Current Treatment Options in Neurology (2011) 13:371379

DOI 10.1007/s11940-011-0127-8

Epilepsy

Treatment of Depression
in Patients with Epilepsy
Katherine H. Noe, MD, PhD1
Dona E. C. Locke, PhD2
Joseph I. Sirven, MD1,*
Address
1,*
Department of Neurology, Mayo Clinic in Arizona,
5777 East Mayo Boulevard, Phoenix, AZ 85054, USA
Email: sirven.joseph@mayo.edu
2
Department of Psychiatry and Psychology, Mayo Clinic in Arizona,
5777 East Mayo Boulevard, Phoenix, AZ 85054, USA

Published online: 7 April 2011

* Springer Science+Business Media, LLC 2011

Opinion statement
In this article, we review the current best evidence for the treatment of depression
in patients with epilepsy. Depression is a common epilepsy comorbidity, but it is
often unrecognized. The most important step in appropriately managing mood disorders in this population is making the diagnosis. Clinical vigilance and routine use
of a validated screening tool can improve detection and quality of care. As is increasingly the case for the general population, persons with epilepsy are often interested in exploring alternative therapies for chronic conditions, including
depression. Unfortunately, the benefit of complementary and alternative therapies
for depression currently is largely unproven for persons with a seizure history, although an early study of exercise for mild depression has shown some benefit. Concerns about drug interactions, side effects, and expense may be barriers to the
prescription of antidepressant medications for people requiring chronic antiepileptic drug (AED) therapy. For this reason, use of an AED with mood-stabilizing properties has appeal and may be appropriate for selected individuals with mild
depressive symptoms. Undue fear of lowering seizure threshold should not preclude
the prescription of an antidepressant medication, as the perceived risks are often
overestimated and rarely outweigh the risk of leaving depression untreated. At
present, the best evidence for efficacy and safety support the use of citalopram,
sertraline, or mirtazapine as initial pharmacotherapy, whereas bupropion should
be avoided. Start low, go slow, and use the lowest effective dose. Cognitive behavioral therapy is a valuable adjunct to antidepressant therapy in this population. For
people with refractory partial epilepsy and refractory depression, vagus nerve stimulation has some appeal, in that it may be beneficial for both conditions, but the
efficacy of vagus nerve stimulation in improving mood in patients with epilepsy
remains unclear.

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Epilepsy

Introduction
Depression is increased in people with epilepsy, with a
lifetime prevalence of about 30% [1]. Patients with epilepsy are three times more likely to be prescribed an
antidepressant medication than the general population, and two times more likely to report suicidal
thoughts [1, 2]. Depression can be diagnosed at any
time during the course of epilepsy and may precede
the first seizure [3]. Multiple studies have demonstrated that depression has a greater negative impact on
health-related quality of life than seizure activity [4].
Furthermore, depression has been associated with
poorer seizure outcomes, increased rates of adverse
effects from antiepileptic drugs (AEDs), and increased
medical costs [4].
Despite the frequency and significance of depression
in persons with epilepsy, it remains underdiagnosed
and undertreated [4]. The causes of underrecognition
of depression in this population are multiple.
Though many will meet the full criteria for major depressive disorder as outlined in the DSM-IV, others
may have dysthymia, atypical features such as psychosis or irritability, or a waxing and waning of
mood that depends on seizure activity. Physicians,
patients, and family members may have difficulty
distinguishing depression from side effects of seizures or AEDs, or they may consider depressed mood

to be a natural consequence of psychosocial limitations imposed by uncontrolled epilepsy. The Neurologic Disorders Depression Inventory for Epilepsy
(NDDI-E), which has been validated as a screening
tool for major depression, avoids some of the confounding effects unique to this population, but few
neurologists use such screening tools as part of routine practice [5].
Even when depression is recognized, there may be
reluctance to treat. Expanding choices of antidepressant medication have increased therapeutic options
(Table 1), but also may have decreased the comfort
of treating neurologists, who may struggle to select
an appropriate antidepressant or may feel unfamiliar
with possible adverse effects. Fear of drug interactions
and exacerbation of seizure activity by the antidepressant medication are also potent barriers to care [4].
Lack of evidence-based guidelines or high-quality
studies specific to the epilepsy population further
add to confusion on best practice. To help guide
the neurologist or internist in managing depression
in patients with epilepsy, this article reviews the scientific evidence for management of depression, including not only conventional antidepressants but
also lifestyle factors, therapy-based interventions,
and surgical avenues.

