Running Head: SLEEP ON IT
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Sleep on It:
A Literature Review of Zolpidem’s Bizarre Side Effects
Katherine A. Hoffman
Barnard College
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Abstract
This paper explores the controversy surrounding zolpidem’s rarer side effects. Zolpidem has
been known to trigger potentially dangerous nocturnal behaviors such as sleep-related eating
disorder, somnambulism, and sleep driving. A review of recent and past literature suggests that
zolpidem’s adverse side effects are not as rare as previously thought. For patients with a history
of mental disorders, brain injuries, parasomnia, and disorders that disrupt sleep, the risk
presented by zolpidem may not be justifiable. Additionally, practitioners should closely monitor
their patients when zolpidem is taken in conjunction with other drugs.
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Sleep On It:
A Literature Review of Zolpidem’s Bizarre Side Effects
Background
Though all humans sleep, its exact purposes remain controversial in the scientific
community. While both Shakespeare and Cervantes related sleeping to death, recent research
contradicts such representations of the brain’s activity during rest and suggests that the human
brain is not as dormant during sleep as previously thought. In fact, some areas of the brain, such
as parts of the amygdala (Nielsen & Stenstrom, 2005), are more active during rest than during
wakefulness. Furthermore, if avoidance of sleep was biologically possible, natural selection
probably would have favored it (Devitt, 2005). This indicates that sleep serves a vital, if
unknown, purpose in everyday life. Even if scientists argue about the exact roles such an activity
plays, the importance of sleep can be experienced outside of the laboratory through the
unpleasant symptoms resulting from a deprivation. Several studies have found that cognitive test
scores drop dramatically as the time spent sleeping also decreases (Abdulla, 2002). Probably no
one is more familiar with the seriousness of sleep loss than Nick Moloney, a solo yacht racer.
Once, after enduring five days without sleep, Moloney almost died due to impaired judgment
(Browne, 2004).
In addition to cognitive deficits, a lack of sleep has been linked to a number of troubling
conditions such as diabetes, hypertension, cardiovascular risk, and stroke. According to David
Dinges, a professor at the University of Pennsylvania, these links increase with more than eight
hours of sleep or less than seven (Tuma, 2006). Patients with sleep apnea are almost two times
more likely to have heart problems or a stoke (Tuma). Sleep and the immune system also appear
to be correlated as four to five hours of sleep a night for about a week result in an abnormally
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high white blood cell count, as if the body is preparing to fight an infection (Flatow, 2007).
Princeton University recently monitored the stress hormone corticosterone in relation to sleep
and found that the amount of time spent sleeping was inversely related to the level of this
hormone. The higher the hormone concentration, the slower the proliferation of brain cells in
specific areas on the hippocampus (“No sleep,” 2007).
These sleep deficit results are important due to the prevalence of insomnia and other
sleep disorders. According to the Mayo Clinc, more than 10% of adults have chronic insomnia
while about a third has experienced insomnia at some point in their lives (“Insomnia,” 2009).
The high incidence of insomnia is even more obvious in the National Sleep Foundation poll,
which indicated that almost 6 out of l0 adult Americans experience at least one symptom of
insomnia a few nights a week (Oh, 2006). While studies have shown that some individuals have
a biological advantage when it comes to sleep, this biological advantage benefits only a minority.
The gene known as adenosine deaminase, thought to induce log-like sleep, has been found in a
paltry 10% of Americans (“To sleep,” 2005) and the unlucky 90% of people remaining must find
sleep naturally, rely on prescription drugs such as Lunesta and Ambien, or take dietary
supplements like melatonin to experience a more satisfying slumber.
Given the findings about sleep deprivation and the pervasiveness of sleep disorders like
insomnia, it comes as no surprise that the pharmaceutical companies have prioritized the
development of hypnotic drugs. The trend towards controlling sleep began with the discovery of
chloral hydrate, which excites the inhibitory gamma-Aminobutyric acid (GABA) receptor
complex, in 1832 (Thornton, 2010). By the mid-20th century, the barbiturates, which bind to
alpha subunit of the GABAA receptor, had replaced chloral hydrate as the preferred sleepinducing medicine (Thornton). Unfortunately, these barbiturates were associated with a high risk
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of dependence and abuse so when the alternative benzodiazepines emerged in the 1970s, they
were hailed as the new sleep method. By 1978, Americans were taking 2.3 billion tablets of
benzodiazepines annually despite mounting concerns about their physically addictive properties
(Thornton).
