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Treatments forDysautonomias

Successful treatment of dysautonomiasusually requires an individualized program,which can change over time.

You should understand that since theunderlying mechanisms often are notunderstood well, treatment is likely toinvolve some trial and error.

Non-Drug Treatments

Several non-drug treatments are used fordifferent types of dysautonomias. Thereasons for a treatment depend on theparticular dysautonomia. Sometimes, theresponses of a patient to a treatment help thedoctor determine the diagnosis. Patients withdysautonomias can feel differently from dayto day, even without any clear reason why.

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This means that if a treatment is tried, it maytake several days to decideon whether thetreatment has helped or not.

Elevation of the Head of the Bed

In patients who have a fall in blood pressure every timethey stand up (orthostatic hypotension), elevation of thehead of the bed at night, by a variety of ways, improvesthe ability to tolerate standing up in the morning.

Salt Intake

High salt intake tends to increase the volume of fluid inthe body. A small percent of this volume is in thebloodstream. Doctors usually recommend a high salt dietfor patients with an inability to tolerate prolongedstanding (chronic orthostatic intolerance) or a fall inblood pressure during standing (orthostatic hypotension).Normally when a person takes in a high salt diet, thekidneys increase the amount of salt in the urine, and thislimits the increase in blood volume. Drugs that promoteretention of sodium by the kidneys, such as Florinef™,are usually required for high salt intake to increase bodyfluid volume effectively.

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Meals

Eating a big meal leads to shunting of blood toward thegut. In people with dizziness or lightheadedness whenthey stand up (orthostatic intolerance) or with orthostatichypotension, it is usually advisable to take frequent smallmeals.

Reducing the amounts of sugars or other carbohydrates inmeals may help manage symptoms.

Compression Hose

Compression hose or other compression garments tend todecrease the amount of pooling of blood in veins when aperson stands. This can decrease leakage of fluid fromthe veins into the tissues and decrease swelling of thefeet. In patients with veins that fill up or leak excessivelyduring standing, compression garments can improvetoleration of prolonged standing. In patients with a fall inblood pressure during standing (orthostatic hypotension),the problem may be less with the veins than with thearteries and arterioles, the blood vessels that carryoxygen-rich blood under high pressure to the organs andlimbs. Wearing compression garments therefore may bedisappointing in the management of orthostatichypotension.

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Coffee

Some patients with dysautonomias feel better drinkingcaffeinated coffee frequently. Others feel jittery oranxious and avoid caffeinated coffee. Still others noticeno effect one way or the other.

Temperature

Patients with dysautonomias often have an inability totolerate extremes of external temperature. When exposedto the heat, patients with failure of the sympatheticnervous system may not sweat adequately to maintain thecore temperature by evaporation of the sweat. Patientswith chronic orthostatic intolerance, such as frompostural tachycardia syndrome (POTS), can have heatintolerance because of loss of blood volume by sweatingor shunting of blood away from the brain. When exposedto cold, patients with sympathetic nervous system failuremay not constrict blood vessels adequately in the skin, sothat the body temperature falls (hypothermia).

Exercise

Patients with dysautonomias sometimes benefit from anexercise training program. Often, however, the trainingdoes not decrease the sense of fatigue.

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As a person exercises, the blood vessels carrying oxygen-rich blood to the exercising muscle (arteries andarterioles) tend to relax, due at least partly to theaccumulation of byproducts of metabolism. Thesympathetic nervous system normally counters thistendency, by increasing the tone of the blood vesselwalls. The blood flow to the exercising muscle thereforeis in a dynamic state of balance. Activation ofsympathetic nerves to the heart during exercise increasesthe force and rate of the heartbeat, and the total amountof blood pumped by the heart in one minute (cardiacoutput) increases. Meanwhile, like squeezing a tube oftoothpaste, pumping of muscle during exercise increasesthe movement of blood from the limbs back to the heart.The increased metabolic activity tends to increase bodytemperature, and sweating, which is stimulatedimportantly by sympathetic nerves to sweat glands,increases the loss of heat by evaporation, helpingmaintain an appropriate body temperature.

If a patient had failure of the sympathetic nervous system,excessive production of byproducts of metabolism, or aform of heart disease where there were an inability toincrease the force or rate of the heartbeat, then the bloodpressure would fall during exercise, producing a sense offatigue or exhaustion.

