Temporal Lobe Epilepsy Confused With Panic Disorder: Implications for Treatment Stephen I. Deutsch, MD, PhD, Richard B. Rosse, MD, Indu M. Sud, MD, and Jessica A. Burket, BS Abstract: A 34-year-old woman with a 9-year history of unprovoked attacks of anxiety and dyspnea associated with symptoms of deper- sonalization and derealization is presented. The attacks increased in frequency and were associated with internal derogatory voices, vivid frightening imagery, and suicidal ideation, leading to 3 emergency psychiatric hospitalizations in a period of less than 3 months. She had been treated unsuccessfully for a presumptive diagnosis of panic disor- der without agoraphobia, prompting a reconsideration of this diagno- sis. Although electroencephalography and magnetic resonance imaging findings were normal, temporal lobe epilepsy was considered and the patient responded rapidly and dramatically to carbamazepine. Panic disorder and temporal lobe epilepsy can be confused with each other; proper diagnosis is necessary for selection of effective pharmacotherapy. Although uncertain, the contribution of sustained exposure to carbon monoxide as an adult may have contributed to the emergence of panic symptoms, which would be an unusual clinical presentation. Key Words: panic disorder, temporal lobe epilepsy, depersonalization, derealization, carbamazepine, carbon monoxide (Clin Neuropharm 2009;32: 160Y162) A case is presented that highlights the importance of rec- ognizing that temporal lobe epilepsy can coexist with panic disorder or present as panic disorder; in the former case, pathophysiologic mechanisms may be shared by the 2 disor- ders. 1Y9 Diagnostic confusion between episodes of panic or ep- ileptic aura with prominent fear is not uncommon even among experienced clinicians because, in addition to fear, both of them may present with tachycardia, fluctuations of blood pressure, diaphoresis, flushing, and depersonalization and derealization. 6 In patients with epilepsy, these symptoms occur both ictally and interictally. 7 Diagnostic difficulties are further exacerbated by the not infrequent presentation of simple partial seizures in the absence of electroencephalographic (EEG) findings and psy- chogenic elaboration of seizure-related phenomena. 7,10 There is an impression that presentations of panic attacks with evidence of autonomic instability such as tachycardia, blood pressure fluctuations, and hyperventilation in patients with temporal lobe epilepsy reflect a pathologic condition lateralized to the right hemisphere. 7 Shared descriptive and phenomenological features of pa- nic disorder and complex partial seizures may be related to ob- servations that nonspecific but definitely abnormal EEG findings occur more frequently among patients with panic disorder and epidemiologic data showing a positive association between life- time prevalence of panic disorder with agoraphobia and seizures in the same persons. 4 Again, the pathologic condition within the temporal lobe, especially amygdala, may be a shared mechanism underlying this descriptive similarity because fear is the most common emotion elicited by focal discharges within this re- gion. 3,4,6,7,11 A substantial percentage of patients with panic disorder and agoraphobia, perhaps as high as one third, mani- fest symptoms of depersonalization and derealization. This pro- file of symptoms resembles that of patients with temporal lobe epilepsy. 4 Thus, feelings of detachment from the environment, unfamiliarity of the external world, and de ´ja ` vu occur commonly among both groups of patients. Panic attacks, however, may also occur in association with generalized seizure disorders, especially absence seizures or petit mal epilepsy that can persist into adulthood. 12 Occasion- ally, the distinction between absence and complex partial sei- zures may be difficult on clinical grounds; this distinction may be made even more difficult when they are associated with panic attacks. The distinction has important implications for pharma- cotherapy because carbamazepine, which may be indicated for complex partial seizures, may worsen and be poorly tolerated in patients with absence seizures. 12 In general, the prevalence of panic attacks is significantly higher among patients with epi- lepsy than the general population. A provocative relationship is emerging between the aura of ictal fear, amygdalar pathology such as hyperexcitability or smaller amygdalar volume, and panic disorder among patients with temporal lobe epilepsy. 3,6Y9,11 Thus, a small, sclerotic, and hyperexcitable amygdala may be a shared common focus of a pathologic condition in at least some patients with temporal lobe epilepsy and panic disorder. The amygdala is a key node in a limbic circuit that is activated by fear imagery provocation in patients with panic disorder; in addition to the amygdala, this circuit includes hippocampus, orbitofrontal cortex, and anterior cingulate. Dyspnea as the predominant ictal phenomenon of a simple partial seizure disorder associated with oxygen desaturation was described in a 56-year-old man with evidence of a right medial temporal lobe lesion on magnetic resonance imaging (MRI) findings. 13 The episodes of dyspnea resolved after treatment with therapeutic blood levels of phenytoin, although brief epi- sodes (G5 seconds) of sensations of Bants crawling[ persisted. The mechanism could relate to respiratory arrest and transient apnea that has been reported in association with stimulation of limbic and temporal lobe regions. Although, as noted, the resolution of the diagnosis is often difficult on clinical grounds and EEG results may be negative, frequent, unprovoked spells of several seconds’ duration, im- paired auditory verbal comprehension, dysmnesic phenomena and aphasia during the spells, absence of agoraphobia, and no family history of panic disorder are more consistent with a di- agnosis of temporal lobe epilepsy. 3 Furthermore, selective se- rotonin reuptake inhibitors (SSRIs), a common and effective CASE REPORT 160 | www.clinicalneuropharm.com Clinical Neuropharmacology & Volume 32, Number 3, May/June 2009 Mental Health Service Line, Department of Veterans Affairs Medical Center; and Department of Psychiatry, Georgetown University School of Medicine, Washington, DC. Address correspondence and reprint requests to Stephen I. Deutsch, MD, PhD, Department of Veterans Affairs Medical Center,50 Irving St, NW, Washington, DC 20422; E-mail: Stephen.deutsch@med.va.gov Copyright * 2009 by Lippincott Williams & Wilkins DOI: 10.1097/WNF.0b013e31818d44fc 9 Copyright @ 200 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.