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SCHIZOPHRENIA and TEMPORAL LOBE EPILEPSY: MORE INFORMATION From MEDSCAPE

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Psychiatric Disorders Associated With Epilepsy

Author: Fahad Salih Algreeshah, MD; Chief Editor: Jose E Cavazos, MD, PhD, FAAN, FANA, FACNS more…

Updated: Oct 28, 2013

Overview

The International League Against Epilepsy (ILAE) and the International Bureau for Epilepsy (IBE) define epilepsy as a disorder of the brain characterized by an enduring predisposition to generate epileptic seizures and by the biologic, cognitive, psychological, and social consequences of this condition. This association may reflect the anatomical and neurobiological source of both epileptic seizures and the behavioral manifestations.

Antiepileptic drugs (AEDs) can play a role in the genesis of psychiatric symptoms; on the other hand, some psychotropic medications can lower the seizure threshold and provoke epileptic seizures.

Indeed, there is a general agreement that the incidence of neurobehavioral disorders is higher in patients with epilepsy than in the general population, although some authors argue that this apparent overrepresentation is due to sampling errors or inadequate control groups. Many, but not all, authors also accept the proposition that the link between neurobehavioral disorders and temporal lobe or complex partial epilepsy is particularly strong.

Go to Epilepsy and Seizures for an overview of this topic. Additionally, go to Psychogenic Nonepileptic Seizures for complete information on this topic.

Factors in the relationship between epilepsy and behavioral disorders

Mechanisms for a relationship between epilepsy and behavioral disorders include the following:

Common neuropathology
Genetic predisposition
Developmental disturbance
Ictal neurophysiologic effects
Inhibition or hypometabolism surrounding the epileptic focus Secondary epileptogenesis

Alteration of receptor sensitivity
Secondary endocrinologic alterations
Primary, independent psychiatric illness Consequence of medical or surgical treatment Consequence of psychosocial burden of epilepsy

Multiple interacting biologic and psychosocial factors determine the risk for the development of either schizophreniform psychoses or major depression in patients with epilepsy, and

behavioral disorders in epilepsy have multiple risk factors and multifactorial etiologies.[1] Role of the neurologist in the psychiatric management of patients with

epilepsy

As neurologists, we tend to focus on seizure control, and psychiatric comorbidities are often underestimated. Recognizing psychiatric manifestations is an area that needs improvement.

Once symptoms are identified, the following questions arise[2] :

Are the symptoms related to the occurrence of seizures (preictal, ictal, postictal)?
Are the symptoms related to AEDs?
Is the onset of symptoms associated with the remission of seizures in patients who had previously failed to respond to AEDs?

Because of the phenomenology of epilepsy, the close association between epilepsy and psychiatry has a long history. The traditional approach to epilepsy care has been to focus on

the seizures and their treatment. Concentrating only on the treatment of the seizures, which occupy only a small proportion of the patient’s life, does not seem to address many of the issues that have an adverse impact on the quality of life of the patient with epilepsy.

Sackellares and Berent stated that comprehensive care of the epileptic patient requires “attention to the psychological and social consequences of epilepsy as well as to the control

of seizures.”[3]

Although undoubtedly important in the care of the patient with epilepsy, advances in neurologic diagnosis and treatment tended to obscure the behavioral manifestations of epilepsy until Gibbs drew attention to the high incidence of behavioral disorders in patients

with temporal lobe epilepsy.[4]
Frequency of psychiatric disorders in patients with epilepsy

It is estimated that 20­30% of patients with epilepsy have psychiatric disturbances.[5]

Of patients with intractable complex partial seizures, 70% may have 1 or more diagnoses consistent with the Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition (DSM­III­R); 58% of these patients have a history of depressive episodes, 32% have

agoraphobia without panic or other anxiety disorder, and 13% have psychoses.[6] The risk of psychosis in patients with epilepsy may be 6­12 times that of the general

population, with a prevalence of about 7­8%; in patients with treatment­refractory temporal lobe epilepsy, the prevalence has been reported to range from 0­16%.[7]

Differences in the rates may result from differences in the populations studied, time periods investigated, and diagnostic criteria.

The most common psychiatric conditions in epilepsy are depression, anxiety, and psychoses. [8, 9, 10, 11, 12, 13] (See the Table below.)

Table. Prevalence Rates of Psychiatric Disorders in Patients With Epilepsy and the General Population (2007 data)[8] (Open Table in a new window)

The psychiatric symptoms characteristic of the neurobehavioral syndrome of epilepsy (ie, Morel syndrome) tend to be distinguished in the following ways:

Atypical for the psychiatric disorder Episodic
Pleomorphic

Psychotic Disorders

Psychotic disorders are severe mental disorders that cause abnormal thinking and perception. Psychotic individuals lose relation with reality. Symptoms generally described as either positive, such as hallucinations, delusions, and disorganized behaviors, or negative, such as diminished range of emotion, reduced speech, and inability to initiate and sustain goal­directed activities.

Vuilleumier and Jallon found that 2­9% of patients with epilepsy have psychotic disorders.[14] Perez and Trimble reported that about half of epileptic patients with psychosis could be

diagnosed with schizophrenia.[15]

The etiology and pathogenesis of psychosis in epilepsy are poorly understood; however, neuroanatomical changes have been observed in patients with psychosis and include the following:

Asymmetry of amygdala and anterior segment of the hippocampus [16]
Rule of hippocampal­amygdala complex in pathogenesis of schizophrenia [17]

Smaller gray matter volume in the left and middle temporal gyri and left posterior superior temporal gyrus [18]

Psychiatric Disorder

Controls

Patients With Epilepsy

Major depressive disorder

10.7%

17.4%

Anxiety disorder

11.2%

22.8%

Mood/anxiety disorder

19.6%

34.2%

Suicidal Ideation

13.3%

25.0%

Others

20.7%

35.5%

Rule of bilateral middle frontal gyrus (prefrontal cortex) in overt psychosis occurring with schizophrenia [19]

Superior temporal cortex and dysfunction of corollary discharges in auditory hallucination [20]

Patients with temporal lobe epilepsy and psychosis of epilepsy have significantly smaller brain volume than people with temporal lobe epilepsy alone, and psychosis of epilepsy is a

distinct nosologic entity differing from schizophrenia.[21]

Kanner states that various classifications have been proposed for the psychoses associated with epilepsy. He asserts that for the neurologist, the most useful might be that which distinguishes among psychoses closely linked to seizures (ictal or postictal psychosis), those linked to seizure remission (alternative psychosis), psychoses with a more stable and chronic course (eg, interictal psychosis), and iatrogenic psychotic processes related to antiepileptic

drugs.[22]

Ictal events

Status epilepticus (ie, complex partial status epilepticus and absence status epilepticus) can mimic psychiatric disorders, including psychosis.

Postictal events

So and colleagues distinguished between postictal psychosis, which is characterized by well­ systematized delusions and hallucinations in a setting of preserved orientation and alertness, as well as postictal confusion. They also distinguished between self­limited postictal

psychosis and the unremitting chronic interictal psychosis seen in long­standing epilepsy.[23] Criteria proposed by Stagno for postictal psychosis include the following[24] :

Psychotic or other psychiatric symptoms occur after a seizure or, more frequently, a series of seizures, after a lucid interval, or within 7 days of the seizure(s)
The event may be psychosis, depression, or elation or may be an anxiety­related symptom

The event is time­limited, lasting days or, rarely, weeks; no significant clouding of consciousness occurs

Logsdail and Toone believe that clouding of consciousness, disorientation, or delirium may be noted, and, if consciousness is unimpaired, delusions and hallucinations are present; a

mixture of both also may be noted.[25]
Clouding should not be attributed to other medical or psychiatric causes (eg, drug

intoxication, complex partial status epilepticus, metabolic disturbance).

Interictal events

Interictal psychotic phenomena, particularly hallucinations and delusions, are common in patients with epilepsy.[26, 27, 28]

Although many etiologies of psychosis in epilepsy have been proposed, the significance of such factors as the type of seizure, epilepsy classification, lateralization of foci, and age at

onset of epilepsy remains uncertain.[29, 30, 31, 32]
Tarulli et al documented cases of patients who had multiple episodes of postictal psychosis

before developing interictal psychosis.[33] They concluded that a progression from postictal to interictal psychosis may be at play and that increased awareness and prompt treatment of postictal psychosis may inhibit or prevent the development of some instances of interictal psychosis.