After exercise, when muscle pumping ceases, the bloodcan begin to pool in the legs or abdomen, while the rateof sympathetic nerve traffic falls to the resting rate. If thedecline in sympathetic nerve traffic did not balance thedecline in production of byproducts of metabolism, then

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the blood pressure would fall after exercise. At the sametime, loss of body fluid via evaporative sweating woulddecrease the blood volume. Patients with a dysautonomiatherefore can feel bad not only during exercise but alsoafter exercise. It is important to stay hydrated and toavoid activities like eating a large meal after exercise,because this can divert already limited blood volume tothe gut.

Perhaps surprisingly, even vigorously healthy, muscular,lean people can have a susceptibility to faint(neurocardiogenic syncope), and it is unclear if exercisetraining in general helps them. On the other hand, somepatients can improve by isometric calf muscle training,where the patient learns to tense calf muscles whenstanding. This tends to decrease the amount of pooling ofblood in the legs.

Pacemakers and Sinus Node Ablation

Insertion of a pacemaker in the heart can help patientswith neurocardiogenic syncope or POTS. This is an areaof active research and some controversy. In some patientswith neurocardiogenic syncope, having a pacemakerinserted may not be a cure, because the low pulse rate atthe time of fainting might not cause and might even bethe result of low blood flow to the brain. On the otherhand, a sudden absence of electrical activity in the heartproduces loss of consciousness within seconds, and inthis setting a pacemaker could be curative.

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Some patients who have a very fast pulse rate undergodestruction of the sinus node pacemaker cells in the heart(sinus node ablation). The doctor must be sure that thefast pulse rate results from a problem with the heart anddoes not result from a compensation by the sympatheticnervous system for another problem, such as low bloodvolume, because eliminating the compensation couldmake the patient worse rather than better.

Neurosurgery

Some patients with chronic orthostatic intolerance havea type of change in the brainstem called Chiarimalformation. This is an anatomic abnormality wherepart of the brainstem falls below the hole in the skullbetween the brain and spinal cord. Neurosurgery cancorrect the malformation, but the orthostatic intolerancedoes not necessarily disappear. This is a controversialtopic, and we recommend that patients seek a secondopinion before agreeing to this procedure.

Constipation or Urinary Retention

Patients with failure of the parasympathetic nervoussystem can have problems with constipation and retentionof urine in the bladder. The constipation is treated non-specifically, with stool softeners, bulk laxatives, and ifneeded milk of magnesia, magnesium citrate, senna, orcascara. Urinary retention can be associated with urinaryurgency and incontinence. Drugs that stimulate receptorsfor acetylcholine, such as urecholine, might be tried.

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Often patients with autonomic failure must learn to self-catheterize to empty the bladder, by inserting a plastic orrubber tube into the urethra and then into the bladder, inorder to obtain relief.

Water Drinking

A relatively recently described tactic to increase bloodpressure in patients with autonomic failure is to drink 16ounces of water or other fluid. Why water drinkingshould increase blood pressure in patients withautonomic failure, when doing so does not affect theblood pressure of healthy people, remains unclear.

Patients with chronic orthostatic intolerance,neurocardiogenic syncope, or POTS often keep a watercontainer with them and sip from it repeatedly during theday. This habit might indicate a tendency to dehydrationand low blood volume, but the meaning of what we callthe “water bottle sign” remains unproven.

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Drug Treatments

Several drug treatments are used fordysautonomias. Some of them are powerfulor can produce bad effects. Patients shouldtake medications only under the supervisionof a doctor with expertise and experience inthe treatment of dysautonomias.

Fludrocortisone (Florinef™)

Florinef™ is a man-made type of drug called a salt-retaining steroid, or mineralocorticoid. Florinef™closely resembles the body’s main salt-retaining steroid,which is aldosterone.

Florinef™ must be taken with a high-salt diet to work.Florinef™ forces the kidneys to retain sodium, inexchange for potassium. Water follows the sodium, andso Florinef™ is thought to increase the blood volume.The patient gains “fluid weight,” and blood pressureincreases. Because of the tendency of Florinef™ to wastepotassium, Florinef™ can cause a fall in the serumpotassium level, which if severe can be dangerous.Patients taking Florinef™ should have periodic checks oftheir serum potassium level, and if it is low take apotassium supplement.

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O

OHO

OHO

O

OH

O

OH

OH

F

Aldosterone

Fludrocortisone(Florinef™)

Florinef™ forces the body to retain salt.

