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Dr. Bob is Robert Hsiung, MD,
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Posted by iforgotmypassword on April 18, 2008, at 20:16:04
wondering how SSRIs cause this harm.
i have been afraid of anything serotonergic for years. i still have permanent EPS, rigidity, akathisia, and twitches. i stopped paxil in early 2002, but it has only gotten worse with time. i did try effexor for a while, a year or so after... but still it has been so long...
i may have had a predisposition, but this has happened to other people too. what is the mechanism?
should i continue to consider drugs that are serotonergic as off-my-list?
Posted by Phillipa on April 18, 2008, at 20:34:41
In reply to how do SSRIs cause EPS, akathisia, perm. damage?, posted by iforgotmypassword on April 18, 2008, at 20:16:04
Don't know what did your doc say? Maybe you just can't take them???? Love Phillipa
Posted by Amigan on April 20, 2008, at 18:50:18
In reply to how do SSRIs cause EPS, akathisia, perm. damage?, posted by iforgotmypassword on April 18, 2008, at 20:16:04
> wondering how SSRIs cause this harm.
Excessive serotonin in the synaptic cleft binds to certain 5-ht receptors and this causes a drop in the release of dopamine.
An indirect decrease of dopamine caused by serotoninergic drugs.> i have been afraid of anything serotonergic for years. i still have permanent EPS, rigidity, akathisia, and twitches.
"permanent EPS" sounds like tardive dyskenisia. It is caused by antipsychotics mainly, not antidepressants.
ADs can cause akathisia and EPS to sensitive people but not permanently, afaik.
Are you sure that you haven't been taking any APs?
Have you ever experienced serotonin syndrome?
Have you ever combined SSRI with contradicted, illicit drugs?> i may have had a predisposition,
Most probable.
> but this has happened to other people too. what is the mechanism?
I can't remember reading a case of TD caused by SSRIs alone. It must be a very rare thing.
> should i continue to consider drugs that are serotonergic as off-my-list?
I can't answer that.
Posted by nevergiveup on April 21, 2008, at 16:46:36
In reply to Re: how do SSRIs cause EPS, akathisia, perm. damage? » iforgotmypassword, posted by Phillipa on April 18, 2008, at 20:34:41
What is EPS? Can akathisia be easily distinguished from GAD?
Posted by Phillipa on April 21, 2008, at 19:26:52
In reply to Re: how do SSRIs cause EPS, akathisia, perm. damage?, posted by nevergiveup on April 21, 2008, at 16:46:36
Maybe this will help. Love Phillipa
From Wikipedia, the free encyclopedia
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Brain: Extrapyramidal system
Medulla spinalis. (Extrapyramidal tracts are labeled "2" in red, at left.)
NeuroNames ancil-623
MeSH Extrapyramidal+tracts
Dorlands/Elsevier s_33/12787420
In human anatomy, the extrapyramidal system is a neural network located in the brain that is part of the motor system involved in the coordination of movement. The system is called "extrapyramidal" to distinguish it from the tracts of the motor cortex that reach their targets by traveling through the "pyramids" of the medulla. The pyramidal pathways (corticospinal and some corticobulbar tracts) may directly innervate motor neurons of the spinal cord or brainstem (anterior horn cells or certain cranial nerve nuclei), whereas the extrapyramidal system centers around the modulation and regulation (indirect control) of anterior horn cells.Extrapyramidal tracts are chiefly found in the reticular formation of the pons and medulla, and target neurons in the spinal cord involved in reflexes, locomotion, complex movements, and postural control. These tracts are in turn modulated by various parts of the central nervous system, including the nigrostriatal pathway, the basal ganglia, the cerebellum, the vestibular nuclei, and different sensory areas of the cerebral cortex. All of these regulatory components can be considered part of the extrapyramidal system, in that they modulate motor activity without directly innervating motor neurons.