Factors in the development of psychosis

The following variables are believed to have particularly strong links to the development of psychotic phenomena in patients with epilepsy:

Family history of psychosis ­ Patients who had a positive family history of psychosis were extremely susceptible to psychosis, so a genetic factor appears to be involved Age at onset of epilepsy ­ Patients with interictal psychosis showed a significantly

earlier onset of epilepsy [34, 35, 36, 37, 38]
Type of seizure ­ The existence of complex partial seizure (mostly temporal lobe

epilepsy) may be strongly associated with interictal psychoses [39, 40]

Intelligence ­ Patients with borderline intellectual functioning tend to develop psychotic symptoms relatively frequently [34, 35]

The risk factors for developing psychosis in epilepsy found in some studies also include the following[41] :

Partial complex seizures, especially with temporal lobe foci The presence of “alien tissue” (eg, small tumors, hamartomas) Mesial temporal lobe gangliogliomas
Left­handedness, especially in women

With regard to the first item above, some authors have noted a predominance of left­sided foci. Frontal lobe epilepsy is also common.

Schmitz et al studied risk factors and classified them by the following system:

Biologic factors
Earlier onset of epilepsy
More severe epilepsy
Psychosocial factors
Disturbed family background
Lack of interpersonal relationships
Social dependency
Professional failure
More frequent temporal lobe and unclassifiable epilepsies and less frequent generalized epilepsies

With regard to the last item above, no significant differences in types of epilepsies between patients with epilepsy and psychosis and patients with epilepsy without psychiatric disease have been found.

Trimble and Schmitz believe that the conclusions presented in the literature on risk factors are highly controversial.[41]

Schizophrenia

In a review study of patients with epilepsy who developed psychosis, Tandon and DeQuardo found that the patients’ psychoses were usually a form of schizophrenia, most commonly

paranoid schizophrenia.[42]
Stagno reported that persistent interictal psychoses of epilepsy and the schizophrenialike

psychoses of epilepsy are distinguishable from schizophrenia in the traditional psychiatric sense by the following[43] :

Lack of negative symptoms of schizophrenia, particularly flattening of affect and personality deterioration
Better premorbid personality
Paranoid delusions

Delusions of reference
More benign and variable course

Treatment

Status epilepticus and ictal abnormalities are treated in the same way as nonpsychiatric epileptic events. Postictal events are treated by improving seizure control.

So et al believe that postictal psychosis remits spontaneously even without treatment but that

the use of effective neuroleptics may shorten the duration.[44] Interictal psychosis is treated with antipsychotic drugs. Medications that lower the seizure threshold should be avoided. Some studies indicate that risperidone, molindone, and fluphenazine may have better profiles than older antipsychotic medications; clozapine has been reported to confer a particularly high risk of seizures.

Forced normalization

Treatment of any of the psychoses of epilepsy should take into consideration the phenomenon termed forced normalization, which is a concept described by Landolt in the 1950s. When the electroencephalogram (EEG) in psychotic patients is normalized, often with anticonvulsant medicines, the psychiatric problem worsens.

Alternative psychosis, or antagonism between seizures and behavioral abnormalities (ie, worsening of behavior with improvement in seizure control), is a similar phenomenon that has been known for a longer time. Forced normalization frequently is described in patients treated

with ethosuximide; anecdotally, however, forced normalization effects have been produced by treatment with most antiepileptic agents, including the newer agents. The mechanism underlying these interesting phenomena is not yet understood. Many authors consider the idea of forced normalization to be somewhat controversial.

Bipolar Affective Disorders

Bipolar affective disorder is chronic psychiatric disease with severe changes in mood with a wide spectrum of clinical manifestations. A number of studies have demonstrated that affective disorders in epilepsy represent a common psychiatric comorbidity; however, most of

the neuropsychiatric literature focuses on depression, which is actually prominent.[45] The incidence of developing bipolar affective disorder in epilepsy is 1.69 cases per 1000

persons­year, compared with 0.07 in the general population.[46]

Bipolar symptoms were 1.6­2.2 times more common in subjects with epilepsy than with migraine, asthma, or diabetes mellitus and are 6.6 times more likely to occur than in healthy subjects. A total of 49.7% of patients with epilepsy who screened positive for bipolar symptoms were diagnosed with bipolar disorder by a physician, nearly twice the rate seen in

other disorders.[47]

Depression

Depression is a mental state or chronic mental disorder characterized by feelings of sadness, loneliness, despair, low self­esteem, and self­reproach. Accompanying signs include psychomotor retardation (or, less frequently, agitation), withdrawal from social contact, and vegetative states, such as loss of appetite and insomnia.

Depression is the most frequent psychiatric comorbidity seen in patients with epilepsy. It is more likely to occur in patients with partial seizure disorders of temporal and frontal lobe

origin. It is also more frequent in patients with poorly controlled seizures.[48]
Two possibilities exist: (1) depression is a reaction to the epilepsy or (2) depression is a part

of the epilepsy.

Mendez et al compared patients with epilepsy to matched controls without epilepsy but with a similar degree of disability from other chronic medical diseases and found that while 55% of the patients with epilepsy reported depression, only 30% of the matched controls reported

depression.[49]
Mendez et al concluded that depression is related to a specific epileptic psychosyndrome.

On the other hand, Robertson concluded that with few exceptions, the phenomenology of the depression to a large degree is not attributed to neuroepilepsy variables; however, not all

studies have found this difference.[50]

In patients with refractory epilepsy, the presence of depression is one of the most important variables to have an impact on their quality of life, even more than the frequency and severity of the seizures.

Several studies have documented that the quality of life improves significantly in patients with epilepsy who are made seizure free. If those patients are excluded, Boylan et al have found

that the quality of life is related to depression but not to degree of seizure control.[51] Despite its high prevalence in patients with epilepsy, depression very often remains

unrecognized and untreated. The reasons for clinicians’ failure to recognize depressive disorders in patients with epilepsy include the following[52] :

Patients tend to minimize their psychiatric symptoms for fear of being further stigmatized
The clinical manifestations of certain types of depressive disorders in epilepsy differ from depressive disorders in patients without epilepsy and therefore are not recognized by physicians
Clinicians usually fail to inquire about psychiatric symptoms
Patients and clinicians tend to minimize the significance of symptoms of depression because they consider them to be a reflection of a normal adaptation process to this

chronic disease [53]
The concern that antidepressant drugs may lower the seizure threshold has generated among clinicians a certain reluctance to use psychotropic drugs in patients with epilepsy

Risk factors for the development of depression in patients with epilepsy include the following:

Temporal lobe (but not frontal lobe) partial complex seizures Vegetative auras
Family history of psychiatric illness, particularly depression Laterality effects, which are controversial

Physiologic factors associated with epilepsy and depression

Decreased serotonergic, noradrenergic, and GABAergic functions have been identified as pivotal etiologic mechanisms in depression and have been the basis for antidepressant

pharmacologic treatments.[54] Decreased activity of these same neurotransmitters has been shown to facilitate the kindling process of seizure foci, to exacerbate seizure severity, and to intensify seizure predisposition in some animal models of epilepsy.

Therefore, parallel changes of serotonin, norepinephrine, dopamine, and GABA may be operant in the pathophysiology of depressive disorders and epilepsy. Jobe et al have presented evidence that some types of depression and some types of epilepsy may be

associated with decreased noradrenergic and serotonergic transmission in the brain.[55] Flor­Henry speculated that depression might be related to right (nondominant) foci, a finding

confirmed by a few other investigators.[56]

Some authors have suggested that elation is associated with right­sided lesions and depression or sadness with left­sided lesions. Most studies that find a relationship between laterality and depression have found depression to be more common with left­sided foci.

Lopez­Rodriguez et al found that major depressive episodes were statistically more frequent in patients with left temporal lobe seizures than in patients with right temporal lobe seizures. [57]

Other authors report no laterality differences in depression rates.

Other factors associated with depression in epilepsy

One of the variables linking depression and epilepsy is a family history of depression.

