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Lemons2lemonade

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  1. Antipsychotics Cause Oh

    in Dysautonomia Discussion

    Posted

    Perhaps this can shed some light on the effects of dopamine and serotonin in pots.

    Antipsychotic Pharmacotherapy and Orthostatic Hypotension

    Gugger, James J. CNS Drugs 25. 8 (Aug 2011): 659-71.

    All antipsychotics are associated with orthostatic hypotension,[1-3] although it is more frequent and severe with certain drugs. The incidence of orthostatic hypotension in patients taking antipsychotics is described below; however, comparison between studies should be done with caution due to significant differences in the demographic profile of each study and differing methods of assessment for orthostasis.

    The largest source of comparative data comes from the CATIE (Clinical Antipsychotic Trials of Intervention Effectiveness) trial, a large, federally funded study comparing the relative effectiveness and tolerability of second-generation antipsychotics with first-generation antipsychotics (represented by the mid-potency phenothiazine, perphenazine). Table I shows comparative rates of orthostatic hypotension in patients participating in phases I-III of CATIE.[4-8] Among atypical antipsychotics, clozapine and quetiapine had the greatest incidence of orthostatic hypotension, as high as 24% and 27%, respectively, because of a high affinity for the α 1 -adrenoceptor.

    Table I. Percentage of patients reporting orthostatic faintness in phases I-III of the CATIE trial [Table omitted.]

    Among the more recently introduced second-generation antipsychotics, iloperidone appears to have the highest incidence of orthostatic hypotension (19.5% compared with 8.3% in patients taking placebo in a pooled analysis of randomized controlled trials),[9] while the incidence of orthostasis with lurasidone and asenapine is less than 2%.[10,11]

    There are much fewer data on the incidence of orthostatic hypotension with first-generation antipsychotics, although low-potency (i.e. agents with low potency at the dopamine D 2 receptor) phenothiazine antipsychotics such as chlorpromazine and

    thioridazine are generally considered the most likely to cause orthostatic hypotension.[3] The incidence of orthostasis in a report of 515 patients taking chlorpromazine was 8%[12] and it was 14.7% in a randomized controlled trial.[13] Almost no quantitative data exist for higher-potency phenothiazine antipsychotics (perphenazine, loxapine, trifluoperazine, fluphenazine) and thiothixene,[1,3,14-18] but they are generally considered to infrequently cause orthostatic hypotension. In the pooled analysis of iloperidone studies mentioned above, the incidence of orthostatic hypotension with haloperidol (used as an active control) was 15.3% compared with 8.3% for placebo.[19]

    Since intramuscular administration generally results in a higher and more rapid elevation of plasma concentrations than oral administration,[20,21] there is likely to be a greater risk of orthostatic hypotension when antipsychotics are administered by the intramuscular route. A large study (n = 2011) evaluated the safety of intramuscular olanzapine relative to other intramuscular antipsychotics (primarily haloperidol). Orthostatic hypotension occurred in 2.4% of patients receiving olanzapine and 4.2% of those receiving any other antipsychotic.[22] Very little data exist for the other intramuscular antipsychotics. In a trial of intramuscular chlorpromazine (dosed at 1 mg/kg with a maximum dose of 100 mg) for the treatment of migraine, 18% (18/100) of patients developed orthostasis.[23] Although the frequency was not defined, orthostasis was the most common adverse effect of chlorpromazine in a trial comparing the efficacy of intramuscular chlorpromazine with intramuscular haloperidol in 50 patients with psychotic agitation; orthostasis was not mentioned as an adverse effect of haloperidol.[24]

    On iloperidone (the antipshyotic that causes the most OH)from Wikipedia

    ...acting upon and antagonizing specific neurotransmitters, particularly multiple dopamine and serotonin receptor subtypes. It is considered an ‘atypical’ antipsychotic because it displays serotonin receptor antagonism, similar to other atypical antipsychotics. The older typicalantipsychotics are primarily dopamine antagonists.

