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среда, 13 июня 2012 г.

Влияние различных антидепрессантов на фазы сна

A clinical consequence of REM suppression can be a change in frequency and intensity of dreaming, as well as a pronounced exacerbation of intense, disturbing dreams related to “REM rebound” on discontinuation. Pulmonary specialists sometimes advocate use of an activating TCA such as protriptyline because it may help suppress REM sleep—when sleep apnea episodes may be accentuated—and also provide benefit for the daytime somnolence that many patients with sleep apnea experience.

The Effects of Antidepressants on Sleep

четверг, 26 января 2012 г.

Психостимуляторы для пожилых больных


Psychostimulants are recognized for their role in managing attention-deficit/hyperactivity disorder
(ADHD), but also have found a treatment niche in conditions such as apathy, fatigue, and depression.
Psychostimulants for older adult

среда, 4 мая 2011 г.

Комбинации антидепрессантов не превосходят по эффективности монотерапию антидепрессантом

The first group took escitalopram (a selective serotonin reuptake inhibitor, or SSRI, brand name Lexapro) and a placebo; the second group received the same SSRI along with bupropion (a non-tricyclic antidepressant, brand name Wellbutrin); and the third group took two different antidepressants: venlafaxine (a tetracyclic antidepressant, Effexor) and mirtazapine (a serotonin norepinephrine reuptake inhibitor, Remeron).

After 12 weeks of treatment, all three groups showed similar remission and response rates: 39 percent, 39 percent and 38 percent, respectively, for remission; response rates were approximately 52 percent in all three groups. After seven months, remission and response rates remained similar in all three groups, but side effects were more frequent in the third group.

Two Antidepressants Appear No Better Than One

вторник, 19 октября 2010 г.

PHQ-9

Table 3. PHQ-9

1. Over the past 2 weeks, how often have you been bothered by any of the following problems?
Not at all (0) Several days (1) More than half the days (2) Nearly every day (3)
a. Little interest or pleasure in doing things
b. Feeling down, depressed, or hopeless
c. Trouble falling/staying asleep, sleeping too much
d. Feeling tired or having little energy
e. Poor appetite or overeating
f. Feeling bad about yourself -- or that you are a failure or have let yourself or your family down
g. Trouble concentrating on things, such as reading the newspaper or watching television
h. Moving or speaking so slowly that other people could have noticed. Or the opposite -- being so fidgety or restless that you have been moving around a lot more than usual
i. Thoughts that you would be better off dead or of hurting yourself in some way
2. If you checked off any problem on this questionnaire so far, how difficult have these problems made it for you to do your work, take care of things at home, or get along with other people?
Not difficult at all Somewhat difficult Very difficult Extremely difficult


Table 4. Interpretation of PHQ-9 Results

Score/
Symptom Level

Treatment

0-4
No depression
Consider other diagnoses
5-9
Minimal
▪ Consider other diagnoses
▪ If diagnosis is depression, watchful waiting is appropriate initial management
10-14
Mild
▪ Consider watchful waiting
▪ If active treatment is needed, medication or psychotherapy is equally effective; consider function score in choosing treatment
15-19
Moderate
▪ Active treatment with medication or psychotherapy is recommended
▪ Medication or psychotherapy is equally effective
20-27
Severe
▪ Medication treatment is recommended
▪For many people, psychotherapy is useful as an additional treatment
▪ People with severe symptoms often benefit from consultation with a psychiatrist
Data from Kroenke K, Spitzer R. Psychiatr Ann. 2002;32:509-521.


A number of combinations have some benefit in selected patients, including:

  • Lithium augmentation at stage 3 of STAR*D resulted in remissions in 15.9%.[84] Lithium in combination with SSRIs and TCAs also has been effective in placebo-controlled studies, most involving small numbers of subjects. Such treatment requires monitoring of lithium levels, because there is a small difference between therapeutic and toxic levels.[85]
  • Thyroid hormone, and particularly triiodothyronine, has been studied for augmentation with the TCAs. In the STAR*D study, at step 3, augmentation with triiodothyronine led to a remission rate of 24.7%.[84] Placebo-controlled studies have involved small numbers of subjects and have had mixed results.[86]
  • A heterocyclic-SSRI combination in 1 small study produced more rapid treatment onset and increased the likelihood of remission.[87] In the study, a combination of fluoxetine and desipramine (a norepinephrine reuptake inhibitor) was more effective in achieving remission than either drug used as monotherapy: 53.8% for the combination, compared with 7.1% and 0%, respectively. However, such combinations can produce the serotonin syndrome, which is potentially life-threatening, and the dose of the heterocyclic must be adjusted using blood levels because SSRIs increase TCA levels through CYP-450 isoenzyme interactions (eg, fluoxetine increases the levels of desipramine 3- to 4-fold).[88] Consequently, this augmentation strategy should rarely be considered in primary care.
  • Mirtazapine has recently been evaluated in combination therapy with an SSRI (fluoxetine), an SNRI (venlafaxine), or bupropion.[89] The investigators found that all 3 combinations were more effective than fluoxetine alone in achieving remission (52%, 58%, 46%, respectively, compared with 25%). In patients who responded, double-blind discontinuation resulted in relapse in about 40%. Of note, treatment was initiated with these combinations, rather than mirtazapine being used as an augmenting agent in those not initially responding.
  • Methylfolate and folate have been used to augment SSRIs, resulting in increased rates of remission, particularly in women.[90] The degree to which the response is due to folate deficiency, and whether methylfolate is of greater benefit due to its increased ability to cross the blood-brain barrier, are subject to further research.
  • Antidepressants and hypnotics have been used together, with early improvement not only in sleep measures, but also in rates of depression remission.[91]
  • Stimulant drugs have been used as augmentation of heterocyclics or SSRIs.[92] Of note, in individuals with comorbid medical illness, amphetamine stimulants should be used with caution, particularly if cardiac disease is potentially present.
Clinical and Pharmacologic Strategies to Achieve Remission in Depression

пятница, 10 сентября 2010 г.

Инверсия аффекта - дозозависимый эффект бупропиона

A switch into mania is a potential risk associated with antidepressant drug use in bipolar affective disorder. Bupropion is believed to be associated with a decreased risk compared with other antidepressant therapies. However, our case report as well as others support the theory that this decreased risk may be due to dosages not exceeding the recommended daily dose (450 mg/d). Doses of bupropion >450 mg/d should be used with caution in depressed patients with bipolar affective disorder.

Mania with bupropion: a dose-related phenomenon?

четверг, 8 июля 2010 г.

STAR*D


The Sequenced Treatment Alternatives to Relieve Depression (STAR*D) trial was a longitudinal, multi-center, 5-year study of common strategies for treating depression. To date, it is the United States’ largest National Institute of Mental Health funded study including over 4,000 patients. This four level trial compared traditional augmentation strategies with switching agents (Slide 2).30-34 Unlike most depression studies, in STAR*D the outcome measure was full remission.
In Level 1, the initial monotherapy phase, citalopram (mean dose of 41.8 mg) was effective at achieving remission for only ~30% of subjects. This finding has been accepted as an accurate reflection of clinical experience with any initial monotherapy. The remaining 70% were randomized to either receive bupropion or buspirone augmentation, or switched to one of three antidepressants as monotherapy—bupropion, venlafaxine, or sertraline. Augmentation resulted in a 30% response, while switching antidepressants resulted in ~20% of patients achieving remission. Level 3 included those non-remitters from Level 2 who were then randomized to either T3 or lithium augmentation, resulting in remission rates of 25% and 16% respectively. A Level 3 switch to nortriptyline (NTP) or mirtazapine (MTZ) was in general less successful than Level 3 augmentation, with 20% of NTP patients and 12% of MTZ patients remitting. Level 4 treatment options (monoamine oxidase inhibitors [MAOIs] or venlafaxine–mirtazapine-combination therapy) were provided to patients who had not responded satisfactorily to previous levels of the treatment protocol, and very few experienced full remission (14% and 7% respectively).12,35


An overall analysis of STAR*D results indicates that the chances of achieving and maintaining remission in patients with difficult-to-treat depression diminishes with every additional strategy needed. Those who fully remit early in the course of treatment have a better chance of remaining well than those who experience only symptomatic improvement. STAR*D does not tell us which treatment works better as a first or second adjunct, simply that the greatest chance of recovery appears to lie with the first two sequential treatments.

The Role of L-methylfolate in Depressive Disorders

четверг, 6 мая 2010 г.

