Can an old TBI cause high beta?

[Guest guest]

As usual, Pete's comments about focal high beta and brain

trauma are direct and practical. I have a few references and comments on my

desktop I thought might share.

Stern and Engel describe " paroxysmal fast activity "

[1] as having two forms - generalized and focal. The focal form can occur with

" posttraumatic epilepsy " [2].  Epilepsy is a word few of us should

ever use, but subclinical seizure patterns actually occur frequently. They

often escape routine EEG, but may appear as brief (0.25-2 second) bursts of

well-formed beta spindling between about 15-30 Hz occurring periodically. Such

bursts are usually only detected by careful attention to the raw EEGs, but they

often show up as spectral peaks on full or mini qEEGs. They are not uncommon

[3]. In my experience failing to control them through the use of a narrow (or

multiple) inhibits is a common reason for problems with NFB. They can easily be

fueled, with serious negative consequences, by synchrony training and by ultra-low

frequency training.

Such paroxysmal fast activity is often correctly described

as an " irritable focus " . The fact that they often occur in

temporal and frontal regions is due to the impact of the bony architecture of

the skull on nervous tissue during trauma.

In the articles/abstracts below you will find an impressive

list of symptoms, both acute and chronic, that may be due to irritable cortical

foci such as beta spindling. The only indicator with mini-Q evaluations may be a

decreased theta to beta ratio. If you observe carefully, you can often detect

several narrow bands of beta spindling on your cascading spectral display. (see

below for abstracts).

Documented consequences of paroxysmal fast activity:

Anxiety

Asperger's Syndrome

Attention Deficits

Autism

Autonomic instability

Bulemia

Concentration poor

Depersonalization

Depression

Dread

Dyspnea

Emotional lability

Fear

Fetishism

Hypersexuality

Impotence

Intermittent explosive disorder

Libido lost

Morality, abandoned

Morality, increased

Panic attacks

Paranoia

Personality disorders

Poor impulse control

Psychosis

PTSD symptoms

Rage

Rapid mood swings

Suicidal ideation

Suicide attempts

Transvestism (spontaneous - not due to transgenderism)

Violence

It is also worth mentioning that focal irritability can often

be reduced by taking GABA. GABA may be contraindicated general seizure activity

(inhibition of inhibition).

Dailey

References:

[1] Stern JM, Engel J. Atlas of EEG patterns. 2005,

Lippincott & Wilkins p 207.

[2] Niedermeyer E. Abnormal EEG patterns: Epileptic and

paroxysmal. In " : Niedermeyer E, Lopes da Silva FR, eds.

Electroencephalography: basic principles, clinical applications, and related

fields. Baltimore: & Wilkins. 199:235-210.

[3] M, et al.  Improving attention in adults and

children - Differing EEG profiles and implications for training. Biofeedback.

Volume 34, Issue 3, pp. 99-105

Related abstracts:

Epilepsy Behav. 2011 Jan;20(1):107-10. Epub 2010 Nov 16.

Fear as the only clinical expression of affective focal

status epilepticus.

Brigo F, Ferlisi M, Fiaschi A, Bongiovanni LG.

Department of Neurological, Neuropsychological,

Morphological and Movement

Sciences, University of Verona, Verona, Italy.

Affective seizures consist of fear, depression, joy, and

(rarely) anger. A correct diagnosis is often delayed as the behavioral

features, like fear, are interpreted as psychiatric disorders. We describe a

patient with affective focal status epilepticus (AFSE) in which fear was the

only clinical manifestation. We present electroencephalographic correlates and

discuss the diagnostic difficulties that can be encountered in similar cases.

AFSE with fear as the only clinical expression may represent a diagnostic

challenge. When fear is the only or the prominent behavioral feature, seizures

may be diagnosed as panic attacks, leading to erroneous therapy. In such

situations, electroencephalography is an essential tool in differentiating

between psychiatric disorders and epileptic events.

PMID: 21084226

Epilepsy Behav. 2010 Dec;19(4):652-5. Epub 2010 Oct 28.

Posttraumatic stress disorder caused by the

misattribution of seizure-related experiential responses.

Cohen ML, Rozensky RH, Zlatar ZZ, Averbuch RN, Cibula JE.

