Panic attacks treatment

CBD has no activity at the CBl or CB2 receptor. It is well known that CBD influences the activity of THC if co-administered [140]. Another effect of CBD is the inhibition of cytochrome oxidase [141], which inversely to its antagonistic activity strongly potentiates THC effects above a certain threshhold. CBD is also active as a mild antipsychotic [142] and was proposed as a treatment for anxiety and panic attacks. The mechanism is not fully understood, but it might be caused by an interference with the endocannabi-... 

The acute phase of panic disorder treatment lasts about 12 weeks and should result in marked reduction in panic attacks, ideally total elimination, and minimal anticipatory anxiety and social anxiety avoidance. Treatment should be continued to prevent relapse for an additional 12 to 18 months before attempting discontinuation. 

The main objectives of treatment are to reduce the severity and frequency of panic attacks, reduce anticipatory anxiety and agoraphobic behavior, and minimize symptoms of depression or other comorbid disorders.48 The long-term goal is to achieve and sustain remission. 

Treatment options include medication, psychotherapy (e.g., CBT preferred), or a combination of both. In some cases, pharmacotherapy will follow psychotherapy treatments when full response is not realized. Patients with panic symptoms without agoraphobia may respond to pharmacotherapy alone. Agoraphobic symptoms generally take longer to respond than panic symptoms. The acute phase of PD treatment lasts about 12 weeks and should result in marked reduction in panic attacks, ideally total elimination, and minimal anticipatory anxiety and phobic avoidance. Treatment should be continued to prevent relapse for an additional 12 to 18 months before attempting discontinuation. 6 49 Patients who relapse following discontinuation of medication should have therapy resumed.49... 

The symptoms of a panic attack are so frightening that an unusually large number of those with panic disorder (in comparison to other psychiatric illnesses) seek treatment on their own accord. However, easily half of those who seek treatment do so in general medical settings such as hospital emergency rooms and the offices of primary care physicians. Easily mistaken for severe and even life-threatening medical conditions such as asthma attacks and heart attacks, panic disorder results in disproportionately higher health care utilization than other anxiety disorders. 

Substance-Induced Anxiety Disorder. Numerous medicines and drugs of abuse can produce panic attacks. Panic attacks can be triggered by central nervous system stimulants such as cocaine, methamphetamine, caffeine, over-the-counter herbal stimulants such as ephedra, or any of the medications commonly used to treat narcolepsy and ADHD, including psychostimulants and modafinil. Thyroid supplementation with thyroxine (Synthroid) or triiodothyronine (Cytomel) can rarely produce panic attacks. Abrupt withdrawal from central nervous system depressants such as alcohol, barbiturates, and benzodiazepines can cause panic attacks as well. This can be especially problematic with short-acting benzodiazepines such as alprazolam (Xanax), which is an effective treatment for panic disorder but which has been associated with between dose withdrawal symptoms. 

General Medical Conditions that Resemble Panic Attacks. Panic attacks are characterized by the abrupt onset of characteristic physical symptoms such as chest pain, shortness of breath, profnse sweating, dizziness, andnansea. Such symptoms may also be caused by severe and even life-threatening medical conditions such as asthma, emphysema, strokes, aneurysms, and heart attacks. It is, in fact, the fear that they re having a heart attack or some other severe medical problem that leads many patients to seek treatment after a panic attack. 

Monoamine Oxidase Inhibitors (MAOIs). Shortly after their introduction, MAOIs, snch as phenelzine (Nardil), were found to reduce the frequency of panic attacks. It became a standard treatment for what is now known as panic disorder nntil snpplanted by the benzodiazepines and SSRIs. Although all MAOIs are presumably effective for panic disorder, phenelzine is the best studied and has been shown to be effective at daily doses ranging from 45 to 90 mg. When used to treat panic disorder, phenelzine should be initiated at a dose of 15mg/day and gradually increased in 15 mg increments until reaching a therapeutic dose. 