A new sleeping pill wasn’t introduced into the market until the United States Food and
Drug Administration (FDA) approved the more selective drug zolpidem in 1992, followed by its
successors zaleplon and eszopiclone in 1999 and 2004 respectively (Thornton). According to
reporter Melissa McNamara, by 2005, more than 26 million prescriptions Ambien, the brand
name for zolpidem manufactured by the French Sanofi-Aventis company, were sold annually for
a profit of more than two billion dollars (2006b). When the patent to zolpidem tartate expired in
the fall of 2006, Sanofi-Aventis distributed a controlled release version of the drug they dubbed
Ambien CR (Oh, 2006). This newer version’s patent will not expire until June 2020, allowing
Sanofi-Aventis to maintain its position as the world’s third largest pharmaceutical company
(Oh). Despite its original intention of treating short-term insomnia, studies indicating that
Ambien produces no signs of tolerance suggest that Sanofi-Aventis is pushing for the approval of
Ambien as a treatment for chronic insomnia as well (McNamara, 2006a).
However, 10 years after its initial launch in the American pharmacology market, journals
and mass media outlets alike began to report on a series of bizarre side effects linked to zolpidem
use (McNamara, 2006b). Short-term amnesia has been linked to the drug and researchers
Wesensten, Balkin, and Belenky found that zolpidem produced memory impairment even when
administered at levels so low that they did not induce sleep (1995). Participants in this study
failed to successfully complete two Weschler Memory Scale Associative Learning sub-tests and
the Buschke test but zolpidem has the capability of triggering anterograde amnesia for more than
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just word associations (Wesensten et al.). Patients using the drug reported eating anything from
raw bacon to salt sandwiches to entire tubs of margarine in their sleep (McNamara). This
unconscious calorie intake has been known to cause a weight gain of more than 100 pounds in
some patients (Thornton, 2010).
In addition to abnormal sleep eating behaviors, some of zolpidem’s rarer side effects
include delusions, euphoria, and hallucinations. Actor Lindsey Lohan blamed the latter for
leading to a life-threatening bathtub incident and she’s not alone. In a three-week clinical trial,
almost four percent of participants taking the controlled release version of Ambien reported
hallucinations (“Ambien,” 2010) and researchers Elko, Burgess, and Robertson found that
selective serotonin reuptake inhibitors may intensify and extend the life of these hallucinations as
well (1998).
Even more troubling than nocturnal binge eating and hallucinations, however, is sleepdriving. United States Representative Patrick J. Kennedy of Rhode Island placed the blame for
his collision near the Capitol in 2006 on Ambien (Pear & Hulse, 2006) while in Denver, a
registered nurse with a previously clean record was charged with careless driving. She
remembers waking up in the middle of an intersection while arguing with police over a fender
bender and wearing only a thin nightshirt despite the winter chill and blames her amnesia and
actions on Ambien (Saul, 2006). Another incident that has been attributed to Ambien involves a
parole officer from South Carolina who woke up in jail to learn he had left his bed and driven
into a tree (Saul). From 1999 to 2004, 187 Wisconsin drivers arrested for traffic violations tested
positive for Ambien (Saul) but more interestingly, the blood work from 53 most extreme cases of
impaired driving in Wisconsin indicated that each driver had tested positive for zolpidem
(McNamara, 2006a). Furthermore, the director of the Minnesota Regional Sleep Disorders
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Center has evaluated 52 separate criminal cases where the defendants have blamed their actions
on drugs. Out of these cases, 50 cases involved Ambien (Thornton, 2010). While prosecutors
have argued that Ambien makes for a convenient alibi, a few medical researchers claim that
sleep-driving is more than just a possibility. In 2006, Dr. Carlos Schenck, a sleep disorder expert
from the University of Minnesota Medical Center, believed that the makers of Ambien should
have printed a stronger warning label (McNamara).
Meanwhile in New York, attorney Susan Chana Lask coined the term “Ambien zombie”
and filed a class-action lawsuit in 2006 against Sanofi-Aventis claiming that more than 1,000
people “suffered injury or damage as a direct result of their Ambien use” (Thornton, 2010). Lask
charged that the pharmaceutical giant did not provide adequate warnings to doctors, patients, and
the public about the possible side effects and said, “The memory loss is the worst part. People do
things for seven hours at a time and they don’t know what they’re doing” (“New York,” 2006).
