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Showing posts with label stress. Show all posts
Showing posts with label stress. Show all posts

Monday, December 2, 2013

Guinea Pig Experiment | Klonopin

Stressed out and not thinking straight has a lot to do with the lack of dopamine that Tardive Dyskinesia patients experience. [source]


I'm trying (with difficulty) to de-stress. I'm trying to figure out how to do that. I believe it's all about figuring out what triggers one to stress. In my case it's too much noise, too much stimulation. I need the calm sometimes and it can seem elusive when I feel overwhelmed and overstimulated. The TV reaches a piercing pitch. The light becomes unbearable. 

I succumbed to temptation, to the easy route. Yesterday and I took the Klonopin that my doctor prescribed for me. I was sad and disappointed in myself all freaking day. Here I advertise not to ingest that chemical stuff and I do the opposite. I just don't think I have another choice.

I tried the Kava Kava at regular intervals during the day, but it just didn't do the trick. I do admit that I could meditate more than once a day, but I need to relax and get into a groove to do this. I decided that a little help couldn't hurt every once in a while just so I can get back to myself and remember that I can beat this thing. Sometimes I need more help than others.

Yesterday was a bad day. I woke up crying. The pain was excruciating even before I awoke. I know what it was, too. It was the result of too much stress. Too much stress kills me, well, almost anyway. The pain began in my wrist, my fingers slowly went numb and then it was hard to hold up my arm. Then the spasms began and my fingers burned, but were also numb at the same time. Holding anything at that moment is an impossibility.

To top that off, yesterday was particularly emotional for me. I'm not always an emotional wreck, but yesterday I had had enough and I was having a "Why me?" morning. What had I done in my life to deserve so much pain? I know that I'm still on the grief scale and I'm alternating between anger, bargaining and depression, but at least I'm past the denial stage. I began to type that I know acceptance will come, but I wonder if with acceptance comes compliance? Compliance is not in this girl's future. EVER.

I took an extremely hot shower. Cried uncontrollably. I had reached my breaking point. So, I took half of a .5mg Klonopin. I felt super relaxed after 20 minutes and within 40 minutes (I think) I fell asleep and slept for two hours straight. It felt so great to be able to sleep. It's been months since I've slept that deeply for that long.

The doctor prescribed .5mg cut in half twice a day. I only took it in the morning yesterday because I was zonked until 3pm yesterday. At 3pm I could've used another one, but I was at work. This morning I decided to take a 1/4 of a .5mg. If I'm going to take this to regulate my stress then I'm going to do it on my terms. I'm going to take the least amount I can. I'm not going to be a fucking zombie. Been there, done that in my heavily medicated days as a misdiagnosed bipolar patient.

And, because I have been there and done that, I feel like I have a wealth of wisdom about what I'm embarking on. Just enough and not too much is the key. I will not be a willing slave to Big Pharma. I'm going to use them and then throw them away. That's the plan anyway.

…………………………………..

Clonazepam Side Effects [source]


Adverse effects[edit]

Very common[edit]

  • Drowsiness[31]
  • Interference with cognitive and motor performance
  • Euphoria (Mostly due to anxiolytic properties)

Less common[edit]

  • Confusion[7]
  • Irritability and aggression[32]
  • Psychomotor agitation[33]
  • Lack of motivation[34]
  • Loss of libido
  • Impaired motor function
    • Impaired coordination
    • Impaired balance
    • Dizziness
  • Cognitive impairments[35]
  • Some users report hangover-like symptoms of being drowsy, having a headache, being sluggish, and being irritable after waking up if the medication is taken before sleep. This is likely the result of the medication's long half-life, which continues to affect the user after waking up.[citation needed]
  • The "hangover effect" some experience not only results from clonazepam's considerably long half-life. Like many other benzodiazepines, when taken as a sleep-aid, clonazepam disrupts or interferes with the brain's delta waves. Delta waves signify the brain's slowest waves (~4 Hz) and occur during Stage 4 sleep, which represents humans' deepest sleep state (our muscles are the most relaxed; breathing slows and becomes shallow), and the stage right before R.E.M. sleep and dreaming (Stage 5). Therefore, upon waking, this disruption of Stage 4 delta wave sleep causes a failure for an adequate brain/body rest or "recharge".[citation needed]
[39][40] While benzodiazepines induce sleep, they tend to produce a poorer quality sleep than natural sleep. Benzodiazepines such as clonazepam suppress REM sleep.[41] After regular use rebound insomnia can occur when discontinuing clonazepam.[42]

