Ritalin is a heavily prescribed (and even more heavily abused) amphetamine based drug normally prescribed in the treatment of ADD/ADHD amongst a great many others.

And whilst I’m no doctor or pharmacist, I have read a great deal into the workings of how it affects the human body, and how it works has no resemblence at all, to how Provigil works.

Whilst Cephalon have been very quiet regarding how Provigil works, its not said to be a big user of “dopamine” receptors in the brain;

The ‘mechanics’ behind giving us a “high”.

Ritalin tweaks these dopamine receptors to such a degree, the consumer can feel jittery when the drug is wearing off, as the body’s dopamine supply is used & exhausted.

Dependence
In people with an addictive personality this can quickly lead to dependence as the user tries to feel better by taking more amphetamine.

But as Provigil pays little or no attention to the dopamine receptors, there are no jitters when the drug wears off, leading to a far more ‘user-friendly’ experience.

For more information, or to ask any questions you may have regarding Provigil/Modafinil, check out the new Facebook group by clicking here .

http://www.provigil-rx.info

The Ultimate Provigil/Modafinil Information Resource – Buy generic provigil today. Order with confidence!!

An autoimmune component has been long suspected in narcolepsy, leading in the mid-1980s to a Japanese study which associated narcolepsy with a specific immune system marker.

In a 1998 breakthrough, narcolepsy was tied to the loss of brain cells located in the hypothalamus that produce the hypocretin neurotransmitters, further implicating the immune system.

This latest discovery moves us closer to understanding what causes this cell destruction.

The article, “Narcolepsy is strongly associated with the T-cell receptor alpha locus,” published in Nature Genetics earlier this week, details the work of a prestigious team of international researchers led by Emmanuel Mignot, MD PhD, Director of Stanford University’s Center for Narcolepsy and Chair of Narcolepsy Network’s Medical Advisory Board. “At last, we now know for sure narcolepsy involves the immune system,” Dr. Mignot says.

Through research spanning several continents and involving three distinct ethnic groups, a tight association has now been found between narcolepsy and a genetic mutation in the “T-cell receptor alpha locus,” a region on human chromosome 14. T-cells are the immune system’s vehicle for identifying and attacking foreign bodies such as bacteria and viruses. In an auto-immune disorder, these cells may mistakenly attack the body’s own cells. Further research is needed to determine the precise role of this mutation in the development of narcolepsy.

Narcolepsy is an often misunderstood and debilitating sleep disorder characterized by excessive daytime sleepiness, overpowering sleep attacks and fragmented nighttime sleep. It also includes the REM-related symptoms of cataplexy – a loss of muscle tone triggered by sudden emotional stimuli, which is unique to narcolepsy – and hallucinations and/or sleep paralysis upon falling asleep and/or waking. Symptoms vary in number and severity from one person to another, as does response to available treatments. For some, narcolepsy is mildly inconvenient. For others, it can be disabling.

People with narcolepsy greet each new development with renewed hope for the future.

The first-line medications for treating the symptoms of narcolepsy (Provigil and Xyrem) have only become available within the past decade or so. While they have significantly improved the quality of life for many, patients may still experience limiting residual symptoms. As awareness of narcolepsy grows both in the public arena and within the medical community, time to diagnosis is decreasing. As a result, the narcolepsy patient population includes an increasingly higher percentage of children, adolescents and young adults. Patricia Duffin Higgins, RN, President of Narcolepsy Network, says “It is especially for these young people that we must keep alive hope for the development of more effective treatment options and if not a cure, at least the ability to identify those at risk for developing narcolepsy and the means to prevent it in future generations. Dr Mignot gives us that hope: This [latest finding] is opening the door for preventive therapies.”

“People with narcolepsy are so very fortunate to have cutting-edge researchers committed to solving the mysteries of our disorder. It is no surprise to us that this latest finding provides a new and novel model for research in over 100 other unsolved immune-related disorders,” Higgins states. Narcolepsy Network strongly encourages its members to participate in research studies and has facilitated several events over the past two years at which participants were able to donate blood for this and other DNA studies.

