Category Archives: MSA

The Parkinson’s Disease Foundation (PDF) hosted a symposia on Parkinson’s on July 18, 2008.  The overall topic is “Mind, Mood and Body: Understanding Nonmotor Symptoms of PD.”  Here’s a link to the archived recording of the symposia:

event.netbriefings.com/event/pdf/Archives/nonmotor/register.html

The second speaker, Dr. Matthew Menza, gave a good presentation on the topic of “Emotional and Cognitive Aspects of Parkinson’s Disease.”

Even though this presentation was focused on PD, some references are made to LBD.  And, of course, there are emotional and cognitive aspects to all of the atypical parkinsonism disorders.

The most important thing I got from Dr. Menza’s presentation is that SSRIs should *not* be considered as the first line treatment in dealing with depression in PD.  A recent study showed that an old antidepressant, nortriptyline (Pamelor), performed better than Paxil, an SSRI.  Other drugs that are similar to nortriptylnie are Cymbalta and Effexor.

Of the atypical parkinsonism disorders, the only antidepressant that has been studied is Elavil (amitriptyline) in PSP.  Otherwise, I’m not aware of any studies.  You might take this recent PD research to your MD to find out if his/her recommendation would change based upon the new info.

Dr. Menza spent some amount of time on antipsychotics.  He explained that there was good data to recommend Clozaril and that in some studies Seroquel performed no better than the placebo.

He did talk about Lewy Body Dementia a couple of times, but I didn’t think his description was very good.  (Dr. Menza is a neurologist and psychiatrist.)

These are my notes from his presentation and his answers to the questions directed to him.  Of course it’s much better to watch the video yourself.

Robin

Robin’s notes from:

Emotional and Cognitive Aspects of Parkinson’s Disease
Matthew Menza, M.D., Prof. of Psychiatry and Neurology, Robert Wood Johnson Medical School

Non-motor symptoms of PD include:
* sleep disturbances, fatigue, and excessive daytime sleepiness
* depression
* drug reactions, including psychosis and impulsivity
* mild cognitive impairment to dementia

The non-motor symptoms have become the focus of research because they are so important to how patients feel day to day.

Depression:  about 40% have some.  It has a major impact on quality of life and functioning (faster progression of motor symptoms; greater decline in cognitive skills; greater decline in ability to care for self).  Depression often precedes the PD diagnosis.

Symptoms of depression include:  sadness, lack of appetite, sleep problems, lack of interest and motivation, fatigue, crying spells, etc.  Some of these symptoms are seen in PD without depression.  (6:22)

Depression is very inter-related with anxiety (worrying about things in an excessive way).  Anxiety is a common symptom in PD.

What causes depression in PD?  Probably a mix of neurochemical changes in the brain that accompany PD and the stress of living with an illness.

We encourage people to get involved in support groups.  There’s a lot of knowledge in SGs about handling day to day problems.  SG members may have common wisdom that MDs may not know about.

Try relaxation techniques to help yourself forget worries and get to sleep.  Even counting sheep.

Psycho-therapies are being modified and written expressively for those with PD.  Best to find a psychiatrist or psychologist who has experience with PD.

Exercise is a good treatment for depression.

NIH funded an 8-week trial of PD and paroxetine CR (an SSRI), nortriptyline (a tricyclic), and placebo.  This is the largest and first of placebo-controlled studies on antidepressants and PD.  This study is not yet published.  (Other studies are in the works.)  Big improvement in depression for both anti-depressants but nortriptyline was much better than paroxetine.  [paroxetine CR = Paxil CR; nortriptyline = Pamelor]  Nortriptyline affects both serotonin and norepinephrine in the brain.  Paroxetine affects only serotonin.  This study calls into question the use of SSRIs as first line treatment in PD.  Two other newer drugs that affect both serotonin and norepinephrine are Cymbalta and Effexor.  Paxil was effective for some in the study.  (23:48)

Sleep problems in PD are more common than would be expected from age alone.  50-75% of people with PD have trouble with sleep.  In their current study, sleep was the #1 predictor of quality of life (even more than motor problems).  The most common sleep problem is difficulty staying asleep (74-88% of patients).  Other problems:  poor quality sleep, difficulty falling asleep, muscle movements (PLMS and RLS; up to 15%), sleep apnea (up to 12%), RBD, morning headaches.

