Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Email this article to a Colleague Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to My Articles & Searches Download to citation manager Citing Articles via Google Scholar Articles by Daly, K. A. Articles by Knopman, D. Search for Related Content PubMed Citation Articles by Daly, K. A. Articles by Knopman, D.

Seizure Disorder Is in the Differential Diagnosis of Panic Disorder

Received September 22, 1999; revised December 1, 1999; accepted February 4, 2000. From the University of Minnesota, Departments of Psychiatry and Neurology, Medical School, Minneapolis, Minnesota. Address reprint requests to Dr. Daly, University of Minnesota, Department of Psychiatry, Medical School, F256/2B West, 2450 Riverside Avenue, Minneapolis, MN 55454-1495.

Key Words: Seizure

Differentiating between complex partial seizure disorder and psychiatric illness is challenging in psychiatric practice. Although seizure disorder occurs in 0.5%–2% of the general population,^1,2 the incidence of seizure disorder in psychiatric inpatients across all diagnoses is 1.0%– 4.0%.³ Distinguishing the symptoms of seizure disorder from those of psychiatric illness may be difficult because of the occasional similarity in presentation for these conditions.

Clinicians rely on the patient's presenting diagnosis when treating psychiatric disorders and often assume that psychiatric symptoms such as panic or anxiety result from psychiatric disorders. Neurologic referral is highly dependent on a psychiatrist's ability to detect subtle signs and symptoms of a neurologic disorder. The case of Mr. A. provides an example of a psychiatric patient who required such consultation in order for his presenting symptoms to be adequately explained and treated. The purpose of this case report is to highlight the role of neurologic pathology in the presenting problems of some psychiatric cases.

Case Report

Mr. A. is a 22-year-old man who presented for medication management for bipolar affective disorder. He reported that as an infant he had experienced a febrile seizure. At age 2 he had been diagnosed with panic disorder by his family physician. Mr. A. reported that his panic attacks lasted from 5 to 15 minutes, occurring after he fell asleep. By age 15, the panic attacks occurred nightly. He reported that during the attacks he experienced impending doom, depersonalization, tachycardia, and dyspnea. He was first treated for panic disorder around age 15, receiving nortriptyline (75 mg qd) from a practitioner at a community mental health center. Although his panic attacks resolved, Mr. A. still complained of episodic problems with concentration and memory. The latter problems were not addressed medically and treatment with nortriptyline was discontinued when the patient was 17 years old. By age 18, Mr. A.'s symptoms recurred nightly. He started again on nortriptyline with symptom remission. Nortriptyline was discontinued because of orthostatic hypotension.

Mr. A. remained symptom free until age 20 when, following the breakup of a significant relationship, Mr. A. began to experience panic attacks, paranoia, and insomnia and felt that he was "walking in a dream." Shortly after this, Mr. A. reported that he began to abuse alcohol, engaged in some self-injurious behavior (cutting), quit his job and school, and traveled through the southwestern United States and Mexico. His erratic behavior led to hospitalization and a diagnosis of bipolar affective disorder. Records reflect that the attending psychiatrist was also suspicious of these nocturnal episodes as possibly indicating seizure disorder. A routine magnetic resonance imaging (MRI) revealed cortical dysplasia in the right frontal cortex. An electroencephalogram (EEG) recorded paroxysmal slowing, which was activated by hyperventilation. This activity was noted to be bilaterally synchronous with right frontal accentuation. Mr. A.'s seizure was attributed to alcohol withdrawal. Mr. A.'s bipolar affective disorder was treated with carbamazepine (500 mg qd).

Mr. A. remained stable for 8 months and returned to college; however, he became depressed. A psychiatrist in private practice treated Mr. A.'s depression with buproprion (150 mg bid). Mr. A. reported improvement in his mood and resolution of insomnia. Because of his alcohol abuse and history of self-injurious behavior, he was also treated with risperidone and given the additional diagnosis of borderline personality disorder. Following this treatment, his self-injurious behavior and alcohol abuse ceased.

We evaluated Mr. A. approximately 9 months after he had been stabilized on buproprion and risperidone. At that time, Mr. A. was receiving weekly dialectical behavioral therapy aimed at treating borderline personality disorder. He reported mood swings, irritability, infrequent panic attacks, anomia, and depersonalization. He denied suicidal ideation, insomnia, self-injurious behavior, and substance abuse. His mental status exam was unremarkable. A carbamazepine level was obtained and was 6.2 (therapeutic range from 4 to 12). We continued all medications: buproprion (150 mg bid), carbamazepine (200 mg bid), and risperidone (0.5 mg qhs). Given his symptoms of anomia, depersonalization, and his history of an abnormal EEG and MRI, Mr. A. was referred to a neurologist. A sleep-deprived EEG was obtained and was normal. However, the neurologist believed that Mr. A.'s history and presentation were consistent with a diagnosis of complex partial seizure/disorder.