Occasional[edit]

Rare[edit]

  • Psychosis[52]
  • Incontinence[53][54][55]
  • Liver damage[56]
  • Paradoxical behavioural disinhibition[7][57] (most frequently in children, the elderly, and in persons with developmental disabilities)
    • Rage
    • Excitement
    • Impulsivity
    • Worsening of seizures

Long term effects[edit]

The long term effects of clonazepam can include depressiondisinhibition, and sexual dysfunction.[58] Long-term use of benzodiazepines is also associated with cognitive impairments that can persist for at least six months post-withdrawal, but it is unclear whether these impairments take more than six months to abate or if they are permanent. Benzodiazepines may cause or worsen depression.[7]

Withdrawal-related[edit]

  • Anxiety, irritability, insomnia, tremors
  • Potential to exacerbate existing panic disorder upon discontinuation
  • Seizures[59] similar to delirium tremens (with long-term use of excessive doses)
Benzodiazepines such as clonazepam can be very effective in controlling status epilepticus, but, when used for longer periods of time, some potentially serious side-effects may develop, such as interference with cognitive functions and behavior.[60] Many individuals treated on a long-term basis develop a form of dependence known as "low-dose dependence," as was shown in one double-blind, placebo-controlled study of 34 therapeuticlow-dose benzodiazepine users — physiological dependence was demonstrated by flumazenil-precipitated withdrawal.[61] Use of alcohol or otherCNS depressants while taking clonazepam greatly intensifies the effects (and side-effects) of the drug. Side-effects of the drug itself are generally benign, but sudden withdrawal after long-term use can cause severe symptoms.

Tolerance and withdrawal[edit]

Like all benzodiazepines, clonazepam is a benzodiazepine receptor agonist.[62][63] One third of individuals treated with benzodiazepines for longer than four weeks develop a dependence on the drug and experience a withdrawal syndrome upon dose reduction. High dosage and long term use increases the risk and severity of dependence and withdrawal symptoms. Withdrawal seizures and psychosis can occur in severe cases of withdrawal and anxiety and insomnia in less severe cases of withdrawal. Gradual reduction in dosage reduces the severity of the benzodiazepine withdrawal syndrome. Due to the risks of tolerance and withdrawal seizures clonazepam is generally not recommended for the long-term management of epilepsies. Increasing the dose can overcome the effects of tolerance but tolerance to the higher dose may occur and adverse effects may increase. The mechanism of tolerance includes receptor desensitisation, down regulation, receptor uncoupling and alterations in subunit composition and alterations in gene transcription coding.[7]

Tolerance[edit]

Tolerance to the anticonvulsant effects of clonazepam occurs in both animals and humans. In humans, tolerance to the anticonvulsant effects of clonazepam occurs frequently.[64][65] Chronic use of benzodiazepines leads to the development of tolerance with a decrease of benzodiazepine binding sites. The degree of tolerance is more pronounced with clonazepam than with chlordiazepoxide.[66] In general, short-term therapy is more effective than long-term therapy with clonazepam for the treatment of epilepsy.[67] Many studies have found that tolerance develops to the anticonvulsant properties of clonazepam with chronic use, which limits its long term effectiveness as an anticonvulsant.[68]

Withdrawal[edit]

Abrupt or over-rapid withdrawal from clonazepam may result in the development of the benzodiazepine withdrawal syndrome, causing psychosis characterised by dysphoric manifestations, irritability, aggressiveness, anxiety, and hallucinations.[69][70][71] Sudden withdrawal may also induce the potentially life threatening condition status epilepticus. Antiepileptic drugs, benzodiazepines such as clonazepam in particular, should be reduced slowly and gradually when discontinuing the drug to reduce withdrawal effects.[50] Carbamazepine has been trialed in the treatment of clonazepam withdrawal and has been found to be ineffective in preventing clonazepam withdrawal status epilepticus from occurring.[72]

Special precautions[edit]

