As time went on I needed more and more At this point I was switched to. MomOf taken for 2 to 5 years December 18, I would constantly get short of breath and feel like I was having a heart attack because my heart would pound so hard in my chest. It happened so often I knew what it was and even try to stop it and calm myself down before it got too bad, which rarely worked.
Long story short and after years of dealing with this issue I switched my PCP and was given Clonazepam to try. It actually worked right away after getting my dose fixed to 1 mg as needed and I've hardly had an issue since. Stephen 79 taken for 2 to 5 years December 4, If you have anxiety find another way to deal with it. It's not worth it trust me. I had to stop taking it when I started suboxone, and my panic attacks came back.
Being off it is the worst feeling I can imagine. It made me realize how much it helps with anxiety and panic. Jdschmid taken for 5 to 10 years November 25, It has done wonders for my anxiety, panic, and constant worrying. It actually makes me concentrate better at the task at hand. I was able to study and get my GED after dropping out of high school many years ago. I got my confidence back and regained my positive thoughts. I also take Sertraline mg.
But Clonazepam is my go to for panicky situations. I've been taking it on and off for years It actually is better then Xanax because it lasts longer throughout the day and is not as sedating for me. I'd say its the safer of the Benzos. I was on Zoloft 50mg at the time for Panic Disorder and it worked beautifully for over ten years, but just stopped. I went from a high functioning manager to a terrified mess afraid to leave the house. Got myself to a psychiatrist, she prescribed 1mg daily taken in two doses and it was a godsend.
Got on another antidepressant, citalopram, which did the trick. I was able to slowly taper off the klonopin with no side effects. Recently I've been having some rebound anxiety I'm in medical school: Sunshine November 19, SSRI's don't work well for me. It also calms me down so I can think better. If I take more than a normal dose of Klonopin, it could make me sleepy, but other than that, no side affects. And I have the option to not take it if I don't need it.
I hope l-methyl folate will be even better once I figure out how to use it without a bad reaction. Don't take Klonopin if you get addicted to drugs". TBAgs November 18, The time it takes to kick in is excruciating - one and a half hours. It only makes anxiety more upfront. If you have panic you need Xanax! My Dr said no to my Xanax only having been prescribed 15 in 3 years and only taking for extreme events. Now my life has turned upside down thanks to this worthless medicine.
If you truly have panic and can wait 2 hrs for relief I admire you. Ramey bh November 5, I have been on it before 20 years ago. I avoided since it because it's a benzo, but if I don't get treated successfully, I believe, as does my therapist, my prognosis is poor. I encourage all to try all other pathways; only if they fail should you consider klonopin.
Unrelenting anxiety and panic attacks are not acceptable in my circumstances. The depression and grief led to anxiety and eventually panic. Completely unable to function. Minutes seemed like hours. A struggle to get through each day. Only to like awake all night. At one point got a total of 4 hours of sleep over 5 days. A total wreck about to be institutionalized. Reached crisis mode and was given Klonopin - 1.
A true life saver. Not worried about tapering later. Klonager taken for less than 1 month October 28, Panic taken for 6 months to 1 year October 27, But one night I went to the mental health emergency room because I couldn't deal with this illness anymore and this physician prescribe me Clonazepam since and the panic attacks stopped finally , it's and still using them! Greatful to God taken for 10 years or more October 8, It reminds me as well to just say calm: In my 30's during the 90's I was given every a-typical anti-psycotic by psychiatrists.
The reactions to these medications were severe. I went to the ER numerous times with TD, lock jaw and mostly Severe Akethesia- restless pacing, inability to sit down, panic attacks. I could not eat, or sleep, a sense of impending doom, and lost weight. As noted by Curtis and colleagues, these include the possibility that effect sizes could be artificially inflated, as those participants who drop out may do so due to lack of treatment response [ Curtis et al.