Tricyclic Antidepressants (TCAs). The TCAs, particularly imipramine (Tofranil), were also discovered soon after their introduction to be effective in the treatment of panic attacks. Imipramine, the best-studied TCA in the treatment of panic disorder, is most often helpful at daily doses of 150-250 mg, though it must be started at 10-25 mg, usually at bedtime, and gradually increased over 2-4 weeks. Although they are not as well studied, many clinicians prefer to use the secondary amine TCAs, desipramine (Norpramin) and nortriptyline (Pamelor), because they have milder side effects than imipramine. Clomipramine (Anafranil), though probably the TCA with the greatest side effect burden, is often said to be most effective in patients with refractory disease. 

Like the MAOIs, TCAs are hindered by a delayed onset of action that can be especially intolerable for those with frequent and severe panic attacks. When starting treatment, TCAs, like SSRIs, may also produce a transient nervousness that is especially uncomfortable for those with panic disorder. When this occurs, the starting dose should be reduced by half, and the pace of subsequent dose increases should be even slower than usual. Because they produce prominent side effects and can be dangerous in overdose, TCAs are also now reserved for patients unresponsive to other treatments. Refer to Chapter 3 for a more extensive discussion of the TCAs. 

Benzodiazepines. The introduction of the benzodiazepines represented a significant advance in the treatment of panic disorder. In contrast to MAOIs and TCAs, the benzodiazepines begin to provide relief the very first day of treatment, and many patients experience a complete response by the end of the second week of therapy. All benzodiazepines should theoretically alleviate the symptoms of a panic attack at comparable doses, but the benzodiazepines of choice are alprazolam (Xanax, Xanax XR) and clonazepam (Klonopin). It likely is not coincidental that these two are among the highest potency benzodiazepines. However, they differ considerably from a pharmacokinetic standpoint. If clonazepam is the tortoise of benzodiazepines, then alprazolam is the hare. 

Beta Blockers. Beta blockers such as propranolol (Inderal) and atenolol (Tenormin) act by blocking the activity of the neurotransmitter norepinephrine. They have been nsed in the treatment of patients with panic disorder in an effort to alleviate the physical (antonomic) symptoms of the panic attack, bnt they proved no better than placebo and have no place in the treatment of panic disorder. 

Clonidine (Catapres). Like the beta blockers, clonidine acts by reducing norepinephrine activity, though by a different mechanism. Studies show that clonidine can provide early relief from the symptoms of a panic attack, but patients unfortunately relapse with continued treatment. Therefore, clonidine is not used in the treatment of panic disorder. 

Acute Phase Treatment. The short-term objective when treating panic disorder is to optimize symptom relief. This primarily consists of reducing the severity and frequency of panic attacks but also includes the anticipatory anxiety and secondary... 

The hrst-line treatments for panic disorder are (1) cognitive-behavioral therapy (CBT), (2) benzodiazepines, and (3) SSRIs/SNRls. Each of these three treatment modalities can be nsed independently or in combination. The selection of the primary treatment depends on several factors inclnding severity and frequency of the panic attacks, comorbid illnesses, and patient preference. 

Phenothiazines have a diverse use in medicine. They are primarily used as antipsy-chotics. Despite the fact that they do not cure the disease, they reduce psychotic symptoms to a point where the patient is provided with a better sense of reality. Phenothiazines are sometimes used for relieving severe anxiety, especially in panic attacks caused by dependence on amphetamines or lycergic acid diethylamide (LSD). Phenothiazines are used for alleviating behavioral problems in children that do not respond to treatment of other agents. Phenothiazines are sometimes used during the preoperational period because they relieve anxiety, control nausea, hiccups, diarrhea, and also cause muscle relaxation. 

Table 2 Sensitivity to treatment of experimentally induced panic attacks...

Salkovskis P, Jones D, Clark D (1986) Respiratory control in the treatment of panic attacks replication and extension with concurrent measurement of behaviour and pC02. Br J Psychiatry 148 526-532... 