Department of Clinical and Health Psychology, College of

Public Health and Health Professions, University of Florida, Gainesville, FL

32610-0165, USA. mlcohen@...

Patients with temporal lobe seizures sometimes experience

what Hughlings described as " dreamy states " during

seizure onset. These phenomena may be characterized by a re-experiencing of

past events, feelings of familiarity (déjà  vu), and hallucinations. In

previous reports, patients have been aware of the illusory nature of their

experiences. Here, however, the case of a patient with a documented 37-year

history of temporal lobe epilepsy who is not aware is described. Fifteen years

ago, the patient saw visions of traumatic autobiographical events that he had

never previously recalled. He believed them to be veridical memories from his

childhood, although evidence from his family suggests that they were not. The

patient's psychological reaction to the " recovery " of these traumatic

" memories " was severe enough to qualify as posttraumatic stress

disorder (PTSD). To our knowledge, this is the first report  of PTSD caused by

the misattribution of mental states that accompany a seizure.

PMID: 21035405

Neurol Clin. 1993 Feb;11(1):127-49.

Behavioral changes associated with epilepsy.

Devinsky O, Vazquez B.

Department of Neurology, New York University Medical Center,

New York.

Epilepsy can be accompanied by changes in cognition,

personality, affect, and other elements of behavior. There is no single

epileptic constitution or personality complex. A unifying theme to the behavior

in epilepsy is diversity. As one looks at the behavioral traits reported in

epilepsy, a specific and consistent pattern is lacking. Rather, extremes of

behavior are accentuated: sometimes in one direction, often in both directions.

Changes in emotional state  are prominent among behavioral features in

epilepsy. Some authors describe a prominent deepening or increase in

emotionality, whereas others identify a global decrease in emotional life and

content. Emotional lability is also reported. Sexuality and libido are

typically decreased, but fetishism, transvestism, exhibitionism, and

hypersexual episodes also occur. Concerns over morality may be lacking or

exaggerated. Patients may be irritable and aggressive or timid and apathetic. The

impressive list of people with epilepsy in politics, religion, arts, and

sciences suggests a positive expression of this behavioral spectrum. Psychosis,

depression, paranoia, and personality disorders may represent a negative pole

of epilepsy-related behavioral changes. The most important aspect of behavioral

changes in epilepsy for physicians is to recognize and treat dysfunctional

behavior. Depression is a common problem that is often unrecognized and

untreated. Other treatable problems include impotence, anxiety, panic attacks,

and psychosis. Identifying risk factors will, it is hoped, assist in developing

methods to prevent these disorders.

PMID: 8441366

 

Ann N Y Acad Sci. 1990;602:67-96.

Effect of diaphragmatic respiration with end-tidal CO2

biofeedback on respiration, EEG, and seizure frequency in idiopathic epilepsy.

Fried R, Fox MC, Carlton RM.

Hunter College, City University of New York, New York 10021.

Breathing rate (RR), end-tidal percent CO2, and EEG were

obtained in three groups: psychiatric referral subjects presenting with

anxiety, panic phobia, depression and migraine; a group of idiopathic seizure

sufferers; and a group of  asymptomatic controls. Virtually all the noncontrol

subjects were found to show moderate to severe hyperventilation and the

accompanying EEG dysrhythmia. The seizure group subjects were taught

diaphragmatic respiration with end-tidal percent CO2 biofeedback. The training

normalized their respiration and altered their EEGs and seizure frequency.

PMID: 2122789

 

Z Kinder Jugendpsychiatr Psychother. 2009

May;37(3):203-7.

[Panic attacks simulated by occipital lobe seizures].

[Article in German]

Stolle M, Sieben C, Püst B.

Deutsches Zentrum für Suchtfragen des Kindes- und

Jugendalters (DZSKJ), Psychosoziales Zentrum am Universitätsklinikum

Hamburg-Eppendorf. m.stolle@...

Eleven-year-old was admitted to a child and

adolescent psychiatry day hospital with symptoms of an anxiety and panic

disorder, and compulsive and self-harmful behavior. The patient described

detailed threatening scenic sequences that caused her to feel panicky. They

symptoms could be classified as epilepsy with visually dominated seizures of

the occipital lobe. In addition to pharmacological treatment with oxcabazepine,

extensive multimodal interventions as part of the child and adolescent

psychiatric day hospital treatment program helped all family members to

understand and handle the seizures. Eight weeks after initiation of treatment,

was seizure-free. Complex partial epilepsy can be mistaken for

primary child-psychiatric disorder.