Антидепрессанты при БАР

"Although some might argue that the precise relative risk of antidepressant-induced mania or hypomania is unknown (eg, considering intervening factors such as the natural illness course), recent literature suggests that the emergence of mania or hypomania can be reasonably attributed to antidepressant use in no more than 10% to 25% of patients with bipolar disorder"

"One large randomized trial showed comparable antidepressant efficacy with a mood stabilizer plus adjunctive venlafaxine (43%) vs sertraline (55%) vs bupropion (49%) over 10 weeks,14 but the lack of a mood stabilizer monotherapy comparison group limits the ability to anticipate whether adjunctive antidepressants increase response or remission rates more than mood stabilizers alone. Adjunctive imipramine,13 paroxetine,12,13,15 and bupropion12 yield no greater improvement in depressive symptoms than is seen with optimally dosed mood stabilizers alone."

"The largest dataset on this topic—the randomized controlled data from Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD)12—found that the risk for treatment-emergent manic switch with paroxetine or bupropion was almost identical (about 10%) with or without an FDA-approved antimanic agent.

In a retrospective study, Henry et al6 found that cotherapy with lithium but not divalproex or carbamazepine protects against antidepressant-induced mania, and that switch rates to mania were the same whether or not an antidepressant was taken with an anticonvulsant. In a naturalistic retrospective study (n=158), Bottlender et al24 revealed that mood stabilizers (lithium, carbamazepine, or divalproex) prevented switches from depression to mania during treatment with TCAs but not SSRIs or MAOIs.

I favor incorporating lithium or other antimanic agents in the regimens of patients with bipolar depression not primarily to guard against antidepressant-induced mania but more for pharmacodynamic synergy—complementary mechanisms of action that collectively may produce more substantial antidepressant effects—especially when the patient’s illness course has included manic or hypomanic features in the preceding year."

"Wehr et al25 reported that antidepressants may accelerate cycling frequency (ie, inter-episode durations become shorter) in a small subgroup (N=10) of patients. By contrast, use of TCAs was not more likely in the weeks preceding shifts from depression to mania or hypomania in a 14-year follow-up study of bipolar rapid cycling from the NIMH Collaborative Depression Study.26 In fact, rapid-cycling patients spent more weeks depressed when taking lithium without a TCA than with."

Antidepressants in bipolar disorder: 7 myths and realities

вторник, 22 декабря 2009 г.

SNRIs Anti-depressants

Trazodone (Desyrel) inhibits serotonin reuptake in addition to blocking certain types of serotonin, norepinephrine, and histamine receptors. Histamine is a both a biological chemical involved in immune responses as well as a neurotransmitter. In low doses, Trazodone can be used as a sleep aid, especially for people who experience insomnia as part of their depression. Side effects of Trazodone include: allergic reactions, irregular heartbeat, prolonged and painful erection, drowsiness, fatigue, lethargy (exhaustion), psychomotor retardation (slow movements), lightheadedness, dizziness, difficulty concentrating, confusion, impaired memory, disorientation, excitement, agitation, anxiety, tension, nervousness, restlessness, insomnia, nightmares, anger, hostility and, rarely, hypomania, visual distortions, hallucinations (sensing things that aren't really there), delusions (false, fixed beliefs), and paranoia (suspicious fear).

Buproprion (Wellbutrin) is often a first choice treatment for Major Depressive Disorder. This medication is just as effective as SSRIs in treating depressive symptoms, with less risk of weight gain and sexual side effects. In addition to serotonin and norepinephrine, buproprion also inhibits dopamine reuptake. The most common side effects of buproprion are dry mouth, constipation, headaches, and insomnia. Care must be taken when using buproprion at higher doses, as it has been known to cause seizures.

Venlafaxine (Effexor) is often used for the treatment of depressive illnesses, but large numbers of studies demonstrating treatment success are lacking. In addition to inhibiting serotonin reuptake, venlafaxine inhibits norepinephrine and dopamine reuptake. Venlafaxine does not interfere with other brain chemicals, which makes it less "messy" and more powerful than other antidepressants. Some evidence suggests that venlafaxine relieves depressive symptoms more quickly than other medications with fewer side effects, and that it can be combined safely with other medications. However, more research is necessary to substantiate these claims.

Nefazodone (Serzone) inhibits serotonin reuptake by blocking a particular type of serotonin receptor. Serzone is sedating, and is useful for relieving anxiety and severe insomnia. Furthermore, sexual side effects are mild, if any. Unfortunately however, nefazodone is a strong inhibitor of liver enzymes and should be used cautiously. Many medications are metabolized in the liver, and functional liver enzymes are essential to proper liver functioning and overall health.

