Keywords
“Is it a panic attack or is it ictal panic?” This question illustrates one of the examples of the borderlands between epilepsy and psychiatric disorders. The similarities of the clinical manifestations of the 2 types of paroxysmal episodes have resulted in frequent diagnostic errors.
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Indeed, it is not infrequent for simple partial seizures of mesial temporal lobe origin presenting as panic episodes to be treated as panic attacks until the patient develops a secondarily generalized tonic-clonic seizure or is witnessed to have a complex partial seizure.In epilepsy, psychiatric symptoms are classified into periictal and interictal in relation to their temporal occurrence to seizures.
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Periictal symptoms are of 3 types: preictal (preceding a seizure), ictal (presenting as a seizure), and postictal (occurring within 120 hours of a seizure). Interictal symptoms occur independently of seizures. Often, ictal and postictal panic can be identified in the same patient suffering from interictal panic attacks. Furthermore, interictal symptoms can worsen in severity during the postictal period.- Kanner A.M.
Peri-ictal psychiatric phenomena: clinical characteristics and implications of past and future psychiatric disorders.
in: Ettinger A. Kanner A.M. Psychiatric issues in epilepsy: a practical guide to diagnosis and treatment. 2nd edition. Lippincott Williams and Wilkins,
Philadelphia2007: 321-345
The involvement of common neuroanatomical structures and the pathogenic role played by the same neurotransmitters (serotonin [5-HT], γ-aminobutyric acid [GABA]) probably explain the similar clinical manifestations and relatively high comorbidity between periictal panic symptoms and interictal panic disorders (PDs). This article reviews these data and provides practical strategies that can be used in the differential diagnosis and treatment of ictal and postictal panic episodes and panic attacks.
Epidemiologic aspects
Whereas ictal panic is the classic expression of anxiety symptoms presenting as a simple partial seizure, postictal panic is a seizure-related symptom that often goes unrecognized but is relatively frequent. Ictal panic is the most frequent type of simple partial seizures, presenting primarily with psychiatric symptoms and corresponding to 60% of all psychiatric auras.
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, Postictal panic has been identified in 10% of 100 consecutive patients with treatment-resistant partial epilepsy, occurring during the postictal period (defined in this study as the 72 hours following a seizure or cluster of seizures) of more than 50% of their seizures and having a median duration of 24 hours.7
In that same study, 39% of patients reported postictal symptoms of agoraphobia.Epileptic patients have been found to suffer more frequently from interictal PD than nonepileptic people. For example, one population-based study performed in Canada found a 12-month prevalence rate of interictal PD to be 5.6%, almost 3-fold higher than in nonepileptic subjects (2%).
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A prevalence of 5.1% was found in a prospective study of 97 patients with treatment-resistant epilepsy.Ictal panic has been typically associated with partial seizure disorders of mesial temporal origin.
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However, seizures of frontal lobe origin have also been associated with ictal panic.13
When the seizures involve the orbitofrontal cortex in the nondominant hemisphere, they may present with sudden panic-stricken screams, with nonverbal screams or verbal vocalizations of “help me…help me,” or “Oh my God!” These differ from the classic ictal panic in that the ictal panic occurs in the setting of complex partial seizures and patients are not aware of the distressing affect and associated phenomena, which include complex automatisms. Seizures of parietal lobe origin have also been associated with ictal panic on rare occasions. For example, Alemayehu and colleagues14
reported 2 cases with ictal panic originating from the right parietal lobe where a brain tumor was identified. Intracranial monitoring documented correlations between the symptoms of fear and restricted regional parietal cortical discharges. Surgical resections of the lesions (1 total and 1 subtotal) resulted in either complete recovery or improvement.Pathophysiology
Do ictal panic and PDs share common pathogenic mechanisms? The similarity of clinical semiology between these 2 types of paroxysmal events (see later discussion) and the relatively high comorbidity of interictal PD in patients with ictal panic may be explained by the existence of common pathogenic mechanisms operant in both conditions. These conditions include (1) structural and functional abnormalities of common neuroanatomical structures and (2) disturbances of the function of common neurotransmitters, including 5-HT and GABA.
Abnormalities in Common Neuroanatomical Structures
Panicky symptoms are typical of temporal lobe epilepsy (TLE) of mesial temporal origin with particular involvement of the amygdala. In fact, electric stimulation of the amygdala produces many of symptoms of panic attacks (eg, intense fear, dizziness, nausea, tachycardia, chest pain, and depersonalization).