The elderly metabolise benzodiazepines more slowly than younger individuals and are also more sensitive to the effects of benzodiazepines even at similar blood plasma levels. Doses for the elderly are recommended to be about half of that given to younger adults and given for no longer than 2 weeks. Long-acting benzodiazepines such as clonazepam are not generally recommended for the elderly due the risk of drug accumulation.[7]
Caution in the elderly: increased risk of impairments, falls and drug accumulation. Benzodiazepines also require special precaution if used in pregnant, alcohol- or drug-dependent individuals and individuals with comorbid psychiatric disorders.[73] Clonazepam is generally not recommended for use in elderly people for insomnia due to its high potency relative to other benzodiazepines.[74]
Caution in children: Clonazepam is not recommended for use in those under 18. Use in very young children may be especially hazardous. Of anticonvulsant drugs behavioural disturbances occur most frequently with clonazepam and phenobarbital.[73][75]
Caution using high dosages of clonazepam. Doses higher than 0.5 – 1 mg per day are associated with significant sedation.[76]
Clonazepam may aggravate hepatic porphyria.[77][78]
Caution in chronic schizophrenia. A 1982 double blinded placebo controlled study found clonazepam increases violent behavior in individuals with chronic schizophrenia.[79]

Interactions[edit]

Clonazepam decreases the levels of carbamazepine,[80][81] and likewise clonazepam's level is reduced by carbamazepine. Azole antifungals such asketoconazole may inhibit the metabolism of clonazepam.[7] Clonazepam may affect levels of phenytoin (diphenylhydantoin) by decreasing,[80][82] or increasing.[83][84] In turn Phenytoin may lower clonazepam plasma levels, by increasing the speed of clonazepam clearance by approximately 50% and decreasing its half-life by 31%.[85] Clonazepam increases the levels of primidone,[83] and phenobarbital.[86]
Combined use of clonazepam with certain antidepressantsantiepileptics such as phenobarbitalphenytoin and carbamazepine, sedativeantihistaminesopiatesantipsychotics and alcohol may result in enhanced sedative effects.[7]

Warnings[edit]

Clonazepam, like other benzodiazepines, will impair one's ability to drive or operate machinery. The central nervous system depressing effects of the drug can be intensified by alcohol consumption and therefore alcohol should be avoided while taking this medication. Benzodiazepines have been shown to cause both psychological and physical dependence. Patients physically dependent on clonazepam should be slowly titrated off under the supervision of a qualified healthcare professional to reduce the intensity of withdrawal or rebound symptoms.

……………………………………

Experiment Details:


Day 1: 1/2 .5 mg
Side Effects : Tired and relaxed

Day 2: 1/4 .5 mg in the morning, and 1/2 .5mg at night
Side Effects: Tired and loss of libido
Note to Self: Don't take more than once a day.

Day 7: 1/4 .5 mg in the morning, and 1/2 .5mg at night
Effectiveness: I haven't had any major pain for FIVE days!
Side Effects: Sadness
Note to Self: Skip the morning dose unless the pain returns.

Day 37: 1/2 .5 mg morning and night
Side Effects: Fatigue.
Note to Self: Just had a pain storm that lasted five days. Haven't been pain free since Day 10. I need to get off this medicine, but will continue taking them for one more month to conclude my experiment.

Conclusion: 


I stopped taking Klonopins at the end of June. I have continued to progress despite being on them, so decided to discontinue use. My body needs to be clean to rid itself of all impurities and it can't be clean with a pharmaceutical in it. All pharmaceuticals are plant derivatives spliced with chemicals that are toxic.

Wednesday, November 13, 2013

Research | Tardive Dyskinesia

Prognosis: "there is no known cure or treatment option to improve symptoms. In fact, many physicians will simply opt to change the patient's medications or eliminate medication use altogether although, ultimately, symptoms of tardive dyskinesia may not improve". [Source]
What Tardive Dyskinesia is:
Antispychotics cause the disorder which is mainly characterized by involuntary movements more often in the face and hands.