Drawbacks in the use of cannabinoids in treating tics include side effects such as short-term memory impairment, poor hand—eye coordination, and impairments in attention, time and space perception. Withdrawal can be associated with restlessness, anxiety, depression, tremor and insomnia. There is also some evidence that THC use can precipitate or exacerbate psychotic symptoms. Muller-Vahl and colleagues reported no deterioration in verbal or visual memory, reaction time, intelligence, sustained attention, divided attention, vigilance or mood, with the use of THC [ Muller-Vahl et al.
However, there was some evidence for increased OCSs and a trend towards increased phobic anxiety. A number of nonpharmacological treatments can be used to treat patients with TS of moderate severity. One behavioural technique which may help with tics is exposure plus response prevention therapy. Tics are suppressed for prolonged periods of time, in order for patients to learn to habituate to associated premonitory urges.
Verdellen and colleagues showed that this method could reduce tics according to observation and YGTSS ratings and that this treatment was equally effective to the more widely applied technique of habit reversal training [ Verdellen et al. Although focusing attention on tics may increase inhibitory effort leading to exacerbation [ Robertson and Stern, ], Verdellen and colleagues reported no evidence for a rebound effect after exposure plus response prevention therapy sessions [ Verdellen et al.
The effectiveness of habit reversal training has been evaluated more thoroughly [for a review, see Himle et al. Habit reversal training may also help with vocal tics, as shown by Woods and colleagues [ Woods et al. Studies by Azrin and colleagues have also provided favourable evidence. Beneficial effects were apparent in both children and adults, in both motor and vocal tics and in tic severity and frequency. A study of 22 adults [ Azrin et al. One clear limitation associated with this behavioural technique is that tics in one part of the body may be replaced by tics in another part [ Robertson and Stern, ].
Long-term evaluation of treatment outcome is therefore necessary. Botulinum toxin botox inhibits localized release of acetylcholine leading to reduced muscle activity. When used to treat tics, it is administered directly into the muscle group involved in the motor tic, or into the laryngeal muscles for vocal tics. Although some studies report a lack of efficacy [ Chappell et al. These include cases involving patients with self-injurious symptoms [ Aguirregomozacorta et al.
In relation to vocal tics, botox has been shown to help coprolalia and accompanying premonitory sensations [ Scott et al. The efficacy of botox for phonic tics was also illustrated by a prospective, nonrandomized study carried out by Porta and colleagues which investigated the effectiveness of vocal cord injections of botox for phonic tics [ Porta et al. Seventy patients 29 aged 10—16, 41 aged 19—55 were assessed 15 days after treatment and then a further four times over the next year following the injection of botox into the vocal cords.
Candidates for surgical treatment include patients exhibiting life-threatening self-injurious symptoms or severe tics that lead to significant functional impairment. Patients who fail to respond to many other forms of intervention may also be considered. The most common invasive technique for tics is DBS of the thalamus or globus pallidus.
Activation of the implanted electrode leads to a localized paradoxical decrease in neural activity in the site of implantation. Although this form of treatment is still in its infancy, studies have provided encouraging evidence for the effectiveness of this technique in ameliorating tics. Many studies have investigated the effectiveness of DBS of the medial thalamus for tics. Another study of five patients [ Maciunas et al.
In a larger sample of 18 patients, Servello and colleagues reported evidence of good tic reduction at 3—17 months post treatment, although on a few occasions, surgery led to complications [ Servello et al. DBS of the globus pallidus has also been shown to improve tics. Houeto and colleagues compared DBS of the globus pallidus interna GPi and centromedial parafascicular nucleus of the thalamus [ Houeto et al.
The centromedian parafascicular nucleus of the thalamus and ventromedial GPi were targeted in three patients who participated in a controlled, double-blind, randomized, crossover study [ Welter et al. No advantage was apparent when both regions were targeted together. DBS also reduced self-injurious behaviour and impulsiveness. Not all studies report complete success.
After treatment, at 3- and 6-month follow up there was almost complete resolution of motor and vocal tics at rest, but recurrence of vocal tics on speaking. An important finding was that the patient felt that surgery had not improved his QoL overall, although he did prefer the stimulator to be switched on. The side effects that have been reported after DBS of the thalamus include drowsiness and changes in sexual behaviour [ Visser-Vanderwalle et al. Electroconvulsive therapy ECT is most often applied to treat depressive disorders, but a few case reports have documented potential effectiveness in treating TS.