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In patients with primary PD, volumetric measurements of mesial temporal structures have demonstrated a smaller volume of the amygdala. For example, Massana and colleagues
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measured the volumes of amygdalae, hippocampi, and temporal lobes in 12 drug-free symptomatic patients with primary PD and 12 case-matched healthy controls. Patients with PD had bilateral smaller volumes of the amygdala than the controls, but no differences were found in either hippocampi or temporal lobes. In a separate study, Cendes and colleagues16
performed magnetic resonance imaging (MRI) volumetric measurements of amygdala and hippocampus in 50 patients with intractable TLE. Among them, 17 patients (34%) had a clear history of ictal panic accompanied by a rising epigastric sensation as the initial manifestation of their habitual attacks. The amygdala volumes in this group were significantly smaller (mean, 2131.6 mm3) than the volumes of the 33 patients without these symptoms (mean, 2561.5 mm3). Both patient groups had smaller mean amygdala volumes when compared with normal controls (mean, 2828.2 mm3). Postoperative pathology correlated well with volumetric atrophy.Evidence of a pivotal role of the amygdala in anxiety disorders has been also suggested by data from animal models. For example, the central nucleus of the amygdala has been found to be primarily responsible for mediating fear (emotional reaction to aversive events) and anxiety (the apprehension of an imminent aversive event) in the fear-conditioning animal model of anxiety.
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Furthermore, stimulation of this nucleus resulted in fearlike responses (reminiscent of symptoms of panic attacks in humans) such as freezing, shivering, and autonomic nervous system activation, including tachycardia and increase in blood pressure. On the other hand, bilateral lesions of the central nucleus of the rabbit amygdala have resulted in loss of the fear-induced tachycardia to a conditioned auditory fear stimulus,18
whereas lesions of the central nucleus of the rat eliminated a fear-potentiated startle response.19
Structural abnormalities of mesial structures are not restricted to the amygdala but have been found in hippocampal formations and parahippocampal gyri and have resulted in smaller total volumes of the temporal lobes. Thus, Massana and colleagues
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investigated the gray matter density in 18 outpatients with PD and 18 healthy subjects using a voxel-based morphometry approach. They found that gray matter density of the left parahippocampal gyrus was significantly lower in patients with PD compared with healthy subjects. In a separate study, Vythilingam and colleagues21
measured the volume of the temporal lobes and hippocampi in 13 patients with primary PD and 14 healthy control subjects. They found that the mean volume of both temporal lobes was significantly smaller in PD compared with healthy subjects, but there was no significant difference in the volume of the hippocampi between the 2 groups.Uchida and colleagues
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conducted volumetric studies of temporal lobe structures in 11 patients with primary PD and 11 controls matched for age, sex, handedness, socioeconomic status, and years of education. They found that in patients with PD, the mean volume of the left temporal lobe was 9% less than that of controls; although the mean volume of the right temporal lobes were also less, the difference only reached a trend (7%, P = .06). Furthermore, there was a trend in the difference of the volumes of the right amygdala (8%, t21 = 1.83, P = .08), left amygdala (5%, t21 = 1.78, P = .09), and left hippocampus (9%, t21 = 1.93, P = .07) in patients when compared with controls. Of note, these investigators found a positive correlation between left hippocampal volume and duration of PD (r = 0.67, P = .025), with recent cases showing more reduction than older cases.Functional abnormalities have been demonstrated in temporal and extratemporal lobe structures. First, positron emission tomographic (PET) studies conducted in healthy humans demonstrated increased perfusion in the amygdala when they were shown images of fearful as opposed to happy faces.
