PANIC ATTACKS
IN THE DIFFERENTIAL DIAGNOSIS AND TREATMENT OF RESISTANT EPILEPSY
Márcio
A. Benik, M.D.,* Ph.D., Fábio M. Corregiari, M.D., and Ivan Mário
Braun, M.D.
The
authors present four patients displaying panic disorder and a history of epileptic
seizures to illustrate difficulties regarding differential diagnosis between
epileptic seizures and panic attacks. The cases describe the aversive properties
of epileptic seizures, the role of visual seizure-triggering stimuli as phobic
cues, and the effectiveness and safety of clomipramine treatment of panic attacks
as an adjunct to concurrent antiepileptic medication. Depression and Anxiety
15:190-192, 2002. @ 2002 Wiley-Liss, Inc.
Epileptic
seizures and panic attacks may display similar symptoms despite distinct pathophysiologies.
Fear and anxiety can occur before, during, or after epileptic phenomena [pariente,
1991]. Gloor [1982] reports that fear is the emotion most commonly associated
with temporal lobe seizures. Seizures of insular and amygdala origin may also
display auto- nomic symptomatology [Delgado-Escueta et al., 1986].
Differential
diagnosis is usua11y simple because simple partial seizures displaying fear,
anxiety, or autonomic features genera11y progress to complex partial seizures
and/or generalize at some time [Young, 1995]. On the other hand, epileptic
patients tend to attribute a11 ictal phenomena to epilepsy and comorbid panic
disorder may be unrecognized [Weissman, 1990]. We report four patients who
had their panic attacks misdiagnosed as treatment-resistant seizures, but
who responded we11 to adjunctive clomipramine.
CASES
HISTORIES
CASE
1
Mrs.
C., 30 years old, had a 19-year history of secondarily generalized partial
seizures with visual symptomatology ("a bright point that increases until
it becomes big, round, and ye11ow"), progressing occasiona11y to tonic-clonic
fits. Seizures could be visua11y triggered by flashes and car headlights.
At 15, she began avoiding situations where her seizures could be constraining
or dangerous. She feared she "would make a scene," that "nobody would help,"
or that she would "lose her identity." She used to write her name on various
parts of her body before facing public situations alone. Anticipatory anxiety
eventually progressed to "fear attacks." This involved shortness of breath,
tingling in her hands, palpitations, marked derealization, and a strong fear
of losing control of herself. These attacks increased in frequency and were
related to exposure to feared situations such as public and crowded places
or places where strong visual stimuli were expected. Spontaneous panic attacks
began at 20. She came to us displaying daily panic attacks. Her symptoms improved
with clomipramine (CMI) 40mg/day in addition to her antiepileptic medication
[carbamazepine (CBZ) 1,200 mg/day].
CASE
2
Mr.
C., a 32-year-old truck driver, had a 10-year history of secondarily generalized
simple partial seizures with visual symptoms: "a black point rotating as a
boomerang, growing larger and larger and becoming yellow and green as it came
closer," progressing occasionally to tonic-clonic seizures. His partial seizures
could be visually triggered (e.g., by black a1id white pavements). Such stimuli
turned him anxious and he began avoiding them. Once, he felt anxious while
driving, saw the road growing alternately small and large, and felt palpitations
and shortness of breath. He was first prescribed diphenylhydantoin (DPH),
which was later replaced by phenobarbitone (PB). When he came to us at age
30, he was taking CBZ 600 mg/day. He was prescribed CBZ 800 mg/day to prevent
residual seizures. He was very anxious, got up every morning feeling his head
heavy, his body floating, and felt palpitations many times a day. The thought
of the possibility of having a seizure worsened his anxiety. He also reported
avoidance of crowded places, tunnels, and entering the sea. A diagnosis of
agoraphobia without panic attacks (but with panic symptoms) was added. Eleven
months later, his seizures were controlled but his anxiety symptoms progressed
to spontaneous panic attacks, twice a week. CMI was prescribed up to 200mg/day
and after 5 months his panic attacks disappeared. Exposure treatment was initiated
for residual agora- phobic avoidance.
CASE
3
Mrs.
P., a 34-year-old teacher, displayed one febrile convulsion at 2. She was
treated with PB until 21, even though she had no more seizures. At 30, she
reported the appearance of sudden events during which she lost her ability
to concentrate due to reverberation of words in her mind, concurrently with
feelings of desrealization and bodily symptoms, such as tingling in the fingers
and lips, tremors. and palpitations. Her neurologist asked for 5 subsequents
EEGs, two of them displaying "right-anterior temporal irritative activity."
Her CAT scan was norrnal. She was prescribed CBZ up to 2,600 mg/day, without
results. Clonazepam and PB were added, her symptoms remaining unchanged. When
neurosurgery was considered, she left medical treatment, trying acupuncture
and psychotherapy for two years. She came to us displaying daily attacks,
mostly situational, in classroom or public transportation, but also spontaneous
attacks triggered by emotions, memories, or bodily sensation of arousal. She
was always monitoring her heartbeat because she feared attacks. A diagnosis
of panic disorder with agoraphobia was made, and initial treatment with CMI
20 mg/day led to marked decrease in both frequency and intensity of attacks
after three weeks.