Boyer W (1995) Serotonin uptake inhibitors are superior to imipramine and alprazolam in alleviating panic attacks a meta-analysis. Int Clin Psychopharmacol 10 45-49 Brady K, Pearlstein T, Asnis GM, Baker D, Rothbaum B, Sikes CR, Farfel GM (2000) Efficacy and safety of sertraline treatment of posttraumatic stress disorder a randomized controlled trial. JAMA 283 1837-1844... 

In patients with panic disorder, basal ANP concentrations are lower when compared to healthy control subjects, but ANP concentrations are faster and more pronounced during experimentally induced panic attacks (Kellner et al. 1995). In line with these findings, there is evidence for an anxiolytic activity of ANP in humans ANP decreases CCK-4-induced panic anxiety in patients with panic disorder (StrOhle et al. 2001) and healthy control subjects, and attenuates HPA system activity by decreasing ACTH and cortisol stimulation (Wiedemann et al. 2001). Modulation of ANP concentrations or nonpeptidergic ANP receptor ligands maybe ultimately used in the pharmacological treatment of anxiety disorders, such as panic disorder. 

StrOhle A, Pasini A, Romeo E, Hermann B, Spalletta G, di Michele F, Holsboer F, Rupprecht R (2000) Fluoxetine decreases concentrations of 3a,5a-tetrahydrodeoxycorticosterone (3a,5a-THDOC) in major depression. J Psychiatr Res 34 183-186 StrOhle A, Kellner M, Holsboer F, Wiedemann K (2001) Anxiolytic activity of atrial natriuretic peptide in patients with panic disorder. Am J Psychiatry 158 1514-1516 StrOhle A, Romeo E, di Michele F, Pasini A, Yassouridis A, Holsboer F, Rupprecht R (2002) GABAA receptor modulatory neuroactive steroid composition in panic disorder and during paroxetine treatment. Am J Psychiatry 159 145-147 StrOhle A, Romeo E, di Michele F, Pasini A, Hermann B, Gajewsky G, Holsboer F, Rupprecht F (2003) Induced panic attacks shift GABAA receptor modulatory neuroactive steroid composition. Arch Gen Psychiatry 60 161-168 Szapiro G, Vianna MRM, McGaugh JL, Medina JH, Izquierdo I (2003) The role of NMDA glutamate receptors, PKA, MAPK, and CAMKII in the hippocampus in extinction of conditioned fear. Hippocampus 13 53-58... 

Panic disorder. Sixty-six panic disorder patients were included in a study. All of whom met the DSM-IV diagnosis of panic disorder (n = 45) or panic disorder with agoraphobia ([PDA] n = 21). Twenty-four patients experienced their first panic attack within 48 hours of cannabis use and then went on to develop panic disorder. All the patients were treated with paroxetine (gradually increased up to 40 mg/day). The two groups responded equally well to paroxetine treatment as measured at the 8 weeks and 12 months follow-up visits. There were no significant effects of age, sex, and duration of illness as covariates with response rates between the two groups. In addition, panic disorder or panic disorder... 

Uniabeied Uses Treatment of anxiety, depression, panic attacks... 

The efficacy of beta-blockers in the symptomatic relief of anxiety in adults has been established in over a dozen controlled trials (Neppe, 1989). In a number of countries, beta-blockers have been licensed for the treatment of anxiety disorders. Somatic manifestations of anxiety such as palpitations, diaphoresis, and tremor, rather than core psychological symptoms, were particularly responsive to beta-blocker treatment. In comparative trials that included patients with severe anxiety and panic attacks, the antianxiety effect of beta-blockers was, however, somewhat less powerful than that of benzodiazepines (Lader, 1988), with the exception of a small trial that compared alprazolam to propranolol (Ravaris et ah, 1991). Head-to-head comparisons of beta-blockers and selective serotonin reuptake inhibitors (SSRIs) are lacking. Performance and stress-related anxiety that may affect public performers, such as musicians or people taking an examination or giving a speech, seems to be particularly suited for beta-blocker treatment (Lader, 1988). Beta-blockers may be given on an as-required basis 1-2 hours before the stressful situation. 

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