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Likewise, PET studies targeting the 5-HT1A receptor have demonstrated involvement of temporal and extratemporal limbic structures. For example, in one study of 9 symptomatic untreated patients with PD, 7 patients who recovered on selective serotonin reuptake inhibitor (SSRI) medication and 19 healthy volunteers underwent PET scan using the 5-HT1A tracer 11C-WAY-100635.24
In comparison with controls, both presynaptic and postsynaptic 5-HT1A receptor binding was reduced in patients, with the most significant reductions being in the raphe, orbitofrontal cortex, temporal cortex, and amygdala. In recovered patients, presynaptic binding was reduced but there was no significant reduction in postsynaptic binding. In another study of 16 unmedicated symptomatic outpatients with PD (7 of whom also suffered from a mood disorder of mild severity) and 15 matched healthy controls, PET studies were performed to target the 5-HT1A receptor with the selective 5-HT1AR radioligand 18F-trans-4-fluoro-N-2-[4-(2-methoxyphenyl)piperazin-1-yl]ethyl]-N-(2-pyridyl)cyclohexanecarboxamide (FCWAY).25
A reduction in binding of 5-HT1A receptor was found in the anterior cingulate, posterior cingulated, and raphe in patients compared with controls. The binding of 5-HT1A receptors did not differ between patients with PD and patients with comorbid depression, whereas the latter differed significantly from controls in that 5-HT1A receptor binding was reduced in cingulate and raphe nuclei.Disturbances of the Function of Some Common Neurotransmitters
5-HT has been found to play an important pathogenic role in PD and epilepsy.
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The role of 5-HT in PD can be appreciated in the data from the PET studies discussed earlier. Furthermore, the prophylactic effect of SSRIs and tricyclic antidepressant imipramine 5-HT in PD is an expression of the pathogenic role of 5-HT.28
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The pathogenic role of 5-HT in epilepsy has been demonstrated in various animal models of epilepsy, illustrated in particular by the genetically epilepsy prone rat whose brain reveals deficits in serotonergic arborization and decreased postsynaptic 5-HT1A receptor density in hippocampus.
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Conversely, drugs that enhance serotonergic transmission, such as the SSRIs sertraline and fluoxetine cause a reduction in seizure frequency in a dose-dependent manner that correlates to the extracellular thalamic serotonergic thalamic concentration. In addition, an antiepileptic effect of 5-HT1A receptors has been correlated to a membrane hyperpolarizing response, which is associated with increased potassium conductance in hippocampus-kindled seizures in cats and in intrahippocampal kainic acid–induced seizures in freely moving rats.33
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The pathogenic role of 5-HT in epilepsy has been reviewed in greater detail elsewhere.35
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GABA is another neurotransmitter with important pathogenic roles in PD and epilepsy. It is a neurotransmitter that promotes the inhibition of neuronal excitability through the chloride ion channels. In fact, several of the commonly used antiepileptic drugs (AEDs) such as benzodiazepines, barbiturates, tiagabine, and vigabatrin exert their antiepileptic effect by increasing synaptic GABA concentrations.
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Furthermore, the convulsant agent pentylenetetrazol (a model for generalized seizures) blocks GABAA receptor function and facilitates the development of anxiety symptoms.38
It has been suggested that anxiety disorders may be caused by defective neuroinhibitory processes that are mediated in part through GABA. In patients with PD, the pathogenic role of GABA is suggested by the induction of panic symptoms with the benzodiazepine antagonist flumazenil39
; these data are also supported by the demonstration of widespread decreased binding of flumazenil to benzodiazepine receptor in patients with PD.40
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The question is then raised whether downregulation of these receptors is a consequence of exposure to stress or whether a preexisting low level of benzodiazepine receptor density may be a genetic risk factor for the development of stress-related anxiety disorders.Clinical presentations:(distinguishing ictal panic, panic attack and postictal panic)
It is not unusual that patients with ictal and/or postictal panic are mistakenly diagnosed as suffering from a PD. Yet a careful history can usually provide enough clues to reach the correct diagnosis, which are summarized in the following sections.
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Duration
Ictal panic is a very brief event lasting less than 30 seconds. It may evolve into a complex partial or secondarily generalized tonic-clonic seizure, which may last between 60 and 90 seconds on average. Yet, rarely, partial complex status epilepticus associated with isolated fear has been reported.
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In such cases, panic symptoms may last for hours, intermixed with a confusional state. In contrast, the duration of panic attacks can range between 5 and 20 minutes and at times may persist for several hours. Postictal panic can appear within 120 hours of a seizure or cluster of seizures and was found to have a median duration of 24 hours and to range between 1 and 120 hours.Intensity of the Panic Experience
The sensation of fear in ictal panic is mild to moderate and rarely reaches the intensity of a panic attack. In fact, Williams
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described ictal fear as unnatural rather than seeming more reality based. In contrast, panic attacks are characterized by a very intense fear or panic often referred as a “feeling of impending doom.”46
It is not infrequent for patients to become extremely apprehensive about experiencing another panic attack that may then lead to the development of a full-blown agoraphobia. In postictal panic, the intensity of the fear sensation is closer to that of ictal panic.Timing of Occurrence
Ictal panic can occur in awake and sleep states, whereas panic attacks rarely occur out of sleep.