Narcolepsy Network is a non-profit patient support organization representing all Americans with narcolepsy as well as the less common diagnosis of idiopathic hypersomnia (excessive sleepiness of unknown origin). Narcolepsy is a life-long disorder, with symptoms usually presenting in adolescence, and diagnosis often delayed until the second or third decade. Even with treatment, narcolepsy limits patients in many all aspects of life.

- – - -

CONTACT: Eveline Honig, MD MPH

Executive Director

Narcolepsy Network

914-741-5680

ehonig@narcolepsynetwork.org

“I was conscious, but I couldn’t move,” remembers the mum-of-three. “The one bonus was that the entire Cambridge United squad were in there, back in the days when Dion Dublin was on the team.

They waited with me until the ambulance came: all the other girls were jealous!”

The collapse was, explains Louise, a symptom of narcolepsy – a rare and chronic sleep disorder. Affecting an estimated five in every 10,000 people, it’s a neurological condition which causes a wide range of disabling symptoms (everything from extreme fatigue to cataplexy, sudden loss of muscle control).

Diagnosed when she was just 19, Louise has battled narcolepsy all her adult life.

She relies on daily amphetamines – between six and eight tablets a day – to keep her going. And there is no cure.

“You learn to live with these things,” explains Louise, 39. “You have to really, don’t you? And I always said I wouldn’t let narcolepsy get the better of me.

“You have to live your life and make the most of every day. And I’ve got lots to be grateful for – like my three lovely sons.”

Louise first showed signs of narcolepsy in her mid to late teens. Fidgety at school, she admits it was hard to concentrate in class. And, exhausted, she often spent most of the weekend in bed. By the time she got her first job, aged 17, Louise was feeling drowsy almost all the time; as soon as she got home at night, she’d be out like a light.

“Sometimes I’d go to bed on a Friday and literally couldn’t get out of bed all weekend,” she remembers. “My parents would say ‘How can you be so lazy?’ – they got really cross. I lost friends over it too:

when they came to collect me for a night out I was never ready, because I’d have fallen asleep on my bed. “And I noticed that, when I was at work, my writing sometimes started to trail off; it looked like a child’s writing. I knew there was something wrong. And I wasn’t going to give up until I’d found out what it was.”

Referred to Addenbrooke’s, Louise was tested for all kinds of things, from anaemia to hormone imbalance. But, for a whole year and a half, doctors couldn’t get to the bottom of her problems. “You start to think you’re being a div, that you’re going barmy,” admits Louise.

It wasn’t until she had her first cataplexic episode – when her mouth began to twitch uncontrollably – that everyone began to take Louise seriously.

“My mum actually thought I was having a stroke,” she adds.

Then, after a consultation with a student doctor, narcolepsy was diagnosed.

“They did a tissue typing test which confirmed it,” Louise explains. “It was a bit scary; I’d never even heard of this thing. But, more than anything, it was a relief – a relief to finally know what was wrong.”

Sent to a London hospital, for a further two weeks of tests, Louise then started medication: first a herbal caffeine supplement and then, when that failed, amphetamines – the primary ingredient in Ecstasy. “I’ve been taking them for 20 years now,” she says. “They’re Class A drugs, basically. But they enable me to live a normal life.”

Taking up to eight amphetamines a day means the Cambridge mum is awake – and on the go – from dawn until dusk. There are, she says, certain side-effects, such as early morning palpitations. But without the pills, Louise would struggle to keep her eyes open.

When the drugs wear off, in the evening, she becomes instantly drowsy. “Who else do you know that falls asleep eating their dinner?” asks Louise, laughing. “My head just drops and I end up with my chin in gravy or tomato sauce . . .

“While the kids are awake, I’m awake. I manage by being constantly on the go: I can’t sit down to watch telly, not even EastEnders, because I just fall asleep. So I do the cleaning, do a bit of decorating . . .

“The sad thing is that whenever I do get time to myself I can’t enjoy it – I’m asleep.

