buy xanax Q&A

Antidepressant withdrawal effects do not indicate addiction in the strict medical sense, but are rather the results of the brain attempting to reach neurochemical stability after an abrupt change. The exact mechanism of SSRI discontinuation syndrome is unknown, and may be a variety of factors. Continuing research on discontinuation/withdrawal syndrome has attributed SSRI discontinuation syndrome to electrophysiological changes in the brain (particularly on the 5-HT receptor), and electrophysiological changes in the body (nerve growth factor) in the absence of the SSRI, as well as dopamine dependency, and an over-excited immune system.
The central nervous system (CNS) adapts to the presence of psychoactive drugs. Such adaptation commonly involves the readjustment of neuroreceptors to compensate for the acute pharmacological action of the medication. Desired drug effects may be mediated by such compensatory changes which may explain the delayed onset of therapeutic effect of antidepressants. This adaptation theory also explains why withdrawal symptoms and signs can occur on the discontinuation of such medications as clearance of drug can occur at a rate faster than the brain can readjust to the absence of medication. Hence, pharmacodynamic and pharmacokinetic factors contribute to the risk of a withdrawal syndrome. Pharmacodynamic factors explain why withdrawal syndromes are often a class issue and why the administration of a drug in the same class often relieves withdrawal symptoms. Formal studies have not characterized the relative risk.
One theory states that SSRI discontinuation syndrome is associated with a rostral anterior cingulate Cho/Cre metabolite ratio decrease that may reflect dynamics of rostral anterior cingulate cortex (ACC) function.
The ACC appears to play a role in a wide variety of autonomic functions, such as regulating heart rate and blood pressure, and is vital to cognitive functions, such as reward anticipation, decision-making, empathy, and emotion. Neuroscientists indicate the dorsal anterior cingulate cortex is primarily related to rational cognition while the ventral is more related to emotional cognition.
A separate study demonstrated that changes in regional central blood volume of left prefrontal cortex and left caudate nucleus correlate with the emergence of discontinuation symptoms and increased Hamilton Depression Rating Scale after interruption of paroxetine treatment. The findings supported the hypothesis that brain regions implicated in depression, with extensive serotonergic innervation, would exhibit changes in activity associated with emergence of symptoms following drug discontinuation. Cerebral blood volume maps were obtained via dynamic susceptibility functional magnetic resonance imaging (fMRI).
There is speculation concerning the possibility of a temporary deficiency of synaptic serotonin with abrupt withdrawal of an SSRI. This deficiency is compounded by the fact that down-regulated receptors will remain in their relatively hypoactive state for days to weeks. This is believed to result in antidepressant discontinuation syndrome directly or indirectly via downstream effects on other neurotransmitter systems (e.g., norepinephrine, dopamine, and g-aminobutyric acid) implicated in depressive and anxiety disorders.
Another possible mechanism is by inhibition of dopaminergic neurotransmission.
Patients should be advised of the elimination half-life times on their specific medication, and patients should be aware if changing from a long half-life medication such as fluoxetine, to a shorter one, that taking their dose regularly becomes much more important. Patients taking fluoxetine can often miss several doses without noticing any discomfort, but the shorter halflife of other SSRIs such as venlafaxine, paroxetine, duloxetine, escitalopram oxalate and sertraline (ranging approximately 10 hours) means that a single missed dose may cause withdrawal symptoms.
The condition may be avoided by either recommencing the original, and/or lesser dose of the SSRI (or a similar SSRI), or slowly reducing the dosage over several weeks or months. While slowly reducing the dosage does not guarantee that a patient will not experience the discontinuation syndrome, it is considered a safer method than abrupt discontinuation. Gradual discontinuation, or tapering, or titration, can be accomplished by breaking pills into parts or using a graduated oral syringe with the liquid form.
Treatment is dependent on the severity of the discontinuation reaction and whether or not further antidepressant treatment is warranted. In cases where further antidepressant treatment is required then the only step required is restarting the antidepressant; this is usually the case following patient noncompliance with the drug. If antidepressants are no longer required, treatment depends on symptom severity. Mild reactions may only require reassurance. Moderate cases may require symptom man

Brain shivers are a relatively common side effect of various anti-depressants. They are usually strongest when you are just starting, coming off them or changing doses. They generally aren’t dangerous but if they don’t go away after a week or two on the medication, speak to your Doctor.
Unfortunately, there is no good way to treat them. If you have just started the drug, give your body a week or two to get used to it. Or speak to your Doctor.
Good luck!

i take xanax as well for panic disorder .. you will have a tingling sensation on your face and head and yes it does cause your brain to feel” funny” lightheaded etc. i take a large dose of 3 mg per day yeah you do and will tend to be slightly foggy i take mine at night so i can sleep awake refreshed but groggy You really should talk to your md about these symptoms