A greater frequency of depression has been found in patients with seizures originating in limbic structures; also, a frontal lobe dysfunction has been associated with depression.

The quality of life is often suboptimal for patients with epilepsy, and this may adversely affect mood.[58, 59, 60, 61, 62]

Increased financial stress, life stressors, and poor adjustment to seizures are predictive of increased depression.[63]

The lack of control over the illness may be an additional risk factor for depression.[64, 65]

Depression in epilepsy may also result from iatrogenic causes (pharmacologic and surgical).

The AEDs most frequently associated with iatrogenic depressive symptoms include the following[66] :

Phenobarbital Primidone Vigabatrin Levetiracetam Felbamate Topiramate

Depressive disorder can also occur following the discontinuation of AEDs with positive psychotropic properties, such as carbamazepine, oxcarbazepine, valproic acid, and lamotrigine.

Frequency of depression in epilepsy

In patients with epilepsy, the reported rates of depression range from 8­48% (mean 29%, median 32%); the prevalence of depression in the general population ranges in different

epidemiologic studies from 6­17%.[67]
In a study of patients with epilepsy who were admitted to a psychiatric hospital, Betts found

that depression was the most common psychiatric diagnosis.

Williams studied 2000 patients with epilepsy and found that depressed mood was part of the attack in 21. According to Williams, depressed mood was the second most common emotion

constituting part of the attack, with fear being the most common.[68] Others have found similar results.

Characteristics of depression in patients with epilepsy

Characteristics of patients with epilepsy who also have depression include the following:

Fewer neurotic traits
More psychotic traits
Higher trait and state anxiety scores
More abnormal affect and chronic dysthymic disorder High hostility scores, especially for self­criticism and guilt Sudden onset and brief duration of symptoms

Perhaps 10­20% of persons with epilepsy have a peri­ictal prodrome consisting of depressed­irritable mood, sometimes with anxiety or tension and headaches. Although Williams noted in his patients that the mood disturbance would persist for 1 hour to 3 days

after the ictus, postictal affective syndromes have received little attention in the literature.[68] Blumer has defined an interictal dysphoric disorder in patients with epilepsy in which

symptoms tend to be intermittent.[69]
On average, the patients tend to have 5 of the following symptoms (range 3­8):

Depressed mood Anergia
Pain
Insomnia

Fear
Anxiety
Paroxysmal irritability Euphoric moods

Kanner has noted that the symptoms of depression in patients with epilepsy are different from those in patients without epilepsy. He believes that patients with epilepsy who are felt to warrant antidepressant therapy often do not meet formal DSM criteria for a mood disorder and concludes that the problem of depression in epilepsy may be underestimated by using

screening instruments designed for use in psychiatric patients.[70]

Kanner continued with this research using the DSM­IV criteria. Most symptoms presented with a waxing and waning course, with symptom­free periods. He referred to this form of depression as “dysthymic­like disorder of epilepsy.”

Caplan et al believe that depression in children and adolescents with epilepsy tends to have a different presentation from that seen in adults with epilepsy, although some adolescents with depression may present with a syndrome similar to that seen in adults. They reported that children with depression often do not appear sad and that the depression may be

manifested by the following[71] :

Irritability Oppositionality Aggression Anger

For this reason, special instruments are used to assess depression in children.

Thome­Souza et al reported that depression in children with epilepsy may be underdiagnosed and untreated for longer periods than in adults. They found that 70.5% of children and adolescents in the study had psychiatric disorders and that the most frequent psychiatric disorder in children was attention­deficit/hyperactivity disorder (ADHD) and the most frequent psychiatric disorder in adolescents was depression. They found that family

history was also an important determinant in mood disorders in children and adolescents.[72]

Preictal symptoms of depression

Categorizing depression in patients with epilepsy as depression occurring peri­ictally (preictally, ictally, or postictally) and interictally may be useful.

Preictal symptoms of depression are believed to present as symptoms of irritability, poor frustration tolerance, motor hyperactivity, and aggressive behavior in children with epilepsy.

However, very few studies have been performed in the literature.[73]

Ictal symptoms of depression

Ictal symptoms are the clinical expression of a simple partial seizure. Psychiatric symptoms occur in approximately 25% of auras. The most frequent symptoms include feelings of

anhedonia, guilt, and suicidal ideation.[74]

Postictal symptoms of depression

Postictal symptoms of depression have been recognized for a long time, but they have been poorly studied in a systematic manner.[75]

Interictal symptoms of depression

For patients with epilepsy to experience depressive episodes that fail to meet any of the DSM­IV­TR criteria is not unusual. Kraepelin and Bleuler were the first to describe affective symptoms of prominent irritability, intermixed with euphoric mood, fear, and symptoms of

anxiety, as well as anergia, pain, and insomnia.[76, 77, 78]
In 1986, Mendez et al used the term atypical depression in epilepsy patients using the DSM­

III­R criteria.

Treatment

The treatment of mood disorders in patients with epilepsy includes reevaluation of the anticonvulsant regimen, cautious but aggressive use of antidepressants, and psychotherapy.

First and foremost, treatment involves seizure control with appropriate anticonvulsant therapies. A phenomenon analogous to alternative psychosis, worsening of behavior with better seizure control, has been reported in epilepsy­associated mood disorders.

There is evidence that some anticonvulsant therapies, including vagus nerve stimulation, valproate, gabapentin, carbamazepine, and lamotrigine, also have antidepressant effects and may prove effective in treating depression in patients with epilepsy. Phenobarbital is known to produce depression.

According to Schmitz, vigabatrin has been linked to psychoses and to major depression, and phenytoin has been associated with toxic encephalopathies.[79]

McConnell and Duncan cite some patients in whom phenytoin had been linked to depression and mania. A case has been made that the GABAergic drugs may be associated with an

increased incidence of psychiatric problems.[80]

However, antidepressants may be necessary to effectively treat depression in these patients. When an antidepressant is prescribed, the epileptogenic potential, adverse effects, and drug interactions must be evaluated. Selective serotonin reuptake inhibitors (SSRIs) such as citalopram (owing to its lack of drug interactions) and multireceptor­active compounds such as nefazodone or venlafaxine are suggested as first­line treatments. Bupropion, maprotiline, and clomipramine should be avoided.

Virtually all non–monoamine oxidase inhibitor (MAOI) antidepressants have been reported to lower the seizure threshold. In the treatment of epilepsy­related depression, priority should be given to optimizing seizure control, since improved psychosocial functioning tends to accompany seizure remission. Antidepressants may manifest convulsant and anticonvulsant effects. Maprotiline and amoxapine have the greatest seizure risk; doxepin, trazodone, and fluvoxamine appear to have the lowest risk.

Electroconvulsive therapy is not contraindicated and may prove effective for epilepsy patients with severe, treatment­resistant, or psychotic depression.

It is imperative that depression be recognized and treated in patients with epilepsy. Further prospective studies of new treatment options for depression in this patient population are

needed.[81]

Mania

In a carefully selected series of patients with epilepsy, Williams found that only 165 of 2000 patients had complex, including emotional, ictal experiences.[82]

Of those 165 patients, only 3 described elation. Mania and hypomania are rare in association with epilepsy.

Manic­depressive illness is also rare; of 66 patients with epilepsy and major depression, only 2 had bipolar disorder. This rarity is probably, to some degree, secondary to the antimanic effect of drugs such as carbamazepine and valproate. However, mania was uncommonly associated with epilepsy even before the use of modern antiepileptic drugs.

Suicidal Behaviors

Suicidality (completed suicide, suicide attempt, and suicidal ideation) is significantly more frequent among people with epilepsy than in the general population.[81, 83, 84, 85, 86, 87]

The risk of suicide in the general population averages about 1.4%. Depression is one of the psychiatric disorders that increases the risk of suicide. The risk of suicide in depressed patients is believed to be around 15%.

On average, the risk of suicide in patients with epilepsy is about 13% (prevalence rate ranges from 5­10 times that of the general population). Although some authors question its methodological and patient selection techniques, most authors cite Barraclough’s meta­ analysis, which revealed that the risk of suicide in patients with temporal lobe epilepsy is

increased to as much as 25­fold that of the general population.[88]
Even so, depression remains underrecognized and untreated. The relationship between

epilepsy and suicidality is complex and multifactorial.