Contents [hide]
1 Extrapyramidal symptoms
1.1 Disorders
1.2 Treatment for extrapyramidal symptoms
2 See also
[edit] Extrapyramidal symptoms
The extrapyramidal system can be affected in a number of ways, which are revealed in a range of extrapyramidal symptoms such as akinesia (inability to initiate movement) and akathisia (inability to remain motionless).Extrapyramidal symptoms (EPS) are the various movement disorders such as tardive dyskinesia suffered as a result of taking dopamine antagonists, usually antipsychotic (neuroleptic) drugs, which are often used to control psychosis, especially schizophrenia. Other antidopaminergic drugs like the antiemetic metoclopramide or the tricyclic antidepressant amoxapine can also cause extrapyramidal side effects.
[edit] Disorders
The best known EPS is tardive dyskinesia (involuntary, irregular muscle movements, usually in the face). Other common EPS include akathisia (restlessness), dystonia (muscular spasms of neck - torticollis, eyes - oculogyric crisis, tongue, or jaw; more frequent in children), drug-induced parkinsonism (muscular lead-pipe rigidity, bradykinesia/akinesia, resting tremor, postural instability; more frequent in adults and the elderly),Although Parkinson's Disease is primarily a disease of the nigrostriatal pathway and not the extrapyramidal system, loss of dopaminergic neurons in the substantia nigra leads to dysregulation of the extrapyramidal system. Since this system regulates posture and skeletal muscle tone, a result is the characteristic bradykinesia of Parkinson's.
Extrapyramidal symptoms can also be caused by brain damage, as in athetotic cerebral palsy, which is involuntary writhing movements caused by prenatal or perinatal brain damage.
[edit] Treatment for extrapyramidal symptoms
Anticholinergic drugs are used to control neuroleptic-induced EPS, although akathisia may require beta blockers or even benzodiazepines. If the EPS are induced by a typical antipsychotic, EPS may be reduced by dose titration or by switching to an atypical antipsychotic, such as aripiprazole, ziprasidone, quetiapine, olanzapine, risperidone or clozapine. These medications possess an additional mode of action that is believed to negate their effect on the nigrostriatal pathway, which means they are associated with fewer extrapyramidal side effects than "conventional" antipsychotics (chlorpromazine, haloperidol, etc.).Commonly used medications for EPS are benztropine (Cogentin), diphenhydramine (Benadryl), and trihexyphenidyl (Artane).
Posted by Phillipa on April 21, 2008, at 19:36:43
In reply to Re: how do SSRIs cause EPS, akathisia, perm. damage?, posted by nevergiveup on April 21, 2008, at 16:46:36
Wiki on GAD. Love Phillipa
Generalized anxiety disorder (GAD) is an anxiety disorder that is characterized by excessive, uncontrollable and often irrational worry about everyday things, which is disproportionate to the actual source of worry. This excessive worry often interferes with daily functioning, as individuals suffering GAD typically catastrophise, anticipate disaster, and are overly concerned about everyday matters such as health issues, money, family problems, friend problems or work difficulties.[1] They often exhibit a variety of physical symptoms, including fatigue, headaches, muscle tension, muscle aches, difficulty swallowing, trembling, twitching, irritability, sweating, and hot flashes. These symptoms must be consistent and on-going, persisting at least 6 months, for a formal diagnosis of GAD to be introduced. [1] Approximately 6.8 million American adults experience GAD, affecting about twice as many women as men.[2]
Contents [hide]
1 Diagnosis
2 Prevalence
3 Potential Causes of GAD
4 Treatment
4.1 SSRIs
4.2 Other Drugs
4.3 Benzodiazepines
4.4 Herbal
4.5 Cognitive behavioral therapy
5 GAD and Comorbid Depression
6 See also
7 Notes
8 References
9 External links
[edit] Diagnosis
According to the Diagnostic and Statistical Manual IV-Text Revision (DSM-IV-TR), the following criteria must be met for a person to be diagnosed with Generalized Anxiety Disorder.Excessive anxiety and worry (apprehensive expectation), occurring more days than not for at least six months, about a number of events or activities (such as work or school performance).
