Stimulants side effects

Although all patients with depression should undergo a thorough medical evaluation, no specific tests are required before SSRI therapy is initiated. The usual starting doses of SSRIs are summarized in Table 2-1. These standard doses should be decreased by 50% in patients with hepatic disease and in elderly persons. In addition, patients with panic disorder or significant anxiety symptoms are often intolerant of the initial stimulating side effects that commonly occur with SSRI use. In these cases, the initial dose should be decreased... 

A partial list of stimulant side effects is outlined in Table 6-2. Common side effects (such as insomnia, nervousness, nausea, decreased appetite, stomachaches, and headaches) tend to be transient and diminish with time or medication discontinuation. Using the lowest effective dose, taking the medications with meals, and avoiding doses late in the day help minimize these side effects as well. 

Table 11.5 provides descriptions of stimulant adverse reactions from the clinical and research literature that are consistent with the brain-disabling principle. A broad array of stimulant side effects in fact provides the primary effects of the drug. 

Breggin, P. (1992b). A case of fluoxetine-induced stimulant side effects with suicidal ideation associated with a possible withdrawal syndrome ( crashing ). International Journal of Risk and Safety in Medicine, 3, 325—328. 

Researchers have discovered that there are two types of monoamine oxidase enzyme MAO-A and MAO-B, each located in different regions of the body. Older MAOIs, such as Nardil, inhibit both versions of monoamine oxidase, resulting in increased serotonin and norepinephrine inside the cell (and also leakage into the synapse, thus activating receptors). Increases in serotonin and noreinephrine receptor activation can lead to several over-stimulating side effects. These central nervous system effects include tremors, insomnia, agitation, and occasionally, precipitation of a mania in patients with bipolar depression. 

Advances in immunology during the last part of the twentieth century have continued at a rapid rate and cytokines and immune cells having specific markers continue to be defined. A number of natural and synthetic immunotherapeutic agents have been discovered that can modulate components of the normal or aberrant immune system, through stimulation or suppression. However, most of these substances also have inherent adverse side effects. 

Initial attempts to treat AD using direct cholinergic agonists were limited by low efficacy and side-effect issues (140—142). Thus trials using RS-86 (25), oxotremorine [70-22-4] (26), arecoline [63-75-2] (27), and pilocarpine [92-32-7] (28) to treat AD were equivocal (Eig. 5). However, the identification of multiple subtypes of muscarinic receptors has stimulated a search for subtype specific muscarinic agonists which may limit side effects while increasing efficacy. 

Normally, dietary tyramine is broken down in the gastrointestinal tract by MAO and is not absorbed. In the presence of MAOI, however, all of its potent sympathomimetic actions are seen. Other side effects of MAOI include excessive CNS stimulation, orthostatic hypotension, weight gain, and in rare cases hepatotoxicity. Because the monoamine oxidase inhibitors exhibit greater toxicity, yet no greater therapeutic response than other, newer agents, clinical use has been markedly curtailed. The primary use for MAOIs is in the treatment of atypical depressions, eg, those associated with increased appetite, phobic anxiety, hypersomnolence, and fatigues, but not melancholia (2). 

Compounds available in the United States are Hsted in Table 1. Whereas they vary in degree, all of them share similar HabiUties of cardiovascular side effects, the potential for central nervous system (CNS) stimulation, the development of tolerance, and abuse potential. AH, with the exception of ma2indol, are derivatives of phenethylamine. The introduction of an oxygen atom on the -carbon of the side chain tends to reduce CNS stimulant properties without decreasing the anorectic activity. Following the Federal Controlled Dmg Act of 1970, dmgs were classified into one of five schedules according to medical utiUty and abuse potential. 

The Class I agents have many similar side effects and toxicities. The anticholinergic side effects include dry mouth, constipation, and urinary hesitancy and retention. Common gastrointestinal (GI) side effects include nausea, vomiting, diarrhea, and anorexia. Cardiovascular adverse effects are hypotension, tachycardia, arrhythmias, and myocardial depression, especially in patients with congestive heart failure. Common central nervous system (CNS) side effects are headache, dizziness, mental confusion, hallucinations, CNS stimulation, paraesthesias, and convulsions. 

Figure 10-5. Transient transmission changes AV/Po in PPV for different lime delays between the pump and probe pulse. The pump pulse is a 100 fs laser pulse at 325 nm obtained by frequency doubling ol amplified dye laser pulses, (a) and (b) correspond to different sides of a PPV-film. The spectra in (a) were obtained lor the unoxidized side of the sample while the set of spectra in (b) was measured for the oxidized side of the same sample. The main differences observed are a much lower stimulated emission effect for the oxidized side. The two bottom spectra depict the PL-spectra for comparison. The dashed line indicates the optical absorption (according to Kef. (281).

Antidepressants are used in the treatment of neuropathic pain and headache. They include the classic tricyclic compounds and are divided into nonselective nor-adrenaline/5-HT reuptake inhibitors (e.g., amitriptyline, imipramine, clomipramine, venlafaxine), preferential noradrenaline reuptake inhibitors (e.g., desipramine, nortriptyline) and selective 5-HT reuptake inhibitors (e.g., citalopram, paroxetine, fluoxetine). The reuptake block leads to a stimulation of endogenous monoaminer-gic pain inhibition in the spinal cord and brain. In addition, tricyclics have NMDA receptor antagonist, endogenous opioid enhancing, Na+ channel blocking, and K+ channel opening effects which can suppress peripheral and central sensitization. Block of cardiac ion channels by tricyclics can lead to life-threatening arrhythmias. The selective 5-HT transporter inhibitors have a different side effect profile and are safer in cases of overdose [3]. 

Stimulation of appetite and weight gain has frequently been observed as a side effect of long-term therapy with various psychoactive drugs. Prominent examples not... 

BAYK8644 is a DHP with Ca2+ channel activating properties. Although some therapeutic effects can be envisaged for such drugs (such as stimulation of glucose-dependent insulin secretion, positive inotropy), severe side effects are also predicted from animal studies (dystonic neurobehavioral syndrome, hypertension, arrhythmias), which currently prevents their clinical development. 

Historically the only melanocortin peptide to be used clinically is the parent hormone from which all these peptides are derived from namely ACTH (see above). It has also been used in the treatment infantile spasms for epilepsy, where it is administered as an intramuscular injection only over a 2-12 weeks period. Obvious side effects include weight gain, puffy face, high blood pressure and an increased risk of infection and should never be administered to patients with diabetics, renal or heart failure. ACTH is also used as a stimulation test to measure adrenal cortex activity, i.e. production of cortisol and is used to ascertain whether someone has Addison s disease. 

---