Psychiatric adverse events, including symptoms of depression and anxiety, have been reported with the use of several AEDs, particularly barbiturates (phenobarbital and

primidone), topiramate, tiagabine, zonisamide, vigabatrin, and levetiracetam.[89, 90, 91, 92]

The incidence of suicidal phenomena linked to specific AEDs has not been systematically well studied. These data may either reflect the natural course of an underlying, recurrent psychiatric illness with no real effect from AEDs or could suggest that AEDs lower the threshold for manifesting psychiatric symptoms in individuals who are vulnerable because of a genetic or historical predisposition to psychiatric disorders.

Frequent risks associated with suicidality include the following[81] :

Current or past history of mood and anxiety disorders
Family psychiatric history of mood disorders, particularly of suicidal behavior Past suicidal attempts

In January 2008, the US Food and Drug Administration (FDA) issued an alert regarding the association between suicidality and AEDs, having concluded that there was a statistically significant, 1.8­fold increased risk of suicidality with exposure to AEDs. This conclusion was based on the results of a meta­analysis that included data from 199 randomized clinical trials of 11 AEDs: carbamazepine, felbamate, gabapentin, lamotrigine, levetiracetam, oxcarbazepine, pregabalin, tiagabine, topiramate, valproate, and zonisamide. The meta­ analysis encompassed 43,892 patients treated for epilepsy, psychiatric disorders, and other disorders, predominantly pain.

In the study, suicidality occurred in 4.3 of 1,000 patients treated with AEDs in the active arm, compared with 2.2 of 1,000 patients in the comparison arm. The results of this meta­analysis

must be considered with great caution, and more research is necessary.[81, 93, 94]
The FDA has decided to insert suicide warnings in the package inserts of all AEDs; thus,

physicians need to identify patients with increased risk of suicide.[95] Anxiety Disorders

Anxiety is an experience of fear or apprehension in response to anticipated internal or external danger, accompanied by muscle tension, restlessness, sympathetic hyperactivity, and/or cognitive signs and symptoms (hypervigilance, confusion, decreased concentration, or fear of losing control).

Anxiety is common in patients with epilepsy; of 49 patients with epilepsy attending a tertiary epilepsy care center, 57% had high­level anxiety.

Anxiety in patients with epilepsy can be ictal, postictal, or interictal.

GABA is the most important inhibitory transmitter in the central nervous system. Evidence suggests that the abnormal functioning of GABA receptors could be of great importance in

the pathophysiology of epilepsy and anxiety disorders.[82, 81]

Differentiating between spontaneous fear and reactive fear (ie, reaction to the knowledge that a seizure may occur) can be difficult. Panic disorder can produce paroxysmal symptoms, which can be confused with epileptic events and may go unrecognized in patients with epilepsy. Anxiety also may be related to nonepileptic attack disorder.

Symptoms of anxiety in epilepsy

Symptoms of anxiety in epilepsy may result or be exacerbated by psychological reactions, including responses to the unpredictability of seizures and restrictions of normal activities.

This results in low self­esteem, stigmatization, and social rejection.[1, 83, 84] According to Goldstein and Harden, epileptic events can produce symptoms indistinguishable from those

of primary anxiety disorder.[85]

Fear and anxiety are often associated with simple partial seizures. Torta and Keller estimated that fear occurs as an aura in as many as 15% of patients,[11] and Goldstein and Harden concluded from several studies that fear is one of the most common ictal emotions.[85]

Ictal anxiety symptoms manifest as fear or panic, sometimes with other characteristics of temporal discharges, such as depersonalization and déjà vu, as well as other psychological

and autonomous phenomena.[1, 86]

Anxiety in association with type of epilepsy and frequency of seizures

The highest rates of psychiatric comorbidities, including anxiety, are reported in patients with chronic, refractory seizure disorders.[1, 83, 86, 87]

Interestingly, however, Goldstein et al found that patients with epilepsy with high seizure frequency had lower anxiety scores than did patients with lower seizure frequency.[88]

The risk of anxiety is higher in focal (more frequent in temporal lobe) epilepsy than in generalized epilepsy. In patients with temporal lobe epilepsy, Trimble et al reported that 19% of the patients were diagnosed with anxiety and 11% were diagnosed with depression.

Edeh and Toone found that patients with temporal lobe epilepsy scored higher for anxiety than did those with focal, nontemporal lobe epilepsy.[4]

Anxiety can also be seen in frontal lobe epilepsy.

Ictal and interictal anxiety

Anxiety in epileptic patients may occur as an ictal phenomenon, as normal interictal emotion or as part of an accompanying anxiety disorder, as part of an accompanying depressive disorder, or in association with nonepileptic, seizurelike events as part of an underlying primary anxiety disorder.

Interictal anxiety has a great influence on the quality of life of patients, since most of them have a permanent fear of new discharges. Torta and Keller have estimated that as many as 66% of patients with epilepsy report interictal anxiety. Goldstein and Harden proposed 2 major psychological mechanisms for this, as follows:

Fear of seizure recurrence (seizure phobia) Issues surrounding locus of control

They concluded that documented cases of actual seizure phobia are rare but that a sense of dispersed locus of control can cause profound problems in patients with epilepsy.

Treatment

Several studies have shown that pregabalin, used as an adjunct for partial seizures, has been an effective, rapidly active, and safe treatment for generalized anxiety disorder.

Research

Although, as shown above, studies looking into the association between anxiety and epilepsy have been performed, because of the difficulty in separating the anxiety that accompanies a chronic disease from pathologic anxiety, studies investigating anxiety in epilepsy have nonetheless been relatively few.

Personality Disorders

Personality disorders in epileptic patients can cause abnormal behavior that can have a direct impact on seizure control and quality of life. The question of the relationship has a long history and remains controversial. In 1975, Woxman and Geschwind described a syndrome consisting of circumstantiality (excessive verbal output, stickiness, and hypergraphia), altered sexuality, and intensified mental life in a patient with temporal lobe epilepsy. It was called

Geschwind syndrome.[89]

Bensan and Herman reported that data are insufficient to state with certainty that a consistent pattern of behavioral changes occur in patient with temporal lobe epilepsy. The complex partial epilepsy should not be diagnosed on the basis of the presence of Geschwind

syndrome without any paroxysmal episodes that can be proven to be epileptic.[90]

The link of personality disorders to epilepsy was not only seen in temporal lobe epilepsy. Trinka et al found that personality disorders were present in 23% of patients with juvenile

myoclonic epilepsy.[91]

Trimble has summarized the data and concluded that the personality profile of a patient with epilepsy can be explained by a complex combination of the effect of (1) dealing with a chronic illnesses, (2) AED effects, (3) and temporal lobe pathology. He supported that certain personality disturbances in epilepsies should be viewed as associated with cerebral

abnormalities that also lead to seizures.[92] Attention­Deficit/Hyperactivity Disorder

Attention­deficit/hyperactivity disorder (ADHD) is another psychiatric comorbidity in patients with epilepsy and is more common in children. The co­occurrence may result from altered neurobiological mechanisms involved in early brain development.

The incidence of ADHD is about 7.76 cases per 1000 person­years in patients with epilepsy and 3.22 in patients without epilepsy. The incidence of epilepsy is 3.24 cases per 1000

person­year in patient with ADHD and 0.78 in those without ADHD.[93]
A neuropsychiatrist may find difficulty in differentiating impaired attention secondary to

absence of seizure and attention deficit as a phenotypical representation of ADHD.

Many AEDs can cause symptoms mimic ADHD, and the most common implicated are the GABAergic drugs such as barbiturates, benzodiazepines, and vigabatrin.

Methylphenidate can cause aggravate seizures in patients with ADHD, although generally it is considered safe in those who are seizure free.[94]

Psychotropic Effects of Antiepileptic Drugs

Knowledge about the psychotropic effects of AEDs is crucial and yet very limited in the epilepsy population. Evidence suggests that lamotrigine and the vagal nerve stimulator may have antidepressant properties that could be of use in light of common comorbid depression.

Carbamazepine, valproate, lamotrigine, and possibly oxcarbazepine may have mood stabilizing properties. Gabapentin, pregabalin, and tiagabine may have anxiolytic benefits.