RBD (REM behavior disorder) is a particular concern.  PD accounts for 27% of RBD cases.  32% had injured themselves and 64% had assaulted their spouse.  Acting out dreams.  Can be a few vocalizations or something more dramatic.  People are reluctant to talk to MDs about this.  There’s a good treatment for RBD that works most of the time.

Excessive daytime sleepiness (EDS) occurs in up to 51% of PD patients.

Sleep attacks (sudden onset of sleep, usually without much warning) are associated with nearly every dopaminergic medication but especially Mirapex and Requip.  3.8% of PD patients had sudden attacks while driving.  Some still debate whether these attacks are caused by these drugs or EDS.

Sleep disturbances in PD may be related to nocturia (frequent need to urinate at night), pain, dystonia, akinesia, difficulty turning, etc.  Sleep is regulated by adrenergic, serotonergic, cholinergic, and various peptidergic symptoms which are disrupted (variably) in PD.  Depression is a major risk factor.  Dopaminergics can also worsen sleep (produce arousal and suppress REM).  (33:00)

Treatment of sleep disturbances includes:  exercise, sleep hygiene, intermittent use of sleep meds (Lunesta, Ambien, etc).  Some medications may help daytime sleepiness including Provigil, Ritalin (an older stimulant), and sometimes amantadine (Symmetrel).

Sleep hygiene:  regular sleep hours; avoid excess time in bed; regular get-up time regardless of sleep quality; avoid daytime naps (of 2 hours in length; 15 minutes is OK); use bed for sleep or sex; relaxation; physical activity; sunlight in morning; bedroom quality (noise, temperature, humidity); avoid evening stimulants; avoid large evening meals.  If you are worrying, get out of bed.  (36:34)

Two categories of unusual behaviors that sometimes accompany meds given for PD:  psychosis (hallucinations and delusions); impulse control disorders (including gambling, binge eating, buying, hypersexuality).

Psychosis is rare in untreated PD.  Can be caused by all PD meds though psychosis is somewhat more frequent with dopaminergic receptor agonists.  Biggest risk factor for developing psychosis is memory impairment.

Hallucinations (seeing something that isn’t really there) occurs in approximately 30% of PD patients.  Usually these are mild.  The problem is when hallucinations are frightening.

Delusions (belief that isn’t shared by other people in your world) occur in 3-17% of patients.  Can cause major problems and be very disruptive.  Generally later in illness when memory begins to fail.  Typically persecutory (eg, fear of being poisoned, infidelity).  Please bring these up with your MD.

There was just a large study on impulse control behaviors just discussed.  Seem to occur more frequently with Mirapex and Requip but can also occur with Sinemet.  (42:03)

In the face of these problems (psychosis or impulse control disorders), the first thing MDs do is reduce the dopamine medication.  “Motion-emotion conundrum.”  If reducing the parkinson meds doesn’t solve the problem, then MDs look to antipsychotics.  (43:08)  The first antipsychotic given is Seroquel.  If that doesn’t work, then Clozaril is tried.  Clozaril requires a weekly blood sample.  Clozaril is very effective.  (43:42)

In early PD, most develop a little of what could be described as “mild cognitive impairment.”  This is impairment of tasks requiring the frontal lobe of the brain — planning, judgment, and recall memory.  This doesn’t cause major problems.  Dopamine replacement leads to some improvement.  (44:39)

The more difficult thing is the more serious memory impairment that happens later in the disease.  Quite a few people develop this.  This is not Alzheimer’s.  This is much, much slower in development than Alzheimer’s, and generally less severe.  There are trials out there looking at the typical AD drugs (such as Exelon) in PD.  In one study, Exelon had a slightly positive response, and some with PD can take this drug.  It’s worth trying.  There is a question if Namenda will work.

Dealing with cognitive impairment includes:  household safety (and preventing wandering), reminders as to the structure of the house, day care, in-home help.

