Anxiety clonidine

Detoxification is more successful when the patient is transitioned from a stable methadone dose with the support of ongoing therapy than when the patient comes directly from the street for detoxification from heroin. Some practitioners believe that detoxification with clonidine can be more rapid than with methadone, at least on an outpatient basis. One important hmitation of clonidine is that, although it suppresses autonomic signs of withdrawal, subject-reported symptoms, such as lethargy, restlessness, insomnia, and craving, are not well relieved (Charney et al. 1981 Jasinski et al. 1985). Anxiety may... 

Fyer AJ, Liebowitz MR, Gorman JM, et al Effects of clonidine on alprazolam discontinuation in panic patients a pilot study. J Clin Psychopharmacol 8 270—274,1988 Garvey MJ, Tollefson GD Prevalence of misuse of prescribed benzodiazepines in patients with primary anxiety disorder or major depression. Am J Psychiatry 143 1601-1603, 1986... 

The answer is a. (Hardman, p 789. Katzung, pp 162—163.) Withdrawal of clonidine, particularly doses greater than 1 mg/d, is well known to cause such a syndrome (including severe hypertension, tachycardia, anxiety tremor, headache, abdominal pain, and sweating), even after one or two missed doses. 

Alternative pharmacological approaches Clonidine, an o2 adrenergic agonist, has been employed as adjunctive therapy to assist in smoking cessation. However, results have been mixed or the effects small (Gourlay et al. 1994 Hilleman et al. 1993 Franks et al. 1989). Buspirone (BuSpar) is a 5-HTlA partial agonist with anxiolytic effects. It has been tested as a treatment for smoking cessation because anxiety is a prominent feature of nicotine withdrawal (Farid and Abate 1998). To date, results have been mixed and more controlled research is needed. 

Noradrenaline is the neurotransmitter most closely associated with the peripheral and central stress response (Figure 9.5). There is experimental evidence to show that drugs such as yohimbine that block the noradrenergic autoreceptors (e.g. on cell bodies and nerve terminals) and thereby enhance noradrenaline release cause fear and anxiety in both man and animals. Conversely, drugs that stimulate these autoreceptors (as exemplified by clonidine) diminish the anxiety state because they reduce the release of noradrenaline. Benzodiazepines have been shown to inhibit the fear-motivated increase in the functional activity of noradrenaline in experimental animals, but it is now widely believed that the action of the benzodiazepines on the central noradrenergic system is only short term and may contribute to the sedative effects which most conventional benzodiazepines produce, at least initially. Nevertheless, altered noradrenergic... 

Few studies have examined noradrenergic function in patients with phobic disorders. In patients with specific phobias, increases in subjective anxiety and increased heart rate, blood pressure, plasma NE, and epinephrine have been associated with exposure to the phobic stimulus (Nesse et al. 1985). This finding may be of interest from the standpoint of the model of conditioned fear, reviewed above, in which a potentiated release of NE occurs in response to a reexposure to the original stressful stimulus. Patients with social phobia have been found to have greater increases in plasma NE in comparison to healthy controls and patients with panic disorder (Stein et al. 1992). In contrast to panic disorder patients, the density of lymphocyte a-adrenoceptors is normal in social phobic patients (Stein et al. 1993). The growth hormone response to intravenous clonidine (a marker of central a2-receptor function) is blunted in social phobia patients (Tancer et al. 1990). 

Effects of early environmental adversity on HPA mediation of neurodevelopment have also been demonstrated in non-human primates (Coplan et al., 1995). Corticotropin-releasing hormone (CRH) intracerebro-ventricular administration in rhesus monkeys that had been separated from their mothers produced behavioral inhibition and increases in ACTH and cortisol. Coplan et al (1995) presented evidence for persistently elevated cerebrospinal fluid concentrations of corticotropin-releasing factor (CRF) in grown macaques that had been reared by mothers in unpredictable environmental conditions. Further studies in adversely reared adult monkeys demonstrated an inverse relationship between mean CRF concentrations and GH response to clonidine (Coplan et al., 2000). In light of evidence that reduced GH response to clonidine has been shown in other anxiety disorders (Charney and Bremner, 1999), Coplan et al. (2000) hypothesize that GH response to clonidine may inversely reflect trait-like increases of central nervous system CRF activity. Data linking childhood anxiety to growth deficits are consistent with this view (Pine et al., 1996). Activity, of the HPA axis, as related to early environmental... 

Two different patterns of clonidine-induced cardiovascular complications have been described (Swanson et ah, 1995). One is characterized by decreased pulse and BP, often with associated EKG changes, fatigue, and sedation, and responds to a decrease in dosage. The other presents with tachycardia, tachypnea, with or without fever, anxiety, panic, and acute mental status changes, and is often associated with a missed dose or an abrupt taper. This pattern often responds to reinstituting the dosage and slowly tapering as necessary. 

Inattentiveness, impulsivity, hyperactivity 50% will continue to manifest the disorder into adulthood Stimulants (70% response for uncomplicated ADHD caution in patients with tic disorders) TCAs (70% response, first line for patients with comorbid MD or anxiety disorders, and for patients with ADHD + tics) requires serum levels and cardiovascular monitoring Bupropion Clonidine, guan-facine (first line for patients with ADHD + tics) MAOIs Combined pharmacotherapy for treatment-resistant cases... 

Perry, 1994 Clonidine 0.05-0.1 mg bid Open-label = 17 Improvement in anxiety, arousal, concentration, mood, impulsivity ... 

The medical management of other childhood anxiety disorders has included the use of BZDs, antihistamines, b -adrenergic blockers, and clonidine (152,... 

FIGURE 8—13. If an alpha 2 agonist such as clonidine, is administered, it will have much the same action as norepinephrine (NE) itself both at somatodendritic alpha 2 autoreceptors and at terminal alpha 2 autoreceptors. This action is that of reducing both neuronal impulse in NE neurons and release of NE from noradrenergic axon terminals. Thus, alpha 2 agonists will decrease the symptoms associated with anxiety, especially the autonomic symptoms of dilated pupils, tachycardia, tremor, and sweating. 

Clonidine (Catapres) is another drug used to treat opiate addiction. It can relieve the anxiety, runny nose, salivation, sweating, abdominal cramps, and muscle aches of opiate withdrawal. Side effects are dry mouth, dizziness, and drowsiness. Clonidine is initially taken at 0.8-1.2 mg a day, maintained for a few days, and then gradually decreased. Combined with the opiate blocker naltrexone, clonidine can allow a more rapid detoxification (the removal of morphine from the body). Detox in a single day can be accomplished by heavy sedation or anesthesia while giving naltrexone to an unconscious addict. This controversial method has not been studied in controlled trials. 

One of two common treatment approaches is to combat withdrawal symptoms by treating them with appropriate medications. A drug commonly used in withdrawal treatment is clonidine, a medication most often used to lower blood pressure. For people going through withdrawal, clonidine may help lessen some symptoms. A variety of other drugs also may be used to deal with symptom-specific complaints. Examples include ibupro-fen for headaches, muscle, joint, or bone pain, and mild tranquilizers to combat anxiety and/or insomnia. 

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