Four single case reports to date [ Karadenizli et al. Two patients had comorbid depression, one had comorbid OCD and one experienced self-injurious tics. ECT could have a less-specific therapeutic effect in TS by altering stress levels, or could indirectly reduce dopamine levels by increasing serotonin [ Bloch, ]. However, it remains to be shown if this approach could be effective in ameliorating tics in pure TS. In addition, no data is available to support the usefulness of this approach with adolescents and it is unlikely to be appropriate for use with children.
The limitations of this approach also include side effects such as short-term memory problems and benefits may not be durable. Until better-controlled studies have been conducted this approach may be best reserved for cases involving severe depression. A few preliminary studies investigating the therapeutic effectiveness of repetitive transcranial magnetic stimulation rTMS have reported a favourable outcome [e.
Treatment also resulted in reduced scores on scales assessing depression and OCSs and therapeutic effects were still present after 3 months. Another randomized, blinded, crossover study assessed the efficacy of rTMS 1 and 15 Hz over prefrontal cortex or motor cortex in eight patients with TS. There were minimal side effects and no worsening of tics. Tic symptoms improved significantly overall during the week of the study. However, a single-blind, placebo-controlled, crossover repetitive trial [ Munchau et al.
Further controlled studies are needed to determine the effectiveness of rTMS, especially for more severe tics. The advantages of this technique include fewer and milder side effects e. Drawbacks include the likelihood of purely ephemeral benefit and the fact this approach requires multiple treatment sessions [ Bloch, ]. The evidence we have reviewed relating to pharmacological treatments indicates that dopamine antagonists may lead to the most reliable treatment response, but also pose the greatest drawbacks in terms of side effects.
There is strong evidence supporting the efficacy of neuroleptics in the successful treatment of tics. Some reports suggest that pimozide and fluphenazine can be as efficacious as haloperidol and less toxic. Overall, however, the use of these agents can lead to a greater risk of adverse effects such as extrapyramidal symptoms than atypical antipsychotics.
One more favourable option is risperidone, which has the most supportive evidence for efficacy and is appears safer than neuroleptics. A number of studies provide evidence for efficacy for olanzapine and quetiapine. Clozapine, however, is associated with less supportive evidence and the potentially serious side effect of agranulocytosis. Benzamides can be effective and their use is rarely associated with extrapyramidal side effects.
However, the risk of hyperprolactinaemia may lead to caution, and more data is crucial to enable a more thorough evaluation of the merits of these agents. Clonidine appears to be a safe option, although a few studies dispute its efficacy. An additional benefit of this medication is that it could be useful in more complex cases of TS, as individuals who respond to this drug may also experience improvements in ADHD symptoms, aggression and OCSs. Benzodiazepines can also show good efficacy but should be prescribed with caution due to associated tolerance and potential for addiction.
Associated sedation may also be a troublesome side effect. A variety of other agents have the potential to be viable treatments and compel further investigation in order for their utility to be fully determined. These include tetrabenazine, levetiracetam, topiramate and cannabinoids. Tetrabenazine may be an effective medication and is less likely to lead to weight gain than atypical antipsychotics.
Although there is conflicting evidence of efficacy, this agent may be the least problematic in terms of side effects. There is some good evidence for the efficacy of cannabinoids, but concerns about the possibility of some potentially serious side effects e. In relation to nonpharmacological treatments, there is much evidence in support of the efficacy of both behavioural and surgical techniques.
It is vital that behavioural options are available for younger patients and those who are sensitive to pharmacological interventions. Habit reversal training is a safe choice, but may not be of benefit in the long term in patients whose tics move to new body regions. There is also a clear issue of compliance, as patients are actively involved in home practice between sessions. There is a considerable amount of evidence in favour of botox for vocal and specific motor tics, although it is difficult to conduct controlled studies.