Mirtazapine (Remeron) blocks serotonin and norepinephrine reuptake. Mirtazapine is sedating, and has the disagreeable side effect (for most) of weight gain in comparison with other SSRIs. Although few studies clearly demonstrate Mirtazapine's usefulness in treating unipolar depression, this medication may be a good option for people who have experienced significant weight loss during their depressive episodes.

Antidepressants for Major Depression - Selective Serotonin and Norepinephrine Reuptake Inhibitors (SNRI)


"Why does this matter? Because the two scales used to rate depression in this study, the Hamilton Scale and the Montgomery-Asberg Scale, both count reduced appetite and sleeplessness as symptoms of depression. If you're on mirtazapine, you're unlikely to have either problem - you'll be more worried about the exact opposite, insatiable hunger and drowsiness. So mirtazapine could reduce your total score on these scales even if it didn't change your mood. I have no idea to what extent this is a factor in these results, but it could be important."

Two Drugs Are Better Than One?

понедельник, 14 сентября 2009 г.

предикторы эффективности антидепрессантов

A new medical test — called a biomarker test — appears to help predict a patient’s response to a specific antidepressant. The test is non-invasive, painless and fast, taking about 15 minutes. Six electrodes (which measure brain activity) are placed around the forehead and on the earlobes (the electrodes don’t hurt — they are only measuring devices).

Here’s what the study found:

Subjects were then randomly assigned to continue with escitalopram or were given a different drug. A total of 73 patients who remained on escitalopram were tracked for 49 days to see if their results matched the prediction of the ATR biomarker. The ATR predicted both response and remission with an accuracy rate of 74 percent, much higher than any other method available.

The researchers also found that they could predict whether subjects were more likely to respond to a different antidepressant, bupropion, also known as Wellbutrin XL.

Test Predicts Depression Medication Response

вторник, 11 августа 2009 г.

Резистентное к лечению биполярное расстройство



In acute mania, antidepressants should be discontinued immediately. The focus should be on using evidence-based treatments for mania. Although lithium is not recommended for mixed episodes or for patients with many previous episodes, lithium and divalproex are often used before an atypical antipsychotic because they are thought to be safer with long-term use.
The most commonly recommended nonstandard treatments for treatment-resistant mania are clozapine and ECT, which have been shown to have efficacy.A combination of clozapine and ECT has also been suggested.
Several novel treatments have been studied using an augmentation approach in combination with standard treatments for treatment-resistant mania. These include donepezil, gabapentin, topiramate, mexiletine, and intravenous magnesium sulphate. The reported efficacy in these uncontrolled reports is confounded by the continuation of the previous treatments. One exception is tamoxifen, which, like lithium and valproate, inhibits protein kinase C and was found to have antimanic efficacy superior to placebo.
However, antidepressants (other than fluoxetine in combination with olanzapine) have not been shown to be efficacious in acute bipolar depression and may be associated with switching. In particular, antidepressants with norepinephrine activity including tricyclics and serotonin-norepinephrine reuptake inhibitors may have a greater risk of inducing switching than SSRIs.
For treatment-resistant acute bipolar depression, the dopaminergic agonist pramipexole and the wakefulness-promoting agent modafinil have been shown to have efficacy greater than placebo as augmentation to standard treatments.4,26 Other pharmacotherapies have been studied in uncontrolled augmentation, including donepezil, bupropion, riluzole, gabapentin, levetiracetam, and aripiprazole. Two brain-stimulating therapies—magnetic seizure therapy and repetitive transcranial magnetic stimulation (TMS)—have been studied as well.
Other approaches include augmentation with hypermetabolic thyroid supplementation, diltiazem, aripiprazole, topiramate, gabapentin, mexiletine, levetiracetam, and chromium, as well as vagus nerve stimulation. Efficacy has also been reported for levetiracetam monotherapy and a combination of topiramate and clozapine.

Treatment-Resistant Bipolar Disorder

четверг, 9 июля 2009 г.

Treatment of Sexual Side Effects: Antidotes

Treatment of Sexual Side Effects: Antidotes

A variety of antidotes have been reported to treat SSRI-induced sexual dysfunction effectively; however, virtually all the data on these agents are derived from open case reports and case series. Insofar as sexual function improvement may be responsive to placebo effects, it is impossible to estimate the true efficacy of these antidotes.[27]

Most of these antidotes either have serotonin-blocking properties (especially 5HT-2 antagonistic effects) or augment catecholamine activity, especially that of dopamine. The antiserotonergic antidotes are cyproheptadine, buspirone, nefazodone, and mianserin. Medications enhancing dopaminergic tone include amantadine, bupropion, and stimulants, with yohimbine showing noradrenergic effects. Among the reported antidotes, the only 2 without antiserotonergic effects or catecholaminergic activity are gingko biloba and urecholine.