PMID: 19415605

 

BMJ. 1993 Mar 13;306(6879):709-10.

Epilepsy mistaken for panic attacks in an adolescent

girl.

Laidlaw JD, Khin-Maung-Zaw.

Department of Child and Adolescent Psychiatry, Gloucestershire

Royal Hospital.

Complex partial seizures are a form of focal epilepsy

associated with impairment of consciousness. The clinical presentation of such

seizures is diverse, which can lead to misdiagnosis. We describe the case of a

17 year old woman who was referred to our service for treatment of panic

attacks.

PMID: 8471931

J Clin Psychiatry. 1995 Aug;56(8):358-62.

EEG abnormalities in patients with atypical panic

attacks.

Weilburg JB, Schachter S, Worth J, Pollack MH, Sachs GS, Ives

JR, Schomer DL.

Department of Psychiatry, Massachusetts General Hospital,

Boston 02114, USA.

BACKGROUND: Panic attacks and certain partial seizures have

phenomenologic similarities which suggest that they may somehow be related. No

evidence of such  a relationship, however, was found when the routine EEGs of

patients with panic attacks were examined. METHOD: Fifteen subjects with

atypical panic attacks who met DSM-III-R criteria for panic disorder agreed to

have routine followed by prolonged ambulatory EEG monitoring with sphenoidal

electrodes. Fourteen subjects actually underwent monitoring; 1 had a panic

attack during premonitoring routine EEG. RESULTS: Focal paroxysmal EEG changes

consistent with partial seizure activity occurred during panic attacks in 33%

(N = 5) of the 15 subjects; 2 (40%) of the 5 subjects with panic-related EEG changes had normal

routine EEGs. Multiple attacks were recorded before panic-related EEG

changes were demonstrated in several subjects. CONCLUSION: It may be necessary

to monitor the EEG during multiple panic attacks  to reveal an association

between atypical panic attacks and epileptiform EEG changes.

PMID: 7635852

 

J Neuropsychiatry Clin Neurosci. 1993 Winter;5(1):50-5.

Focal paroxysmal EEG changes during atypical panic

attacks.

Weilburg JB, Schachter S, Sachs GS, Worth J, Pollack MH,

Ives JR, Schomer DL.

Department of Psychiatry, Massachusetts General Hospital,

Boston 02115.

Atypical panic attacks include features such as focal

paresthesias or sensory distortions, but attempts to demonstrate a relationship

to partial seizures have  been unsuccessful. Two patients with atypical panic

attacks had attacks during EEG monitoring: one during a routine EEG in the EEG

laboratory, the other at home during ambulatory monitoring. Focal paroxysms of

sharp wave activity appeared on  both patients' EEGs coincident with the

spontaneous onset of panic attack symptoms. Both patients remained conscious.

The correlation of focal paroxysmal EEG changes with panic attack symptoms suggests

that these attacks were produced  by partial seizure activity. Further study of

the relationship between panic attacks and seizures is indicated.

PMID: 8428135

 

Nervenarzt. 1999 Mar;70(3):206-15.

[Limbic ictus as a condition for anxiety attacks].

[Article in German]

Gallinat J, Hegerl U.

Psychiatrische Klinik, Ludwig-Maximilians-Universität

München.

Episodes of anxiety have been reported to be the most common

psychological symptoms in patients with partial seizures. They may occur

before, during and after seizures and can also appear in isolation without any

convulsive symptoms.  The epileptic anxiety syndrome is strikingly similar to

panic attacks, and panic  disorder is an important differential diagnosis. The

close relationship between epileptic seizures and panic attacks is of special

interest for a better pathophysiological understanding of panic attacks. In the

literature an epileptiform neuronal activity is discussed as a possible

underlying mechanism for panic disorder. The finding that anxiety was the most

common experiential phenomenon produced by electrical stimulation of amygdala

and hippocampus with depth electrodes points in this direction. PET has

demonstrated abnormalities of  hippocampal structures during the nonpanic state

of patients with panic disorder. In addition, some EEG studies have

demonstrated a high incidence of epileptiform  EEG patterns in patients with

panic disorder with or without agoraphobia. This was the reason why several

investigators proposed that a subset of panic attacks  may be related to

abnormal epileptiform neuronal activity in the limbic system. The size of this

subset is difficult to determine because discharges in the depth of the limbic system often cannot