Treatment
Diet and lifestyle
&

&

Physical activity has been suggested as an intervention for persons

with mild depression [6, Class III], but it has not been well studied in
the epilepsy population. A single 12-week, prospective, randomized
study of supervised exercise versus current level of activity in 23
adults with epilepsy found improvement in mood as assessed by a
self-administered checklist [7, Class III].
Complementary and alternative medicine is increasingly used for
many disorders, often without the knowledge of those prescribing
traditional medical care. For people with a chronic medical condition, alternative medications may seem like a cheaper, safer, or
more natural alternative to prescription medications. In a survey of
persons with epilepsy, over 40% reported using botanical medications, but worrisomely, almost half believed that the herbal medication had resulted in increased seizures [8]. St. Johns wort
(Hypericum perforatum) is a popular herbal treatment for depression
and has shown some promise in placebo-controlled trials [9], Class

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Noe et. al

373

Table 1. Commonly prescribed antidepressant medications

Tricyclic antidepressants
Amitriptyline
Desipramine
Doxepin
Nortriptyline
SSRIs
Citalopram
Escitalopram
Fluoxetine
Paroxetine
Sertraline
SNRIs
Desvenlafaxine
Duloxetine
Venlafaxine
Atypical antidepressants
Bupropion
Mirtazapine
SNRIs serotonin-norepinephrine reuptake inhibitors, SSRIs selective serotonin reuptake
inhibitors.

&

II]. St. Johns wort has not been specifically evaluated in people with
epilepsy, and it carries some potential risk because induction of hepatic cytochrome P450 enzymes may alter serum AED levels [10,
Class IV]. St. Johns wort has also been reported to cause serotonin
syndrome when used in conjunction with serotonin reuptake
inhibitors [10, Class IV].
Serum folate levels have been negatively correlated with depression
scores in two case series of adults with epilepsy [11, 12; Class IV]. The
effect of folate supplementation on mood in the epilepsy population, however, has not been investigated beyond one report of positive outcome in four patients [13, Class IV].

Pharmacologic treatment
Antiepileptic drugs
&

Role as mood stabilizers: Several antiepileptic drugs are used as

mood stabilizers, most notably valproic acid, lamotrigine, and carbamazepine. Lamotrigine has been shown to have positive effects on
mood in people with epilepsy in two randomized, double-blind
trials of 7 to 8 weeks of therapy and in several open-label prospective
studies [14, Class II]. The effect of other AEDs on mood has been
inconclusively assessed at this time. An expert consensus statement
from the Epilepsy Foundation of America suggests the use of an AED
with positive psychotropic properties, such as lamotrigine, as therapy
for mild depressive symptoms [4, Class IV].

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Epilepsy

&

Role in causing suicidality: In 2008, the U.S. Food and Drug Ad

ministration (FDA) released a safety alert for increased risk of suicidal
behavior or ideation with AEDs as a class, based on a meta-analysis of
placebo-controlled AED trials [15, Class II]. This report led to a change
in the labeling of all AEDs, requiring a warning about the risk of suicidal
thoughts or suicide. The meta-analysis was controversial in the epilepsy
community, however, based on the small number of total events in the
combined studies, concern about lack of significant effect when AEDs
were evaluated individually, and failure to include many older AEDs in
the analysis. Others argued that the observed effect of AEDs on suicidality may have been blunted, as many of these studies excluded persons with significant or active psychiatric disease, including a history of
suicidal behavior. Several investigations published in the past year have
attempted to clarify this important topic, but the debate is far from
settled. Patorno et al. evaluated risk of suicide, attempted suicide, or
violent death in nearly 300,000 patients prescribed an anticonvulsant,
identified from a pharmacy database in the United States [16, Class II].
They reported an increased risk with gabapentin, lamotrigine, oxcarbazepine, and tiagabine as compared with topiramate, but only a minority of patients were taking these medications for epilepsy. The study
was criticized because of its inability to control for prescription patterns
affected by mood, chronic pain, and substance abuse. A large study of a
cohort of over 5 million patients in a general practice database from the
UK found no increased risk of suicide in patients with epilepsy taking
AEDs, but it did note an association for those with depression without
epilepsy [17, Class II]. A case-control study of 44,300 patients with
epilepsy from the United Kingdom General Practice Research Database
found an increased risk of suicidal behavior in those taking drugs defined as newer AEDs with a high potential for depression (levetiracetam,
tiagabine, topiramate, vigabatrin), but not with other newer AEDs,
older AEDs, or barbiturates [18, Class II]. In the same cohort, when
the effect of individual drugs was analyzed, only current use of levetiracetam was linked to an increased risk for suicidal thoughts or behavior
[18]. It is hoped that future studies will better clarify the risks for
mood of individual drugs, as well as the role of depression treatment in
modifying these risks.