I can’t have a nice hot bath, or paint my nails, or call my friends on the phone in the evening. The last time I went to the cinema was when I was 15.”

Louise says her health was at its worst when Aaron, her eldest son, was tiny.

Living alone, a young single mum, her drug regime wasn’t working properly; suffering from exhaustion, she developed what she describes as “automatic behaviour”.

Absentmindedly, she did all kinds of things – from putting laundry in the freezer to, on one memorable occasion, drinking bleach. “I burned my mouth, it was horrible,” she remembers. “That was quite scary.”

Since then, medication has helped bring Louise’s condition under far better control. And Aaron, now 15, is, she says, a great source of support. “When I nod off over dinner he’ll wake me up,” laughs Louise.

Louise went on to have two more boys with her current partner: Lee, eight, and Jay, two. She had to stay on her meds throughout all her pregnancies which was, she admits, a real worry; after two decades on amphetamines, Louise says she could be at risk of an enlarged heart herself (and has just had a scan which, thankfully, pronounced her fit and well).

“Without the pills I wouldn’t be able to function really,” continues Louise. “I wouldn’t be able to look after the kids, because I wouldn’t be able to stay awake.”

Lee has ADHD (attention defecit and hyperactivity disorder), meaning he has behavioural problems and is always incredibly active. It’s a challenge for any mum; for Louise it can be totally debilitating.

Thanks to her medication, Louise can drive. But she refuses to get behind the wheel in the evening, because that’s when her pills wear off – and the inevitable drowsiness kicks in. “I know what could happen,” adds Louise. “And there is no way I’d put my kids and other people at risk.”

As well as taking the pills, Louise has learned to manage her condition, within reason, herself. She steers clear of warm, dark environments, which are more likely to lull her to sleep.

And she can pretty much control the cataplexy, which is triggered by emotions, such as anger or amusement. As soon as Louise detects an attack (usually thanks to a tingling sensation) she removes herself from the source of the emotion – and mentally calms herself down.

Although she had to quit work in her early 20s because of her illness, Louise has always been keen to do voluntary jobs:

until a couple of years ago, she was city councillor for King’s Hedges.

“I am proud of that,” she adds. “But I’m a real believer in getting on with things.

Either you get out there and live your life, or you spend it sitting on the sidelines.”

http://www.cambridge-news.co.uk

The gene has a known role in the immune system, which strongly suggests that autoimmunity, in which the immune system turns against the body’s own tissues, plays an important role in the disorder.

“The link between narcolepsy and autoimmunity was proposed decades ago, but efforts to verify it have failed repeatedly.

Current findings leave little doubt that autoimmunity plays a role,” says Merrill Mitler, Ph.D., a program director with the National Institute of Neurological Disorders and Stroke (NINDS).

The study was funded principally by NINDS, with additional support from the National Institute of Mental Health (NIMH), the National Heart, Lung and Blood Institute (NHLBI), and the National Institute of Allergy and Infectious Diseases (NIAID), all components of NIH.

The new study, which appears today in Nature Genetics, focused on narcolepsy with cataplexy – a sudden loss of muscle tone that can cause a person to collapse, with or without falling asleep.

About 1 in 2,000 Americans have narcolepsy-cataplexy. The symptoms of narcolepsy-cataplexy have been shown to result from the death of a small group of brain cells that normally regulate the sleep-wake cycle by releasing chemicals called hypocretins.

Genetic and environmental factors both clearly play a role in narcolepsy-cataplexy. Until now, the best evidence for autoimmunity as a cause of the disorder was the discovery that nearly everyone with the disorder has unique variants of a gene called HLA-DQB1*0602. This is one of the genes that encodes HLA proteins, which dot the surface of the body’s cells and help the immune system identify foreign proteins. Some researchers theorize that the HLA variants found in people with narcolepsy-cataplexy predispose them to an autoimmune reaction that destroys their hypocretin-producing cells.