The neurologist's findings, along with the fact that Mr. A. reported anxiety, irritability, and dissociation associated with subtherapeutic carbamazepine levels, led us to increase his carbamazepine dose to 400 mg bid. With the increase in carbamazepine, Mr. A. maintained a serum level of 6. In addition, risperidone and buproprion, which theoretically in high doses could precipitate seizures, were tapered and discontinued.

Following this change in therapeutic regimen, Mr. A. reported stable mood and a return to both employment and college. After being stable for about 1 year, Mr. A. is now followed by a neurologist.

Discussion

The symptoms of complex partial seizures and panic disorder can be similar, making them difficult to clinically differentiate. Effective treatment of complex partial seizures obviously requires that the diagnosis be considered. Because of the low diagnostic yield, it is impractical to order 24-hour video/EEG monitoring for all panic disorder patients in order to rule out a diagnosis of seizure disorder.⁴ Cases like Mr. A., consistent with the elevated base-rate for neurologic disorder among psychiatric patients,³ make clear the need for identifying psychiatric patients who could have a seizure disorder. A detailed history and presentation can provide important indicators as to the presence of seizure disorder, as detailed below.

Past Medical History. In contrast to seizure disorders, which frequently present in childhood, first onset for panic disorder is typically in early adulthood. An initial clue that Mr. A. may have an underlying seizure disorder was the presentation of his first panic attack in early childhood.

Seizures that first begin in childhood can remit for a period of many years before resurfacing as a recurrent seizure disorder. Therefore, even when panic-like episodes begin at a typical age, a remote history of seizures should alert the psychiatrist of a possible neurological disorder.

A history of febrile seizures in childhood, along with an abnormal EEG in Mr. A., increased the likelihood that his symptoms could be associated with a seizure disorder.

Presenting Symptoms. Both partial complex seizures and panic disorder share the following characteristics: rapid onset, brief in duration, nocturnal episodes during slow-wave sleep as well as typical symptoms that accompany episodes include disorientation, impulsivity, and hallucinations and may occur during delta-wave sleep. Some researchers^3,5 have suggested that these characteristics can be used to distinguish a complex partial seizure from an episode of panic; however, distinguishing between the disorders in this way is limited because partial complex seizures can occur subcortically and escape detection. Frequently, medical conditions such as cerebrovascular disease, cardiovascular disease, and endocrinologic disorders are mistakenly diagnosed as either seizure disorder or panic disorder.^6,7 Therefore, it is critical that the clinician carefully explore the possibility of other potentially life- threatening illnesses before making a diagnosis and treating the patient for either panic or seizure disorder.

Associated Symptoms. Although highly controversial, some neurologists believe that patients with complex partial seizure disorders may have more "viscous" personalities, tend to be interpersonally clingy, and speak redundantly and circumstantially.⁸ On the other hand, panic disorder patients frequently are more anxious, have more phobias, and have avoidant behavior patterns.⁹ In fact, only about 5% of those with panic disorder are without a phobia, with agoraphobia being the most common.¹ Therefore, in the case of Mr. A., the absence of a phobia did not support the diagnosis of panic disorder.

Looking beyond the features of panic, it is possible that Mr. A.'s "mania" may have been an interictal affective response stemming from a seizure disorder.¹⁰ Barczak¹⁰ reported three interictal cases of hypomania, which persisted for days without diminished levels of consciousness following EEG documentation of temporal lobe seizures. Interictal hypomania is rarely reported; however, its occurrence is a consideration given that electroconvulsive therapy (ECT) "induced" seizures elevate mood.

Family History. Primary seizure disorders are heritable. An individual's overall risk of developing complex partial seizure disorder is 8% for siblings of an affected sibling and 6.7% for individuals who have a parent with a history of complex partial seizures.¹¹ Therefore, a patient who has a first-degree relative with a history of epilepsy strongly supports a seizure disorder diagnosis. Unfortunately, because Mr. A. was adopted as a young child from a foreign country by a couple from the United States, he was unable to provide any history concerning his biological family.

Medication Responsiveness. Panic disorder and seizure disorder can be distinguished empirically via patients' response to pharmacological treatment. Panic disorder is expected to resolve with anxiolytic drugs but not anticonvulsant drugs, and seizure disorder is expected to resolve with anticonvulsant drugs but not anxiolytics.⁵ In the case of Mr. A., bupropion, a typical antidepressant, was administered without improvement of his depersonalization and anomia episodes. Bupropion could be contraindicated in individuals with a lowered seizure threshold.⁵ Failure to respond or worsening of symptoms in response to conventional psychiatric treatment is also evidence against panic disorder, which makes an alternative diagnosis such as partial complex seizures more likely.