be seen in the scalp EEG. Concerning the hypothetical pathophysiological

mechanism of panic disorder therapeutic measures  were taken with antiepileptic

agents. The best results were obtained for valproic acid. It seems to be

reasonable to make a therapeutic trial with antiepileptic medication after nonresponse

to standard pharmacotherapy.

PMID: 10231807

 

Eur Child Adolesc Psychiatry. 1999 Sep;8(3):237-9.

Panic disorder or temporal lobe epilepsy: A diagnostic

problem in an adolescent girl.

Pegna C, Perri A, Lenti C.

Istituto di Scienze Neurologiche e

Psichiatriche dell'lnfanzia e dell'Adolescenza, Via Besta 1, Milano, Italia.

Similarities in the clinical presentation of panic disorder

and temporal lobe epilepsy suggest that the two disorders are related and can

lead to difficulties  in a differential diagnosis. We describe the case of a

young girl suffering from  paroxysmal anxiety, derealization-depersonalization

and autonomic symptoms, lasting from seconds to several minutes; these episodes

were very frequent and disabling. The interictal EEGs and MRI were normal.

After having diagnosed panic  disorder based mainly on the duration of the

attacks and the family history, a pharmacological treatment was started.

PMID: 10550706

 

Clin Neuropharmacol. 2009 May-Jun;32(3):160-2.

Temporal lobe epilepsy confused with panic disorder:

implications for treatment.

Deutsch SI, Rosse RB, Sud IM, Burket JA.

Mental Health Service Line, Department of Veterans Affairs

Medical Center, Washington, DC 20422, USA. .deutsch@...

A 34-year-old woman with a 9-year history of unprovoked

attacks of anxiety and dyspnea associated with symptoms of depersonalization

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 disorder without agoraphobia, prompting a

reconsideration of this diagnosis. 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.

PMID: 19483484

 

J Psychiatry Neurosci. 1993 Jan;18(1):46-8.

Absence seizures associated with panic attacks initially

misdiagnosed as temporal lobe epilepsy: the importance of prolonged EEG

monitoring in diagnosis.

McNamara ME.

Department of Psychiatry, Brown University, Providence,

Rhode Island.

While temporal lobe epilepsy is often considered in the

differential diagnosis of patients with anxiety or panic disorders, other types

of epilepsy can confound the presentation or treatment of adults with panic

disorders. The cases of two patients are presented who were initially thought

to have temporal lobe epilepsy  producing panic attacks, but who were

subsequently found to have primary generalized seizures. The clinical

implications are discussed.

PMCID: PMC1188475

 

BMJ. 2001 Apr 7;322(7290):864.

Distinguishing between partial seizures and panic

attacks. Psychotic and behavioural symptoms are also common in elderly

patients.

Dale MC.

PMCID: PMC1120028

 

J Neurol Neurosurg Psychiatry. 2001 Feb;70(2):186-91.

Fear as the main feature of epileptic seizures.

Biraben A, Taussig D, P, Even C, Vignal

JP, Scarabin JM, Chauvel P.

Service de Neurologie, CHU Pontchaillou, Rue

Henri Le Guilloux, Rennes, France. Arnaud.Biraben@...