There are gaps in that theory, however, says Emmanuel Mignot, M.D., Ph.D., director of the Center for Narcolepsy at Stanford University School of Medicine in Palo Alto, Calif., and a Howard Hughes Medical Institute investigator. Dr. Mignot discovered the link between narcolepsy and the hypocretins, and helped establish the link to the HLA system. HLA proteins are found in many tissues including the brain, where they may affect brain development, he says.

HLA variations, however, do not fully account for narcolepsy-cataplexy. Dr. Mignot led a genome-wide association study to search for other genes associated with narcolepsy-cataplexy. These studies involve scanning the genome – the entire set of DNA – for small differences between people who have a disorder and people who do not. Dr. Mignot’s study included more than 4,000 individuals, all of whom had the HLA variants that predispose to narcolepsy-cataplexy but only about half of whom had the disorder. Participants were recruited so that many genetic groups were represented. Subjects were from the United States and eight countries in Europe and Asia; hundreds were African-American, Korean, and Japanese, groups known to have a high incidence of the disorder.

The researchers discovered that in addition to unique HLA variants, people with narcolepsy-cataplexy are also more likely to have unique variants of the TCRA gene, which encodes a receptor protein on the surface of T cells. T cells are the mobile infantry of the immune system. In concert with the HLA proteins, the T cell receptor enables T cells to recognize and attack foreign invaders, such as bacteria and viruses. Changes to the T cell receptor could increase the likelihood that the cells will direct their attack against the body.

The findings of Dr. Mignot’s group indicate that narcolepsy-cataplexy is linked to autoimmunity and involves T-cells. The research could lead to new approaches to prevention and treatment. One possibility may be preventing the disorder by stopping the effects of the autoimmune process. “If we can define the changes in the T cell receptor associated with narcolepsy-cataplexy, we might be able to develop drugs that block the protein’s abnormal activity and prevent the onset of the disorder,” says Dr. Mignot. Current treatments such as stimulant drugs for combating daytime sleepiness and antidepressants for cataplexy are only able to control symptoms, and do not address the underlying loss of hypocretin cells.

It is important to note that this study, like most genome-wide association studies, did not identify genetic variants that directly cause narcolepsy-cataplexy. Instead it identifies groups that are more likely to show narcolepsy-cataplexy and groups that are less likely to show the disorder. In people with the HLA variants that predispose to narcolepsy-cataplexy, there is about a 20-fold higher frequency of the disorder if variants in the TCRA gene are present. It is yet to be known which people with the genetic variants will go on to develop narcolepsy-cataplexy.

Other risk factors for narcolepsy-cataplexy remain to be discovered, and Dr. Mignot’s findings could provide clues to their identity. For example, further studies to characterize the T cells in people with narcolepsy-cataplexy could help reveal whether specific environmental factors – such as infections – contribute to the disorder. Dr. Mignot’s findings also could lead to a better understanding of other autoimmune diseases where HLA genes are known to play a role, such as multiple sclerosis and type 1 diabetes.

http://www.hindu.com/

Apparently, offender numbers have shown a marked rise over the last four years even though according to the governments own board of expert advisors, cannabis use has dropped since it was intially declassified to a class C substance back in 2004. Confused?

According to the government, this rise in offences is due to how the police were able to deal with people found in possession of cannabis under the new class C category. Which begs the question; what difference does that make exactly?

Of course the real reason cannabis enforcement is higher than it has been for many years is as a result of the public relations campaign the government have undertaken in the run up to the ill-advised reclassification which took place in January of 2009.

Lets face it if you influence a nations press to write about wellington boots every day for two years at the end of the campaign wellington boot sales are going to be showing a healthy up-turn. Its not called public relations for nothing. Just ask Julie Myerson.

So its fair to assume with all of the news coverage regarding prescription drugs such as narcolepsy treatment Provigil and ADD treatment Ritalin, its fair to assume the same thing is going to happen. The numbers of people who are using these drugs, (and who are finding themselves in trouble for doing so illegally, or ‘off-label’ as our American cousins quaintly like to call it) is going to increase.