It’s important to educate yourself about psychiatric issues.  Sometimes you have to educate your physician about psychiatric issues in PD.  (46:39)

Question: Is bipolar a precursor to PD?
Answer:  I don’t think so but on the other hand certainly people with PD can develop bipolar disorder (though this would be unusual).  Bipolar disorder hits people early in life.  (48:00)

Question:  Can you elaborate on Lewy bodies?
Answer:  In Lewy body disease, there is wide distribution of Parkinson’s pathology across the brain.  This is a variant of PD where the cognitive impairment and memory impairment progresses much, much more rapidly than in normal PD.  And the individuals are much more sensitive to the adverse side effects of PD.  It’s a much more rapidly progressive illness than normal PD.  Not much is known about LBD.  It can be quite a trial.  (49:10)

Question:  What were the side effects related to nortriptyline?  (50:06)
Answer:  The newer antidepressants are better tolerated.  Surprisingly, nortriptyline (an older med) was well tolerated.  There was more constipation in the nortriptyline group.  Our lesson from the study:  don’t start with an SSRI.  (51:13)

Question:  When will a cure happen?
Answer:  Someday there will be a cure.  But what do you do now?  We need research on the problems we are having right now.  (51:56)

Question:  Can you comment on the French clozapine study?
Answer:  There have been two well-controlled Clozaril trials showing Clozaril is better than placebo for psychosis.  Weekly blood draws for six months can be a problem for some.  Some of the Seroquel trials did not show that Seroquel was any better than placebo.

Question:  Can we view panic reactions as a behavioral equivalent of a motor tremor?
Answer:  I suppose you could look at them that way.  Sometimes those with anxiety have panic attacks.  I don’t know if it’s the same neurochemically.

Question:  Depression vs. anger.  Can anger be a stimulus?
Answer:  Anger can motivate people to make changes in behavior.  If people are having a lot of anger, it’s usually based on relationships and chronic problems.  Counseling may be helpful in determining cause of anger.  Is the anger a personality change?

Question:  What determines sexual dysfunction?  Compared to what you used to do?  Frequency?
Answer:  These problems are happening in people who are older, some of whom have less interest in sex.  Autonomic dysfunction can contribute.  There are also relationship issues.  If something has dramatically changed compared to the past, then we look to some cause (medication?) for the problem.  (56:09)

Question:  If a person with PD is on bipolar meds, and needs an antidepressant, is there a conflict?  Are they more likely to become manic?  Any connection?
Answer:  This is complicated.  Lithium (a bipolar med) can sometimes not be at all well-tolerated in PD.  Med changes have to be made.  But there are some bipolar meds that those with PD can take.  Depression would be seen as a function of bipolar disorder.  In bipolar disorder, we generally try not to use antidepressants because this can worsen the mania.  But we do use them in conjunction with a mood stabilizer.  (58:10)

Question:  My husband becomes agitated and anxious.
Answer:  Agitation can be many things.  Impulsivity can be a personality change.  Is there a change in impulsivity?

Question:  How effective is Remeron for depression in PD?
Answer:  We have no idea.  Remeron is a new kind of antidepressant.  It works differently than Paxil, Prozac, that class.  Remeron tends to be very helpful with sleep.  It has a lot of antihistaminic and anticholinergic effects so it can make constipation worse.  Each antidepressant needs to be studied individually:  does this drug work in this person?

Question:  Is depression in PD hereditary?  (00:48)
Answer:  We don’t know.  We think that in non-PD depression has a hereditary component (“somewhat more likely” to develop PD).  Many people, however, with no family history develop depression, and many people with a family history of depression who never develop it.  Is there something different about PD and depression compared to PD without depression?  We don’t know but it’s a good question.

The Parkinson’s Disease Foundation (PDF) hosted a symposia on Parkinson’s on July 18, 2008.  The overall topic is “Mind, Mood and Body: Understanding Nonmotor Symptoms of PD.”  Here’s a link to the archived recording of the symposia:

event.netbriefings.com/event/pdf/Archives/nonmotor/register.html

The first speaker, Dr. Ron Pfeiffer, gave a wonderful presentation on the topic of “When Parkinson’s Interferes with Gastrointestinal, Urological, Sexual and Other Functions.”

Even though this presentation was focused on PD, lots of references are made to MSA.  And, of course, GI, urological, and other symptoms appear in all of the atypical parkinsonism disorders.

I’d heard Dr. Pfeiffer speak twice previously.  There was one new item from him:  To treat irritative urinary symptoms, he prefers the newer anticholinergics (Sanctura, Enablex, Vesicare — the first two are unlikely to cross the blood-brain barrier) compared to the older ones (Ditropan, Detrol, Levsin, Urispas, Pro-Banthine).  Tricyclics such as Tofranil can be used.

