The Pickle Jar

SuN

.:~**~.~**~.~**~:.
fuck u imageshack, that was some damn good gore :(
 

Seph

Retired Account
CUNTS !!! FTW!!!!
 

SuN

.:~**~.~**~.~**~:.
A type of impulse control disorder, pyromania is an impulse to deliberately start fires to relieve tension and typically includes feelings of gratification or relief afterward. Pyromania is distinct from arson, and pyromaniacs are also distinct from those who start fires because of psychosis, for personal, monetary or political gain, or for acts of revenge. Pyromaniacs start fires to induce euphoria, and often fixate on institutions of fire control like fire stations and firefighters.

Behavior modification is the usual treatment for pyromania. Other treatments include seeing the patient's actions as an unconscious process and analyzing to help the patient get rid of the behavior. Often, this treatment is followed by a more psychodynamic approach that addresses the underlying problems that generated the negative emotions causing the mania.
The prognosis for treatment is generally fair to poor. Treatment appears to work in 95% of children that exhibit signs of pyromania, which include family therapy and community intervention. Selective serotonin reuptake inhibitors (SSRIs) are also used to treat this condition. Studies have also shown there are therapeutic benefits associated with playing out the mania in a simulated environment.

Pyromania is a rare disorder, and the incidence of it is less than one percent in most studies; also, pyromaniacs are a very small proportion of psychiatric hospital admissions. Pyromania can occur in children as young as age three, but it is rare in adults and rarer in children. Only a small percentage of children and adolescents arrested for arson have pyromania. Ninety percent of those diagnosed with pyromania are male. Based on a survey of 9,282 Americans using the Diagnostic & Statistical Manual on Mental Disorders, 4th edition, impulse-control problems such as gambling, pyromania and compulsive shopping collectively affect 9% of the population. And a 1979 study by the Law Enforcement Assistance Administration found that only 14% of fires were started by pyromaniacs and others with mental illness.

Pyrophilia is a relatively uncommon paraphilia in which the patient derives gratification from fire and fire-starting activity. It is distinguished from pyromania by the gratification being of a sexual nature.
While the erotic focus immediately raises the diagnostic issue of pyromania, the Diagnostic and Statistical Manual of Mental Disorders IV classifies this disorder as an impulse-control disorder, with nothing to indicate or suggest an overlap between this disorder and the paraphilias.

Other than the purposeful act of fire-setting itself, there is no mention of the possibility that the tension or affective arousal experienced before the act; the fascination with, interest in, or attraction to fire and its situational contexts (for example, paraphernalia, uses, consequences); or the pleasure, gratification, or relief when setting, witnessing, or participating in the aftermath of fires might be sexual in nature or even contain a sexual arousal component.

Some described cases of pyrophilia do not include behaviors commonly associated with pyromania, such as being a regular “watcher” at fires in his neighbourhood; setting off false alarms; deriving pleasure from institutions, equipment, and personnel associated with fire, spending time at the local fire station, setting fires in order to be affiliated with the fire department; and either showing indifference to the consequences to life and property caused by the fire or deriving satisfaction from the resulting destruction of property. Sexual gratification need not involve actual fire; arousal or masturbatory aids may include fantasies or talk of setting a fire. In other instances, the patient may derive arousal primarily from setting or watching their fire.

Pyrophilia has been diagnosed in very few instances, and is not fully accepted by the general psychological community.
 

SuN

.:~**~.~**~.~**~:.
An acquired brain injury (ABI) is brain damage caused by events after birth, rather than as part of a genetic or congenital disorder. It usually affects cognitive, physical, emotional, social or independent functioning and can result from either traumatic brain injury (e.g. physical trauma due to accidents, falls, assaults etc.) or nontraumatic injury derived from either an internal or external source (e.g. stroke, brain tumours, infection, poisoning, hypoxia, ischemia, encephalopathy or substance abuse). Most definitions of ABI exclude neurodegenerative disorders.

Acquired brain injury is not to be confused with intellectual disability. People with a brain injury may have difficulty controlling, coordinating and communicating their thoughts and actions, but they retain their intellectual abilities. However, the intellectual abilities of a person with a brain injury are likely to be interfered with by the aforementioned thought coordination and communication difficulties, which can make it difficult for them to express themselves in a manner intelligible to others, which in turn might offer the perception of a damaged intelligence to others, even though such is not the case.