At the top of the pile currently is the anti-narcoleptic Provigil, made by US pharmaceutical giant Cephalon. A company which employs around 3000 employees and is said to be worth just under $5 billion US dollars, and on a personal note its worth mentioning I didn’t even know what Provigil was until two weeks ago, and now I really want some.

Cephalon has been in the news recently regarding a number of patent disputes, after a number of smaller pharma’s decided to create their own versions of Cephalon’s brain drug Provigil (generic name Modafinil).

In 2003 Cephalon took a number of these drug companies to court over patent infringements. Surprisingly Cephalon was unsuccessful and had to negotiate outside of the courts. In a bid to recoup some of their losses from Modafinil, Cephalon instigated a number of licensing deals to cover future manufacture of a drug which was being marketed so aggressively even the US military was buying it in by the container load in a bid to keep its exhausted fighter pilots in the air.

From this point forth the marketing ‘focus’ was moved from being an anti-narcoleptic, to being a “stay awake” mood brightener, and in 2007 the company was hit with an intoxicating fine of $425 million dollars for illegal marketing practices relating to off-label promotion of modafinil, (there’s that term ‘off-label’ again).

Today Provigil/Modafinil continues to dominate the prescription drug news, and for a number of different reasons.

On the one hand we hear of students, doctors, truck drivers etc. Anyone in fact who works long hours or night-shifts, visiting their doctor and asking for Provigil for their ‘narcolepsy’. Apparently all it takes is a straight face while you ask for it, and your wish is my command. Or rather your doctors command.

Provigil/Modafinil is being prescribed by the truck load, and even the driver of the truck delivering it is most-likely on Provigil too.

But the whole distasteful saga has taken something a sinister turn of late.

From being hailed as a wonder drug on its creation, it now appears all of those students and truckers merrily crunching Provigil tic-tacs in between chain-drinking cups of espresso, may be getting addicted.

To a drug which was supposed not to affect the part of the brain involved in the reward-chain? How does that work?

The big marketing angle for Provigil was the fact it tip-toed around the brains dopamine receptors, where as other stimulants such as Methylphenidate, AKA hard-assed amphetamine based ADD/ADHD treatment Ritalin, stamped all over the dopamine receptors with hobnail boots on, giving the user the uncomfortable ‘crash landing’ as they came down off their 48 hour drug-induced stay-awake-athon.

Anyone who has overdosed on strong coffee whilst going without sleep will know the feeling of getting ‘the jitters’ all too well.

But now it appears all that good news which was released on the initial release of provigil, could well have been wrong. So much for clinical trials.

But not to worry, because as luck would have Cephalon is about to bring a new, safer drug to market, called Nuvigil, and at this stage if you can see a pattern forming here, have another cup of coffee to reward yourself, and read on.

Nuvigil, (generic name Amodafinil) is a new flavour of Provigil which received FDA aproval in the US on June 15th 2007, and before rushing out to buy yourself a chemistry set and knocking up your own version, Cephalon have secured this patent until 2023 so don’t even go there.

Apparently Amodafinil is a ’stimulant-like’ drug which is being aimed as a treatment for bi-polar depression, conditions associated with schizophrenia, as well as chronic fatigue syndrome associated with Parkinsons disease and MS, amongst a great many others.

Far be it for me, a simple truck driver with very red eyes to point fingers, but I do find it something of a coincidence that with a new drug to find a market for, all of a sudden the super-safe Provigil, is no longer super-safe. Far from it in fact, and a quick ‘Google’ will turn up all sorts of ‘if’s buts and maybes’s’, without actually telling us the information we need.

Is Provigil dangerous and addictive, or is it not?

The truth of the matter is, it doesn’t matter.

There has been so much news coverage regarding Provigil, a drug which generates around $500 million US every year, that its markets are safe. If this wasn’t the case there would be no illicit heroin market lets face it?

But the real issue here, is the readiness of the worlds press to undertake global marketing and publicity for a product which is by its creators own admission, unsafe, as they can’t tell the public whether they will become addicted or not. Only that they might, (or might not).