CASE
4
Mrs.
N., 32 years old, had a 22-year history of simple partial seizures with psychic
symptomatology progressing to type 2 [Delgado-Escueta, 1979] complex partial
seizures, which occasionally generalized. She reported a feeling of "fear
or disgust," followed by loss of consciousness and automatisms. Her seizures
could be visually triggered by patterns like black and white pavements. At
16, she reports having had her first tonic-clonic seizure and an increase
in the frequency of partial seizures. At 17, she started feeling daylong bodily
sensations of anxiety such as sweating, shortness of brea1:h, and tingling
in fingers, associated with fear of having a seizure. Sometimes similar symptoms
preceded a seizure. She began avoiding crowded streets, shopping centers,
supermarkets, and public transportation. At 24, at a party, she suddenly felt
frightened, desperate, and experienced fear of dying, associated with palpitations
and tingling in her fingers. These attacks increased, occurring up to 3 times
a day, mainly in social situations but also during sleep. She was prescribed
DPH, which was later replaced by CBZ 600 mg/day. Her agoraphobic avoidance
increased until she became housebound. Ten months later she was taking CBZ
1900 mg/day and displayed less than one complex seizure a month and no generalized
ones. Nevertheless, she was very anxious and her agoraphobic symptomatology
had not decreased. She was referred to us and was taught to distinguish the
presumptive anxious symptoms from the partial seizures and a diagnosis of
panic attacks with agoraphobia was added. After 2 months with CMI up to 100
mg/ day and exposure treatment, she displayed marked improvement in both avoidance
behavior and panic symptomatology.
DISCUSSION
Panic
attacks are brief, paroxysmal, and self-limited phenomena. Such a description
also suits epileptic fits well. Epileptic patients with panic attacks may
therefore be misdiagnosed as having uncontrollable epilepsy, especially if
their fits also have symptomatology similar to those of panic disorder. Less
commonly, but as seen in patient 3, subjects with a history of childhood epileptic
seizures may have panic symptomatology appearing during adulthood misinterpreted
as a relapse of the former.
Some
epileptic patients become anxious in anticipation of facing public places
and situations. Victoroff [1994] who studied candidates for epilepsy surgery,
found that 32% had histories of agoraphobia without panic or other anxiety
disorders. Although this leads to mainly situational panic attacks, the daylong
anticipatory anxiety may lead to non-situational panic attacks as seen in
patients 1,2, and 4. Seizure-triggering visual stimuli may also cause unpleasant
sensations in normal subjects [Wilkins, 1984] and therefore could act as aversive
stimuli.
Edlund
[1987] proposed that panic attack patients with atypical symptomatology associated
with abnormal EEG findings might benefit from CBZ or alprazolam therapy instead
of tricyclic antidepressants (fCA). According to Lishman [1998], even though
atypical symptomatology may suggest a specific organic underlying etiology
in psychiatric disorders, the finding of an abnormal interictal EEG does not
warrant a diagnosis of epilepsy, so the use of CBZ instead of TCA is not justified
based on such pathophysiological assumptions alone. Indeed, our patients,
though having both EEG abormalities and a history of epileptic seizures, did
benefit from CMI in addition to their antiepileptic therapy.
Acknowledgements.
We thank Dr. Jessie M. Navarro for the EEG analysis and Dr. Silvia C. Bronisser
for clinical assistance.
REFERENCES
Delgado-Escueta
AV: 1979. Epileptogenic paroxysms and clinical correlations. Neurology 29:1014-1022.
Edlund
MJ, Swann AC, Clothier J. 1987. Patients with panic attacks and abnormal EEG
results. AmJ Psychiatry 144:508-509.
Gloor
P, Oliver A, Quesney LF, Andennann F, Horowitz S. 1992. The role of the limbic
system in experimental phenomena of temporallobe epilepsy. Ann Neuroll2:129-144.
Pariente
PD, Lepine JP, LellouchJ. 1991. Lifetime history of panic attacks and epilepsy:
na association from a general population survey. J Clin Psychiatry 52:88-89.
VictoroffJ.
1994. DsM-m.R psychiatric diagnoses in candidates for epilepsy surgery: lifetime
prevalence. Neuropsychiatry Neuropsy- thol Behavioral Neurol 7:87-97.
Weissman
MM. 1990. The hidden patient: unrecognized panic disorder. J Clin Psychiatry
51 :5-8.
Wilkins
A, Nimmo-Smith I, Tait A, McManus C, D~lla Sala S, Til1ey A, Arnold K, Barrie
M, Scott S. 1984. A neurological basis for visual discomfort. Brain 107:987-1017.