Fundamentally, our brains enable us to accomplish three things--to think, to move, and to feel. An acquired brain injury can disrupt cognitive processing, physical activity and social functioning.

–The ABI Handbook[1]

While research has demonstrated that thinking and behavior may be altered in virtually all forms of ABI, brain injury is itself a very complex phenomenon having dramatically varied effects.[1] No two persons can expect the same outcome or resulting difficulties. The brain controls every part of human life: physical, intellectual, behavioral, social and emotional. When the brain is damaged, some part of a person's life will be adversely affected. Even a mild injury can sometimes result in a serious disability that will interfere with a person’s daily functioning and personal activities for the rest of their life. Such interferences require a major life adjustment around the person's new circumstances, and making that adjustment is a critical factor in recovery and rehabilitation.[1] While the outcome of a given injury depends largely upon the nature and severity of the injury itself, appropriate treatment plays a vital role in determining the level of recovery.
 

SuN

.:~**~.~**~.~**~:.
Electroconvulsive therapy (ECT), also known as electroshock, is a well-established, albeit controversial, psychiatric treatment in which seizures are electrically induced in anesthetized patients for therapeutic effect. Today, ECT is most often used as a treatment for severe major depression which has not responded to other treatment, and is also used in the treatment of mania (often in bipolar disorder), and catatonia.[1] It was first introduced in the 1930s[2] and gained widespread use as a form of treatment in the 1940s and 1950s; today, an estimated 1 million people worldwide receive ECT every year,[3] usually in a course of 6–12 treatments administered 2 or 3 times a week.

Electroconvulsive therapy can differ in its application in three ways: electrode placement, length of time that the stimulus is given, and the property of the stimulus. The variance of these three forms of application have significant differences in both adverse side effects and positive outcomes. After treatment, drug therapy can be continued, and some patients receive continuation/maintenance ECT. Informed consent is a standard of modern electroconvulsive therapy.[4] Involuntary treatment is uncommon in countries that follow contemporary standards and is typically only used when the use of ECT is believed to be potentially life saving.

There is considerable variability in opinion among experts as to whether ECT is appropriate as a first-line treatment or if its use should be reserved for patients who have not responded to other interventions such as medication and psychotherapy.

The American Psychiatric Association (APA) 2001 guidelines give the primary indications for ECT among patients with depression as a lack of a response to, or intolerance of, antidepressant medications; a good response to previous ECT; and the need for a rapid and definitive response (e.g. because of psychosis or a risk of suicide). The decision to use ECT depends on several factors, including the severity and chronicity of the depression, the likelihood that alternative treatments would be effective, the patient's preference, and a weighing of the risks and benefits.

Some guidelines recommend that cognitive behavioral therapy or other psychotherapy should generally be tried before ECT is used. However, treatment resistance is widely defined as lack of therapeutic response to two antidepressants. The APA states that at times patients will prefer to receive ECT over alternative treatments, but commonly the opposite will be the case.

The APA ECT guidelines state that severe major depression with psychotic features, manic delirium, or catatonia are conditions for which there is a clear consensus favoring early reliance on ECT. The NICE guidelines recommend ECT for patients with severe depression, catatonia, or prolonged or severe mania.
The 2001 APA ECT guidelines say that ECT is rarely used as a first-line treatment for schizophrenia but is considered after unsuccessful treatment with antipsychotic medication, and may also be considered in the treatment of patients with schizoaffective or schizophreniform disorder. The 2003 NICE ECT guidelines do not recommend ECT for schizophrenia.

The NICE 2003 guidelines state that doctors should be particularly cautious when considering ECT treatment for women who are pregnant and for older or younger people, because they may be at higher risk of complications with ECT. The 2001 APA ECT guidelines say that ECT may be safer than alternative treatments in the infirm elderly and during pregnancy, and the 2000 APA depression guidelines stated that the literature supports the safety for mother and fetus, as well as the efficacy during pregnancy.