OBJECTIVES: There are circumstances in which partial

seizures may be misdiagnosed as acute psychiatric disturbances. In particular,

when fear is the prominent feature the patient may be considered for years as

having panic attacks. Eight patients in whom fear was the main symptom of the

seizures are reported on. Patients who had a proved lack of consciousness

during the fits and patients in whom fear was just fear of having a seizure

were excluded. The ictal involvement  of temporal limbic and frontal structures

in those patients with fear of particular intensity was studied. METHODS: The

localisation of the epileptogenic zone was assessed by prolonged interictal EEG

recordings as well as ictal video-EEG recording of at least one seizure in

every patient; five had ictal SPECT and four had chronic stereotactic 

implantation of depth electrodes (SEEG). In six patients, a cortical resection

was performed with an Engel's class 1 outcome (minimum 28 months follow up,

except for two patients). RESULTS: Localisations of primary epileptogenic zones

were right temporal in three patients, left temporal in three, bitemporal in

one, and frontal in one. In all cases, diagnosis of epileptic seizures could be

clinically evoked because of  the stereotypy of fits and of associated

symptoms. The association of a fear sensation, autonomic symptoms, and

coordinated behaviour suggests disturbance of  a particular system. The SEEG

data argue for temporolimbic and prefrontal lobe involvement in the expression

of ictal fear. CONCLUSIONS: In intense ictal fear, with coordinated behaviour

and autonomic features, the discharge may involve or interfere with a

physiological complex information processing network. This network involves

orbitoprefrontal, anterior  cingulate, and temporal limbic cortices.

PMCID: PMC1737203

 

Adv Neurol. 1991;55:97-111.

Neurobiological evidence for epilepsy-induced interictal

disturbances.

Engel J Jr, Bandler R, Griffith NC, Caldecott-Hazard S.

Department of Neurology, UCLA School of Medicine 90024.

It is not in the best interest of persons with epilepsy to

deny the possibility that seizures could cause enduring behavioral

disturbances. Rather, it is essential to pursue clinical and animal investigations

in order to identify any such changes that might occur and to elucidate their

mechanisms. Many testable hypotheses can be developed from existing evidence.

Antiepileptic medication may  produce interictal behavioral disturbances in

patients with epilepsy by indirect  mechanisms. Some aberrant behaviors could

be due to medication-induced systemic disorders, neuroendocrine dysfunction, or

REM deficit, whereas depression following successful treatment with drugs, as

well as with surgery, may be related more specifically to cessation of

seizures. The underlying neuropathological process also induces neurological

and mental deficits, but it is not always possible to differentiate those

behavioral disturbances due to destructive effects of the lesion from those due

to recurrent epileptic seizures. Behavioral disturbances are associated more

frequently with epileptogenic lesions in limbic structures than with those

elsewhere in the brain, but a relationship between hemispheric lateralization

of the epileptogenic lesion and specific interictal behavioral symptoms remains

controversial. When considering the effects of seizures per se on interictal

behavior, it is important to realize that some " interictal "

behavioral disturbances may actually be ictal events. Prolonged affective,

autonomic, and psychic disturbances can occur in clear consciousness with

unilateral limbic seizures that are not associated with scalp  EEG changes.

When epilepsy is acquired as a result of cerebral damage, the epileptogenic process

takes time to develop before spontaneous seizures appear. It is more reasonable

to assume that this progressive process continues than to postulate that it

stops completely at the time the first seizure occurs. Epilepsy-induced

protective homeostatic mechanisms that act to terminate ictal events, prevent

ictal spread, and maintain the interictal state may also disrupt  interictal

function. Furthermore, seizures could indirectly influence interictal  behavior

as a result of their effects on neuroendocrine function and sleep. Because of

confounding biological factors, it is difficult to document the association of

any epilepsy disorder, by itself, with progressive behavioral disturbances in

humans. Secondary epileptogenesis, protective homeostatic mechanisms, and

epilepsy-induced disturbances in development can be readily demonstrated,

however, in experimental animal models. In experimental animals, endogenous

opoids are released during seizures and mediate some postictal behaviors. A

physiological dependency on high levels of endogenous opioids released during

seizures could produce depression as a withdrawal symptom interictally or when

seizures no longer occur as a result of successful therapy.  Experimental

animal models of depression exist to test hypotheses concerning pro- and

antidepressant effects of epileptogenesis.(ABSTRACT TRUNCATED AT 400 WORDS)

PMID: 2003426

 

J Am Acad Child Adolesc Psychiatry. 1997 Sep;36(9):1295-8.

Case study: seizure disorder presenting as panic disorder

with agoraphobia.

Lee DO, Helmers SL, Steingard RJ, DeMaso DR.

Department of Psychiatry, Emory University School of

Medicine, Atlanta, GA 30322, USA.