Cyproheptadine is an antihistamine with antiserotonergic properties that has been reported for over a decade to reverse antidepressant-induced sexual dysfunction. Only case reports and case series attest to its efficacy.[13,42-44] Effective doses range from 2mg to 16mg. In the most recent and largest case series, 12 of 25 patients described improvement in sexual function when treated with cyproheptadine (mean dose, 8.6mg).[13] Anorgasmia is the sexual side effect most often reported to be alleviated by cyproheptadine. Cyproheptadine is effective when taken either on an as-needed basis (typically, 1 to 2 hours before intercourse) or on a regular basis.

However, cyproheptadine's utility is often limited by its potential side effects. Excessive sedation and the reversal of the therapeutic effect of the antidepressant are major problems that limit its usefulness. Effectively treated depression and bulimic symptoms have been reported to reemerge soon after cyproheptadine was started.[42,45-48] This reversal of therapeutic effects is itself reversible upon discontinuation.

Buspirone is a serotonin-IA partial agonist typically prescribed to treat persistent anxiety. One case series reported that buspirone reversed both decreased sexual interest and orgasmic dysfunction caused by SSRIs.[49] Most patients using buspirone to treat sexual dysfunction take it daily. The dosage is the same as that used for anxiety (15mg to 60mg daily). The mechanism of action of buspirone in treating sexual dysfunction may be reduction of serotonergic tone via stimulation of presynaptic autoreceptors or the alpha-2 antagonist effects of one of buspirone's major metabolites, 1-pyrimidinylpiperazine.

Nefazodone and mianserin are antidepressants with strong postsynaptic blocking properties. In one case report, nefazodone 150mg taken 1 hour prior to sexual activity completely reversed sertraline-induced anorgasmia.[50] Mianserin, an antidepressant with 5HT-2 and alpha-2 adrenergic antagonist properties, is available in many countries but not in the US. It has been reported to reverse serotonin reuptake inhibitor-induced sexual dysfunction in 9 of 15 patients.[51] Mirtazapine is similar in its biological activity to mianserin and might also be effective in reversing sexual side effects. No case reports or case series have yet been published attesting to this, although clinicians have described such an effect. The putative capacity of mianserin and mirtazapine to reverse sexual side effects can be attributed either to their serotonergic activity or presynaptic alpha-2 activity.

Amantadine, a dopamine agonist, is used both as an antiviral agent and as a treatment for Parkinson's disease. It has been shown in a number of small case series to reverse anorgasmia.[13,52-54] Reported effective doses have ranged between 100mg to 400mg taken either on a daily or as-needed basis. In the most recent case series, 8 (42%) out of 19 patients with SSRI-induced sexual dysfunction improved with amantadine 200mg daily.[13] Given dopamine's consistent effect as a neurotransmitter involved in sexual arousal, a number of other dopamine agonists have been explored as treatments for sexual side effects.[2,55,56]

Bupropion is another commonly touted antidote for SSRI-induced sexual dysfunction.[57,58] It is assumed that the mechanism of action by which bupropion reverses sexual side effects is its weak dopamine agonism. The evidence for bupropion's efficacy is scant, except for unpublished, anecdotal reports, one case report,[57] and a case series[58] in which 31 (66%) of 47 patients showed improvement when bupropion was added to the regimen along with the serotonergic antidepressant. Most patients (18/31) with a successful outcome responded to as-needed use of bupropion 75mg to 150mg. Libido, arousal, and orgasmic difficulties were all effectively reversed. Fifteen percent of treated patients stopped taking bupropion because of its stimulation side effects. It is unclear whether bupropion doses need to be somewhat lower than usual when added to fluoxetine or paroxetine, to compensate for pharmacokinetic interactions resulting in increased bupropion levels.[59]

Stimulants, such as methylphenidate, D-amphetamine, and pemoline, are reported to reverse a variety of sexual side effects caused by SSRIs or MAOIs.[60-62] Low doses of 10mg-25mg of methylphenidate or D-amphetamine have been effective. One should add stimulants to an MAOI with extreme caution because of the risk of a hypertensive episode. However, use of an MAOI/stimulant combination has been shown to be safe in a case series.[63] SSRI/stimulant combinations show no similar risks.