Surgery may be appropriate for severe, treatment refractory patients. The evidence of the efficacy of DBS is encouraging, although the target of surgery is open to debate. While behavioural interventions are perhaps the safest treatment method and should be offered whenever possible, the therapeutic power of a number of pharmacological options establishes these agents as promising first-line treatments for tics. Medication selection will partly depend on the age of the patient, as younger children may be more vulnerable to the toxicity of agents.
Clonidine could therefore be the best agent to prescribe initially, based on the mild and infrequent nature of side effects, which include postural hypotension and minor anticholinergic effects. Another benefit of this drug is the evidence suggesting that it can help with other behavioural symptoms linked to ADHD [ Leckman et al. For adults, stronger medications may also be tolerated.
The efficacy of risperidone is well established and may be needed for tics of moderate severity. If the patient needs to discontinue treatment due to adverse effects, an alternative similar option is aripiprazole. These agents offer a good compromise between efficacy and toxicity. They are less toxic than neuroleptics and perhaps as effective. Some patients may not respond to the above agents, or exhibit severe tics that lead to greater distress and functional impairment.
In such cases, haloperidol or sulpiride may be considered. Careful monitoring of treatment response and gradual titration of dose are particularly critical with the prescription of these agents, due to the possibility of more significant side effects hyperprolactinaemia and extrapyramidal symptoms. The use of these agents may also be well justified in cases involving self-injurious behaviour.
If not well tolerated, a viable alternative is botox injection. Studies have shown this approach can be useful in treating specific tics through localized muscular action, so could be useful in patients with severe cervical tics. Botox may also be useful in cases where vocal tics or coprolalia are the primary problem. For behavioural symptoms involving rage and aggression, studies have indicated that clonidine, sulpiride or risperidone may be beneficial.
It may be possible to combine certain medications for tics with agents that specifically target severe OCD symptoms. Examples of safe combinations include atypical antipsychotics and SSRIs. The presence of particular comorbidities may make certain treatment options for tics less likely to be effective. For example, patients with comorbid ADHD could find it more difficult to remember to take medication or more anxious patients could feel their tics are exacerbated due to increased focus on them during habit reversal training.
In cases where comorbid conditions may cause more distress and impairment than tics, their treatment is of prime importance. However, treating comorbid conditions may also have the potential to lead to some improvement in tics. While medications such as SSRIs may be unlikely to have any direct mechanism of action that improves tics, their effective treatment of a comorbid condition will reduce stress, which characteristically exacerbates tics.
For example, if significant symptoms of OCD are present, amelioration of these may help reduce anxiety levels and improve mood, leading to reductions in tic severity or frequency. Despite encouraging findings, many studies documenting the investigation of treatment efficacy for tics are far from flawless in terms of their design and methodology. These limitations are likely to contribute to the conflicting reports of efficacy and tolerability of treatments.
One critical difficulty is that studies vary in the approach they employ to assess efficacy. For example, effectiveness may be considered in terms of the percentage of patients whose symptoms improve, or by the mean percentage improvement in tic severity or frequency across the treatment group. Some treatments may be considered most effective if they are associated with changes in functional impairment. Enhanced scientific rigour is crucial for the advancement of knowledge in this area.
Placebo control is clearly necessary, as some studies have shown placebo to be associated with as much improvement in tics as an active agent. Double-blind studies are well motivated but are limited by the possibility that significant treatment effects could always lead participants to work out which condition they are undertaking. Artificially inflated effect size may also occur when participants drop out of studies because they do not experience any treatment benefits.
More fundamental problems arise due to the nature of tics. Long-term studies are encouraged by the finding that tics tend to follow a waxing and waning course, which could obscure treatment effects. In relation to tic severity, some interventions may be effective only in mild cases, whereas others may only show an effect in patients with more severe tics who have the potential to exhibit improvement across a wider scale.
Other potentially interacting factors are age-related hormone changes. Future research should employ stringent tests of efficacy, and randomized, double-blind, placebo-controlled trials should be conducted whenever possible. Trials conducted over longer timescales will give further insight into the durability of treatment response. Particularly useful investigations will be those that systematically compare the effectiveness of different treatments in independent samples grouped according to variations in symptom severity, comorbidities or other pertinent behavioural problems.
