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There is no magic pill to cure dysphagia.

There are plenty of medications that can cause difficulties eating

and swallowing.

When we evaluate a person’s eating and swallowing function,
we have to put on our critical thinking caps, be detectives,
and collaborate with the team. To determine if there may be a
drug-induced dysphagia, we discuss symptoms and medications
with the patient/family/caregivers, medical team, psychiatrists,
pharmacists, and nurses. Lethargy, cognitive impairment,
inattention, distractibility, tremors, dry mouth, discoordination,
oral and pharyngeal delays in swallowing, food getting stuck,
burning sensation and odynophagia, drooling, dysphonia, weak
cough, aspiration, and inability to manage secretions could all
potentially be “blamed” on medications.
In this blog, I will cover some medications that Speech-
Language Pathologists (SLPs) working with adults should have
in their radar. First, I will discuss how Sinemet could relieve
symptoms of dysphagia in patients with Parkinson’s Disease
when used correctly. Second, I will cover three groups of
medications that could cause side effects which could elevate
risks for dysphagia and aspiration, particularly in geriatrics
(keep in mind the mnemonic of ABA).

1. A medication that can relieve symptoms that lead to

In the case of Parkinson’s Disease, there are case studies to
show that the delivery of Levodopa (L-dopa is the agonist in
Sinemet, which is Carbidopa/Levodopa) on an empty stomach
one hour prior to a meal can significantly improve swallow
function. Fonda, et al. (1995) noted the following: reduction in
oral tremor, reduction in laryngeal tremor during swallow,
improvements in total swallow time, reduction in laryngeal
penetration with solids/liquids, and reduction in aspiration with
liquids. I recall testing a patient with Parkinson’s Disease with a
Modified Barium Swallow and noting significant dysphagia and
aspiration. She commented during the study that the team had
kept her completely NPO for the study, including not giving her
the morning Sinemet dose. Fortunately, we were able to abort
the study, call the nurse in the ICU and have her come down
and administer the Sinemet. Not surprisingly, when the study
resumed after one hour, the patient’s swallow function returned
to within functional limits.
We should pay close attention to medications during our
evaluation. We can use our electronic medical record systems
to track administrations and timing. The Sinemet especially
needs to be on an empty stomach at least 30 minutes before a
meal, as it is absorbed in the small bowel. The rate of
absorption can be affected by delayed gastric emptying and
competition with food in the stomach (particularly amino acids).
We should also keep in mind that Sinemet can cause dry mouth,
so the clinician and team can monitor for this issue.

2. ABA = Anticholinergics, Benzodiazepines, and

Maybe you have heard the medical team talking about
Anticholinergics, “Benzos,” “typical” and “atypical”
antipsychotics. SLPs need to be ready to discuss these
medications with the medical team.
A. What do the doctors mean by Anticholinergic effects?
Anticholinergics work by blocking the neurotransmitter
acetylcholine and interrupting the “parasympathetic nerve
impulses in the central and autonomic nervous system” (per
Priff & Harold, 2005, in Pharmacology: A 2-in-1 Resource for
Nurses, pg 36). They can be used to treat spastic conditions of
the GI tract or urinary tract, motion sickness, extrapyramidal
symptoms caused by other drugs, sinus bradycardia, and more.
The main issue related to swallowing function is that many
anticholinergics are antimuscarinic agents. This effect can
cause decreased mucous and saliva production in the nose,
mouth and throat, causing a dry mouth that could also elevate
risk for dental caries.
Examples of common anticholinergics with antimuscarinic
Benzatropine (Cogentin – counteract the parkinsonian features
caused by antipsychotic medications)
Chlorpheniramine (Chlor-trimeton)
Dicyclomine (Dicycloverine)
Dimenhydrinate (Dramamine)
Diphenhydramine (Benadryl, Advil PM, Unisom, Sominex)
Doxylamine (Restavit, for insomnia)
Ipratropium (Atrovent)
Tiotropium (Spiriva)
However, the side-effects are much greater than simply a dry
mouth, and many can affect a patient’s ability to safely
consume meals. For example, other potential side effects
include: decreased coordination, memory loss, confusion,
disorientation, inability to sustain attention, illogical thinking,
visual disturbances and more. The elderly are at greater risk for
falls with anticholingergics due to sudden drops in blood
pressure upon standing (orthostatic hypotension). Geriatrics
with long-term use of anticholinergics have shown to be at risk
for mental and physical decline, with increased risk for death.
Wikipedia reported on this mnemonic for the cluster of
common side-effects (From “Anticholinergic Toxidrome” in Life
in the Fast Lane):

