerns a 44-year-old woman who experienced 5 similar motor vehicle accidents, the last 3 causing severe PTSD episodes of over 6 months each, despite multiple pharmacotherapies. Following a 6th accident, severe PTSD symptoms reemerged. Forty-eight hours after this trauma, propranolol (60 mg) orally, twice a day (1.75 mg/kg/day) was begun, and the PTSD symptoms were rapidly and markedly reduced. The Clinician-Administered PTSD Rating Scale score was reduced from an initial 86 to 56 by 11 days posttrauma. To our knowledge, this is the first report of the effects of propranolol treatment on reemergent PTSD symptoms. Propranolol may be particularly efficacious in the prevention of initial or reemergent PTSD symptoms.
Biol Psychiatry. 2002 Jan 15;51(2):189-92.
Pilot study of secondary prevention of posttraumatic stress disorder with propranolol.
Pitman RK, Sanders KM, Zusman RM, Healy AR, Cheema F, Lasko NB, Cahill L, Orr SP.
Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02129, USA.
BACKGROUND: Preclinical considerations suggest that treatment with a beta-adrenergic blocker following an acute psychologically traumatic event may reduce subsequent posttraumatic stress disorder (PTSD) symptoms. This pilot study addressed this hypothesis. METHODS: Patients were randomized to begin, within 6 hours of the event, a 10-day course of double-blind propranolol (n = 18) versus placebo (n = 23) 40 mg four times daily. RESULTS: The mean (SD) 1-month Clinician-Administered PTSD Scale (CAPS) score of 11 propranolol completers was 27.6 (15.7), with one outlier 5.2 SDs above the others' mean, and of 20 placebo completers, 35.5 (21.5), t = 1.1, df = 29, p =.15. Two propranolol patients' scores fell above, and nine below, the placebo group's median, p =.03 (sign test). Zero of eight propranolol, but six of 14 placebo, patients were physiologic responders during script-driven imagery of the traumatic event when tested 3 months afterward, p =.04 (all p values one-tailed). CONCLUSIONS: These pilot results suggest that acute, posttrauma propranolol may have a preventive effect on subsequent PTSD.
Int J Neuropsychopharmacol. 2001 Dec;4(4):377-83.
Beta-Adrenergic blockade and emotional memory in PTSD.
Reist C, Duffy JG, Fujimoto K, Cahill L.
Department of Psychiatry, VA Healthcare System, Long Beach, CA 90822, USA. firstname.lastname@example.org
Emotional arousal has been shown to enhance memory, an effect that is blocked by propranolol suggesting that the noradrenergic system is important in the mechanism action. Because PTSD has as prominent features heightened arousal and distressing memories, the current study was undertaken to examine whether PTSD subjects differed from controls in emotional enhancement of memory. Seventeen subjects with PTSD and 21 controls received either placebo or 40 mg of propranolol prior to exposure to either an emotionally arousing or emotionally neutral, narrated slide story. Recall, measured 1 wk later, for the arousing story was enhanced and this effect was reduced by propranolol. PTSD and control subjects did not differ in the acquisition and retention of memories under emotionally arousing or emotionally neutral conditions, nor were differential effects of propranolol observed between the two groups.
J Neurosci. 1999 Aug 1;19(15):6623-8.
Attenuation of emotional and nonemotional memories after their reactivation: role of beta adrenergic receptors.
Przybyslawski J, Roullet P, Sara SJ.
Neuromodulation et Processus Cognitifs, Institut des Neurosciences, Centre National de la Recherche Scientifique, Unite Mixte de Recherche 7624, Universite Paris VI, 75005 Paris, France.
A memory trace in its active state is susceptible to interference by amnesic agents, such as hypothermia and electroconvulsive shock, and by NMDA receptor antagonists, suggesting that a time-dependent consolidation process occurs each time a memory is reactivated. The role of beta noradrenergic receptors in reconsolidation in rats was examined in both a positively reinforced radial maze task and a footshock-reinforced conditioned emotional response task. For the former, rats were trained over several days in a spatial reference memory task and received a single reactivation trial followed by propranolol. A temporally graded impairment was observed when propranolol treatment occurred after the memory reactivation trial. In the emotional task, memory impairing effects of propranolol were greater when the drug was administered after a reactivation trial than when administered immediately after the initial training. These results suggest that reactivation of memory triggers a beta receptor-dependent cascade of intracellular events, recapitulating that which occurs during initial postacquisition consolidation, thus permitting reorganization of the existing memory as a function of new information in the retrieval environment. This remarkable lability of an active memory trace provides a new basis for pharmacotherapeutic intervention in such syndromes as Posttraumatic Stress Disorder. beta adrenoreceptor antagonists may be promising pharmacological agents for attenuating debilitating memories at the time of their controlled reactivation.
Am J Dis Child. 1988 Nov;142(11):1244-7.
Propranolol treatment for childhood posttraumatic stress disorder, acute type. A pilot study.
Famularo R, Kinscherff R, Fenton T.
Department of Psychiatry, Harvard Medical School, Boston.
We report 11 cases of posttraumatic stress disorder. Each child had been physically abused or sexually abused or both and presented in an agitated, hyperaroused state. Using a B-A-B (off-on-off) medication design in a clinical setting, the children were treated with the beta-adrenergic antagonist propranolol. Scores on an inventory of symptoms of posttraumatic stress disorder indicated that patients exhibited significantly fewer symptoms while receiving medication than either before or after they received medication.