The person finds it difficult to control the worry.
The anxiety and worry are associated with three (or more) of the following six symptoms (with at least some symptoms present for more days than not for the past 6 months). Note: Only one item is required in children.
restlessness or feeling keyed up or on edge
being easily fatigued
irritability
muscle tension
difficulty falling or staying asleep, or restless unsatisfying sleep
difficulty concentrating or the mind going blank#
Symptoms can also include nausea, vomiting, and chronic stomach aches.The focus of the anxiety and worry is not confined to features of an Axis I disorder, e.g., the anxiety or worry is not about having a panic attack (as in panic disorder), being embarrassed in public (as in social phobia), being away from home or close relatives (as in Separation Anxiety Disorder), gaining weight (as in anorexia nervosa), having multiple physical complaints (as in somatization disorder), or having a serious illness (as in hypochondriasis), and the anxiety and worry do not occur exclusively during post-traumatic stress disorder.
The anxiety, worry, or physical symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
The disturbance is not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition (e.g., hyperthyroidism) and does not occur exclusively during a Mood Disorder, a Psychotic Disorder, or a Pervasive Developmental Disorder.
Symptoms can also include nausea, vomiting, and chronic stomach aches.[edit] Prevalence
The World Health Organization's Global Burden of Disease project did not include generalised anxiety disorders.[3] In lieu of global statistics, here are some prevalence rates from around the world:Australia: 3 percent of adults[3]
Canada: Between 3-5 percent of adults[4]
Italy: 2.9 percent[5]
Taiwan: 0.4 percent[5]
United States: approx. 3.1 percent of people age 18 and over in a given year (6.8 million)[2][edit] Potential Causes of GAD
Some research suggests that GAD may run in families[6], and it may also grow worse during stress. GAD usually begins at an earlier age and symptoms may manifest themselves more slowly than in most other anxiety disorders[7]. Some people with GAD report onset in early adulthood, usually in response to a life stressor. Once GAD develops, it can be chronic but can be managed if not all but alleviated with proper treatment.[8]
[edit] Treatment[edit] SSRIs
Main article: Selective serotonin reuptake inhibitor
Pharmaceutical treatments for GAD include selective serotonin reuptake inhibitors (SSRIs),[9] which are antidepressants that influence brain chemistry to block the reabsorption of serotonin in the brain.[10] SSRIs are mainly indicated for clinical depression, but are also effective in treating anxiety disorders.[9] Common side effects include nausea, sexual dysfunction, headache, diarrhea, among others. Common SSRIs prescribed for GAD include:fluoxetine (Prozac)
paroxetine (Paxil)
escitalopram (Lexapro;Cipralex)[edit] Other Drugs
imipramine (Tofranil)
venlafaxine (Effexor)
Buspirone (BuSpar)
Venlafaxine (Effexor) is a serotonin-norepinephrine reuptake inhibitor (SNRI). SNRIs, a class of drugs related to the SSRIs, alter the chemistries of both norepinephrine and serotonin in the brain. Imipramine (Tofranil) is a tricyclic antidepressant (TCA). TCAs are thought to act on serotonin, norepinephrine, and dopamine in the brain. Buspirone is a serotonin receptor agonist belonging to the azaspirodecanedione class of compounds.