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Postictal panic is typically reported in awake states.Stereotypic Features
Ictal panic is a stereotypic paroxysmal event, whereas panic attacks may or may not be stereotypic, with respect to duration and associated symptoms. Likewise, postictal panic episodes may or may not be stereotypic in their clinical manifestations and duration.
Associated Symptoms
Unresponsiveness
Typically, patients with ictal panic may be partially or totally aware of their surroundings; in the former scenario, patients report that their concentration is affected during and around the ictus after which they must exert greater effort to achieve the same cognitive tasks. When ictal panic evolves to a complex partial seizure, patients become unaware of their surroundings. Yet in complex partial seizures of mesial temporal origin in the nondominant hemisphere, responsiveness may be preserved and patients may continue interacting with others in a coherent manner during the ictus but become amnesic to the event when questioned postictally. Conversely, in panic attacks, the patients’ awareness of their surroundings and responsiveness is typically preserved; yet, in the case of severe panic attacks, the patients may be overwhelmed by the sensation of impending doom to the point where they may not be able to report what is going on around them. In addition, a panic attack associated with profound hyperventilation could also conceivably lead to a “subjective perception” of loss of consciousness. In postictal panic episodes, patients are fully aware of their surroundings.
Autonomic symptoms
These symptoms are present in panic attacks and ictal panic. Among these symptoms, paroxysmal salivation is a pathognomic autonomic symptom in seizures of mesial temporal or insular origin; it has never been reported in panic attacks or postictal panic. Salivation may often be copious and associated with nausea and vomiting, particularly in ictal panic originating in mesial temporal structures in the nondominant hemisphere. Postictal nausea or vomiting has been reported in some patients.
Chest discomfort including chest pain, palpitations, and hyperventilation is a common symptom in ictal panic and panic attacks.
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, Of note, intense hyperventilation in panic attacks can lead to carpal spasms that can be confused with dystonic posturing of seizures of temporal lobe origin. All these symptoms may also be present in postictal panic.Symptoms of derealization, depersonalization, déjà vu, and jamais vu
These symptoms are characteristic of ictal activity of mesial temporal origin and are often associated with ictal panic. Yet they may also occur in primary or interictal panic and generalized anxiety disorders.
Age of Onset
Ictal fear can begin at any age, although they are more likely to occur after late childhood or early adolescence. On the other hand, PD usually begins in late adolescence or early adulthood, but onset in the 30s and even 40s is common. In fact, PD in childhood presents as school phobia.
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Symptoms that are suggestive of panic attacks and begin in older age groups should be vigorously investigated for the possibility of a seizure disorder. Data on postictal panic in childhood are not available.Psychiatric comorbidities
Recognition of the semiology of ictal panic, panic attacks, and postictal panic is pivotal to reach an accurate diagnosis. Yet it is important to remember that these episodes do not occur in an isolated manner. For example, patients with ictal panic have a high risk of suffering as well from an interictal PD and generalized anxiety disorder. For example, in a study of 12 consecutive patients with ictal panic, Mintzer and Lopez
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found a comorbid PD in 4 patients (33%). One of these patients developed panic attacks only after epilepsy surgery and another worsened after surgery, whereas the other 2 had panic attacks that were not related to any surgical procedure. Two patients had other anxiety disorders, and 8 patients (67%) had current or past depression independent of the presence of PD.Furthermore, ictal panic is associated with an increased risk of postsurgical mood disorders in patients undergoing a temporal lobectomy. For example, Kohler and colleagues
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compared 22 patients with ictal panic and matched groups with other auras and no auras. Neurologic and neuropsychological evaluations before, 1 to 2 months after, and 1 year after temporal lobectomy were reviewed for mood and anxiety disorders and psychotropic medication treatment. Most patients in the 3 groups experienced mood and anxiety disorders before surgery. Mood and anxiety disorders declined in the control but not in the ictal fear group after surgery. Presence of auras at 1 year after surgery was not related to psychiatric outcome. Postoperative mood and anxiety disorders were more common in patients with persistence of seizures and in those in the ictal panic group who were seizure free.Likewise, patients with PD are likely to suffer from generalized anxiety and depressive disorders and patients with ictal panic and PD often experience postictal panic episodes, which in addition to the panic symptoms may be associated with other symptoms of anxiety and depression.