Little wonder then, that the world is currently in the teeth of a prescription drug epidemic which grows exponentially year on year, and there’s not a thing we can do about it.

In the meantime, we have hard and fast evidence regarding a cure for a large number of cancers, which the press simply refuse to cover, and the government won’t let us have access to, even though the drug in question has never been credibly linked to a single death..ever.

There’s no doubting the pharmaceutical industry does a fantastic job in improving the quality of life for many millions of people every single year. But the fact their products are readily available on a million websites, and to absolutely anyone who has access to a credit card number is no accident.

Even worse is the fact government’s seem ill-prepared to anything about this, whilst in the meantime sending over-zealous police forces in to kick peoples doors down simply for growing a cannabis plant or two.

Something’s just not right about it all and I can’t quite put my finger on it.

Provigil-RX.Info

A new study from the Montreal Neurological Institute (MNI) at McGill University demonstrates interestingly, that sleep-wake states are regulated by two different types of nerve cells (neurons), melanin-concentrating hormone (MCH) neurons and orexin (Orx) neurons, which occupy the same region of the brain but perform opposite functions.

The MNI study is the first to discover that MCH neurons are activated during sleep and could thus be important in regulating the sleep state. The study, published in this week’s issue of the journal Proceedings of the National Academy of Sciences (PNAS), provides deeper understanding of the sleep-wake cycle and vital insight into the basis of sleep disorders such as narcolepsy and possibly also other diseases such as depression and Parkinson’s.

Sleep is regulated by processes in the brain in response to how long we are awake in addition to the light/dark cycle controlled by the circadian rhythm.

With Drs. Oum Hassani and Maan Gee Lee, Dr. Barbara Jones at the MNI were studying a structure in the brain called the lateral hypothalamus (LH) known to be critical for maintaining wakefulness.

MCH neurons, co-distributed with Orx neurons, constitute less than 10% of the LH.

Previous studies have shown that Orx neurons are essential for maintenance of the awake state. These neurons are active in the waking state and turn off during sleep and in their absence, animals and humans experience narcolepsy with cataplexy or sudden loss of muscle tone.

However, the role of MCH neurons was until now, unclear. Evidence from earlier knockout studies suggested that MCH neurons might play a different role than Orx neurons in regulating activity and sleep-wake states.

Therefore the team at the MNI set up experiments to study the function of MCH neurons during the sleep-wake states.

“Remarkably, what we found is that MCH neurons are actually silent during waking, which is a surprising finding especially in this wake-promoting region of the brain.

The neurons fire during sleep, and are most active during REM sleep,” says Dr. Barbara Jones, neuroscientist at the MNI and principal investigator in the study. “Our study markedly demonstrates that MCH neurons discharge in a reciprocal manner to the Orx neurons across the sleep-wake cycle.”

Dr. Jones and colleagues used their expertise to apply and develop a difficult technique which allowed them to selectively record, label and thus identify a nerve cell containing a particular chemical. This allowed them to isolate the functions of the MCH and Orx cells even though they comprise less than 10% of the nerve cells in the LH.

The reciprocal profiles and roles of the Orx and MCH neurons could be significant in the manifestation of sleep disorders.

It is possible that narcolepsy, which occurs with the loss of Orx neurons, is provoked in part by the MCH neurons that remain intact in the narcoleptic patients. A growing body of research shows that regular and normal sleep is necessary for overall health; regulating hormone levels, blood pressure, metabolism, alertness, mood, and consolidating memory.

This study presents potential therapeutic avenues and targets for the treatment of various sleep disorders including the development of drugs that will act on receptors for Orx and MCH, to stimulate or block these receptors accordingly.

(Source: McGill University: Proceedings of the National Academy of Sciences: March 2009)

http://www.virtualmedicalcentre.com

“About 20 percent of adults in the United States report a level of daytime sleepiness sufficient to interfere with daily activities, and excessive daytime sleepiness is the leading symptom of patients presenting to sleep clinics,” writes J.F. Pagel, MD, MS, from Rocky Mountain Sleep Disorders Center in Pueblo, Colorado.