Also, he mentioned an important difference between MSA and PD:  “In PD, there can be sympathetic enervation to the heart is impaired.  (36:48)  In fact, it’s almost gone.  This doesn’t affect the functioning of the heart.  This may be useful in distinguishing PD from MSA because in MSA and in vascular parkinsonism the heart is normal.  (38:10)  This can be useful but it’s not sensitive enough.”

And I will relay his warning about Reglan:  “Don’t ever let an MD put you on Reglan, which works well but is terrible for those with PD.”  I think this caution would apply to those dealing with atypical parkinsonism disorder as well because the problem with Reglan is that it depletes dopamine.

These are my notes from his presentation and his answers to the questions directed to him.  Of course it’s much better to watch the video yourself.

Robin

Robin’s notes from:

When Parkinson’s Interferes with Gastrointestinal, Urological, Sexual and Other Functions  (he starts speaking at 1:48)
Ron Pfeiffer, M.D., Neurology, University of Tennessee Health Science Center

Non-motor features of PD:
* abnormalities of sensation
* behavioral changes
* sleep disturbances
* abnormalities of respiratory function
* autonomic dysfunction –> the focus of his presentation
* fatigue

The autonomic nervous system might be called the automatic nervous system.  It handles functions we don’t have to think about including:
* gastrointestinal –> he’ll spend most of his time here
* cardiovascular
* urological
* sexual
* thermoregulatory
* respiratory

In PD, things go wrong with the autonomic nervous system.

Gastrointestinal (starts at 5:00) dysfunction was described by James Parkinson.  GI symptoms include:
* salivary excess
* dysphagia
* nausea
* decreased frequency of bowel movements
* defecatory dysfunction
* weight loss

It had been thought that GI dysfunction was due to problems in the substantia nigra (midbrain).  Braak proposes that PD changes start in two other areas of the brain:  the olfactory center and the medulla (brain stem).  The medulla affects the vagus nerve, which controls a lot of the autonomic system.

Within the GI system, there’s another nervous system that controls the gut.  This is called the enteric nervous system.  Braak found alpha-synuclein deposition in the stomach.  So maybe PD originates not in the brain but in the stomach!  Maybe PD is transported from the stomach to the brain via the vagus nerve.  Dopamine deficiency can also be found in the enteric nervous system.

Weight loss in PD occurs in 52%.  (11:10)  May precede diagnosis.  Average weight loss is 7.2 lbs. (but 22% lose > 28 lbs!).  Reason is unclear:  reduced energy intake (but calorie intake is similar) or increased energy expenditure?

Excess saliva is experienced by 70-78% of PDers.  Saliva production is actually decreased.  Reasons saliva accumulates:  decreased swallowing frequency and efficiency, tendency for mouth to be open, stooped posture.

Treatment of excess saliva:
* anticholinergics: but these can make saliva more tenacious and viscous; systemic administration probably best avoided; sublingual atropine ophthalmic solution; can cause urinary retention and memory problems; [his slide says this but he didn’t discuss it:  glycopyrrolate avoids CNS but not peripheral AEs] * intraparotid botox: but there’s risk of pharyngeal muscle weakness
* antiparkinson medication: to improve swallowing efficiency
* gum and hard candy: very useful in a social situation
* tympanic neurectomy: he doesn’t recommend this (dubious benefit)

Dysphagia in PD occurs in 30-82%, according to questionnaires.  MBS (modified barium swallow) shows *some* abnormality in 75-97% though patients may be clinically asymptomatic.  In MBS, a barium-laced liquid, pudding, and cookie are swallowed.  MBS views mouth and throat, not esophagus.  Any phase of swallowing may be affected.

Complications of dysphagia:  (17:18)
* some degree of aspiration is present in 15-56% of those with PD.  Not necessarily full scale aspiration.  Aspiration = something getting past vocal cords.
* clinically silent aspiration present in 15-33%.  Coughing or choking when eating may be a clue.
* any abnormality increases risk of pneumonia.
[his slide says this but he didn’t discuss it:  * one particular abnormality (vallecular residue) present in 88% of patients without dysphagia.]