"They are often mistaken for psychiatric disturbances and patients may be shunned. During episodes of dystonia, opposing muscles that should relax contract. This can result in a limb that appears distorted. One of the most common manifestations is an ankle that twists and won't bear weight. In some cases, muscle groups that should be uninvolved in the activity being attempted will get involved. The result can be shoulders that swing violently during walking or an entire arm and shoulder that cramp and contort while the hand is holding a pen. In some instances, the opposing hand/arm/shoulder may also contort in a perverse sympathy." [Source]

Tardive dystonia is a syndrome of sustained muscle contractions, frequently causing either (a) twitching and repetitive movements, or (b) abnormal postures (14). Blepharospasm, grimacing, torticollis, retrocollis, and the Pisa syndrome are characteristic movements of tardive dystonia. [The Treatment of Tardive Dyskinesia

Antipsychotics work by blocking dopamine receptors along three pathways, and over the long-term, these pathways become increasingly dysfunctional (at least in a high percentage of patients.) The dysfunction in the basal ganglia leads to tardive dyskinesia. The dysfunction in the limbic system and the frontal lobes leads to tardive psychosis and tardive dementia.

So, the antipsychotics blocked my dopamine and as a result, I now have TOO little dopamine


Dopamine is defined as a catecholamine. This means that it is a hormone functioning as a neurotransmitter. The body's nervous system is a sophisticated communication network with the brain sending signals to the various systems through electrochemical impulses. These signals travel through the nerves to the terminals, where they interface with receptors on the surface of cells. In order for those signals to pass from the nerve endings, or synapses, to the cell receptors, dopamine — in very specific amounts — must be present. Dopamine also affects emotional state, perceptions, behavior and cognitive thinking. 
This paper proposes that the neuropsychiatric symptoms of tardive dyskinesia, akathisia and pseudoparkinsonian tremor are modulated by a noradrenergic pathway that projects from the locus coeruleus to the linbic system. -AND- Noradrenergic modulation of the limbic system by way of the locus coeruleus accounts for a number of clinical observations, such as the worsening of tardive dyskinesia by stress, the greater risk for tardive dyskinesia in patients with affective disorder, the time-of-onset of tardive dyskinesia, and the coexistence of tardive dyskinesia and pseudoparkinsonism. [source]

The influence of stress on dopamine receptors: 

Besides the qualitative approach to coping with stress, what bodily mechanisms are responsible for dealing with anxiety? The nervous system is almost solely credited with this task. The complex interaction system between billions of individual neurons facilitates large number of behaviors that result due to inputs originating inside and outside the organism. Spaces between neighboring neurons are called synapses, and one way in which they communicate is by sending chemical signals called neurotransmitters across the presynaptic membrane to the postsynaptic membrane. Years of nervous system research have determined that stress activates the neurotransmitter, dopamine. [source]

Although some alternatives and dopamine agonists (drugs that help to restore normal levels of dopamine) have been of some use in treating tardive dyskinesia, the best treatment found thus far is prevention. [source]

Holistic Solutions for Tardive Dyskinesia:

  1.  1,600 IU of vitamin E [Source]
  2. Vitamin B6 [source]
  3. Ginko biloba, 240 mg/day [source]
  4. Tarvil Amino Acids [source]
  5. Cannabis Oil {[One Study Only for Tardive Dyskinesia] [The afore mentioned study in PubMed] [Cannabis and cannabanoids] [Dr. Sanjay Gupta and Tardive Dyskinesia on Medical Efficacy List] [Cannabis Oil, a Natural Cancer Cure, Natural News
    1. CB1 receptors are found primarily in the brain, to be specific in the basal ganglia and in the limbic system, including the hippocampus. [source]
    2. Cannabinoid receptors are activated by three major groups ofligandsendocannabinoids (produced by the mammalian body), plant cannabinoids (such as THC, produced by the cannabis plant) and synthetic cannabinoids (suchcaas HU-210). [source]
    3. The CB1 receptor is expressed mainly in the brain (central nervous system or "CNS"), but also in the lungsliver and kidneys. [Source]
    4. U.S. National Library of Medicine's take on CBs. [source]
    5. Cannabinoids and Dopamine receptors [source]
    6. However, in the reward circuit, just as in the case of other drugs, more dopamine is released. As with opiates, this paradoxical increase is explained by the fact that the dopaminergic neurons in this circuit do not have CB1 receptors, but are normally inhibited by GABAergic neurons that do have them. The cannabis removes this inhibition by the GABA neurons and hence activates the dopamine neurons. [source]
    7. This is the ULTIMATE research that advocates for the positive use of cannabis in Tardive dyskinesia patients!