The 1999 U.S. Surgeon General's Report on Mental Health summarized psychiatric opinion at the time about the effectiveness of ECT. It stated that both clinical experience and published studies had determined ECT to be effective (with an average 60 to 70 percent remission rate) in the treatment of severe depression, some acute psychotic states, and mania. Its effectiveness had not been demonstrated in dysthymia, substance abuse, anxiety, or personality disorder. The report stated that ECT does not have a long-term protective effect against suicide and should be regarded as a short-term treatment for an acute episode of illness, to be followed by continuation therapy in the form of drug treatment or further ECT at weekly to monthly intervals.

A 2004 large multicentre clinical follow-up study of ECT patients in New York—describing itself as the first systematic documentation of the effectiveness of ECT in community practice in the 65 years of its use—found remission rates of only 30 to 47 percent, with 64 percent of those relapsing within six months.
ECT on its own does not usually have a sustained benefit. Virtually all those who remit end up relapsing within six months following a course, even when given a placebo.[14] The relapse rate in the first six months may be reduced by the use of psychatric medications or further ECT, but remains high.

Aside from effects in the brain, the general physical risks of ECT are similar to those of brief general anesthesia; the United States' Surgeon General's report says that there are "no absolute health contraindications" to its use.
Immediately following treatment the most common adverse effects are confusion and memory loss. The state of confusion usually disappears after a few hours.
Some patients experience muscle soreness after ECT. This is due to either the muscle relaxants given during the procedure or due to the muscle activity caused by the seizure.

Adverse effects

Aside from effects in the brain, the general physical risks of ECT are similar to those of brief general anesthesia; the United States' Surgeon General's report says that there are "no absolute health contraindications" to its use.[12] Immediately following treatment the most common adverse effects are confusion and memory loss. The state of confusion usually disappears after a few hours.[18][19] Some patients experience muscle soreness after ECT. This is due to either the muscle relaxants given during the procedure or due to the muscle activity caused by the seizure.[20]
[edit] Effects on memory

It is the effects of ECT on long-term memory that give rise to much of the concern surrounding its use.[21] The acute effects of ECT can include amnesia, both retrograde (for events occurring before the treatment) and anterograde (for events occurring after the treatment).[22] Memory loss and confusion are more pronounced with bilateral electrode placement rather than unilateral, and with sine-wave rather than brief-pulse currents. The vast majority of modern treatment uses brief pulse currents.[22] Research by Harold Sackeim has shown that excessive current causes more risk for memory loss, and shocking only the right side of the head protects the left side, which contains the brain's verbal structure.[23]

Retrograde amnesia is most marked for events occurring in the weeks or months before treatment, with one study showing that although some people lose memories from years prior to treatment, recovery of such memories was "virtually complete" by seven months post-treatment, with the only enduring loss being memories in the weeks and months prior to the treatment.[24][25] Anterograde memory loss is usually limited to the time of treatment itself or shortly afterwards. In the weeks and months following ECT these memory problems gradually improve, but some people have persistent losses, especially with bilateral ECT.[9][22] One published review summarized the results of seven studies reporting on perceived memory loss and found that between 29% and 55% of respondents believed they experienced long-lasting or permanent memory changes.[26] In 2000, American psychiatrist Sarah Lisanby and colleagues found that bilateral ECT left patients with persistent impairment for memory of public events as compared to RUL ECT.[21]

Studies have found that patients are often unaware of substantial cognitive deficits induced by ECT.[27][28] For example, in June 2008, a Duke University study[27] was published assessing the neuropsychological effects and attitudes in patients after ECT. Forty-six patients participated in the study, which involved neuropsychological and psychological testing before and after ECT. The study documented substantial cognitive decline after ECT on a variety of memory tests, including "verbal memory for word lists and prose passages and visual memory of geometric designs." The study further found that a significant number of patients erroneously believed that their memory had improved after ECT despite the fact that neuropsychological testing clearly showed the opposite. As stated by the researchers, "Indeed, there was a slight trend towards [patients reporting] improved memory functioning, despite the objective neuropsychological data indicating significantly lower recognition and delayed recall." Based on their findings, the authors issued the following recommendation:

"When ECT is provided to adolescents, the potential impact of such cognitive changes should be discussed with the patients and their parents or guardians in terms of implications for not only the patient’s emotional functioning but cognitive functioning as well, particularly upon his or her academic performance. In summary, we argue that an individual cost-benefit analysis should be made in light of the implications of the potential benefits versus costs of ECT upon improving emotional functioning and the impact that potential memory changes may have on real-world functioning and quality of life."[27]