 Blind as a bat (dilated pupils)

 Red as a beet (vasodilation/flushing)
 Hot as a hare (hyperthermia)
 Dry as a bone (dry skin and mouth)
 Mad as a hatter (hallucinations/agitation)
 Bloated as a Toad (ileus or urinary retention)
 And the heart runs alone (heart racing, tachycardia)

B. What’s up with the Benzos?

Benzodiazepines (i.e., Lorazepam, aka Ativan) may lead to
potentially fatal respiratory depression, per drug label
warnings. They are generally used as anticonvulsants, anxiolytic
(reduce anxiety), muscle relaxants, and sedative-hypnotics.
Benzodiazepines have been noted to significantly increase the
elderly’s risk for cognitive impairment, delirium, falls, fractures,
motor vehicle accidents, and amnesia, per a lecture by Cheryl
Marks, MSN, RN-BC, FNP-BC (2015, November). With our
heightened awareness of delirium prevention recently, I find
that Ativan is almost never used in acute care treatment for the
elderly. Benzos are listed on the BEERS list of inappropriate
medications for older adults, due to the short-term and long-term
adverse side-effects. Priff & Harold (2005) noted that in
geriatric patients with liver disease and/or low serum
albumin tend to experience the neurological side-effects
to a greater degree, such as: drowsiness, confusion,
dizziness, nystagmus, vertigo, dysarthria, tremor, and more.
One can see how those CNS adverse reactions complicate a
stroke eval significantly if the patient received Ativan in the ED
for agitation. These CNS side effects can affect the patient’s
ability to feed himself and eat/swallow safely.
A. Antipsychotics/Neuroleptics/Major Tranquilizers:
This class of medication is used to treat psychotic symptoms
(such as those in schizophrenia), bipolar, major depressive
disorders, delusions, hallucinations, agitation, movement
disorders seen in Tourette’s Syndrome and Huntington’s Chorea,
and even intractable hiccups (Priff & Harold, 2005).
The “conventional” or “typical” antipsychotics are the first
generation of antipsychotic medications and tend to cause a
higher risk for adverse side-effects, such as tardive dyskinesia
and extrapyramidal symptoms. Examples of typical

 Chlorpromazine (Thorazine)
 Loxapine
 Haloperidol (Haldol)

The newer, “novel” or “atypical” antipsychotics supposedly

cause less adverse reactions. Examples of atypical
antipsychotics include:

 Lurasidone (Latuda)
 Risperidone
 Olanzapine (Zyprexa)
 Quetiapine (Seroquel)
 Aripiprazole (Abilify)
 Clozapine

Sokoloff & Pavlakovic (1997) compared two typical

antipsychotics, noting that chlorpromazine may frequently cause
sedation, orthostatic hypotension and anticholinergic effects
(dry mouth and blurred vision). Whereas, Haldol and Loxapine
may increase the risk for:

 Extrapyramidal symptoms
 Neuroleptic Malignant Syndrome (NMS)
 Drug-induced dysphagia

Neuroleptics block dopamine receptors in the basal ganglia.