Florinef™ given to patients with chronic autonomicfailure can cause or worsen high blood pressure when thepatient is lying down. Sometimes the doctor faces adifficult dilemma, balancing the long-term increased risk

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of stroke, heart failure, or kidney failure from high bloodpressure against the immediate risk of fainting or fallingfrom orthostatic hypotension.

Beta-Adrenoceptor Blockers

The main chemical messenger of the sympathetic nervoussystem is norepinephrine (noradrenaline) and of theadrenomedullary hormonal system is epinephrine(adrenaline). Norepinephrine and epinephrine producetheir effects by binding to specific receptors on the targetcells, such as heart muscle cells. There are two types ofreceptors for norepinephrine and epinephrine, calledalpha-adrenoceptors and beta-adrenoceptors.

Epinephrine (adrenaline), which stimulates both alpha-adrenoceptors and beta-adrenoceptors, producesvasoconstriction in most parts of the body, such as theskin, due to stimulation of alpha-adrenoceptors, but withthe important exception of the skeletal muscle, where theblood vessels relax, due to stimulation of beta-adrenoceptors. Because of the relaxation of the bloodvessels in skeletal muscle, stimulation of beta-adrenoceptors tends to decrease the total peripheralresistance. Stimulation of beta-adrenoceptors alsoproduces powerful effects on the heart, increasing theforce and rate of the heartbeat. Because of the effects onthe heart, the amount of blood pumped by the heart perminute (cardiac output) increases, and this increases theblood pressure when the heart is contracting, the systolicblood pressure.

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There are at three types of beta-adrenoceptors, calledbeta-1, beta-2, and beta-3. Beta-1 adrenoceptors andbeta-2 adrenoceptors are present in the human heart, andstimulation of these receptors produces about the sameeffects. In contrast, beta-2 adrenoceptors are much moreabundant in skeletal muscle blood vessels than are beta-1adrenoceptors. This difference may be relevant to thetreatment of neurocardiogenic syncope, as explainedbelow.

Beta-adrenoceptor blockers decrease the pulse rate, theforce of heart contraction, and the systolic bloodpressure. In patients with rapid pulse rates, associatedwith a sense of pounding or irregular beating of the heart(palpitations) or chest pain, beta-adrenoceptor blockersdecrease the heart rate and can help relieve the pain andprevent abnormal heartbeats or heart rhythms; however,in patients where the chest pain results from stimulationof alpha-adrenoceptors in the coronary arteries, beta-adrenoceptor blockers may not help the pain. Thesedrugs also are commonly used to treat long-term highblood pressure (hypertension). Because of decreasedsystolic blood pressure and heart rate, the rate ofconsumption of oxygen by the heart decreases, and thiscan help patients with coronary artery disease.

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Propranolol(Inderal™ )

Nadolol(Corgard™ )

Timolol(Blocadren™ )

Atenolol(Tenormin™ )

Metoprolol(Toprol™ )

Non-Selective Selective

Betaxolol(Kerlone™ )

Here are some beta-blockers. All beta-blockers decrease the rate and force of theheartbeat.

In patients with postural tachycardia syndrome (POTS),the value of treatment with beta-adrenoceptor blockersmay depend on whether the rapid pulse rate when thepatient stands up reflected a primary or compensatoryresponse. If the rapid pulse rate were a compensation foranother problem, such as low blood volume due tobleeding, then blocking that compensation would nothelp the patient. But if the rapid pulse rate were the result

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of an inappropriate, excessive rate of sympathetic nervetraffic to the heart, then blocking the effects of theexcessive nerve traffic would help the patient.

There are two types of beta-adrenoceptor blockers,selective and non-selective. Selective beta-adrenoceptorblockers block beta-1 adrenoceptors, and non-selectivebeta-adrenoceptor blockers block both beta-1adrenoceptors and beta-2 adrenoceptors. A potentiallyimportant difference between these drugs is that non-selective beta-adrenoceptor blockers block the beta-2adrenoceptors in blood vessel walls of skeletal muscle,whereas beta-1 adrenoceptor blockers do not. In patientswith neurocardiogenic syncope and high levels ofepinephrine in the bloodstream, the epinephrine mightstimulate beta-2 adrenoceptors on blood vessels inskeletal muscle. This would relax the blood vessels,decreasing the resistance to blood flow. This in turncould shunt blood away from the brain and towards thelimbs, contributing to lightheadedness or loss ofconsciousness. In such patients, non-selective beta-adrenoceptor blockers might be preferable to selectiveblockers.