For example, controlled trials may determine that specific treatments are more effective for particular subgroups of patients with TS who exhibit coprophenomena, paliphenomena, echophenomena, self-injurious behaviours or emotional dysregulation. Future research should systematically examine data collected for a range of measures assessing tics and tic related symptoms, premonitory urge, self-injurious behaviours, emotional dysregulation, NOSIS and the severity of symptoms related to OCD and ADHD, before and after treatment.
This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors. National Center for Biotechnology Information , U. Ther Adv Neurol Disord. Eddy and Hugh E. This article has been cited by other articles in PMC. Abstract Tourette syndrome TS is a chronic neurodevelopmental disorder characterized by tics: Pharmacological treatments for tics Neuroleptics Some of the medications proven to be most effective in treating tics are neuroleptics, such as haloperidol and pimozide.
Studies investigating the efficacy of neuroleptics in treating tics and identified treatment advantages and disadvantages. Atypical antipsychotics Atypical antipsychotics are more selective dopamine receptor D2 blockers, although they can also affect serotonin. Studies investigating the efficacy of atypical antipsychotics in treating tics and identified treatment advantages and disadvantages.
Aripiprazole The newer antipsychotic aripiprazole has a unique mechanism of action, being a partial agonist, rather than an antagonist, of the D2 dopamine receptor. Other pharmacological agents Benzamides Table 4 shows the efficacy and key advantages and disadvantages associated with a range of pharmacological agents which may be used as an alternative to neuroleptics or atypical antipsychotics when treating tics.
Studies investigating the efficacy of alternative pharmacological agents to neuroleptics and atypical antipsychotics in treating tics and identified treatment advantages and disadvantages. Tetrabenazine Tetrabenazine acts as dopamine antagonist, by reducing the presynaptic storage of monoamines and blocking postsynaptic DA receptors.
Noradrenaline modulating agents The alpha-2 adrenergic agonist clonidine inhibits the release of noradrenaline. GABA modulating agents Some reports suggest that tics may be reduced through the administration of benzodiazepines. Dopamine agonists A few studies have investigated the effects of dopamine agonists on tics. Acetylcholinergic agents A few reports suggest that nicotine could help ameliorate tics. Cannabinoids Muller-Vahl and colleagues have conducted a number of studies investigating the therapeutic benefit of cannabinoids in treating tics.
Behavioural techniques A number of nonpharmacological treatments can be used to treat patients with TS of moderate severity. Invasive techniques Botulinum toxin injections Botulinum toxin botox inhibits localized release of acetylcholine leading to reduced muscle activity. Deep brain stimulation Candidates for surgical treatment include patients exhibiting life-threatening self-injurious symptoms or severe tics that lead to significant functional impairment. Other emerging treatments Electroconvulsive therapy Electroconvulsive therapy ECT is most often applied to treat depressive disorders, but a few case reports have documented potential effectiveness in treating TS.
Repetitive transcranial magnetic stimulation A few preliminary studies investigating the therapeutic effectiveness of repetitive transcranial magnetic stimulation rTMS have reported a favourable outcome [e. Discussion Implications in terms of efficacy and safety The evidence we have reviewed relating to pharmacological treatments indicates that dopamine antagonists may lead to the most reliable treatment response, but also pose the greatest drawbacks in terms of side effects.
Recommended first-line treatments While behavioural interventions are perhaps the safest treatment method and should be offered whenever possible, the therapeutic power of a number of pharmacological options establishes these agents as promising first-line treatments for tics. Recommended treatments for specific cases Some patients may not respond to the above agents, or exhibit severe tics that lead to greater distress and functional impairment.
Methodological limitations and directions for future research Despite encouraging findings, many studies documenting the investigation of treatment efficacy for tics are far from flawless in terms of their design and methodology. Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors. Conflict of interest statement None declared. Parkinsonism Relat Disord J Clin Psychiatry J Pediatr Neurol 5: A waiting-list control group comparison.
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