[edit] Benzodiazepines
Main article: Benzodiazepine
Benzodiazepines (or "benzos") are fast-acting sedatives that are also used to treat GAD and other anxiety disorders.[9] These are often given in the short-term due to their nature to become habit-forming. Side effects include drowsiness, reduced motor coordination and problems with equilibrioception. Common benzodiazepines used to treat GAD include[9]:alprazolam (Xanax)
chlordiazepoxide (Librium)
clonazepam (Klonopin)
diazepam (Valium)
lorazepam (Ativan)[edit] Herbal
Main article: Kava
Kava, a relaxant made from a root only of a relative of the black pepper plant, is effective at controlling anxiety - particularly when used as a short term fast acting drug in combination with CBT (see below). The recommended use is for a support person such as the GAD sufferer's partner or housemate to encourage a dose when anxiety strikes as the patient is often unwilling/unable to dose themselves. Kava is absorbed through most mucous membranes and takes effect in roughly the same time as alcohol. It is a symptomatic relief for anxiety and does not address the fundamental problem, but it does give the patient a reliable mental crutch to work through the core problems. It appears that the required dosage actually decreases with regular use, perhaps as a form of conditioning. Two major advantages of Kava supported therapy are the rapid response of the active ingredients (removing the need for titration) and the lack of withdrawal symptoms. There are no specific contraindications with other chemical treatments, but caution must be observed when the patient is already taking psychoactive drugs. Due to reports of serious liver damage related to the use of kava, many countries, particularly across Europe, have banned the sale of it. The risks and benefits of using kava, as with any drug, must be reviewed and proper caution must be exercised.
[edit] Cognitive behavioral therapy
Main article: Cognitive behavioral therapy
A psychological method of treatment for GAD is cognitive behavioral therapy (CBT), which involves a therapist working with the patient to understand how thoughts and feelings influence behavior.[11] The goal of the therapy is to change negative thought patterns that lead to the patient's anxiety, replacing them with positive, more realistic ones. Elements of the therapy include exposure strategies to allow the patient to gradually confront their anxieties and feel more comfortable in anxiety-provoking situations, as well as to practice the skills they have learned. CBT can be used alone or in conjunction with medication.[9]CBT usually helps one third of the patients substantially, whilst another third does not respond at all to treatment. [12]
[edit] GAD and Comorbid Depression
In the National Comorbidity Survey (2005), 58% of patients diagnosed with major depression were found to have an anxiety disorder; among these patients, the rate of comorbidity with GAD was 17.2%, and with panic disorder, 9.9%. Patients with a diagnosed anxiety disorder also had high rates of comorbid depression, including 22.4% of patients with social phobia, 9.4% with agoraphobia, and 2.3% with panic disorder. For many, the symptoms of both depression and anxiety are not severe enough (i.e. are subsyndromal) to justify a primary diagnosis of either major depressive disorder (MDD) or an anxiety disorder.Patients can also be categorized as having mixed anxiety-depressive disorder, and they are at significantly increased risk of developing full-blown depression or anxiety. Appropriate treatment is necessary to alleviate symptoms and prevent the emergence of more serious disease.[citation needed]
Accumulating evidence indicates that patients with comorbid depression and anxiety tend to have greater illness severity and a lower treatment response than those with either disorder alone.[citation needed] In addition, social function and quality of life are more greatly impaired.
In addition to coexisting with depression, research shows that GAD often coexists with substance abuse or other conditions associated with stress, such as irritable bowel syndrome.[citation needed] Patients with physical symptoms such as insomnia or headaches should also tell their doctors about their feelings of worry and tension. This will help the patient's health care provider to recognize whether the person is suffering from GAD.
Posted by undopaminergic on April 28, 2008, at 20:34:28
In reply to how do SSRIs cause EPS, akathisia, perm. damage?, posted by iforgotmypassword on April 18, 2008, at 20:16:04
Long-term and permanent effects of SSRIs are poorly understood, but probably involve changes in the sensitivity or density of serotonin receptors, and changes in other neurotransmitter systems that are indirectly affected by elevated synaptic serotonin - eg. dopamine.
This may be of interest:
"Chapter 1, The Awakened Giant's Wrath: Risking Brain Damage"
http://www.prozacbacklash.com/pdf/prozBackCh1.pdf
http://www.prozacbacklash.com/
This is the end of the thread.
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