By 2007, the FDA demanded that Sanofi Aventis place harsher warnings on their labels about
complex sleep-related behaviors and urged the company to remind users not to take the pills with
other drugs that suppress the nervous system.
Perhaps a few of these rare side effects can be explained through the pharmacodynamics
and pharmacokinetics of zolpidem. This “z-drug,” which is usually administered orally in pill
form, has a half-life of two to three hours, and takes effect within 15 minutes of ingestion (Salvà
& Costa, 1995). In terms of pharmacodynamics, zolpidem is a functionally discriminating
GABAA receptor agonist with a high affinity for the α1 subtype (Hoque & Chesso, 2009).
Researchers believe that this affinity is responsible for the drug’s sedative-hypnotic and
anticonvulsant activities (Crestani, Martin, Möhler, & Rudolph, 2000). However, it has been
shown to bind with the α2 and α3 subtypes with an intermediate affinity as well (Hoque &
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Chesso). Whether it binds with the α5 subtype with a low affinity or not at all is still up for debate
(Crestani et al.; Hoque & Chesso).
The ω1 type GABA receptors contain the α1 subunit and are found primarily in the brain
while the ω2 GABAA receptors that contain the α2, α3, α4, α5 and α6 subunits are found primarily in
the midbrain and spine (Hoque & Chesso). Zolpidem therefore prefers to bind to the ω1 type
GABAA receptors when compared to the corresponding ω2 types (Itier, Depoortere, Scatton, and
Avenet, 1996). This means that zolpidem preferentially binds to the GABAA-benzodiazepine
receptor complex in the brain which contrasts with lower binding rates in the spinal region. Thus
Ambien and its generic equivalents have a hypnoselective profile and they quiet the “intelligent
faculties” while leaving the “primitive reptilian faculties” relatively untouched (Thornton, 2010).
This means that a “subtle environmental stimulus is more likely to rouse the reptilian brain
without waking the intelligent brain promoting parasomnia” (Thornton).
A more precise model that could explain the parasomniac behaviors of patients taking
zolpidem is the cerebral central pattern generator (CPG) hypothesis. This hypothesis predicts that
there are a series of “neuronal collections in the brain, brainstem, and spinal cord that can control
innate motor behaviors essential for survival” (Hoque & Chesso, 2009). It’s possible that
zolpidem binding may activate some of these CPGs associated with motor patterns like walking
and eating. Furthermore, this theory can explain how activities not necessary for survival, like
driving, might be incorporated into an individual’s unusual nocturnal behaviors. Since some
CPGs may reside in the cortex, zolpidem may also “release cortical patterns associated with
overlearned behaviors” (Hoque & Chesso, 2009). These overlearned behaviors could include
eating and driving leading to dangerous consequences not just for zolpidem user, but for nonusers as well.
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Central question
Due to the potentially dangerous nocturnal behavioral patterns that zolpidem use
presents, a review of current findings regarding these side effects may shed light on who is most
susceptible to zolpidem-induced parasomnia and just how common these sleep-related disorders
are. This information can be useful to clinicians who treat patients for insomnia, lawmakers who
have the jurisdiction to alter penal law, and insomniacs who are considering turning to
prescription medications for help.
Literature review of the prevalence of adverse side effects
Although zolpidem has been under researchers’ scrutiny since the late 1980s,
disagreement regarding the percentage of patients that experience adverse side continues. In
1988, researchers conducting a post-marketing research survey found that one out of 96 patients
(or about 1.04%) developed sleepwalking after taking an unknown dose of zolpidem (Sauvanet
et al.).
Two years later, a survey of 93 surgical patients found that 45% of participants
experienced significantly more anterograde amnesia after 20 milligrams (mg) of zolpidem were
administered when compared to the placebo (Praplam-Pahud, Forster, Gamulin, Tassonyi, &
Sauvanet, 1990). It is interesting to note that patients in this study received twice the
recommended dosage for zolpidem. Considering the surgical preparation context, this makes
sense but nevertheless, questions about the results from using half this dosage remain.