Midodrine (Proamatine™)

Midodrine (Proamatine™) is a relatively new drug thattightens blood vessels throughout the body. That is, it is avasoconstrictor. Midodrine works by stimulating alpha-adrenoceptors in blood vessel walls.

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Midodrine (Proamatine™) is used to treat conditionswhere there is a failure to tighten blood vesselsappropriately, such as when a patient stands up. When aperson stands up, the sympathetic nervous system isnormally activated reflexively, the chemical messengernorepinephrine is released from the sympathetic nerveterminals in blood vessel walls, the norepinephrine bindsto alpha-adrenoceptors in the blood vessel walls, and thestimulation of the alpha-adrenoceptors causes the bloodvessels to constrict (vasoconstriction), increasing theblood pressure.

Midodrine acts like an artificial form of norepinephrine,by stimulating alpha-adrenoceptors directly. In somepatients with a fall in blood pressure when they stand up(orthostatic hypotension), the cause is a loss ofsympathetic nerve terminals, so that there is little or nonorepinephrine to release. In this situation, the alpha-adrenoceptors on the cells in blood vessel wallsaccumulate on the cell surface, and the blood vesselsbecome supersensitive (denervation supersensitivity). Inthese patients, midodrine can be very effective in raisingthe blood pressure.

In using midodrine to treat elderly men with orthostatichypotension, the doctor should be aware that stimulationof alpha-adrenoceptors can worsen symptoms of prostateproblems, such as urinary retention, urgency, anddecreased urinary stream. Alpha-1 adrenoceptor blockersare effective in treating benign prostatic hypertrophy(BPH), and alpha-1 adrenoceptors blockers interferewith midodrine.

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a1

Blood VesselSmo oth Musc le

BLOODSTREAM

MIDODRINE

BP

Midodrine works like artificialnorepinephrine, increasing blood pressure(BP) by stimulating alpha-adrenoceptors inblood vessel walls.

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Clonidine

There are two types of alpha-adrenoceptors, calledalpha-1 and alpha-2. Stimulation of either type ofreceptor in blood vessel walls causes the vessels toconstrict (vasoconstriction).

Clonidine stimulates alpha-2 adrenoceptors. Stimulationof alpha-2 adrenoceptors in the brain decreases the rateof sympathetic nerve traffic. Stimulation of alpha-2adrenoceptors on sympathetic nerve terminals decreasesthe amount of release of the chemical messenger,norepinephrine, from the terminals. Therefore, eventhough clonidine stimulates a type of alpha-adrenoceptor, clonidine normally decreases bloodpressure.

Clonidine works both in the brain andoutside the brain. It decreases the bloodpressure and often causes drowsiness.

There are several uses of clonidine in the diagnosis andtreatment of dysautonomias. In the clonidine suppressiontest, discussed in the section about tests fordysautonomias, clonidine is used to separate high bloodpressure due to increased sympathetic nervous systemactivity from high blood pressure due to a tumor thatproduces norepinephrine and epinephrine, calledpheochromocytoma. In patients with long-term highblood pressure (hypertension) due to excessive release of

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norepinephrine from sympathetic nerve terminals(hypernoradrenergic hypertension), clonidine can bevery effective in lowering the blood pressure. Clonidineis also effective in treating withdrawal from someaddictive drugs.

Clonidine usually causes drowsiness and often causes adry mouth. The sedation from clonidine can limit its use.

Yohimbine

When alpha-2 adrenoceptors in the brain are blocked,this increases sympathetic nerve traffic and increases theamount of norepinephrine release for a given amount ofsympathetic nerve traffic.

Yohimbine blocks alpha-2 adrenoceptors in the brain andon sympathetic nerve terminals, and so it releasesnorepinephrine from the terminals. The releasednorepinephrine binds to alpha-1 adrenoceptors in bloodvessel walls. This causes the blood pressure to increase.

Even though yohimbine blocks alpha-2 adrenoceptors inblood vessel walls, the drug releases so muchnorepinephrine, and there are so many alpha-1adrenoceptors in blood vessel walls, that normallyyohimbine increases the plasma norepinephrine level andincreases the blood pressure.

In patients with chronic autonomic failure and aninability to regulate sympathetic nerve traffic to intact

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a1

Blood Vesse lSmo oth Musc le

Ce l l s

BLOODSTREAM

BP

YohimbineYohimbine

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BRAIN

Sym pathet icNerve

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a2

a2 a2

Yohimbine works both in the brain andoutside the brain. The drug increases bloodpressure and the state of alertness.