    Iloperidone has been shown to act as an antagonist at all tested receptors. It was found to block the sites of noradrenaline (α 2C ), dopamine (D 2A and D 3 ), and

    serotonin (5-HT 1A and 5-HT 6 ) receptors. [1] In addition, pharmacogenomic studies identified single nucleotide polymorphisms associated with an enhancedresponse

    to iloperidone during acute treatment of schizophrenia. [2]

    What I gather from this, is that OH can be caused by blockage of the serotonin and dopamine receptors. Perhaps this is why ssri's help patients with pots.

  11. Sudden Mystery Illness..is It Related To Pots/eds Help!

    in Dysautonomia Discussion

    Posted

    This sounds to me like your immune system is going wacky. The rash is inflammation, and the fever is also an immunorespone. If your wbc count is low though, that wouldn't make a lot of sense. I know this sounds terrible and I pray to god it is not the case, but you might want to get tested for hiv and leukemia. It also could just be the eds attacking your white blood cells. I would think that the low white blood cell count has a lot to do with whatever it is that is going on. Here is a list of causes http://www.mayoclinic.com/health/low-white-blood-cell-count/MY00162/DSECTION=causes Also I am curious, did the motrin help the rash? I hope you feel better and that this resolves itself. Being sick, especially with a fever is never fun.

  16. A Review Of Postural Orthostatic Tachycardia Syndrome

    in Dysautonomia Discussion

    Posted

    A review of postural orthostatic

    tachycardia syndrome

    Sheila Carew, Margaret O. Connor, John Cooke, Richard Conway, Christine Sheehy,

    Aine Costelloe, and Declan Lyons*

    Blood Pressure Unit, Mid Western Regional Hospital, Limerick, Ireland

    Received 4 July 2008; accepted 4 November 2008

    Introduction

    Postural orthostatic tachycardia syndrome (POTS) is defined as a

    sustained heart rate increase of 30 bpm or increase of heart

    rate to 120 bpm within the first 10 min of orthostasis associated

    with symptoms of orthostatic intolerance1–3 and without significant

    orthostatic hypotension (OH).

    Patients with POTS are predominately female (4:1) and relatively

    young,4,5 but can range in age from 15 to 50 years.6 Differences in

    muscle sympathetic nerve discharge characteristics, in the setting

    of sympathetic fibre loss associated with POTS, may contribute

    to the predisposition to and greater prevalence of POTS in

    female individuals.7

    There are no accurate epidemiological studies, but it is estimated

    that in the USA alone, there are millions of people affected

    by POTS.8

    Pathophysiology

    Normal physiology of standing

    When supine, up to 30% of the blood volume is in the thorax.

    During orthostasis, 300–800 mL of blood is gravitated downwards

    from the thorax into the abdomen and lower extremities. Most of

    this pooling into lower limb veins occurs within 10 s. This causes a

    decrease in venous return to the right side of the heart with

    a subsequent reduction in the stroke volume and cardiac output.

    Arterial baroreceptors (carotid sinuses and the aortic arch) and

    cardiopulmonary mechanoreceptors (heart and lung) detect a

    reduction in pulse pressure and stroke volume. Compensatory

    reflexes lead to increased sympathetic nervous system output

    (peripheral arteriolar vasoconstriction) and reduced parasympathetic

    nervous system output (reduced vagal tone to the heart

    with cardio-acceleration). After orthostasis in normal subjects,

    there is a 10–15 bpm increase in heart rate, systolic blood

    pressure remains stable, and diastolic blood pressure usually

    increases (10 mmHg).9

    Postural orthostatic tachycardia

    syndrome

    Postural orthostatic tachycardia syndrome is a clinical manifestation

    of multiple underlying mechanisms. It can be divided into a

    number of overlapping pathophysiological models as follows.