“The prevalence of excessive daytime sleepiness is highest in adolescents, older persons, and shift workers, but assessment of its true prevalence is difficult because of the subjective nature of the symptoms, inconsistencies in terminology, and a lack of consensus on methods of diagnosis and assessment,” Dr. Pagel writes. “Some persons use subjective terminology (e.g., drowsiness, languor, inertness, fatigue, sluggishness) when describing symptoms of excessive daytime sleepiness.”

Excessive daytime sleepiness is one of the most prevalent causes of sleep-related patient symptoms, affecting approximately 20% of the population. Persons with excessive daytime sleepiness generally have poorer health vs adults of similar age. The Stanford Sleepiness Scale and the Epworth Sleepiness Scale are useful tools to screen for excessive daytime sleepiness.

The consequences of excessive daytime sleepiness can be varied and sometimes serious or even fatal, largely because of increased risk for motor vehicle crashes and work-related injuries. Sleep problems contribute to more than 100,000 motor vehicle crashes, resulting in 71,000 personal injuries and 1500 deaths annually, with more than half of single-vehicle crashes involving heavy trucks being fatigue related. Adolescent and young adult male drivers are involved in most sleep-related crashes.

Sleep deprivation, obstructive sleep apnea (OSA), and sedating medications are the most common causes of excessive daytime sleepiness. Other potential causes may include certain medical and psychiatric conditions and sleep disorders, such as narcolepsy, periodic limb movement disorder, and restless legs syndrome. Neurologic causes include head trauma, stroke, brain tumors, encephalitis, and genetic and neurodegenerative conditions.

OSA is a frequent cause of excessive daytime sleepiness, as well as the potentially most dangerous and physiologically disruptive cause. Polysomnography should typically be used to confirm the diagnosis. In patients diagnosed with OSA, possible comorbid conditions of hypertension, diabetes, and coronary disease should be identified and managed. Current prevalence of the risk for, or presence of, OSA is estimated to be 26% to 32% of adults, but this is anticipated to increase.

Sedating medications that may cause excessive daytime sleepiness include alpha- and beta-adrenergic blockers, antiepileptic drugs such as hydantoins and succinimides, antidiarrheal agents, antiemetics, antihistamines, antimuscarinics and antispasmodics, antiparkinsonian agents, antipsychotics, cough suppressants, genitourinary smooth muscle relaxants, opiate agonists and partial opiate agonists, and skeletal muscle relaxants.

Antidepressant medications with sedating effects include monoamine oxidase inhibitors, tricyclics, and selective serotonin reuptake inhibitors. Sedative-hypnotics and anxiolytics include barbiturates, benzodiazepines, and other drugs acting on γ-aminobutyric acid receptors.

The cornerstone of evaluating and managing excessive daytime sleepiness is to identify and treat OSA and/or other underlying conditions. In some patients, the appropriate use of activating medications may be indicated.

Most patients with OSA will experience reduction in symptoms of daytime sleepiness when treated with positive pressure devices, such as continuous positive airway pressure (CPAP) during sleep. There is less evidence supporting effects of medications, dental appliances, surgery, and other treatments of OSA.

For the treatment of excessive daytime sleepiness, modafinil is considered to be the first-line choice of activating agent because of its generally benign adverse effect profile. Because it is pharmacologically distinct from the amphetamines, it has a much lower potential for abuse (schedule IV). In addition to its indication for the treatment of persistent sleepiness associated with OSA in patients already being treated with CPAP, modafinil is also indicated for the treatment of daytime sleepiness in patients with shift work disorder.

As schedule II prescription drugs, the amphetamines are thought to have a high potential for abuse and must therefore be used with caution to promote alertness in sleepy patients. These include dextroamphetamine, methylphenidate, and pemoline. Personality changes, tremor, hypertension, headaches, and gastroesophageal reflux may be associated with amphetamine use.