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terminals, such as in the Shy-Drager syndrome,yohimbine releases norepinephrine from the terminalsand effectively increases the blood pressure. In patientswith neurocardiogenic syncope, yohimbine may preventepisodes of fainting.

Yohimbine can cause trembling, paleness of the skin,goosebumps, hair standing out, an increase in salivation,or emotional changes.

Oral yohimbine is approved as a prescription drug to treatimpotence from erectile dysfunction in men. Yohimbine,in the form of yohimbe bark, can be purchased in healthfood stores.

Intravenous Saline

Inability to tolerate prolonged standing can result fromlow blood volume, excessive pooling of blood in theveins of the legs during standing, or exit of fluid from theblood vessels into the tissues during standing(extravasation). In these situations, infusion ofphysiological saline solution can temporarily improve theability to tolerate standing up. This is also useful fordiagnostic purposes. Some patients with chronicorthostatic intolerance benefit from intravenous salineinfusion given repeatedly by way of a permanentintravenous catheter.

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Saline infusion temporarily increases bloodvolume.

Amphetamines

Amphetamines are chemicals that resemble the drug,dextro-amphetamine, or d-amphetamine.

Amphetamines are in a class of drugs called indirectlyacting sympathomimetic amines. They produce theireffects at least partly by increasing delivery ofnorepinephrine to its receptors, both in the brain andoutside the brain.

By way of effects in the brain, amphetamines increasethe state of arousal and attention, prevent or reversefatigue, decrease appetite, and at high doses increase therate and depth of breathing. By way of effects on thesympathetic nervous system, they increase bloodpressure.

Pseudephedrine (Sudafed™) is structurally a mirrorimage (stereoisomer) of ephedrine. This differencechanges the properties of the drug, producing much lesscentral nervous system stimulation. By releasingnorepinephrine from sympathetic nerve terminals in themucous membranes of the nasal airways, pseudephedrinetightens blood vessels, making them less leaky andthereby relieving nasal congestion.

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NH2

CH3

ab

AMPHETAMINE

N

CH3

OH CH3

a

EPHEDRINE

NH2

CH3

a

OH

PHENYLPROPANOLAMINE

CH3

N

CH3

ab

METHAMPHETAMINE

CH3

ab

CH3

NH2

PHENTERMINE

METHYLPHENIDATE

O OCH3

N

Amphetamines work both inside and outsidethe brain. They increase attention, decreaseappetite, interfere with sleep, and oftenincrease the blood pressure.

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Methylphenidate (Ritalin™), another sympathomimeticamine, is used commonly to treat attention deficit-hyperactivity disorder.

Phenylpropanolamine (PPE) until relatively recently wasused in over-the-counter diet pills, until the discovery ofserious adverse effects such as severe high bloodpressure and stroke.

Phentermine prescribed with fenfluramine (“Phen-Fen”)was an effective combination to decrease weight, untilserious adverse effects of this combination came to light.

In treating patients with dysautonomias, amphetaminesshould be used sparingly, because of the potential fortolerance and dependence. In patients with sympatheticneurocirculatory failure from abnormal regulation ofsympathetic nerve traffic to intact sympathetic nerveterminals, this type of drug releases norepinephrine fromthe terminals and increases the blood pressure. Somepatients with chronic orthostatic intolerance, such asneurocardiogenic syncope, can improve.

Selective Serotonin ReuptakeInhibitors (SSRIs)

SSRIs inhibit a key process that is required forinactivating and recycling the chemical messenger,serotonin. The process is reuptake of released serotoninback into the nerve terminals that store it. SSRIs arewidely used to treat depression, anxiety, and other

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psychiatric or emotional problems. They are also used totreat some forms of dysautonomias.

Procrit™ (Erythropoietin)

Procrit™ (Erythropoietin) is a particular hormone that isused as a drug. Erythropoietin in the body is released intothe bloodstream by the kidneys and acts on the bonemarrow to increase the production of red blood cells.Procrit™ therefore is helpful to treat low red blood cellcounts (anemia), such as in kidney failure. Anemicpatients look pale and feel tired. By mechanisms thatremain incompletely understood, Procrit™ tends toincrease the blood pressure. Some doctors prescribeProcrit™ to treat low blood pressure in patients withchronic fatigue syndrome who have a low red blood cellcount.