There is a risk of depression related to barbiturates and topiramate, and possibly to phenytoin. Underlying depression and anxiety symptoms may be exacerbated by levetiracetam, while psychotic symptoms, albeit rare, have been reported with topiramate,

levetiracetam, and zonisamide.[95]
Psychiatric Disorders and Epilepsy Surgery

Generally, psychiatric outcomes improve or no changes are noted with epilepsy surgery. A history of psychiatric disorders before epilepsy surgery is associated with poorer chance of postsurgical seizure remission. After resective surgery, only patients with good or excellent seizure control had sustained long­term improvement in mood.

Postsurgical patients had higher suicidal mortality rate compared with the general population, and people who continue to have seizures after surgery had a higher suicidal mortality rate,

in contrast to those who were seizure free after surgery (4­5 times).[96] In a series of 26 patients, gamma knife radiosurgery for mesial temporal lobe epilepsy showed no significant

psychiatric changes from preoperative baseline for up to 24 months.[97]
The risk factors for depression after epilepsy surgery include preoperative history of mood

disorders and mesial temporal lobe surgery.

Disturbed behavior may interfere with the preoperative evaluation, and the patient may not be able to provide informed consent for investigation and surgery.

Vagus nerve stimulation showed better responses in patients with chronic major depressive

disorders over 12 months of study.[98, 99] In small studies, Elger et al and Harden et al showed that treatment with vagal nerve stimulation improves depression in epileptics independent of effects on seizure frequency. Vagal nerve stimulation is a useful therapeutic

tool in treatment­resistant depression.[100] Patient and Family Education

For patient education information, see Epilepsy, Depression, Schizophrenia, Bipolar Disorder, and Anxiety.

The following Web sites are useful patient and family education tools:

American Epilepsy Society
Centers for Disease Control and Prevention, Epilepsy
Epilepsy.com
Epilepsy Foundation
Epilepsy Foundation, Communities
MayoClinic.com, Epilepsy
Medline Plus, Epilepsy
National Institute of Neurological Disorders and Stroke, NINDS Epilepsy Information Page

Conclusion

Psychiatric comorbidities in patients with epilepsy are relatively frequent. Despite the high prevalence rates, few data are available. Because of this, the data used are from primary psychiatric disorders, assuming it can be applicable to patients with epilepsy.

Early recognition and management of psychiatric disorders in patients with epilepsy is extremely important, because it improves the quality of life, decreases suicidality, and aids in better seizure control.

Contributor Information and Disclosures

Author
Fahad Salih Algreeshah, MD Head of Neurology Unit, Department of Medicine, King Saud Medical City

Disclosure: Nothing to disclose.

Coauthor(s)
Selim R Benbadis, MD Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida College of Medicine

Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association

Disclosure: UCB Pharma Honoraria Speaking, consulting; Lundbeck Honoraria Speaking, consulting; Cyberonics Honoraria Speaking, consulting; Glaxo Smith Kline Honoraria Speaking, consulting; Sleepmed/DigiTrace Honoraria Consulting; Sunovion Consulting fee None; Supernus Speaking, consulting; Upsher­Smith Grant/research funds None

Specialty Editor Board
Andrew S Blum, MD, PhD Director, Adult Epilepsy and EEG Laboratory, Comprehensive Epilepsy Program, Rhode Island Hospital; Associate Professor of Neurology, The Warren Alpert Medical School of Brown University

Andrew S Blum, MD, PhD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, and Massachusetts Medical Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor­in­Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Chief Editor
Jose E Cavazos, MD, PhD, FAAN, FANA, FACNS Professor with Tenure, Departments of Neurology, Pharmacology, and Physiology, Assistant Dean for the MD/PhD Program, Program Director of the Clinical Neurophysiology Fellowship, University of Texas School of Medicine at San Antonio; Co­Director, South Texas Comprehensive Epilepsy Center, University Hospital System; Director, San Antonio Veterans Affairs Epilepsy Center of Excellence and Neurodiagnostic Centers, Audie L Murphy Veterans Affairs Medical Center

Jose E Cavazos, MD, PhD, FAAN, FANA, FACNS is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, American Epilepsy Society, American Neurological Association, and Society for Neuroscience

Disclosure: LGCH, Inc Ownership interest Consulting

Additional Contributors
Pedro E Hernandez­Frau, MD Clinical Neurophysiology Fellow, Department of Neurology, Tampa General Hospital, University of South Florida College of Medicine

Pedro E Hernandez­Frau, MD is a member of the following medical societies: American Academy of Neurology

Disclosure: Nothing to disclose.

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Art, Brain, Health, Temporal Lobe Epilepsy

Made It Through the Night…PLUS Temporal Lobe Epilepsy versus Schizophrenia

12 Comments

This flower, whose name, Self-Heal or Heal-All, says everything, and it is not insignificant that this was the first wildflower that started me on my Field Botany path, and was also the agent of my natural history conversion experience:

Self-Heal or Heal-all (My first wild flower and the one that changed everything)
Self-Heal or Heal-all (My first wild flower and the one that changed everything)

 

Last night was a very difficult night, as you know.

I did not believe the nurse when she told me this morning that E–, who was an animal lover, would never have killed herself, leaving her beloved parrots to fend for themselves. She said it simply went against the grain of most animal people to kill themselves while their “children” still needed them. It turned out, though it took me a while to “grok” this, that E– apparently died of a combination of diabetes type 1 and asthma. The details are unclear and unnecessary but I was assured by both nurse and the building social worker that it was not suicide. Thank god.

However, early this morning things were not well, and I wonder if what  happened later on was not at work last night as well. Let me explain:

I had an appointment to see my psychiatrist, Dr Angela, at 10 a.m. and as usual I got up to drive myself there, a short distance over the bridge to the next town, maybe 6 miles away tops. It is a trip I have done dozens and dozens of times, perhaps hundreds now.

This time, however, things were different. Halfway there, on a stretch of road — I’m talking back roads not highway — a road that I know like the palm of my  hand, I was suddenly overcome by a feeling, an intense almost nauseating feeling of “jamais vu.” This is the opposite of “deja vu” — that sense that things you have never done have happened before. Jamais vu is the sense that while you are in familiar places or with familiar people, they seem strange or new or utterly unfamiliar. I have had deja vu many times, as have a lot of people, and I think it is a fairly common experience to feel as if something has “happened before” even though it is really a new experience.

 

But never before, at least not since I was ill, severely and neurologically ill, with Lyme disease, have I felt this intense feeling of non-familiarity in a situation that I know I knew very well. I was terrified, if briefly. I was not at all certain where I was. I mean, I kept driving, because my instincts told me to keep going, that my hands would make the proper turns. But my conscious brain had no recognition of where I was and no conscious notion that wherever I was I had ever been before. It was, as I said, terrifying and very, very strange.

Luckily, within minutes things had resolved enough so I knew that I had arrived at the Whole Foods parking lot, which my doctor’s office and the doctors’ complex shares. I still felt very weird. I felt in fact that I was not completely embodied, even though I carried a heavy enough bag to embody or burden down anyone.

When I got to Dr Angela’s office, the first thing i told her was that something was wrong. Yes, I had sent her the email I mentioned here yesterday, but I did not mean that. I meant the foreign feeling, the jamais vu intensity, which though faded still scared me. Thinking back, when i was so ill with Lyme it was actually deja vu, in an incredibly brilliant and vivid form, that afflicted me rather than the alienating jamais vu, but I knew that both deja and jamais vu can be commonly a symptom of either an aura or a seizure itself. Especially the much rarer experience of jamais vu.

I have had several different kinds of seizures in my life, and I have just been taken off Topamax, an anti epilepsy drug I have taken for years. I did this in preparation for a neuro-ophthalmology appointment in October (not sure why I thought it had to be stopped). So i have and had some sense that it was the d/c of this anti-convulsant that was the proximate cause if not the absolute cause for my symptoms.

But I was terrified that this jamais vu would generalize into a full-blown seizure, which I couldn’t bear the thought of. Dr Angela was quite responsive and suggested that I 1) take an immediate Ativan, .5mg as that is reasonably effective as an anticonvulsant, though better IV than oral and 2) when we found that I had stashed 100mg of Topamax in my pill compact, she had me take that as well, figuring I would get back to my usual 200-300mg within a week or two.