[edit] Controversy over long-term effects on general cognition

According to prominent ECT researcher Harold Sackeim, "despite over fifty years of clinical use and ongoing controversy", until 2007 there had "never been a large-scale, prospective study of the cognitive effects of ECT."[29] In this first-ever large-scale study (347 subjects), Sackeim and colleagues found that at least some forms (namely bilateral application and sine wave currents) of ECT "routine[ly]" lead to "adverse cognitive effects," including global cognitive deficits and memory loss, that persist for at least six months after treatment, suggesting that the induced deficits may be permanent.[29][30] The authors also warned that their findings did not suggest that right-unilateral ECT did not also lead to chronic cognitive deficits.

Harold Sackeim can be seen in a videotaped deposition briefly discussing the findings of this study and why, in his opinion, earlier studies had failed to find evidence of long-term harm from ECT.[31] Despite over fifty years of clinical use, Sackeim states that prior to 2001, "the field itself never really had an opportunity to have a discussion about patients who have complaints about long-term memory loss." In this video clip, Sackeim also reveals that at a California ECT conference with 200 practitioners present, when polled as to whether they think ECT can lead to chronic cognitive deficits, two-thirds raised their hands. Sackeim says this was "almost a watershed moment for the field", and was the "first time publicly that the field itself said 'no' to the position that it can't happen."[31][32]

In July 2007, a second study was published concluding that ECT routinely leads to chronic, substantial cognitive deficits, and the findings were not limited to any particular forms of ECT.[33] The study, led by psychiatrist Glenda MacQueen and colleagues, found that patients treated with ECT for bipolar disorder show marked deficits across multiple cognitive domains. According to the researchers, "Subjects who had received remote ECT had further impairment on a variety of learning and memory tests when compared with patients with no past ECT. This degree of impairment could not be accounted for by illness state at the time of assessment or by differential past illness burden between patient groups." Despite the findings of chronic, global cognitive deficits in post-ECT patients, MacQueen and colleagues suggest that it is "unlikely that such findings, even if confirmed, would significantly change the risk–benefit ratio of this notably effective treatment."[33]

Six months after the publication of the Sackeim study[29] documenting routine, long-term memory loss after ECT, prominent ECT researcher Max Fink published a review in the journal Psychosomatics concluding that patient complaints of memory loss after ECT are "rare" and should be "characterized as somatoform disorders, rather than as evidence of brain damage, thus warranting psychological treatment for such disorders."[34] Based on his findings, Fink suggests that, "Instead of endorsing these reports as the direct consequence of ECT, especially in patients who have recovered from their depressive illness, lost their suicidal drive, and have improved social functioning, is it not more useful to accept the complaint as a somatoform disorder, explore the basis in the individual’s history and experience, and offer appropriate supportive treatment?"[34]

Most recent reviews of the literature and other articles continue to characterize ECT as safe and effective.[35][36][37][38][39][40][41][42] For example, in June 2009, Portuguese researchers published a review on the safety and efficacy of ECT in an article entitled, Electroconvulsive Therapy: Myths and Evidences.[35] In their review, the researchers conclude that ECT is an "efficient, safe and even life saving treatment for several psychiatric disorders." In 2008, Yale researchers published a review on the safety and efficacy of ECT in elderly patients.[42] According to the authors, "ECT is well established as a safe and effective treatment for several psychiatric disorders." And in a June 2009 article published in the Journal of ECT, Iranian researchers observe that, "Despite the wide consensus over the safety and efficacy of electroconvulsive therapy (ECT), it still faces negative publicity and unfavorable attitudes of patients and families."[41]

Psychiatrist Peter Breggin, chief editor of the journal Ethical Human Psychology and Psychiatry, is a leading critic of ECT who believes the procedure is neither safe nor effective. In a published article reviewing the findings of Harold Sackeim's 2007 study[29] on the cognitive effects of ECT, Breggin accuses Max Fink and other pro-ECT researchers of having a history of "systematically covering up damage done to millions of [ECT] patients throughout the world."[30] He disagrees with the position that findings of chronic, global cognitive deficits should have no bearing on the risk-benefit ratio of ECT, and he believes it's important to address the "actual impact of these losses on the lives of individual patients." In a section of his paper entitled Destroying Lives, Dr. Breggin writes, "Even when these injured people can continue to function on a superficial social basis, they nonetheless suffer devastation of their identities due to the obliteration of key aspects of their personal lives. The loss of the ability to retain and learn new material is not only humiliating and depressing but also disabling. Even when relatively subtle, these activities can disrupt routine activities of living."[30]

A study published in 2004 in the Journal of Mental Health reported that 35 to 42% of patients said ECT resulted in loss of intelligence.[43] The study also reported, "There is no overlap between clinical and consumer studies on the question of benefit."