    Neuropathic

    This is thought to be associated with partial dysautonomia. The

    evidence in support of this is as follows:

    † Distal anhidrosis of the legs is commonly found on thermoregulatory

    sweat testing and quantitative sudomotor axon reflex

    testing (up to 50% of POTS patients).4,10

    † Ganglionic acetylcholine receptor antibody is positive in

    between 10 and 15% of the cases.4,11

    † There is a blunted increase in post-ganglionic sympathetic nerve

    discharge (muscle sympathetic nerve activity).12 This peripheral

    abnormality might reflect partial dysautonomia. Astronauts

    returning from prolonged exposure to microgravity often

    display a form of orthostatic intolerance with features similar

    to POTS.13 This is felt to be due to abnormal muscle sympathetic

    nerve activity.14

    † It is shown that leg arteriolar vasoconstriction is impaired.

    Therefore, increased arterial inflow can enhance venous filling

    and cause venous pooling, despite the fact that venous capacitance

    is normal.

  17. Experimental Induction Of Panic-Like Symptoms In Patients With Postural Tachycardia Syndrome

    in Dysautonomia Discussion

    Posted

    Found this in my research, thought i would share. Sorry about the vertical text, its from a pdf :)

    Experimental induction of panic-like symptoms in patients with postural tachycardia syndrome

    Khurana, Ramesh K ar_button.gif

    spacer.gif

    . Clinical Autonomic Research spacer.gif16. 6 spacer.gif(Dec 2006): 371-7.

    Abstract

    Patients with postural

    tachycardia syndrome (POTS)

    might be misdiagnosed with panic

    disorder due to shared clinical

    features. The first aim of our study

    was to investigate the relationship

    between symptoms of POTS and

    panic disorder. The second aim

    was to delineate clinical features

    distinguishing symptoms of POTS

    from panic disorder. A total of 11

    patients with POTS and 11 control

    subjects participated in an IRBapproved,

    prospective, placebocontrolled

    study. The experimentally

    induced panic-like symptoms

    of POTS were systematically studied

    using the Acute Panic Inventory

    (API) questionnaire. The

    participants answered the questionnaire

    after each placebo infusion

    and after each of the three

    provoking stimuli: head-up tilt

    test (HUT), isoproterenol infusion

    (ISI), and sodium lactate infusion

    (SLI). API responses were

    summed for each subject at each

    time point of administration.

    Individual API symptoms and

    summed responses were analyzed

    for statistical significance. All

    patients with POTS developed

    symptoms of orthostatic intolerance

    during HUT. Pharmacologically

    induced symptoms

    subjectively mimicked spontaneous

    symptoms in 5 of 11 patients

    during ISI and in none of 11

    patients during SLI. In contrast,

    API scores in these patients

    reached panic threshold in 0 of 11

    following HUT, in 4 of 11 following

    ISI and in 4 of 11 following

    SLI. Individual symptoms analysis

    revealed that significant increase

    in scores was limited to the

    somatic symptoms of palpitations,

    dyspnea, and twitching or trembling.

    In conclusion, the symptoms

    of POTS are

    phenomenologically different and

    clinically distinguishable from

    panic disorder symptoms

    Discussion

    The control results in the current study are consistent

    with previous studies. Balon and colleagues observed

    the production of panic symptoms in response to ISI

    in 4 out of 45 (8.9%) normal control subjects [3].

    Liebowitz et al. reported the occurrence of SLI-induced

    panic in 0–25% of control subjects [23]. Similarly,

    the current study found that no control subjects

    reached panic thresholds as compared with baseline

    API in response to any of the three stimuli.

    The lack of resemblance of SLI-induced symptoms

    with spontaneous symptoms and a significant API

    score elevation above baseline after SLI in only 4 of 11

    patients suggest that POTS symptoms cannot be

    equated with panic symptoms. Both ISI and SLI are

    considered reliable and valid models of panic-induction.

    SLI produces panic in panic disorder patients

    with a sensitivity of 0.85 and specificity 0.77, and ISI

    provokes panic with less sensitivity and more specificity

    [2]. It is possible that panic-like episodes

    occurring with pharmacologic stimuli in POTS patients

    are associated with a subclinical panic disorder

    [10], although the lack of similarity between the induced

    and spontaneous episodes militates against it.