In Switzerland not more than five years later, researchers Ganzoni, Santoni, Chevillard,
Sébille, and Mathy conducted a post marketing research surveillance survey of 1,972 insomniac
patients and found that 1.1% of patients experienced anterograde amnesia or somnambulism
while about 0.4% experience sleepwalking (1995). This anterograde amnesia percentage is far
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less than the 45% found in 1990 while the sleepwalking percentage is much smaller than the
1.04% found in 1988. The dose of zolpidem prescribed could explain some of this discrepancy
but unfortunately, dosages weren’t available. When it comes to anterograde amnesia, the more
personal method of rigorous interviews before and after administration as seen in the PraplamPahud et al. study is far more likely to detect memory gaps than a post-marketing research
survey that relies on the reports of patients, who by the very definition of amnesia, may not
remember experiencing it.
Later, researchers found no significant side effect differences between zolpidem and the
placebo when prescribed at 7.5 mg and 10 mg levels (Roth, Roehrs, & Vogel, 1995). However,
this study was designed to determine zolpidem’s capacity for helping with transient insomnia
and therefore consisted of 462 healthy volunteers and included only one trial period. Past
literature has indicated that healthy patients respond differently to zolpidem when compared to
patients who have a history of parasomnia or other disorders that disrupt regular sleeping
patterns. Furthermore, more and more clinicians are prescribing Ambien or its generic spinoffs
for patients plagued by chronic insomnia. Thus a single trial period does not accurately represent
the usage trends of the patients at large.
In 1993, researchers Cluydts and Deroeck used a variety of scales, including diary
entries, to monitor 651 patients prescribed ten milligrams of zolpidem over the course of three
weeks. Their results indicated that 9.7% of participants experienced adverse side effects. This
study relied solely on the reports of the patients. Such a method is problematic when the drug
being studied has been shown to cause amnesia. In a later clinical surveillance study from 1998,
Hajak and Bandelow followed 16,944 German patients who were prescribed 5-20 mg of
zolpidem. Of the participants studied, 268 listed adverse side effects, which is about 0.7%. This
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is a whole nine percentage points lower than the 1993 study. One possible explanation is the
differing dosages. This later survey included some patients who were taking half the dose
prescribed in the earlier study. Furthermore, this was a clinical surveillance study and as such, an
unknown number of patients may have dropped out due to these adverse side effects.
Furthermore, Cluydts and Deroeck monitored their patients for three weeks (1993) while Hajak
and Bandelow provided no timeline (1998).
A more controlled study, which was placebo controlled and double blind, observed the
memories of 16 healthy volunteers before and after taking zolpidem (Mintzer & Griffiths, 1999).
The researchers found that 15 mg of this nonbenzodiazepine impairs explicit memory following
administration. According to the study, this deficit is especially pronounced when acquiring
contextual information. Moreover, they found that zolpidem enhances memory capacity for
information presented directly before administration. Once again, the problem of focusing on
healthy volunteers remains. Furthermore, considering that zolpidem is intended to be taken just
before bed, clinicians and patients alike may not give these warnings about explicit memory
much weight.
A second study conducted in 2006 also involved 16 volunteers with no history of sleep
disorders. Researchers Berthelon, de Longcamp, Coquerel, and Denise administered 10 mg of
zolpidem to each participant and measured their perception the following morning through a
battery of visual tests. Results indicated that zolpidem did not affect day-after perception.
Driving impairments found in prior studies must therefore be explained through other
deficiencies, such as weakened motor or cognitive capacities. While such a conclusion is valid
for healthy patients who intend to drive the following morning, it might not generalize to patients
with sleep disorders who are especially affected by this z-drug’s side effects.
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While this 2006 study focused on the effects of zolpidem on perception, a study
conducted the following year looked at zolpidem’s effects on the elderly. Verster, Volkerts,
Spence, Alford, and Pandi-Perumal ran a series of battery tests on 35 healthy elderly insomniac
volunteers and who were administered 15 mg of zolpidem. They found that this test group
demonstrated significantly poorer scores on delayed recall tests (2007). However, this result was
not found in the groups administered 5, 10, or 20 mg dosages. Furthermore, their test group of 48
healthy elderly volunteers showed impaired body sway after administration of only five
milligrams of zolpidem. However, no other memory, reaction, recognition, tracking ability, or
scanning impairments were found in either test group. The fact that scores only dipped on
delayed recall tests at the 15 mg dosage points demonstrates the importance that dosage plays in
zolpidem’s vast array of side effects. While the scanning and tracking findings coincide with the
2006 study on perception, the finding of no significant memory impairments besides delayed
recall contradicts Mintzer and Giffiths’ findings in 1999. However, in this more recent study, all
research was conducted the morning after administration instead of directly after allowing
sufficient time for zolpidem’s level to deplete.