A recent article by a neuropsychologist and a psychiatrist in Dublin suggests that ECT patients who experience cognitive problems following ECT should be offered some form of cognitive rehabilitation. The authors say that the failure to attempt to rehabilitate patients may be partly responsible for the negative public image of ECT.[44]
[edit] Effects on brain structure

Considerable controversy exists over the effects of ECT on brain tissue despite the fact that a number of mental health associations, including the American Psychiatric Association, have concluded that there is no evidence that ECT causes structural brain damage.[8][45][20] A 1999 report by the United States Surgeon General states, "The fears that ECT causes gross structural brain pathology have not been supported by decades of methodologically sound research in both humans and animals".[5] However, not all experts agree that ECT does not cause brain damage, and two studies have been published since 2007 finding that at least some forms of ECT may result in widespread, persisting, generalized cognitive dysfunction, which would seem to support claims that ECT causes brain damage.[29][33][46]

A leading critic of ECT, psychiatrist Peter Breggin has published books and reviews of the literature purporting to show that ECT routinely causes brain damage as evidenced by a considerable list of studies in humans and animals.[47] In particular, Dr. Breggin asserts that animal and human autopsy studies have shown that ECT routinely causes ‘widespread pinpoint hemorrhages and scattered cell death.’[46] According to Dr. Breggin, the 1990 APA task force report on ECT ignored much of the scientific literature pointing out the negative effects of electroshock therapy. For example, in 1952 Hans Hartelius conducted and published an animal study on cats entitled Cerebral Changes Following Electrically Induced Convulsions in which a double-blind microscopic pathology examination showed that it was possible to distinguish the 8 shocked animals from the 8 non-shocked animals with remarkable accuracy based on statistically significant structural changes to the brain, including vessel wall changes, gliosis, and nerve cell changes. Based on the detection of shadow cells and neuronophagia, Hartelius determined that there was irreversible damage to neurons associated with electroshock.[46]

Proponents argue that the addition of hyperoxygenation and refinement in technique in the last thirty years has made ECT safe, and a majority of published reviews in recent decades have reflected this position.[48] In a 2004 study designed to evaluate whether modern ECT techniques lead to identifiable brain damage, twelve monkeys underwent daily electroshock for six weeks under conditions meant to simulate human ECT; the animals were then sacrificed and their brains were compared to monkeys undergoing anesthesia alone. According to the researchers, "None of the ECT-treated monkeys showed pathological findings."[49]

There are recent animal studies that have documented significant brain damage after an electroshock series. For example, in 2005, Russian researchers published a study entitled, Electroconvulsive Shock Induces Neuron Death in the Mouse Hippocampus: Correlation of Neurodegeneration with Convulsive Activity. In this study, the researchers found that after an electroshock series, there was a significant loss of neurons in parts of the brain and particularly in defined parts of the hippocampus where up to 10% of neurons were killed. The researchers conclude that "the main cause of neuron death is convulsions evoked by electric shocks."[50] In 2008, Portuguese researchers conducted a rat study aimed at answering the question of whether an electroshock series causes structural changes in vulnerable parts of the brain.[51] According to the authors, "This study answers positively the question of whether repeated administration of ECS seizures can cause brain lesions. Our data are consistent with findings from other animal models and from human studies in showing that neurons located in the entorhinal cortex and in the hilus of the dentate gyrus are particularly vulnerable to repeated seizures."