Diagnostic testing
Electroencephalographic Studies
Although routine electroencephalographic (EEG) studies can help identify epileptiform activity and suggest the presence of a partial seizure disorder, they still cannot identify whether the panic episodes are the expression of ictal panic, postictal panic episodes, or interictal panic attacks. On the other hand, a normal routine EEG study is not unusual in patients with ictal and postictal panic because epileptogenic areas in the amygdala or mesial frontal regions are characteristic for their small electric field that often fails to be detected with scalp recordings. Clearly, when ordering routine EEG studies in these patients, anterior temporal and basal temporal electrodes should be requested to increase the yield of identifying epileptiform activity.
Clearly, a careful description of the events is the best way to reach a diagnosis. However, when there is still confusion, capturing the events on video-EEG (V-EEG) monitoring study may be a solution. Nonetheless, one of the limitations of V-EEG is that simple partial seizures often fail to be detected with scalp recordings and this is a particular problem of epileptiform activity, originating from amygdala because its electric field is characteristically restricted. It is not rare, therefore, that patients with ictal panic may have repeated routine and interictal V-EEG monitoring devoid of any epileptiform activity. Occasionally, even complex partial seizures in which the ictal activity remains restricted to mesial structures fail to be detected with scalp electrodes.
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To minimize this problem, it is advised to use sphenoidal electrodes inserted under fluoroscopic guidance to ensure that the recording electrode tip is positioned immediately below the foramen ovale.55
Estimation of Prolactin Levels
The measurement of postictal serum prolactin levels has been used in the differential diagnosis of epileptic and psychogenic seizures. One limitation is the need to draw samples no later than 15 to 20 minutes after a seizure. Serum concentrations can increase in 30% to 40% of seizures of mesial temporal origin (even in the absence of any obvious change on the surface EEG recording), but a negative result does not rule out the diagnosis.
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A cautionary note is that abrupt or rapid discontinuation of benzodiazepines during the V-EEG study may facilitate the occurrence of panic attacks or epileptic seizures.
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Thus, the use of this medication should be slowly tapered before performing the V-EEG study or lowered only slightly at the time of admission.Brain MRI Studies
The presence of a structural lesion in mesial temporal structures or of a hippocampal atrophy should raise suspicion of ictal panic, particularly when the panic episode evolves into a complex partial seizure. However, as with routine EEG studies, these findings do not exclude the possibility of interictal panic attacks and postictal panic episodes in addition to or in the absence of ictal panic.
Some auxiliary tests should be considered when suspecting a diagnosis of PD.
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These tests include thyroid function tests because hyperthyroid disease should be ruled out. Furthermore, an echocardiography should be considered given the high comorbidity of PD and mitral valve prolapse, which may be associated with the symptoms of pressure in the chest and the bouts of paroxysmal tachycardia. It has been suggested that intravenous sodium lactate infusion could be used as a diagnostic tool to confirm a diagnosis of PD, because this infusion can trigger a panic attack with an 80% to 90% probability in patients with PD, whereas in patients without such history the risk is less than 10%. Yet because a significant percentage of patients with ictal panic may also suffer from comorbid interictal PD, the trigger of a panic attack with sodium lactate may result in the false-negative diagnosis of a seizure disorder.Differential diagnosis
PD and ictal panic should also be distinguished from several medical conditions, particular rare disorders associated with paroxysmal cardiac arrhythmias.,
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These conditions include the Romano-Ward syndrome, the prolonged QT syndrome, carcinoid syndrome, hypoglycemia, pheochromocytoma, and Cushing syndrome. Other conditions to consider include alcohol withdrawal or other sedating drug use withdrawal, illicit drug effects (amphetamines, cocaine, and marijuana-induced tachycardia), vertigo-related disorders, and asthma.Treatment options
Before any treatment strategy is put into place, the following question need to be addressed: Is the panic event the expression of (1) ictal panic only, (2) ictal and postictal panic episodes, (3) comorbid ictal panic with or without postictal panic and interictal panic attacks, or (4) interictal panic attacks only. In addition, careful assessment for comorbid depressive disorders is of the essence either in primary PD, interictal panic attacks, and/or ictal panic.