Oropharyngeal dysfunction diagnosed by:
* MBS
* pharyngeal manometry
* electromyography
* videomanofluroometry

Esophageal dysfunction diagnosed by:
* videofluoroscopy
* endoscopy
* esophageal manometry

Other problems that can affect the esophagus but may have nothing directly to do with PD:  (18:20)
* Zenker’s diverticulum: food collects; bad breath is common; people cough up undigested food hours after eaten; can be treated surgically
* cricopharyngeal bar: muscle that doesn’t relax when swallowing; can be treated surgically
* anterior osteophytes: arthritic changes
* achalasia: enteric nervous system is damaged and constricts down

At 19:32 there’s a good slide and discussion of how to approach diagnosis of dysphagia.

GERD can also affect swallowing.

Nausea in PD occurs in 16% of unmedicated people with PD.  (20:50)
Bloating occurs in 43% of unmedicated people
Gastroparesis (impaired emptying of stomach) may be responsible

Gastroparesis symptoms:  early satiety, sense of bloating, nausea/vomiting, weight loss

If there’s gastroparesis, alternate medication delivery routes can be sought:
* subcutaneous:  apomorphine, lisuride  (used in Europe)
* enteral (jejunal):  levodopa  (used in Europe)
* sublingual:  selegiline
* transdermal:  rotigotine  (only briefly available in US)

Prokinetic drugs can improve gastric emptying:  (23:00)
* dopamine antagonists:  domperidone works the best; this med is not available in the US; “your cagey neurologist” can probably get this medication for you from Canada.  Don’t ever let an MD put you on Reglan, which works well but is terrible for those with PD.
* serotonin 5-HT4 agonists:  Cisapride, Tegaserod, Mosapride, Prucalopride, Renzapride.  None of these is available in the US currently because of potential cardiac injury.

A gastric pacemaker can be placed to treat severe gastroparesis.  This has not been studied in those with PD.

The small intestine has not been studied in PD.  The clinical consequences of small intestine dysfunction are unclear.  Could this lead to abdominal bloating?  Could this lead to altered nutrient absorption, thereby causing weight loss?

Constipation = colonic inertia.  Decreased bowel movement frequency.  (25:12)
Defecatory dysfunction is more common than constipation, though he’s not sure everyone has found that.

The Honolulu Asian Aging Study showed that people who had less than one BM per day had:
* twice the likelihood of getting PD as compared to someone who had one BM per day, and
* four times as likely to get PD as compared to someone who had two or more BMs per day.
Unclear if this means that the presence of PD was evident years before the symptoms or if decreased bowel frequency has something to do with the etiology of PD.

Colon transit time is prolonged in PD.  Occurs in about 80% of PD patients.  (27:20)

The first step to treating constipation should always be to increase the amount of fiber and fluid one consumes.  (28:48)  Americans almost universally have a fiber-deficient diet.  If adding fiber to the diet doesn’t work, try a supplement.  Eight glasses of fluid a day need to be consumed.  Add a stool softener if that helps.  Next step is Miralax, available OTC.  Can be taken as needed or daily.  Next step is another choice of osmotic laxative.  If all else fails, enemas can be used.  It’s wise to avoid irritating laxatives for fear of damaging the enteric nervous system with prolonged used.

Medications have been looked at to speed up colon transit time:  Cisapride, NT3, Tegaserod, Prucalopride, and Lubiprostone (Amitiza).  Of these, only Amitiza is available.  The others have been withdrawn due to toxicity.  A teacher of his recommends pyridostigmine for this problem.  Surgical treatment is available:  colectomy (removal of part of the colon).

Defecatory dysfunction occurs in 66% of PD patients.  This includes increased straining, painful defecation, and incomplete emptying.  Some muscles are supposed to relax and others contract when having a BM.  In PD, this doesn’t always happen.  There can be insufficient intra-abdominal pressure.  Underlying mechanisms may be due to bradykinesia, rigidity, and dystonia of the sphincters (off-period phenomenon).  You can be tested for this but the tests (including defecography and anorectal manometry) are somewhat exotic.  There really isn’t any proven treatment for this problem.

In PD, there can be sympathetic enervation to the heart is impaired.  (36:48)  In fact, it’s almost gone.  This doesn’t affect the functioning of the heart.  This may be useful in distinguishing PD from MSA because in MSA and in vascular parkinsonism the heart is normal.  (38:10)  This can be useful but it’s not sensitive enough.