Many expert proponents of ECT maintain that the procedure is safe and does not cause brain damage. Dr. Charles Kellner, a prominent ECT researcher and former chief editor of the Journal of ECT states in a recent published interview that, "There are a number of well-designed studies that show ECT does not cause brain damage and numerous reports of patients who have received a large number of treatments over their lifetime and have suffered no significant problems due to ECT."[52] Dr. Kellner cites specifically to a study purporting to show an absence of cognitive impairment in eight subjects after more than 100 lifetime ECT treatments.[53] One of the authors of the cited study, Harold Sackeim, published a large-scale study less than a month after this interview concluding that the type of ECT used in the eight patients receiving the 100 lifetime treatments, bilateral sine wave, routinely leads to persistent, global cognitive deficits[29] (discussed supra). Dr. Kellner states that, "Rather than cause brain damage, there is evidence that ECT may reverse some of the damaging effects of serious psychiatric illness."[52]
[edit] Effects in pregnancy

If steps are taken to decrease potential risks, ECT is generally accepted to be relatively safe during all trimesters of pregnancy, particularly when compared to pharmacological treatments.[54][55][56] Suggested preparation for ECT during pregnancy includes a pelvic examination, discontinuation of nonessential anticholinergic medication, uterine tocodynamometry, intravenous hydration, and administration of a nonparticulate antacid. During ECT, elevation of the pregnant woman's right hip, external fetal cardiac monitoring, intubation, and avoidance of excessive hyperventilation are recommended.[54] Much of the medical literature in this area is composed of case studies of single or twin pregnancies, and although some have reported serious complications,[57][58] the majority have found ECT to be safe.[59] ECT is not performed on the fetus.
[edit] Administration

Informed consent is sought before treatment. Patients are informed about the risks and benefits of the procedure. Patients are also made aware of risks and benefits of other treatments and of not having the procedure done at all. Depending on the jurisdiction the need for further inputs from other medical professionals or legal professionals may be required. ECT is usually given on an in-patient basis. Prior to treatment a patient is given a short-acting anesthetic such as methohexital, propofol, etomidate, or thiopental,[9] a muscle relaxant such as suxamethonium (succinylcholine), and occasionally atropine to inhibit salivation.

Both electrodes can be placed one on the same side of the patient's head. This is known as unilateral ECT. Unilateral ECT is used first to minimize side effects (memory loss). When electrodes are placed on both sides of the head, this is known as bilateral ECT. In bifrontal ECT, an uncommon variation, the electrode position is somewhere between bilateral and unilateral. Unilateral is thought to cause fewer cognitive effects than bilateral but is considered less effective.[9] In the USA most patients receive bilateral ECT.[60] In the UK almost all patients receive bilateral ECT.[61]

The electrodes deliver an electrical stimulus. The stimulus levels recommended for ECT are in excess of an individual's seizure threshold: about one and a half times seizure threshold for bilateral ECT and up to 12 times for unilateral ECT.[9] Below these levels treatment may not be effective in spite of a seizure, while doses massively above threshold level, especially with bilateral ECT, expose patients to the risk of more severe cognitive impairment without additional therapeutic gains.[62] Seizure threshold is determined by trial and error ("dose titration"). Some psychiatrists use dose titration, some still use "fixed dose" (that is, all patients are given the same dose) and others compromise by roughly estimating a patient's threshold according to age and sex.[60] Older men tend to have higher thresholds than younger women, but it is not a hard and fast rule, and other factors, for example drugs, affect seizure threshold.