Traditional antidepressants
Evidence for efficacy: Unfortunately, few studies of the efficacy of conventional
antidepressants have focused on people with epilepsy. Khn et al. published a retrospective study of 75 adults with temporal lobe epilepsy and comorbid major
depression who were identified from an inpatient epilepsy service, comparing
outcomes for treatment with citalopram, mirtazapine, and reboxetine [19, Class
IV]. At 20 to 30 weeks, there was a 40% reduction in symptoms of depression, and
15% to 20% of patients overall were in remission. The dropout rate was about
10% in each group but was significantly greater for mirtazapine than for citalopram or reboxetine. No patients had worsening of seizure control. Kanner et al.

Complex Partial Seizures and Depression

Noe et. al

375

examined the efficacy of sertraline in 97 adults with epilepsy and depressive disorder in a prospective, open-label study [20, Class III]. Sertraline was initiated at
25 to 50 mg per day and titrated as needed to 200 mg per day. At 1 year of followup, 54% of patients had complete resolution of symptoms. There have been two
small, open-label, prospective studies of citalopram in the epilepsy population.
The first, using flexible dosing in 43 patients with major depression, reported a
65% response rate (defined as a 50% reduction in depression rating scale score)
at 2 months [21, Class III]. The second examined low-dose citalopram (20 mg/d)
over 4 months for patients with at least mild depression and found improvement
in both depression score and improved seizure control [22, Class III]. An expert
consensus statement from the Epilepsy Foundation of America suggests initial
monotherapy with citalopram, escitalopram, venlafaxine, or mirtazapine; if that
therapy is ineffective, a transition to an alternative agent from this list as monotherapy is appropriate [4, Class IV]. Major depression that fails to respond to
two trials of an antidepressant or is associated with suicidal ideation is best referred to a psychiatrist.

&

Effect on seizure threshold: Fear of seizure exacerbation by antide

pressants is a common cause of undertreatment in persons with epilepsy
[4, 23]. Most of our current understanding of the risk of seizures comes
from studies of patients without epilepsy or from case reports of antidepressant overdose. A meta-analysis of FDA phase II and phase III trials of
psychotropic drugs performed from 1985 to 2004, involving over 75,000
patients, found an increased incidence of seizures with bupropion (0.6%)
versus placebo, but not with other antidepressant medications [24, Class
III]. Interestingly, antidepressants as a class were associated with a decreased incidence of seizures versus placebo, with an incidence of seizures
in the treatment arm of 0.3% or less for all antidepressants evaluated,
except for bupropion [24, Class III]. A prospective study of higher-dose
bupropion (200450 mg/d) over 2 months found a 0.36% rate of seizures [25, Class III]. Based on these and other reports, bupropion is not
recommended as first-line or second-line therapy for epilepsy patients [4,
Class IV].
& There are limited data on seizure outcomes for patients with preexisting
epilepsy, who are likely to be at higher risk of antidepressant-induced
events. In a retrospective study of 57 adults with epilepsy and mood disorders who were treated with conventional doses of psychotropic medication per usual practice, one third had decreased seizures and one quarter
had increased seizures over 2 months of therapy, suggesting an inconsistent
effect [26, Class IV]. Trials of sertraline, citalopram, mirtazapine, and
reboxetine in patients with epilepsy have also failed to demonstrate significant exacerbation of seizures [1922; Class IIIIV]. Drug interactions,
titration schedule, and antidepressant dose may all affect seizure outcomes.
It is best to follow the old adage of starting with low doses and proceeding
with slow dose titration to the lowest effective final dosage. If seizure exacerbation is observed, either the antidepressant or the AED can be adjusted. Concerns regarding the possibility of seizure exacerbation must be
weighed against the costs of untreated depression for each individual.