Seizure disorders can produce anxiety that is almost

indistinguishable from psychiatric disorders. There are few reports of

adolescents with seizure disorders that produce fear. The first case of an

adolescent female who presented with panic disorder and agoraphobia which was a

consequence of seizure activity is reported. Careful diagnostic evaluation and

correlation with video electroencephalography were important in distinguishing

seizure activity from panic disorder.

PMID: 9291732

 

Compr Psychiatry. 1989 Nov-Dec;30(6):489-97.

Dyscontrol syndrome: long-term follow-up.

Monroe RR.

Department of Psychiatry, University of land School of

Medicine, Baltimore 21201.

This is a 38- to 57-month follow-up of 50 patients referred

for drug-activated electroencephalograms (EEG) because of the suspicion that a

limbic complex partial seizure was a crucial mechanism behind their episodic

behavior. Hence, an anticonvulsant regimen might be an effective therapeutic

option. The primary referral diagnoses were intermittent explosive disorder (N

= 33) panic disorder (N = 6), or formes frustes of epilepsy (N = 11). None of

the patients had a significant history of typical seizures and previous routine

EEGs had all been normal. Twenty nine patients also had a second axis I and

three a second axis II  diagnosis. On the basis of EEG findings, as well as a

symptom checklist of dyscontrol behavior and a history of episodic disorders, I

recommended an anticonvulsant regimen in 39 patients; this was initiated by the

referring psychiatrist in 25. Of the 11 patients for whom no anticonvulsant was

recommended, three were nevertheless placed on such a regimen. At the end of

the  follow-up period, 12 patients were still on this regimen, eight were on

other regimens that probably raised seizural thresholds, and 10 were treated

with antidepressants, antimanic, antipsychotic, or anti-anxiety medications.

Twenty were not receiving any medication. An analysis of the diagnostic

procedure and the response to the various regimens, including psychotherapy,

did not demonstrate any reliable data that would aid the clinician in selecting

the appropriate regimen. However, of the 20 patients on regimens that raised

seizural threshold, 10 reported marked and six reported moderate improvement.

PMID: 2510965

 

J Neuropsychiatry Clin Neurosci. 1991 Summer;3(3):321-9.

Limbic system dysrhythmia: a diagnostic electroencephalogram

procedure utilizing  procaine activation.

Ryback RS, Gardner EA.

Associated Mental Health Professionals, College Park,

land.

A diagnostic method is presented that makes it possible to

distinguish patients who are most likely to show a positive response to

treatment with anticonvulsant  medication, thereby cutting across many

DSM-III-R diagnoses. Patients are evaluated to determine whether they exhibit

at least 4 of 12 groups of symptoms,  and the local anesthetic procaine is

used, along with an electroencephalogram (EEG) to evaluate for omega band

activity (30-50 Hz) of at least 50 microvolts or approximately three times

baseline values in the anterior temporal leads. This method was studied in 145

patients with varying diagnoses. Eighty-three percent of patients who were

symptom- and procaine-positive responded to anticonvulsants. Specific

application to patients with attention-deficit hyperactivity disorder, bipolar

disorder, and panic disorder is made. This method may provide a basis for identifying

subpopulations of anticonvulsant-responsive patients who often are considered

treatment-resistant.

PMID: 1821249

 

J Nerv Ment Dis. 1984 Oct;172(10):625-7.

Complex partial seizures presenting as a psychiatric

illness.

Stern TA, Murray GB.

A 36-year-old woman was treated for a wide variety of

psychiatric illnesses over  a span of two decades before a diagnosis of complex

partial seizures was made. Her history included poor impulse control, rage

attacks, multiple suicide attempts, rapid mood swings, depression, and

psychotic episodes. Bulimia, panic attacks, severe obsessive-compulsive

symptoms, and multiple somatic complaints were also present. In retrospect,

these symptoms could be attributed to complex partial seizures with cognitive

and affective symptomatology, automatisms, and psychosensory symptoms, and were

controlled by anticonvulsant medications. Therefore, so-called

" purely " psychiatric disorders should not be diagnosed before a

diagnosis of limbic epilepsy (however, this might be labeled, e.g., complex

partial seizure, psychomotor seizure, psychical seizure, or temporal lobe

epilepsy) has been considered.

PMID: 6481348