Examples of extrapyramidal or parkinsonian signs are: akathisia
(restlessness), dystonia, tremors, rigidity, bradykinesia, masked
face, lack of automatic body movements. Neuroleptic-induced
parkinsonism, occurs in 12-45% of patients, especially in
elderly, per Casey (1993). The bradykinesia and muscle rigidity
may be the cause of the oropharyngeal dysphagia and
aspiration, speculated Sokoloff & Pavlakovic (1997). The side-
effects may occur at very low doses, but become more severe at
higher doses.
There are many case reports in the literature of neuroleptics
causing dysphagia. Sokoloff & Pavlakovic (1997) presented a
case of a patient with dementia whose symptoms of agitation
were not controlled by his baseline Haldol and Thioridazine, and
he was changed to Loxapine, which was increased to 5mg two
times a day. After a week, the patient started choking and
became congested. The Modified Barium Swallow Study (MBSS
or videofluoroscopy) showed: reduced mastication, tongue
pumping, reduced tongue range of motion, reduced tongue base
movement (likely due to rigidity), reduced bolus control,
delayed initiation of pharyngeal swallow, reduced laryngeal
movement, residue in valleculae and pyriforms after the swallow
with penetration on this residue, and silent aspiration on thin
liquids. The repeat study over 2 weeks after medication was
discontinued showed significant improvements.
Sliwa & Lis (1993), Dziewas, et al. (2007), and Hughes, et al.
(1994) showed similar issues with Haldol, with dysphagia
complicated by aspiration pneumonia and weight loss. Hughes
(1994) also noted that haloperidol produced a bradykinesia of
the swallowing process. The MBSS showed: poor bolus control,
reduced laryngeal elevation, decreased epiglottic inversion,
reduced cricopharyngeal opening, residue in the pyriforms, and
aspiration with liquids. Similar to many case reports, the repeat
MBSS two weeks after the removal of Haloperidol showed a
resolution of the dysphagia.
Unfortunately, many studies regarding neuroleptic drug-
induced dysphagia are case studies only. As noted by
Aldridge & Taylor’s systematic review in 2012, when excluding
commentaries and single case reports, most studies do not
use instrumental assessments to determine the
frequency of dysphagia in this population of adults with
mental illness. Only one study in 1969 by Hussar, et al. used
“cineradiographic evaluation of swallowing with thin barium
mixture,” and they found 46% of patients with schizophrenia
had dysphagia (Aldridge & Taylor, 2012, page 128). Many other
studies, using only interviews and retrospective analysis of
medical records, of course found lower incidences of dysphagia
What do you think of when you hear Haldol?
I heard a nurse describe it as “Vitamin H”!
It is perceived as a quick and effective fix for that patient who is
climbing out of bed and at risk for self-injury. What is needed is
a multidisciplinary approach to think critically about this
medication’s risks and benefits.
When I think about Haldol, I recall my own case reports of
patients who have acutely developed slurred speech, pooling
and drooling of secretions, and difficulty swallowing. I have seen
patients who have received too much Haldol end up intubated in
the ICU. I have also performed Modified Barium Swallow
Studies, showing severe dysphagia in the presence of Haldol,
only to resolve after two weeks off of Haldol.
I also recall how Haldol, invented in the 1950’s, seemed to go
out of favor in the late 1990’s. It is interesting how many papers
on the topic are from that time. However, Haldol seems to be
enjoying a recent resurgence within the last 5-10 years. These
trends may be due to the increased focus on delirium prevention
in the last 10 years.
Prophylactics and Prevention of Delirium:
I often hear physicians discussing the use of Haldol as the
pharmacologic intervention of choice to control agitation in
patients with delirium, in order to avoid benzodiazepines
and other sedative hypnotics. At times it is the drug of
choice due to its reduced anticholinergic side-effects (Sevris,
1996). Other times it is chosen for its ease of availability and
administration in oral, IV and IM forms.
Haldol is not only being used to control agitation in a patient
who already has delirium, it is also being
usedprophylactically to prevent post-op delirium in geriatric
surgery patients (e.g., Kalisvaart, et al., 2005; Wang, et al.,
2012). However, the doses are very low and for a very short
duration. Kalisvaart, et al., used 1.5mg/day preoperatively and
continued this for only 3 days postoperatively. They found no
significant reduction in the incidence of delirium, only in the
duration of the delirium and the length of stay. Wang, et al.,
only administered 0.5mg, followed by 0.1mg/hour for only 12
hours, for a total of 1.7mg. They noted the incidence of delirium
during the first 7 days was 15.3% in the Haldol group and
23.2% in the placebo group. It should be noted that some of
their measures reported as significant were of minimal
functional difference (i.e., mean length of ICU stay at 21.3
hours for Haldol group versus 23 hours for control group).
The take-home message here is that these doses were very
small and not in combination with a cocktail of other
sedating medications. This is not the neurologically impaired
agitated patient in the ICU receiving Clozapine, Zyprexa and
Haldol. This is not that patient who receives 15 mg a day of
Haldol who shows an inability to manage secretions.
Do Atypical/Novel Antipsychotics Cause Less Side
I recall a neurologist comparing Haldol to Zyprexa, as he
said: “Haldol is like banging your head into a brick wall,
and Zyprexa is just using one brick.” Atypical antipsychotics
are thought to cause less EPS side effects, but it is not so
simple, as the medications may have other side effects that
need to be avoided. One major issue with atypical antipsychotics
is that they can cause cardiovascular side effects ofQT interval
prolongation and life-threatening arrhythmias (Priff & Harold,
Zyprexa is also used for its convenient orally disolvable tab.
(Zyprexa is also known as Olanzapine, which is in the category
of “atypical,” “novel”, or 2nd generation antipsychotics.)
Prolonged use of Zyprexa can cause similar side-effects of EPS
and dysphagia. I recall a patient who was on newly taken off
Cymbalta and placed on Zyprexa and he showed severe
oropharyngeal dysphagia on a Modified Barium Swallow, with
silent aspiration and poor sensation of his diffuse bilateral
pharyngeal residue that did not clear after 4 swallows. When
retested after 3 weeks off Zyprexa and onto Seroquel (another
atypical antipsychotic), he had at least a functional swallow with
slight modifications and strategies. Larsen, et al. (2010) found
that one 5mg dose of Zyprexa pre-operatively and one 5mg
dose post-operatively reduced the incidence of delirium, but
the delirium lasted longer and was more severe in the
Zyprex group when compared to the placebo.
Sico & Patwa (2011) reported a case of Risperidone-induced
dysphagia with bulbar palsycharacteristics in a 58 year old
male with a psychotic disorder, but intact mental status. The
only change in medications was the addition of Risperidone 2
weeks prior to his dysphagia onset. All other laboratory and
neurological examinations ruled-out other causes. His modified
barium swallow study showed severe oropharyngeal dysphagia
with hypomotility, oropharyngeal residue after the swallow and
aspiration. Additionally, his voice was dysphonic; he had facial
diplegia with weakness of eye closure; he had minimal palatal
elevation with an absent gag reflex; but he did not have
extrapyramidal symptoms such as bradykinesia, rigidity or
tremor. His prolactin levels were found to be high and he
developed gynecomastia. During a hospitalization, only his
risperidone was discontinued (his baseline medications of
methadone and clonazepam were continued). Within 9 days off
risperidone, his gag reflex returned and he was started on a soft
diet. After 1 month his dysphagia and other bulbar symptoms
completely resolved, and he started to gain weight. After 3
months, his gynecomastia resolved and prolactin levels returned
to normal.
Even information released by the drug Seroquel (aka,
Quetiapin fumarate, which is another “atypical” antipsychotic
used to treat major depressive disorder, bipolar, and
schizophrenia) states that it is not approved for use in psychotic
conditions related to dementia, and it may increase the risk of
death in older adults with dementia-related conditions.
Is the Focus on Delirium Prevention Leading to Overuse
of Neuroleptics?
Are we preventing delirium while increasing the risk for
neuroleptic malignant syndrome (NMS), Tardive Dyskinesia
(TD), extrapyramidal symptoms, dysphagia, pneumonia and
death due to pneumonia?
Nagamine (2008) compared the typical antipsychotic, Haloperidol, versus an atypical
antipsychotic, Risperidone, and found that patients on Haloperidol had a reduced production
of Substance P, which was correlated with an inhibition of the swallow and cough reflexes.
Nagamine concluded that patients on haloperidol are at increased risk for aspiration, aspiration
pneumonia and mortality, especially among elderly patients with dementia and
neuropsychiatric illness.