Yohimbine is available with or without a prescription (and with unclear purity) in health food stores. It is an alkaloid from the bark of Corynanthe yohimbi (family, Rubiaceae) and has been used for decades to reverse erectile dysfunction.[64-66] Its efficacy in treating sexual dysfunction may be associated with its ability to block presynaptic alpha-2 adrenergic sites, leading to enhanced adrenergic tone.[65] A variety of sexual side effects have been reported to be alleviated by yohimbine in doses ranging from 2.7mg to 16.2mg daily, prescribed either on a regular 5.4mg 3 times daily basis or on an as-needed basis with single doses up to 16.2mg.[13,67-69] In the largest case series, 17 (81%) of 21 patients showed improvement of sexual side effects when treated with yohimbine (mean dose, 16.2mg).[12]

Typical side effects associated with yohimbine include anxiety, nausea, flushing, urinary urgency, and sweating. Yohimbine has been the subject of the only double-blind, placebo-controlled study to evaluate treatment of sexual dysfunction occurring as a drug side effect.[27] Unfortunately, the placebo effect was marked, showing a minimal drug-placebo difference with yohimbine given at a dose of 5.4mg 3 times daily. Yohimbine is also available in lower potency without a prescription. The purity, potency, and safety of these preparations, however, are unknown.

Bethanechol is a cholinergic agonist that has occasionally been useful in reversing sexual dysfunction associated with TCAs and MAOIs.[70-73] Typical doses are 10mg to 20mg as needed or 30mg to 100mg daily in a divided dose. Potential side effects with bethanechol include diarrhea, cramps, and diaphoresis. No reports have evaluated or suggested the efficacy of bethanechol for treating SSRI-induced sexual side effects.

Gingko biloba is an herbal extract reported to reverse a variety of sexual dysfunctions associated with antidepressants. Information about gingko's ability in this regard is derived from the experience of 1 clinician presenting a large case series.[74] The response rate was greater than 80%, with doses ranging from 60mg twice daily to 120mg twice daily (mean daily dose, 207mg). Reported side effects include gastrointestinal upset, lightheadedness, and stimulation effects. Because gingko may inhibit platelet-activating factor, caution should be used in considering its use by any patient with a bleeding diathesis. The mechanism by which gingko might alleviate sexual dysfunction is unknown.

http://www.medscape.com/viewarticle/430614_5

четверг, 2 июля 2009 г.

Антидепрессанты короткого действия в терапии БАР с быстрой сменой фаз

"I have found that in bipolar patients with extreme diurnal variation of mood (characterized by severe a.m.-hour depression followed by significant brightening in the evening), the non-time-release preparations of medications, such as bupropion and venlafaxine, given in low doses in the a.m. hours only can be very helpful and less likely to cause manic switching. Conversely, the long-acting preparations of the same medications tend to cause a reversal of diurnal variation, with improvement in the a.m. hours and agitation in the p.m. hours. It might turn out that short half-life reuptake inhibitors have a place in treating bipolar depression. Other relatively short-acting agents, such as atomoxetine, may also fall into this category."

The Use of Short Half-Life Antidepressants in the Treatment of Bipolar Depression

вторник, 28 апреля 2009 г.

Seroquel, Wellbutrin Used For Highs In Prison

As I've reported before, Seroquel is often used by prisoners--and some civilians in the outside world--to get stoned in prison and apparently so too is Wellbutrin, the well-known anti-depressant. The Wellbutrin bit is news to me.

Things have gotten so out of hand in Santa Clara County, California that prison officials there have almost completely halted giving them to inmates and the state prison system in the state has followed suit.

Seriously, two of the top-selling psych meds in the world can be crushed and snorted to produce a high, or more of a low in Seroquel's case.

"Corrections officials throughout the country have long suspected that some inmates were either using the pills to get loaded, or "cheeking" them in order to later sell them to other prisoners to chop up and snort. Seroquel is an anti-psychotic that produces a hypnotic effect, and Wellbutrin is an antidepressant some liken to speed...."

"'It definitely goes on,' said John Madsen, secretary of the California Association of Alcoholism and Drug Abuse Counselors. 'Say someone is addicted to cocaine but can't get it. They'll try the next best thing. When it comes to drugs, addicts will find themselves doing just about anything.'"

Keep in mind that Seroquel is on the verge of gaining FDA approval for depression and anxiety, indications that would make the drug even more widely available than it already is and would inevitably lead to even more abuse in America.