    Goetz and colleagues (1996) used API questionnaires

    to evaluate subjective ratings and symptoms in

    panic disorder patients before and during SLI. Controlling

    for baseline symptoms levels, these investigators

    found that the symptoms most strongly

    associated with panic were desire to flee (0.70), fear of

    losing control (0.57), afraid in general (0.49), and

    dyspnea (0.48). These psychological symptoms were

    determined essential for the diagnosis of lactate-induced

    panic [15]. Balon and colleagues (1990) compared

    symptom responses to ISI in subjects with and

    without panic disorder and found that fear of going

    crazy, fear of dying, and shortness of breath best

    discriminated between panic and non-panic [3]. In

    our POTS patients, neither pharmacologic stimulus

    produced increased API scores in the cognitive psychological

    symptoms essential to the diagnosis of

    panic disorder, such as fear of dying, fear in general,

    and fear of going crazy. Our POTS patients demonstrated

    a significant increase in palpitations, dyspnea,

    and twitching or trembling, which are all somatic

    symptoms. Palpitations were more prominent with

    ISI, and trembling or twitching was more prominent

    with SLI. This study, therefore, does not support the

    phenomenologic equivalence of panic disorder in

    POTS patients.

    The current data suggest that, for a majority of

    POTS patients, panic-like symptoms are phenomenologically

    unrelated to panic disorder symptoms.

    Despite clinical similarities that can lead to misdiagnosis,

    several characteristics may be helpful in distinguishing

    POTS patients from panic disorder

    patients. First, a prior history of panic disorder may

    be absent in POTS patients. Second, panic-like

    symptoms in POTS patients are precipitated mostly

    by change to an upright posture. Third, particular

    panic symptoms such as fear of dying, fear in general,

    sense of unreality, and feeling detached are infrequently

    reported. Fourth, physical and psychophysiological

    symptoms usually cease with recumbency.

    Fifth, distinct differences in personality patterns exist

    between these two groups of patients. A psychological

    assessment using the Minnesota Multiphasic Personality

    Inventory questionnaire demonstrated that T

    scores for manifest anxiety were in the normal range

    in POTS patients [21]. Sixth, sudomotor and other

    autonomic abnormalities may be demonstrable in

    these patients [19].

    It is not known why patients with POTS present

    with panic-like symptoms. POTS may act as organic

    precipitant of these symptoms as previously described

    in patients with various medical disorders such as

    hyperthyroidism and hypoglycemia [33]. These patients

    may be vulnerable based on innate biological

    factors and anxiety sensitivity index [5, 16].

    375

  19. Poll On Presentation

    in Dysautonomia Discussion

    Posted

    I feel like the head pressure indicates a more systemic vasoconstriction problem rather than simply poor vasoconstriction in the abdomen or legs. When we bend over, blood starts pooling in our heads, which means to me that the veins in the head also aren't constricting or returning blood properly. We are like sand timers!!!

  23. Iv Saline Did Nothing

    in Dysautonomia Discussion

    Posted

    Naomi, I always ask for 2 liters. It seems to do much more than one. The other thing that seems to really help is a slow dispersal rate from the iv. For example 1 liter per hour with 2 liters total. I have to tell them to slow it down all the time because they think it is pointless and are just trying to get me out of there. If they do it quickly, I seem to urinate it all out. Another thing to note is that the first time they gave me saline was in the hospital. Two bags, slowly, before they wheeled me down for a ttt, as per the cardiologists orders. The ttt still showed pots but my blood pressure went up significantly from the laying sitting standing bp they did in my room that morning--my hr dropped from 170 to 130.

  25. Weird Feeling

    in Dysautonomia Discussion

    Posted

    Just curious, for everyone, what are the changes that happen that make you feel this way as far as taste, touch, smell, hearing, vision? A lot of people are saying surreal, what is it about the scene that is surreal( the speed of the moment, the lighting, the detail, the placement of objects)?

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