There is wide variation in ECT use between different countries, different hospitals, and different psychiatrists.[9] International practice varies considerably from widespread use of the therapy in many western countries to a small minority of countries that do not use ECT at all, such as Slovenia.[64] Guidelines on the use of ECT are stringent in the USA and the UK. Modern standards are not always followed throughout the world and not all countries that use ECT have written technical standards. The use of both anesthesia and muscle relaxants is universally recommended in the administration of ECT. If anesthesia and muscle relaxants are not used the procedure is called unmodified ECT. In a minority of countries such as Japan,[65] India,[66] and Nigeria,[67] ECT may be used without anesthesia. WHO has called for a worldwide ban on unmodified ECT and the topic is currently being debated in countries like India. The practice has been recently abolished in Turkey's largest psychiatric hospital.[68] A major difficulty for developing countries in eliminating unmodified ECT is a lack of trained anesthesiologists available to administer the procedure.[69] A small minority of countries never seek consent before administering ECT. This significantly uneven application of ECT around the world continues to make ECT a controversial procedure.
United States
In the USA, a survey of psychiatric practice in the late 1980s found that an estimated 100,000 people received ECT annually, with wide variation between metropolitan statistical areas.[71] Accurate statistics about the frequency, context and circumstances of ECT in the United States are difficult to obtain because only a few states have reporting laws that require the treating facility to supply state authorities with this information.[72] One state which does report such data is Texas, where in the mid-1990s ECT was used in about one third of psychiatric facilities and given to about 1,650 people annually.[10] Usage of ECT has since declined slightly; in 2000–01 ECT was given to about 1,500 people aged from 16 to 97 (in Texas it is illegal to give ECT to anyone under sixteen).[73] ECT is more commonly used in private psychiatric hospitals than in public hospitals, and minority patients are underrepresented in the ECT statistics.[9] In the United States, ECT is usually given three times a week; in the UK, it is usually given twice a week.[9] Occasionally it is given on a daily basis.[9] A course usually consists of 6–12 treatments, but may be more or fewer. Following a course of ECT some patients may be given continuation or maintenance ECT with further treatments at weekly, fortnightly or monthly intervals.[9] A few psychiatrists in the USA use multiple-monitored ECT (MMECT) where patients receive more than one treatment per anesthetic.[9] As of 2007, electroconvulsive therapy practice is not officially regulated in the USA, and the education of physicians in its prescription and administration has been described[citation needed] as poor. Electroconvulsive therapy is not a required subject in US medical schools and not a required skill in psychiatric residency training. Privileging for ECT practice at institutions is a local option, no national certification standards are established, and no ECT-specific continuing training experiences are required of ECT practitioners.[74]
United Kingdom
Eighty-one percent had a diagnosis of mood disorder; schizophrenia was the next most common diagnosis. Sixteen percent were treated without their consent.[77] In 2003, the National Institute for Clinical Excellence, a government body which was set up to standardize treatment throughout the National Health Service, issued guidance on the use of ECT. Its use was recommended "only to achieve rapid and short-term improvement of severe symptoms after an adequate trial of treatment options has proven ineffective and/or when the condition is considered to be potentially life-threatening in individuals with severe depressive illness, catatonia or a prolonged manic episode".The NICE guidance, as the British Medical Journal editorial points out, is only a policy statement and psychiatrists may deviate from it if they see fit. Adherence to standards has not been universal in the past. A survey of ECT use in 1980 found that more than half of ECT clinics failed to meet minimum standards set by the Royal College of Psychiatrists, with a later survey in 1998 finding that minimum standards were largely adhered to, but that two-thirds of clinics still fell short of current guidelines, particularly in the training and supervision of junior doctors involved in the procedure.[81] A voluntary accreditation scheme, ECTAS, was set up in 2004 by the Royal College, but as of 2006 only a minority of ECT clinics in England, Wales, Northern Ireland and the Republic of Ireland have signed up.
It is widely acknowledged internationally that obtaining the written, informed consent of the patient is important before ECT is administered. The World Health Organization, in its 2005 publication "Human Rights and Legislation WHO Resource Book on Mental Health," specifically states, "ECT should be administered only after obtaining informed consent."[84]
To demonstrate what he believes should be required to fully satisfy the legal obligation for informed consent, one psychiatrist, working for an anti-psychiatry organisation, has formulated his own consent form[85] using the consent form developed and enacted by the Texas Legislature as a model.[86]

In the UK, in order for consent to be valid it requires an explanation in "broad terms" of the nature of the procedure and its likely effects.[87] One review from 2005 found that only about half of patients felt they were given sufficient information about ECT and its adverse effects,[88] and another survey found that about fifty percent of psychiatrists and nurses agreed with them.[89]
 

SuN

.:~**~.~**~.~**~:.
[YOUTUBE]<object width="480" height="385"><param name="movie" value="http://www.youtube.com/v/yI0_w9aV8G0&hl=en_US&fs=1&color1=0x402061&color2=0x9461ca"></param><param name="allowFullScreen" value="true"></param><param name="allowscriptaccess" value="always"></param><embed src="http://www.youtube.com/v/yI0_w9aV8G0&hl=en_US&fs=1&color1=0x402061&color2=0x9461ca" type="application/x-shockwave-flash" allowscriptaccess="always" allowfullscreen="true" width="480" height="385"></embed></object>[/YOUTUBE]
 
Top