L-Dihydroxyphenylserine (L-DOPS)

L-Dihydroxyphenylserine (L-DOPS) is a type of chemicalcalled an amino acid. It is very closely related chemicallyto L-dihydroxyphenylalanine (Levodopa, L-DOPA),which is an effective drug to treat Parkinson’s disease. L-DOPA works by being converted in the brain to thecatecholamine, dopamine. L-DOPS works by beingconverted to the closely related catecholamine,norepinephrine. Since norepinephrine is the chemicalmessenger of the sympathetic nervous system, L-DOPScan provide norepinephrine even in the absence ofsympathetic nerve terminals.

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a1

B lood Vesse lSmooth Musc le

Cel l s

BLOODSTREAM

BP

L-DOPS

NE

LAAAD

VMAT

L-DOPS

LAAAD

NE

Uptake-1

VMATNE

LAAADNE

BRAIN

Sym pathet i cNerve

Endings

L-DOPS is converted to norepinephrineboth inside and outside the brain.

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L-DOPS could increase delivery of norepinephrine to itsreceptors by at least three mechanisms. One is fromuptake of L-DOPS into cells such as in blood vesselwalls, followed by conversion of L-DOPS tonorepinephrine that is speeded up by the enzyme, L-aromatic-amino-acid decarboxylase (LAAAD). Thenorepinephrine exits the cells and binds to its receptorson the cell membrane. A second mechanism is fromuptake of L-DOPS into sympathetic nerve terminals,again followed by conversion of L-DOPS tonorepinephrine. The norepinephrine is taken up intostorage vesicles and released in response to sympatheticnerve traffic. The norepinephrine exits the nerveterminals and binds to its receptors on cells in bloodvessel walls. A third mechanism is from L-DOPSentering the brain, followed by conversion of L-DOPS tonorepinephrine. The norepinephrine stimulates anincrease in the rate of sympathetic nerve traffic, resultingin release of norepinephrine from the sympathetic nerveterminals. By all three mechanisms, L-DOPSadministration would lead to stimulation of alpha-adrenoceptors in blood vessel walls, causing the vesselsto constrict and increasing the blood pressure.

L-DOPS is currently an investigational drug. It has greatpromise to treat a fall in blood pressure when the patientstands up (orthostatic hypotension) or prevent fainting.A potential problem with using L-DOPS to treatorthostatic hypotension in patients with Parkinson’sdisease is that the patients often are treated at the sametime with Sinemet™. Sinemet™ is a combination of L-DOPA and carbidopa. The carbidopa interferes with the

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conversion of L-DOPA to dopamine. Since carbidopadoes not enter the brain, the combination results inincreased delivery of DOPA to the brain and increasedproduction of dopamine. Carbidopa also interferes withthe conversion of L-DOPS to norepinephrine. This wouldbe expected to prevent or blunt the hoped-for increase inblood pressure by L-DOPS treatment.

Bethanecol (Urecholine™)

Bethanecol is a drug that stimulates receptors foracetylcholine, the chemical messenger of theparasympathetic nervous system.

Urecholine™ increases production ofsaliva, increases gut activity, and increasesurinary bladder tone.

Bethanecol increases the muscle tone of the bladder,digestive motions of the gut, and salivation. It may beuseful to treat urinary retention or constipation in patientswith chronic autonomic failure, but no formal study ofthis has been reported yet.

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Drug Goal of TreatmentFlorinef™ Increase blood volume

=Fludrocortisone Increase blood pressureProamatine™ Tighten blood vessels

=Midodrine Increase blood pressurePrevent fainting

Beta-Blocker Decrease heart rateDecrease blood pressure

Decrease adrenaline effectsPrevent fainting

Procrit™ Increase blood count(=erythropoietin) Increase blood pressure

Amphetamines Tighten blood vesselsIncrease alertness

Desmopressin Tighten blood vessels“NSAID” Tighten blood vesselsOctreotide Tighten blood vessels in gutSSRI Improve mood, allay anxiety“Tricyclic” Improve moodXanax™ Increase sense of calmness

(=Alprazolam) Improve sleepCatapres™ Decrease blood pressure

(=Clonidine) Improve sleepUrecholine™ Increase salivation

(=Bethanecol) Improve gut actionImprove urination

Yohimbine Increase blood pressure

Different centers use different drugs from along “menu” to treat dysautonomias.