Fortunately, others are noticing the overuse of antipsychotics

too. See this quick article on
Please also see this more in depth FDA warning regarding “increased
mortality in elderly patients with dementia-related
psychosis,” regarding Haldol injection (for immediate release)
and Haldol Decanoate injection (IM).
There seems to be a lack of consistency in recommendations for
Haldol’s usage. One can read warnings on the drug label and
from the FDA that this drug is not recommended for the
elderly, especially in treating dementia-related psychosis.
However, I was at a talk on delirium last year, and Haldol was
listed first in a chart of medications that can be used to manage
agitation in the elderly with delirium, especially when the
behavior is threatening to self or others. The
textbook, Pharmacology: A 2-in-1 Reference for Nurses,
specifically reports that conventional antipsychotics are used to
calm agitated geriatric patients.
When using Haldol to control acute agitation related to delirium,
neurological disease or dementia-related psychosis, the risks are
elevated. Because Haldol takes 30-90 minutes to work,
there is a significantrisk of giving additional doses within
that time. There is a risk of using additional medications if the
Haldol is perceived as not effective (i.e., combinations with
Zyprexa or Ativan can elevate the risk for adverse reactions
from Haldol). One of the side-effects of Haldol at high doses
is akathisia (restlessness), but agitation and restlessness are
often symptoms trying to be treated with Haldol. What
symptoms are we treating and what have we caused?
Does the “benefit” of Haldol outweigh the risks? We have to ask:

 Do we need a quick medication fix due to a lack of available

non-pharmacological interventions (i.e., delirium prevention
strategies, staff availability to be a sitter, and
calming/relaxation techniques)?
 Can the patient tolerate the elevated risk for prolonged
lethargy, aspiration on secretions, dysphagia, and poor oral