“The use of activating agents is inappropriate in hypersomnolent patients with untreated OSA — although daytime sleepiness may be improved with these agents, the patient remains at risk from the pathophysiologic consequences of untreated OSA,” Dr. Pagel writes.

Specific clinical recommendations for practice, all rated level of evidence B, are as follows:

• Treating patients who have OSA with CPAP therapy is associated with decreased daytime sleepiness and a reduced risk for motor vehicle crashes.
• In patients with OSA who are already being treated with CPAP, modafinil therapy has been associated with reduction in symptoms of persistent sleepiness. Modafinil also appears to reduce daytime sleepiness in patients with shift work disorder.

“The physician treating patients with excessive daytime sleepiness (or patients using drugs likely to affect driving performance) has the responsibility to make a clinical assessment of the patient’s overall risk of unsafe driving, and to document driving recommendations and precautions,” Dr. Pagel concludes. “A physician should report patients who fail to comply with treatment, particularly high-risk persons such as airline pilots, truck, bus, and occupational drivers, and those with a history of recent sleepiness-associated incidents.”

http://www.medscape.com

According to the National Institute of Mental Health, about 3 to 5 percent of the general population has the disorder, which is characterized by agitated behavior and an inability to focus on tasks.

Methylphenidate also is occasionally prescribed for treating narcolepsy.

Health Effects
Methylphenidate is a central nervous system (CNS) stimulant. It has effects similar to, but more potent than, caffeine and less potent than amphetamines. It has a notably calming effect on hyperactive children and a “focusing” effect on those with ADHD.

Recent research at Brookhaven National Laboratory may begin to explain how methylphenidate helps people with ADHD.

The researchers used positron emission tomography (PET – a noninvasive brain scan) to confirm that administering normal therapeutic doses of methylphenidate to healthy, adult men increased their dopamine levels.

The researchers speculate that methylphenidate amplifies the release of dopamine, a neurotransmitter, thereby improving attention and focus in individuals who have dopamine signals that are weak, such as individuals with ADHD.

When taken as prescribed, methylphenidate is a valuable medicine. Research shows that people with ADHD do not become addicted to stimulant medications when taken in the form prescribed and at treatment dosages.

Another study found that ADHD boys treated with stimulants such as methylphenidate are significantly less likely to abuse drugs and alcohol when they are older than are non-treated ADHD boys.

Because of its stimulant properties, however, in recent years there have been reports of abuse of methylphenidate by people for whom it is not a medication.

Some individuals abuse it for its stimulant effects: appetite suppression, wakefulness, increased focus/attentiveness, and euphoria.

When abused, the tablets are either taken orally or crushed and snorted. Some abusers dissolve the tablets in water and inject the mixture – complications can arise from this because insoluble fillers in the tablets can block small blood vessels.

Trends in Ritalin Abuse
At their June 2000 meeting, members of NIDA’s Community Epidemiology Work Group (CEWG)* shared the following information.

The abuse of methylphenidate has been reported in Baltimore, mostly among middle and high schools students; Boston, especially among middle and upper-middle class communities; Detroit; Minneapolis/St. Paul; Phoenix; and Texas.

When abused, methylphenidate tablets are often used orally or crushed and used intranasally.

In 1999, 165 methylphenidate-related poison calls were made in Detroit; 419 were reported in Texas, with 114 of those involving intentional misuse or abuse.

On Chicago’s South Side, some users inject methylphenidate (this is referred to as “west coast”). Also, some mix it with heroin (a “speedball”) or in combination with both cocaine and heroin for a more potent effect.

Because stimulant medicines such as methylphenidate do have potential for abuse, the U.S. Drug Enforcement Administration (DEA) has placed stringent, Schedule II controls on their manufacture, distribution, and prescription. For example, DEA requires special licenses for these activities, and prescription refills are not allowed. States may impose further regulations, such as limiting the number of dosage units per prescription.

For more information on the entire spectrum of popularly abused prescription drugs, check out the following link;

http://www.prescription-drug-abuse.org