Ictal Panic and Postictal Panic
The treatment of ictal and postictal panic consists on the eradication of epileptic seizures, initially with AEDs, and a presurgical evaluation must be considered if seizures persist after 2 monotherapy trials with AEDs at optimal doses. The choice of AED has to factor in the presence of comorbid mood and anxiety disorders, including panic attacks. In such cases, AEDs with positive psychotropic properties should be chosen first (eg, carbamazepine, oxcarbazepine, lamotrigine, valproic acid, and pregabalin). Of these AEDs, pregabalin has been found to be effective in the treatment of generalized anxiety disorders, whereas valproic acid has yielded therapeutic effects in PD.
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Likewise, AEDs known to have negative psychotropic properties, including barbiturates, topiramate, levetiracetam, zonisamide, and vigabatrin, should be used with extreme caution because these AEDs may worsen the comorbid mood and anxiety disorders.
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Tiagabine is a GABAergic AED that has been used by psychiatrists in the treatment of anxiety disorders but may be associated with increased risk of depressive episodes.Anterior temporal lobectomy is the most frequently performed surgical procedure in patients with ictal panic. The therapeutic yield has ranged between 50% and 70% of freedom from disabling seizures (complex partial and secondarily generalized tonic-clonic seizures). However, total seizure freedom that includes no ictal panic has been reported in 30% to 40% of case series. If anterior temporal lobectomies are performed, patients need to be monitored for postsurgical psychiatric complications presenting as mood and anxiety disorders.
Panic Attacks
Either as an expression of primary or interictal PD, panic attacks are treated with antidepressant medications of the SSRI and serotonin-norepinephrine reuptake inhibitor (SNRI) families.
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Comorbid mood, generalized anxiety disorders, and various types of phobias, in particular agoraphobia, are relatively frequent in patients with PDs; antidepressant drugs with therapeutic efficacy in panic, generalized, and mood disorders should be considered in the presence of these comorbidities. These drugs and their efficacy are listed in Table 1. Cognitive behavior therapy can be effective in any and all of these conditions, and behavior therapy should be recommended in cases of agoraphobia or simple phobias.Table 1Efficacy of SSRIs and SNRIs in primary depression and anxiety disorders
| Antidepressant Drugs | Efficacy | ||
|---|---|---|---|
| Depression | Panic Disorder | Generalized Anxiety | |
| SSRIs | |||
| Paroxetine | + | + | + |
| Sertraline | + | + | + |
| Fluoxetine | + | + | + |
| Citalopram | + | + | + |
| Escitalopram | + | + | + |
| SNRIs | |||
| Venlafaxine | + | + | + |
| Duloxetine | + | – | + |
It should be noted, however, that there are no data on the use of duloxetine in patients with epilepsy, although the author has used it in more than 50 patients with poorly controlled epilepsy without any worsening of seizures (Kanner AM, unpublished data, 2009).
Because the therapeutic response of antidepressant drugs may not be apparent for 4 to 6 weeks, the use of a benzodiazepine, such as alprazolam or lorazepam, can be considered as a bridge for a 6-week to 8-week period. The goal of treatment must always be the achievement of total remission of panic attacks (and other types of comorbid anxiety or mood disorders, when present). To that end, clinicians must not hesitate to use effective doses of psychotropic drugs in combination with cognitive behavior therapy or behavior therapy.
Safety of Antidepressant Drugs in Patients with Epilepsy
The concern of a proconvulsant effect of antidepressant drugs has been one of the most frequent causes of undertreatment of patients with epilepsy with a mood or anxiety disorder. Yet antidepressants can cause seizures when given at toxic doses, or in patients in whom the drug metabolism is slow, which can result in high serum concentrations at standard doses. In fact, among all antidepressant drugs available, only 4 have been found to have a relatively high proconvulsant risk.
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These drugs include bupropion, maprotiline, clomipramine, and amoxapine, whereas none of the SSRIs and SNRIs have been found to increase this risk.Summary
The distinction between ictal panic and interictal panic attacks can be difficult to make and can result in diagnostic errors. The presence of comorbid occurrence of all these types of events must be considered. Ictal and postictal panic and interictal and primary panic attacks share common symptoms but differ with respect to duration and association with other symptoms. A careful assessment, including an accurate history of comorbid medical conditions and medications, is often sufficient to distinguish these events. Diagnostic testing including EEG, neuroimaging, and/or estimation of prolactin levels can be of additional help to the clinician to reach an accurate diagnosis, optimize treatment option, and improve outcome.
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Disclosures: A.M.K. has received research grant funding from Glaxo-Smith-Kline, Novartis, and Pfizer. He has received honoraria for serving as a consultant to Pfizer.
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