The appointment went — well, I don’t remember much about it, frankly. All I recall is leaving, promising to get a cup of coffee before I drove home, then realizing once I got to the parking lot that there was no way I could drive, coffee or not. I felt simply too weird. And weirded out. Too scared of having a full blown seizure, whether temporal lobe or otherwise to get in the car.

To my great luck, when I contacted my case manager, Rebecca, who works in next town over, she was immediately available and came to pick me up. That was a huge relief. I didn’t even have to wait more than 5 minutes. More, the Whole Foods grocery store people didn’t bat an eyelash when I asked if I could leave my car in the lot overnight.

Later on, Tim went and got my car for me, so I didn’t even have to do that. I simply went home and took a  nap. When I got up I felt at least ten times better. Not so weird, not so seizure-y. Less scared, and finally able to be convinced that the huge balloon of misery and terror from last night was just that, a balloon, a mistaken notion…a fiction. I was wrong, that was all. Even though the conviction and certainty felt as real as anything, they were only FEELINGS, and as so many people including my brother assured me, those feelings would change if I hung in there.

Lo and they did change and have changed. Thank heavens.

 

Now it occurs to me that perhaps even that huge balloon of certainty may have been seizure-related. I don’t have any real reason to think otherwise. I know, I know, my shrink brother has his theories. But I felt so UN-conflicted about it, so hugely convinced, that the explanation of seizure activity, comparable to the certainty that I “have never been here before” of jamais vu even though I knew I had, and also knew, as I said, that I had not caused the putative suicide…this explanation simply makes more sense and feels  “more right” to me. After all, why would I suddenly feel like I did anything to E— who was not all that important to me, or no more than anyone else in the building really. It felt morever just so hugely compelling, in precisely the same way that impending doom feeling of a temporal lobe seizure feels — it isn’t real but it is unshakable, utterly unshakable.

I don’t know, of course. The shrinks — and I include Dr Angela and my brother — would like to make it all about me, all about my conflicts and my mental illness however they want to define that. But I wonder now how much my ongoing (but unofficially diagnosed, that is, only by psychiatrists) TLE has affected me all along. I wrote about this conflict, this contamination of any schizophrenia diagnosis with temporal lobe epilepsy, and months ago. It seems strange that so many have “both”…|

Nevertheless, I have never had my seizure feelings checked out, largely because I do not want anyone curtailing my voluntary driving. And I don’t like doctors having that power over me. I also do not trust them to take me seriously, as a NON-psychiatric patient. I do take AEDs to prevent olfactory hallucinations, (NOT as mood stabilizers) and such, but why see a neurologist who might tell me I can’t drive a car for any length of time when I have never even had a fender bender from this? Or who might, and this would feel just as bad, tell me it is “all in my mind” not in my brain…!

Art and artwork, depth perception, portraits, Temporal Lobe Epilepsy, Vision, Vision therapy

Vision Therapy, Art and Wonder

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The following may repeat some of what I have written before, though expressed rather differently. I “purloined” it from a letter I wrote to someone I once knew, who I hope will forgive me if he ever visits this blog and recognizes it here.

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Life continues to present many challenges, which both the poetry book and Mary’s introduction to WE MAD CLIMB SHAKY LADDERS illuminate , I suppose, in some detail. But among the thrills and wonders of these last few years of recovery are two that are related to one another but which I would never have dreamed of in relation to me.

I speak of vision, one — of depth perception —  and two, of art. I don’t know if you have heard of the recent science memoir by Sue Barry called, Fixing My Gaze, in which she describes her strabismus  and her work in vision therapy. Apparently the book has become quite popular, at least around here, after a review in the Hartford Courant (Barry lives not far from Northampton, MA). Strangely enough, I have been writing for the past year about, among other things, my own experience in vision therapy trying to achieve stereopsis .  I believe I must have had “3-D vision” at some point, since I did not have strabismus as a child. At least not to the same extent as Barry, and I think I did when very young “see” what others said they saw through those Viewmaster toys (you must remember those binocular viewers with the “3-D” slides?). My later lack of 3-D vision never bothered me, apparently, and I never knew that I was missing anything, until I developed frank double vision about four or five years ago. My optometrist told me I probably had had unrecognized intermittent exotropia since childhood, but that my eye muscles had been somewhat stronger then and so my vision had stayed single. She could not say however if it had indeed been binocular, that is to say that I had used both eyes in seeing.. In any event, it was only when I was given prism glasses in 2008 and in February suddenly experienced brief, brief flashes of stereopsis that I understood what most people see, what I had in  fact  gone for so long without seeing. The world was suddenly, achingly more beautiful than — well, than anyone else seemed to recognize:

The first time on the Broad Street Green I passed the huge tree with its bark “sticking out” I was stunned, stopping dead in my tracks to stare at the reddish burnt sienna ridges that had suddenly leapt out at me. Stark, knifelike and jagged, the crusty surface was backlit by an early setting sun in such a way that  it all seemed limned with light. A gentle roughness edged the troughs and depressions. Spawned from the cortex wood, the bark strained and stretched. I could scarcely believe how the air gently touched and tasted each indentation and projection of bark — as if saying, “I love you, I love every inch of you and my kisses, my airy bearhug proves it.” Just as surely as I knew the air loved that bark, I knew that space, the “emptiness” that cups and holds everything in its place safely,  adores matter. This struck me as neither bizarre nor even uncommon, only obvious. What was strange and unfortunate to me was the fact that no one I spoke to about this experience seemed to know what I was talking about…

I cannot tell you (or anyone else for that matter, except perhaps Sue Barry, or Oliver Sacks) how much “space loves us” and everything it touches. Space is what gives us as a gift to ourselves..And when I saw it, saw space for the first time I fell in love with matter, and with the hollows and shapeliness of everything. I wanted to do nothing but gaze upon the world without touching it or or talking for at least a week…I wanted to walk around in silent solitude, experiencing space without interruption, to see without the interposing of frivolous conversation how incredible it was that you write words with pens held above the paper; that when you see a sign or a billboard, there is — and you are as certain of this as of any delusion —the knowledge that there is  flatness to it, and that “more space” lies beyond it…Someone’s nose which reaches out in space is far more interesting than their voice, and the way a hand extends outward can be the most lovely thing seen…Indeed, I would tell people quite spontaneously how beautiful they looked, the way their noses projected from their faces, or their hands suddenly coming out at me…

Oh, it is so impossible to convey the sheer — well, even now there are no words for this, no words beyond that single inadequate word, beauty, for which there seems to be no useful synonym. All I can say is that while I felt no better about myself, I certainly fell in love with the substance of the world! Who can say, What is the matter with the world? Seriously? All is the world is the matter, and that matter is more exquisitely lovely and worthy of being preserved than even many principles — Free trade, capitalism, rugged individualism above socialism in any and all forms etc —  Americans feel they have  a right to hold so dear…
As for Art? In my cooler moments I reduce it to “medicine”, to symptomatology…thinking perhaps this amazing talent, so unexpected and newfound, has merely to do with the Temporal Lobe Epilepsy or seizure disorder with which I was diagnosed after having ECT about 3-5 years ago. I don’t know. (I read in SEIZED by Eve La Plante that not only are there personality changes but one can acquire sudden artistic abilities and interests, almost full-blown after developing TLE..so who knows?) Perhaps not. In any event, (I should mention that this is my theory little mentioned to anyone at all…Not sure to whom I should talk…) starting in 2007 I took up lifesize papier mache sculpture in a serious way, and just a week ago suddenly, VERY suddenly, discovered that I could paint portraits, just like that…I had never done a portrait before, rarely even tried to draw, had always said I couldn’t draw or paint for beans. Then one instant I felt drawn to paint (with which I had always decorated my papier mache, with swirls and colors but not true representational painting) and to doing “real art”. I “decided” I would paint a young man, and then went ahead and fearlessly did so (see first attachment)…Since then I have done one portrait a day. Some imaginary, some from photos…And I have no idea, had no idea I could do so at all! Frankly, ditto the sculpture, though I am getting used to that ability now that I have several to my name…(see two other attachments for examples of earliest pieces).
I hope you won’t mind all this “Wow is me” stuff…I’m not usually so impressed with myself, I assure you. However, while I am at it, I want to send you three newer poems. I actually dislike most of the illness poems in the book, and want you to see what I have been doing more recently,  since the DIVIDED MINDS book was finished in 2003. I hope these poems speak for themselves. The “Epithalamion” one got a lot of chuckles, and ought to, when read properly (best out loud). I read it at my twin’s wedding. “To the Reader” will be the first poem in my second book, the opener, though perhaps not as “welcoming” as “How to read a Poem”.  And the vision therapy one is about what I have been doing in order to regain stereopsis. Which by the way really works, vision therapy that is, despite the skepticism of most ophthalmologists, who never bother to try it out, just condemn and contemn it out of hand, because it is done by ODs not MDs….VT has to be continually practiced though or like me you can lose the ground you gained after a while. Now I struggle to gain it back. I vow to  keep practicing. I do not think I can go without the exercises not after having gotten my eyes to do what they should do. It is so discouraging now to be back at nearly square one, I must admit…