Potential Solutions:
The medical team frequently looks to Cogentin (Benzotropine)
as an antiparkinsonian medication to alleviate the parkinsonian
symptoms. However, this has significant anticholinergic side-
effects as noted above.
Discontinuation of the offending medications can lead to
resolution of the dysphagia, but it may take days to clear out of
the body and weeks for full resolution of the symptoms of the
drug-induced dysphagia. Haldol stays in the system after the
medication has been discontinued, with a half-life of 14-26
hours in IV form and 14-37 hours when given orally in
healthy individuals. It is metabolized in the liver and excreted
in the feces and urine. The elderly and/or those with liver and
kidney disease may have an even greater issue with slow
clearance of the medications.
Unfortunately, tardive dyskinesias (TD) can be persistent and
even irreversible, as the antiparkinsonian medications do not
resolve them. Per the FDA report above: “The risk (for
persistent TD) appears to be greater in elderly patients on high-
dose therapy, especially females.”

In closing, I want to stress the fact that it may not be just one
medication that is the culprit for your patient’s difficulty eating
and swallowing. The medical team also needs to consider the
issue ofpolypharmacy. Regarding the issue of
polypharmacy, check out this interview with Dr Holly Holmes, from
University of Texas, Houston. She spoke on the implications of
polypharmacy in the elderly at the SIOG 2015 (International
Society of Geriatric Oncology). She notes that polypharmacy
may be taking over 5-10 medications, but the main issue is that
the patient may be “taking more drugs than is indicated.” She
notes that polypharmacy can cause falls, cognitive impairment,
and delirium.
Hospitalized elderly patients, especially those who are critically
ill, have an elevated risk for developing delirium (up to 56%
during hospitalization and up to 87% during ICU stay per Dr
Kennedy, 2015, October). Per Kennedy’s talk, hospitalized
patients over the age of 65 with delirium have increased
risks for complications within the hospitalization, such

 prolonged length of stay (which often means prolonged

bedridden status),
 3-times greater risk for functional decline, and
 3 times greater risk for nursing home placement after
hospitalization (Kennedy, 2015, October).

Add to this the side effects of medications like

anticholinergics, benzos and antipsychotics. Then you have
significantly increased the risk for adverse consequences, such
as a drug-induced-dysphagia-related aspiration pneumonia.
During the post-operative course for an elderly patient, the risk
is also high for cognitive impairments, increased pain, anxiety
and medical complications, per Marks (2015, October). Marks
advised to avoid the following medications in older adults:

 Benzodiazepines
 Muscle relaxants (i.e., Flexeril)
 Antihistamines (i.e., Diphenydramine, aka, Benedryl has a
long half-life and should be avoided in the elderly)
 Tricyclic Antidepressants or TCAs (due to anticholinergic
effects, orthostatic hypotension, and sedation). Wilson &
Mottram (2004) noted the following common side effects with
TCAs: dry mouth, drowsiness, dizziness and lethargy. TCAs
have been replaced now by SSRIs (Selective serotonin
reuptake inhibitors, like Celexa and Prozac). However, SSRIs
may still cause nausea, vomiting, dizziness and drowsiness in
some elderly, per Wilson & Mottram (2004).

The speech-language pathologist contributes to the team

by investigating all potential root causes of the
dysphagia. We can have a big impact in this area of potentially
reversible drug-induced dysphagias.
Holmes reminds: “The pharmacist is a vastly underutilized
resource.” The pharmacist can help the team play “which came
first?” Did an increase/change in a medication(s) lead to the
dysphagia and result in a pneumonia? Was the dysphagia
caused by side-effects of confusion, inattention, dry mouth,
and/or parkinsonian symptoms?
Further research is needed to foster a multidisciplinary approach
to minimize adverse effects of medications, especially in
developing non-pharmacological interventions to reduce
agitation and delirium. If pharmacological interventions are
necessary, then “start low and go slow,” per Marks (2015,
October). Close monitoring of the patient is necessary when
adding medications, and many hospitals are now using
pharmacists assigned to the inpatient floors. Patients and
families need to be adequately informed of the risks and
potential benefits of the medications. We need more studies to
delineate the true incidence of dysphagia in the population of
patients taking typical and atypical antipsychotics.
Thank you for reading. I look forward to comments.
FREE pdf of a handy Medications Side-effects Chart that I created. This
is not a complete list of medications that could cause dysphagia-
related side-effects. The chart is meant to be a resource or
guide for the medical speech-language pathologist or other
healthcare professional. It cannot substitute consultation with
appropriate healthcare professionals. The chart covers
medications that may cause dysphagia, including esophageal
dysphagia and gastroesophageal complications, dry mouth, and
central nervous system depression.
See also the FDA search tool for quick access to most drug labels on
FDA approved drug products.

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