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Pharmacokinetic interactions between AEDs and antidepressants

&

Most AEDs and all antidepressants are metabolized in the liver,

making them susceptible to alterations of hepatic cytochrome P450
enzyme activity. Fluoxetine and paroxetine are strong inhibitors of
select hepatic isoenzymes, and duloxetine, bupropion, and high-dose
sertraline are moderate inhibitors. When these are added to hepatically metabolized AEDs, the serum AED level may rise, resulting in
clinical signs of toxicity [27, Class IV]. These interactions have been
reported in small studies, many performed in healthy volunteers
(Table 2). In practice, toxic effects can be avoided by appropriate
adjustment of AED dosing, and if necessary, by monitoring of serum
drug levels before and after the addition of an enzyme-inducing
antidepressant. The enzyme-inducing effect of carbamazepine may
result in lowered serum levels of tricyclic antidepressants, sertraline,
citalopram, mirtazapine, and bupropion [27, Class IV]. When initiating one of these antidepressants, the potential for interaction with
enzyme-inducing AEDs should be considered, but ultimately the
drug dose should be determined by clinical response.

&

Vagus nerve stimulation (VNS) is an approved adjunctive therapy for

medically refractory partial epilepsy. In 2005, VNS was also approved
by the FDA for the treatment of chronic depression in adults that had
failed to respond to four or more adequate trials of conventional
antidepressants. An open-label, nonrandomized trial comparing VNS
plus usual treatment versus usual treatment alone for patients with
such drug-resistant depression reported response rates at 1 year of
13% with usual treatment alone and 27% with the addition of VNS
[28; Class II]. However, a randomized controlled trial failed to note
benefit after 10 weeks of observation [29, Class I]. The utility of VNS
as a treatment for chronic depression in the epilepsy population has
been evaluated in a small study of 20 adults who were implanted
with the device and compared with 20 controls [30, Class III].
Patients in both groups had intractable partial epilepsy, and baseline
assessment demonstrated similar rates of mild depression in both
groups. With a 3-month follow-up, no significant differences in
mood were identified over the study, despite improved seizure con-

Surgery

Table 2. Effects of newer antidepressants on antiepileptic drug (AED) concentrations

Antidepressant

AED serum level

Fluoxetine

Fluvoxamine
Sertraline
increased.
Adapted from Spina et al. [27].

Carbamazepine
Phenytoin
Carbamazepine
Lamotrigine

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377

trol in the VNS group. Therefore, the role of VNS in treating depression in epilepsy remains unclear.

Cognitive behavioral therapy

&

&

&

&

Cognitive behavioral therapy (CBT) typically involves education

about the connections between thoughts, feelings, and behaviors;
problem-solving therapy; behavioral activation; and scheduled engagement in enjoyable activities. The goal of these interventions is to
increase pleasurable and activating experiences while decreasing and
eliminating the cycle of automatic negative thoughts, depressed
mood, and decreased motivation [31].
CBT has been shown to be efficacious in treating depression in the
general adult population, with efficacy rates similar to those of antidepressant medications [32, 33; Class IIIII]. Evidence on the enhanced combined efficacy of medication and CBT together in the
general population is mixed [31]. There is some evidence to suggest
that CBT may provide more protection against relapse in the future
than medication or other kinds of therapy support [34, Class III].
Well-designed clinical trials of CBT specifically in epilepsy patients have
been more limited. Many studies of behavioral interventions such as
CBT in people with epilepsy have focused on seizure frequency, rather
than mood symptoms, as the primary outcome. A Cochrane review on
the topic concluded that there is a possible beneficial effect [of psychological treatments] on seizure frequency (pg. 9), but it recommended caution because of methodologic limitations and small
samples [35]. The same review also indicated that no reliable conclusions can be drawn regarding the effects of psychological interventions on quality of life in people with epilepsy. However, it appears that
educational interventions may be of value (pg. 9).
Recent studies of CBT for depression in epilepsy have been better
designed but still have used samples that are somewhat small. With
that caveat, there is evidence to suggest that CBT reduces depression,
reduces epilepsy-related distress, and improves emotional well-being
in patients with epilepsy [36, Class I; 37, Class IV]. Additionally,
recent preliminary research suggests that CBT with a mindfulness
component may be effectively delivered via Internet or telephone,
and/or in a group format, thereby increasing its accessibility and costeffectiveness [38, Class II; 39, Class IV].

Emerging therapies
&

&

Electroconvulsive therapy (ECT) has been shown to be effective in

treating depression in the general population, but there has been
limited research on its safety and efficacy in patients with epilepsy
[40, 41; Class IV].
Repetitive transcranial magnetic stimulation (rTMS) has been shown
to be safe and effective in treating acute depression [42, Class I], but
it has not been studied in detail in patients with epilepsy.

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Epilepsy

Disclosure
Conflicts of Interest: K. Noe: none; D. Locke: none; J. Sirven: Consulting fees from Novartis, honoraria from
UCB.

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