Recovery, Schizophrenia, Temporal Lobe Epilepsy, Uncategorized

Washington, DC and Beyond

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Before I relate the tale of my trip to DC I hasten to add one addendum to the discussion below on TLE: Dr C said absolutely nothing about schizophrenia and TLE and possible misdiagnosis. Nothing whatsoever. ALL he mentioned was that my ECT apparently triggered — he used the word kindled — classic TLE in my brain, as evidenced by the pattern of onset of the olfactory hallucinations and their response to treatment. ALL the rest of my theorizing about schizophrenia and TLE has come from my own conjectures and readings that have spun off from that one statement and not from a single thing he said or implied. Please understand this. He may not have meant and may never bring up the subject at all…The question remains, Will I?

 

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Now then, about my solo flight, my DC adventure:

On Wednesday, Josephine drove me to New Haven and I took the high speed train, the Acela – going at a rather low rate of speed it seemed to me, most of the way – to Washington DC. The trip down was uneventful, except that in my anxiety to get a seat, I completely forgot to tip the porter who helped me get my bag down and up the  flights of stairs in the station (the escalator wasn’t working). I had a five dollar bill in my pocket all ready for him but at the last minute plum forgot…for which I felt guilty the entire journey right ip until I got back into Jo’s car at the end of it…and even now, a twinge remains.

 

The four and a half hours passed quickly as I had to review the new edits the copy editor had made. It wasn’t announced that we had arrived. People just stood and started getting their things from the overhead rack. I had to ask if we were in Washington. Finally, off the train, I followed where everyone else seemed to be going, managing not to go near the uniforms with the dog, though it occurred to me that maybe it was where I was supposed to go, because I wasn’t going where the cars were, was i? Luckily just then, Sara waved to me from the opposite door , and I saw and recognized her so that misstep was averted…It occurred to me, however, that we have become like a police state, what with armed guards and police dogs standing around in train stations, only supposedly to protect us (after all, they tell you DO NOT TOUCH THE DOG!)

 

That first night we spent just getting caught up on Sara’s recent travels as she is head of an “abroad program” at a university there. Then the next day, I slept till 9 and she went off to work. At noon I was picked up by a friend of Sara’s who drove me, with a few mishaps, to the train again, for my trip to MD to talk to a senior psychology class at a small, private college in a town about an hour outside of Baltimore. During the drive to the school, I began to feel weird — thought it was low blood sugar or simple sleepiness– and asked if we could get some coffee once we got there. I felt too fuzzy to even pay for anything, couldn’t think straight to talk, just eating to prevent myself from fainting. Finally, it was time to go to the class, and so I pulled myself together, took a last bite from my muffin and threw the rest of coffee and muffin away. 

 

In the class I gave my talk and did the Q and A with nothing untoward happening, except that I had to stop when the feelings reoccurred with fatigue near the end, at around 4:15 (the class ended at 4:30 so I made it almost the whole time). All the questions were really good, made me think. The only one I felt I did not do justice to was the one about Lynnie and whether or not she needed therapy and medication (!). If only they knew her and Sal…But in any event, I ought to have explained how psychiatrists are ordinary human beings with ordinary human emotions and flaws and faults, not superhumans, and they get angry and jealous and pissed off etc just as anyone else does. Jealousy in and of itself is not an illness, just an uncomfortable feeling that I know Lynnie has dealt with in her own professional and personal therapy over the years (as I pointed out all psychiatrists see their own therapists first). As for medication, she’d be the first to tell anyone she swears by it, and would not want to do without it!

 

After that class, I was blitzed completely, and could barely sit up straight in the car heading back to Baltimore and the train, and then my head blossomed into a migraine on the train. When I met Sara in the station again in DC I was utterly exhausted. I ate a little supper but basically fell asleep by 9pm and slept through until 9am.

 

Friday we took it easy. We drove around the Capitol area and stopped to walk into the Supreme Court, and walk around the White House. But we didn’t spend a great deal of time anywhere as the light was a brilliant blinding white and the temperature pushing 75°F.  Also, that night I had a poetry reading scheduled at the Potter’s House Sounds of Hope gathering

 

The Potter’s House in DC — a bookstore and home-cooked-food restaurant, with a Let’s All Help Each Other theme…It was great to go in the door and find a seat at the table and know every, or nearly every song sung. I wasn’t scheduled until the last  of the night, and was afraid everyone would leave before then…and they almost did until the MC asked some to stay for “dessert” ie me. So I finally had my reading and I think they liked my stuff…Hope they did, I didn’t hold back or read only easy things at any rate…

 

THe rest of the visit went supremely well, as Sara and I get along great. We ate in an Ethiopian restaurant one night, and at a Spanish open air market for lunch the next day. Only bad aspect of the visit, and it could not be helped, was that I brought a cold with me all unawares, so I was almost, but not quite, miserable the whole time. In point of fact, I was miserable only ONE night of the four, and miserable not a single day there, thanks to Sara’s good company and hospitality, plenty of kleenex and good food, with no pressure at all to do anything (once the class was over with — which was MY pressure entirely).

 

All in all, a great trip. Some paranoia developed on trainride home, with feelings/suspicions/knowledge that the people who sat down next to me in the Acela were accusing me of having stolen one of their tickets…to the point that I started talking to myself and had to get all my things and move seats to somewhere I felt more comfortable. Nowhere really felt comfortable after that, though, since everyone was looking at my book and what I was reading, so I had to switch to a harmless magazine. Finally the guy sitting in the single “disabled” seat at the back of the car got off at Grand Central so I quickly snagged that, having a disabled-discounted ticket myself. Things ought to have calmed then, only then I thought people were looking at me and wondering, Why is she sitting there, she doesn’t look very disabled to me!  I was very glad to detrain at New Haven I will tell you that. But how was I to get my heavy “carry on” wheeled bag down the high stairs at the station? No way was I able to lug it myself, especially not carrying two other bags, and one being my purse/tote bag I could not see leaving it alone while I took the bag by itself.

 

Just then a burly older man, lifting his own carry-on in one hand, stopped and said, Let me get that for you. “Oh, would you? Thank you so very much!” I replied. Without a word, he took my bag by the vertical handle and carried it swiftly down the thirty of more steps to the bottom then walked away before I could thank him again. Oh, what a lovely gesture. I was more relieved than I could say, though it was easy enough for him, and I daresay he is used to doing it. I was very glad to have been today’s recipient of his gallantry! The rest of the way was easy, as I could draw the bag on its wheels and take the escalator the rest of the way. I swear I don’t know how they get away with making these trains to inaccessible to the handicapped. They are practically inaccessible to any but the very young and strong, so far as that goes…And nearly every station had that long staircase leading to the platform, except for, say, DC, which is flat from parking lot to train, and even minus a step getting onto the train  itself.

 

Welp, that was my much anticipated, much worried about adventure and I’d say it went just swimmingly, despite cold and despite migraine and intense fatigue at the middle to the end of every day. One thing I did learn that was helpful was that eating three meals a day was good for me, rather than letting myself forget to eat until late in the evening and then cramming down the calories. Today I even tried to follow the pattern I did with Sara, and started the day with a healthy brakfast of fruit, cereal and yogurt. Then I did what the visiting nurse has suggested for many many months: I set a timer to remind me of lunchtime: I had an onion roll and dried fruit at one o’clock. At 6:00pm or so I plan to have…well, some mix of green beans and onio ns, cheese and soymilk plus strawberries and black berries with yogurt for dessert. Mainly because that is all I have at the moment. Or I will have Irish oatmeal made with soymilk, plus dessert, which would be a lot easier! I hope I can keep this regimen up, as it cannot but help my stamina, if it does nothing else.