The most recent article following zolpidem’s adverse side effects was a retrospective
study conducted in Taiwan which recorded information from 255 patients (Tsai et al., 2008).
Unlike many of the prior studies, Tsai and his fellow researchers also took the reports of family
members and housemates into account and found that 13 patients, or about 5.1%, experienced
adverse side effects. They also found that the anterograde amnesia associated with zolpidem is
dose-dependent and occurs more frequently at dosages exceeding 14 mg. This percentage far
exceeds that of Hajak and Brandelow’s study at 0.7% (1998) but is lower than Cluydts and
Deroeck’s finding at 9.7% (1993). Part of this discrepancy may be due to how each study defined
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“adverse effects” as none of the definitions are consistent. It may also be due to the varying
methods. This latest study also surveyed spouses and housemates leading to a far higher
percentage than the study from 1998. Another confounding factor may be genetics which have
been known to play a role in drug reaction. Participants in the most recent study were Taiwanese
and the participants in the 1998 study were German and it’s possible that this difference in
nationality between the two pools of participants can account for part if not all of the
discrepancy.
Literature review of case studies
While the experimental studies following zolpidem and its rarer side effects are scarce,
there is an abundance of case studies describing its more bizarre side effects such as sleep-related
eating disorder (SRED), somnambulism, sleep-painting, and even hallucinations (“ADRAC
warns,” 2007; “Zolpidem interaction,” 2007). Seven case studies (Chiang & Krystal, 2008;
Dang, Garg, & Rataboli, 2009; Harazin & Berigan, 1999; Hoque & Chesson, 2009;
Morgenthaler & Silber, 2001; Najjar, 2007; Sansone & Sansone, 2008; Sharma & Dewan, 2005)
describe SRED episodes in zolpidem users. In the case report by Chiang and Krystal, both
patients had a history of restless leg syndrome (RLS) and obstructive sleep apnea (OSA). In the
report by Hoque and Chesson, the patient had a history of mild OSA in addition to hypertension,
depression, and hyperlipidemia. Similarly, the patient in Najjar’s study had OSA and depression.
In Morgenthaler and Silber’s case study, all five patients all had RLS and three had OSA. In the
remaining case studies that reported SRED associated with zolpidem use (Dang et al.; Harazin &
Berigan; Sansone & Sansone), all patients were prescribed 10 mg of zolpidem and were between
45 and 51 years of age with no history of sleepwalking and no documented diseases. The most
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notable case of SRED involves a man who drove to his own candy shop to devour sweets while
sleeping—twice (Dang et al.).
Another frequently reported side effect of zolpidem, somnambulism, was reported in five
cases (Lange, 2005; Mendleson, 1994; Sattar, Ramaswamy, Bhatia, & Petty, 2003; Sharma &
Dewan, 2005; Yang, Dollear, & Muthukrishnan, 2005). In both the Mendleson and Lange case
reports, the patients had a history of sleepwalking. Meanwhile, the patient featured in the Sattar
et al. report was taking zolpidem in conjunction with two other drugs. Furthermore, the patients
in the Yang et al. and the Sharma and Dewan studies were diagnosed with a traumatic brain
injury and schizophrenia respectively.
These patterns indicate that zolpidem’s dangerous side effects are more common in
individuals who are plagued by disorders that disrupt normal sleep (like sleep apnea) and in
those with a history of parasomnia. Patients with mental disorders or brain injuries may also be
more vulnerable to these supposedly rare side effects. Additionally, clinicians should take
precautions when prescribing zolpidem in conjunction with other medications.
Conclusion
Current evidence suggests that zolpidem’s adverse side effects such as somnambulism
and SRED are not as rare as previously thought. For patients with a history of mental disorders,
brain injuries, parasomnia, and sleep disorders, the risk presented by zolpidem may not be
justifiable. Furthermore, practitioners should closely monitor their patients when zolpidem is
taken in addition to other drugs.
Future studies incorporating DNA analysis may lead to identification of specific genetic
susceptibilities to such unwanted and dangerous side effects. It’s also possible that different
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formulations of zolpidem, especially with the development and marketing of the extended
release tablets, may present different side effect profiles.
15
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