Conclusion

The case of Mr. A. illustrates the dilemma that clinicians encounter when differentiating between the somatic complaints associated with mental illness and the symptoms of a neurologic disorder or other medical condition. Because it is impractical to request neurological consultation for all psychiatric patients, it is desirable to identify the signs or symptoms that increase the possibility of a neurologic disease, indicate a need for neurologic consultation, and identify patients for whom such consultation is most appropriate.

Imaging techniques such at positron emission tomography, single photon emission computed tomography, and phased array MRI have shown clinical utility in imaging the brain during panic attacks and periods of epileptiform activity.^12–17 Neuropsychiatrists who use these imaging techniques will play an essential role in improving the ability to differentiate between psychiatric disorders and other neurological or medical conditions.

In summary, several features of Mr. A.'s case suggested the need for neurologic consultation to rule out complex partial seizures, including the following: 1) onset of symptoms at age 2; 2) history of febrile seizures; 3) history of prior abnormal EEG and MRI; and 4) atypical response to conventional drug treatment of psychiatric symptoms. Although any of these features alone might not be enough to warrant neurological consultation, a rather strong case for consultation is made when considering the total constellation of Mr. A.'s case.

REFERENCES

1. Robins LN, Reiger DA: Psychiatric Disorders in America. New York, MacMillan, 1991, pp 53–80
2. Kaufman DM: Clinical Neurology for Psychiatrists. Philadelphia, PA, Saunders, 1995, pp 221–261
3. Perrine K, Congett S: Neurobehavioral problems in epilepsy. Neurologic Clinics 1994; 12:129–152[Medline]
4. McNamara ME: Absence seizures associated with panic attacks initially misdiagnosed as temporal lobe epilepsy. J Psychiatry Neursci 1993; 18:46–48
5. Spitz MC: Panic disorder in seizure patients: a diagnostic pitfall. Epilepsia 1991; 32:33–37[Medline]
6. Sheepers B, Clough P, Pickles C: The misdiagnosis of epilepsy: findings of population study. Seizure 1998; 7:403–406[CrossRef][Medline]
7. Winokur G, Clayton P: The Medical Basis of Psychiatry. Philadelphia, PA, Saunders, 1994, p 143
8. Rao SM, Devinsky O, Grafman J, et al: Viscosity and social cohesion in temporal lobe epilepsy. J Neurol Neurosurg Psychiatry 1992; 55:149–152[Abstract/Free Full Text]
9. Katon W, Vitallano P, Anderson K, et al: Panic disorder: residual symptoms after the acute attacks abate. Compr Psychiatry 1987; 28:151–158[Medline]
10. Barczak P, Edmunds E, Betts T: Hypomania following complex partial seizures. Brit J Psychiatry 1992; 152:137–139[Abstract/Free Full Text]
11. Menkes JH: Textbook of Child Neurology. Malvern, PA, Lea & Ferbiger, 1990, pp 602–674
12. Fischer H, Andersson JLR, Furmark T, et al: Brain correlates of an unexpected panic attack: a human positron emission tomographic study. Neuroscience Letters 1998; 251:137–140[CrossRef][Medline]
13. Lewis DH, Ory P, Holmes MD, et al: High-resolution inter-ictal SPET and phased-array MRI in partial epilepsy and an imaging comparison with Video/EEG and outcome correlation. Nuclear Medicine Communications 1998; 19:199–206[Medline]
14. Reiman EM: The application of positron emission tomography to the study of normal and pathologic emotions. J Clin Psychiatry 1997; 58:4–12
15. Blend MJ, DeLeón OA, Jobe TH, et al: Cerebral perfusion SPECT imaging in epileptic and nonepileptic seizures. Clin Nucl Med 1997; 22:363–368[Medline]
16. Rabinowicz AL, Ezequiel S, Beserra F, et al: Changes in regional cerebral blood flow beyond the temporal lobe in unilateral temporal lobe epilepsy. Epilepsia 1997; 38:1011–1014
17. Thompson JE, Castillo M, Kwock L: MR spectroscopy in the evaluation of epilepsy. Magn Reson Imaging Clin N Am 1998; 6:21– 29[Medline]

Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Email this article to a Colleague Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to My Articles & Searches Download to citation manager Citing Articles via Google Scholar Articles by Daly, K. A. Articles by Knopman, D. Search for Related Content PubMed Citation Articles by Daly, K. A. Articles by Knopman, D.

Get information about faster international access.

Privacy Policy

Copyright © 2000 Academy of Psychosomatic Medicine. All rights reserved.

Home | Search | Current Issue | Past Issues | Subscribe | All APPI Journals | Help | Contact Us