Orthostatic hypotension (drop in BP when standing) occurs in 58% of people with PD — in 20% it produces symptoms, while in 38% it produces no symptoms.  Antiparkinson meds can magnify this problem.  Lightheadedness (progressing to fainting) is the typical sensation but there are many others that people don’t realize.  (39:10)  Other symptoms include:  vision problems, impaired thinking, headache in a coathanger distribution, lower back or rear-end ache (because muscles deprived of blood), fatigue or lethargy.

Postprandial hypotension (BP drops after meals) can be triggered by carbohydrates (most likely culprit).  Sitting or standing may exacerbate.  Same symptoms as OH.  May develop within 15 minutes of eating, and may persist up to 3 hours.  In a normal person, eating a meal doesn’t cause BP to drop.  Deal with this by eating smaller meals more frequently.  Or rest/relax after eating until the problem passes.

Urinary dysfunction occurs in 27-39% of those with PD, according to newer studies.  (41:10)  Troublesome incontinence is in 15%.  Symptoms correlate with stage of disease.  Two types:  irritative (most common; consists of overactive bladder contraction) and obstructive.  Characteristics of irritative bladder are:  frequent urination, nighttime urination, urination of small amounts, urgency, and “urge” type incontinence.

To treat irritative symptoms, he prefers the newer anticholinergics (Sanctura, Enablex, Vesicare — the first two are unlikely to cross the blood-brain barrier) compared to the older ones (Ditropan, Detrol, Levsin, Urispas, Pro-Banthine).  Tricyclics such as Tofranil can be used.

Obstructive urinary symptoms include hesitancy and weak urinary stream.  May develop overflow incontinence.  Treatment is more difficult.  Intermittent catheterization is probably going to be the most effective treatment.  (44:05)

Bladder ultrasound can be a useful test to differentiate if this is an overactive or underactive bladder.

Question:  Will a colectomy have an impact on PD symptoms?  (45:45)
Answer:  I don’t think so.

Question:  Can drugs like Flomax be used in women with PD?
Answer:  I don’t think so.

Question:  Any relationship between ulcerative colitis and PD?
Answer:  I’m not aware of any.  Ulcerative colitis is an auto-immune disease.  PD is not an immune-related disease.

Question:  Is there any relationship between PD and sigmoid volvulus?
Answer:  It’s very rare and has to be treated surgically.

Question:  You mentioned injections in Europe to treat nausea and bloating. (48:22)
Answer:  Apomorphine infusions can be used to deliver meds if there’s gastroparesis but this med does not to treat gastroparesis itself.

Question:  What about diarrhea?  (51:12)
Answer:  Generally diarrhea isn’t a problem with PD per se.  Although if a person has severe constipation and gets impacted, eventually stool will liquify and go around the impaction area, and cause diarrhea.  Also, some meds can cause diarrhea.

Question:  My voice is raspy.  It feels tight around my throat.  What is this from?  (51:56)
Answer:  The most common speech problem in PD is a soft, breathy voice because people are not pushing enough air past the vocal cords or the vocal cords may not be closing tightly.  When you say “raspy,” this might be that the vocal cords are spasming.  Lee Silverman Speech Therapy has been developed for those with PD.

Question:  Should someone with PD who has frequent UTIs keep getting meds or does cranberry juice work?
Answer:  If you get an infection, you need antibiotics.  Cranberry juice may prevent UTIs.  If someone continues to get infections, a urologist may put him/her on chronic antibiotic therapy as a preventive measure.

Question:  What about sexual dysfunction?
Answer:  This is common but doesn’t get talked about much.  70% of so men have ED.  ED drugs can drop BP.  44% of men have decreased libido.  Much higher percentage of women have decreased libido.  Not much treatment for decreased libido.

Audience Member Comment:  PDers who drool give good wet kisses.

Question:  Is gall bladder inflammation related to PD?
Answer:  Nothing written about this.

Question:  Is there a portable electrical device to improve bowel function?
Answer:  I’m not aware of anything.

Question:  Bee stings caused my PD symptoms to dissipate.  Twice.  Can you speak to this?  France has been studying this.
Answer:  I’m not aware of anything in the literature about this.  Presumably this is affecting the body’s immune system.

Question:  How does Viagra affect PD or vice versa?
Answer:  Drugs like Viagra can be effective in treating ED but there can be a tendency for these drugs to cause the BP to drop.  It’s not cool to faint when you are trying to get other things done.  If you already have OH, you should probably stay away from these drugs.