Brain, Schizophrenia, Temporal Lobe Epilepsy, Uncategorized

Schizophrenia and Temporal Lobe Epilepsy (cont.)

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In my further reading on TLE I have learned that while “TLE hallucinations” can be ecstatic visions or the sight of threatening people or actually hearing voices, usually they are of brightly colored lights or visual distortions, like objects appearing larger or smaller than usual, hearing music, feeling insects running under one’s skin etc. In addition, there is the awareness that these are hallucinations, though not always. A personality seems to be associated with TLE, some people think, though it is not clear to me how established this is as fact. And some with TLE and without it claim that creativity is directly related to it. Hypergraphia, the compulsion to write, write, write is definitely associated with TLE, along with a compulsion to draw or do art or think/talk about religious subjects. Heightened emotional state but reduced sex drive. Something called “stickiness” is described, which I construe as a kind of tendency to glom onto a person or to exhibit an extreme loyalty. Also, there is seen irritability and gross personality change, rages, a tendency to fly off the handle or perform outrageous acts like stripping in public etc. 

 

In TLE you can have feelings of euphoria and floating as much as feelings of impending doom. A feeling of “rising into something” or of something rising through one’s body is a common concomitant of a TLE seizure or aura. An indescribable feeling according to many.  And you can have psychosis, chronic or acute.

interestingly, while EEG is notoriously poor at picking up TLE, there are often  punctate  signal hyperintensities (precisely the abnormalities I have had at least since Y2K) seen on MRI in those with TLE in the book I am reading — SEIZED, by Eva LaPlante.

Now I do not want to jump the gun, because too many of my symptoms have been chronic and disparate, not following a single pattern of seizure, whereas at least one authority claims that once you have one seizure, all others look similar. Indeed, while you might say that Grey Crinkled Paper arose from a seizure, and the jacksonian seizure with Novocaine were definite, and too the feelings of impending doom were also seizure activity  while I was taking Clozaril and other antipsychotic medications, the others, with different patterns yet, could not have been,since they were more varied even than those. The olfactory hallucinations had to have been seizure  associated too, but then where does it all stop, and where does the notion that one seizure sets the pattern for all others go?

 

And yet even conservatively I myself would count all those instances as seizures even if I were not going to count anything else as seizure-related right now…So  what to make of them, and the fact that ALL were so distinct and different from one another:?

 

Does it make the whole thing, the whole illness over all TLE or schizophrenia? Can you in fact have both, or does having TLE  suggest that the schizophrenia was a misdiagnosis all along?  And how does one know? Certainly, I have one trait that points towards the TLE diagnosis: I do well inbetween “attacks” of either illness, and seem to have not suffered any deterioration in brain function cognitively. Not massively. Though my memory and such is faulty, that is often the case in TLE itself!

I don’t have the slightest idea, but I suppose I will find out as the weeks go on and I continue to discuss it with Dr C, as I anticipate I will. I do plan to  see him once Dr O leaves… I liked him enough to do so at any rate, and I liked this idea enough too, to want to pursue it too. I    t will be very interesting to find out what happens, where it leads…If it redefines me entirely, I wonder how I will feel or deal with it?

 

 

 

Brain, Schizophrenia, Temporal Lobe Epilepsy

Schizophrenia and Temporal Lobe Epilepsy

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I want to begin by quoting two websites on the symptoms of each. First the Mayo Clinic on the symptoms of schizophrenia and then Richard Restak’s excellent article on TLE.

 

Schizophrenia Symptoms

By Mayo Clinic staff

In general, schizophrenia symptoms include:

* Beliefs not based on reality (delusions), such as the belief that there’s a conspiracy against you

* Seeing or hearing things that don’t exist (hallucinations), especially voices

* Incoherent speech

* Neglect of personal hygiene

* Lack of emotions

* Emotions inappropriate to the situation

* Angry outbursts

* Catatonic behavior

* A persistent feeling of being watched

* Trouble functioning at school and work

* Social isolation

* Clumsy, uncoordinated movements

In addition to the general schizophrenia symptoms, symptoms are often categorized in three ways to help with diagnosis and treatment:

Negative signs and symptoms

Negative signs and symptoms represent a loss or decrease in emotions or behavioral abilities. They may include:

* Loss of interest in everyday activities

* Appearing to lack emotion

* Reduced ability to plan or carry out activities

* Neglecting hygiene

* Social withdrawal

* Loss of motivation

Positive signs and symptoms

Positive signs and symptoms are unusual thoughts and perceptions that often involve a loss of contact with reality. These symptoms may come and go. They may include:

* Hallucinations, or sensing things that aren’t real. In schizophrenia, hearing voices is a common hallucination. These voices may seem to give you instructions on how to act, and they sometimes may include harming others.

* Delusions, or beliefs that have no basis in reality. For example, you may believe that the television is directing your behavior or that outside forces are controlling your thoughts.

* Thought disorders, or difficulty speaking and organizing thoughts, such as stopping in midsentence or jumbling together meaningless words, sometimes known as “word salad.”

* Movement disorders, such as repeating movements, clumsiness or involuntary movements.

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Cognitive symptoms involve problems with memory and attention. These symptoms may be the most disabling in schizophrenia because they interfere with the ability to perform routine daily tasks. They include:

* Problems making sense of information

* Difficulty paying attention

* Memory problems

Complex Partial Seizures Present Diagnostic Challenge

Quotes from Richard Restak’s article in Psychiatric Times (Sept 1,1995)

Since the condition [Temporal Lobe Epilepsy] may involve gross disorders of thought and emotion, patients… frequently come to the attention of psychiatrists. But since symptoms may occur in the absence of generalized grand mal seizures, physicians may often fail to recognize the epileptic origin of the disorder.

In most instances, the emotion experienced as part of the seizure is a disturbing one variously described as dread or a feeling of impending doom; in others, the emotion may be experienced as pleasant or euphoric…Descriptions such as “a wave,” “something flowing upward” are often employed.

Controversy continues as to the validity of a so-called temporal lobe personality… Outbursts of irritability, rather than frank violence, are hallmarks of TLE.

[R]are presentations include anorexia nervosa (Signer and Benson 1990), multiple personality (Schenk and Bear.

Most common is a global hyposexuality (deficit of desire and feeling]…

TLE also may be responsible for chronic rather than just acute psychoses. While any of the symptoms of schizophrenia may be encountered, paranoid traits are the most common. TLE patients can be distinguished from schizophrenic patients by the maintenance, when not acutely ill, of warm affect and good rapport…

The treatment of TLE is complicated by the fact that many times improved seizure control via anticonvulsants leads to deterioration of the neuropsychiatric status. Schizophrenia-like epileptic psychoses often emerge when anticonvulsants are normalizing or improving the seizure activity…

While the illness is an epileptic one and treated by neurologists, many neurologists remain unfamiliar with and even uninterested in its neuropsychiatric components. But by ignoring the experiential symptoms, the neurologist deprives the patient of the opportunity to coherently integrate all aspects of the epilepsy. It may also cement the patient’s misconception that in addition to the epilepsy, he or she suffers from a “mental illness.”

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I was going to go into a deeper discussion of this, but cannot at this hour (11:15pm as I must go to bed now. But I plan if I can to do so tomorrow. And if not then, well, then ASAP. Meanwhile, I would have told my schizophrenia.com readers to think back on all that I’d written over the years, and tell ME what is going on…but you cannot do that, not knowing me as well as all that. Needless to say, however, I do think there is reason to suspect that the second diagnosis might have some possible validity, though it is hard to see how all of my symptoms can have been only TLE…But wow, would I be relieved to have a name for it if they were!

TTFN

There is an interesting discussion about schizophrenia and TLE etc here: Schizophrenia and spiritual experiences: Is there a link? http://livewithwonder.wordpress.com/2011/10/19/schizophrenia-and-spiritual-experiences-is-there-a-link/