Center for Behavioral Health Statistics and Quality, Behavioral Health Trends in the United States: Results from the 2014 National Survey on Drug Use and Health (2015). The range of conditions includes depression, which the CDC estimates will soon become the second leading cause of disability in the world…
Folks, below this I post part of Hillary Clinton’s grand Mental Health Care plan, not because I believe in it, but because I want you all to see what our next president has in store for us. And because I hope you noted what the last thirty years have wrought in DAMAGES. Yes, after all the miracul0us advances of SSRI’s and SRI’s and adjunctive atypical anti-psychotics added to these so-called miracle anti-depressants. OOOooh, we have gotten so much healthier on our miracle pills.YES! We have gotten so much better that we now, get this, commit suicide at a rate 24% HIGHER than we did in 1999, In fact we kill ourselves at our highest rate in 30 years.
Well, I am sorry, people, but this is fucking BULLSHIT, just bullshit. You don’t believe me? Okay, i am used to that. No one ever believes me. So go ahead and read what dear Hillary posted in her Mental Health Care Plan below, from the National Institute of Mental Health. Those are not my numbers but right from the NIMH. So let’s go ahead, take our happy pills and tell ourselves we feel better, go right ahead, but what do we do when another buddy kills herself or himself despite the sweet help of his or her neighborhood pusher, er, psychiatrist???
Well, don’t tell me they did not warn us: ANTI- DEPRESSANTS DO NOT WORK THEY KILL. And it is posted very clearly right there, above.
Okay. Being forwarned is only part of the battle, we have to listen and we have to act.
Sorry for being so strident, I am really sorry.
I AM JUST SO ANGRY, SO FUCKING ANGRY AT THE LOUSY BASTARDS THAT DID THIS TO ALL OF US.
Go ahead and discount me, I do not care. But look at the statistic I posted above and ignore the implications at your peril.
______________________
Hillary CLinton’s MENTAL HEALTH CARE PLAN
Federal Support for Suicide Prevention
Suicides, which are usually fueled by mental illness, are rising among numerous population groups, from adolescents and college students[11] to veterans[12] and older adults.[13] The overall rate of suicide increased by 24 percent between 1999 and 2014, and is now at its highest level in 30 years.[14] Over 40,000 Americans die of suicide every year, making it the tenth-leading cause of death nationally.[15] As the former director of NIMH, Dr. Tom Insel, often notes, suicides have 11 victims: the person who dies, and at least 10 people close to them who will never be the same. Hillary believes that suicide is a critical issue that she will prioritize as president. She will:
Create a national initiative around suicide prevention across the lifespan that is headed by the Surgeon General: As president, Hillary will move toward the goal of “Zero Suicide” that has been promoted by the Department of Health and Human Services. She will direct all relevant federal agencies, including HHS, the VA, and the Department of Education, to research and develop plans for suicide prevention in their respective settings, and create a cross-government initiative headed by the Surgeon General to coordinate these efforts. She will also launch a citizen input and feedback mechanism, to enable outside groups to comment on agency recommendations, and explore how we can harness technology to reach out to people who need support.
Encourage evidence-based suicide prevention and mental health programs in high schools. In 2013, a survey of high school students revealed that 17 percent considered attempting suicide in the last year, with 8 percent actually attempting it. The suicide rate among American Indian/Alaska Native adolescents is even higher, at 1.5 times the national average. There are effective ways to respond. It is critical that school districts emphasize evidence-based mental health education, so that students, teachers, and school nurses are aware of the warning signs and risk factors of mental illness and how to address them. The Model School District Policy on Suicide Prevention, released by four leading mental health organizations, includes concrete recommendations that school districts can follow. Hillary will direct the Department of Education to emphasize mental health literacy in middle and high schools and will work with regional and national PTA, school counselor associations, and associations of secondary school principals to encourage school districts to adopt this model policy.
Provide federal support for suicide prevention on college campuses. Hillary believes that every college campus should have a comprehensive strategy to prevent suicide, including counseling, training for personnel, and policies that enable students to take leave for mental health Such multi-layered approaches have a proven track record of decreasing suicides. For instance, the Air Force launched an initiative in 1996 that brought together multiple intervention programs and reduced the suicide rate among Air Force personnel by nearly a third in under a decade. Groups such as the Jed Foundation, American Foundation for Suicide Prevention, the Suicide Prevention Resource Center, and Active Minds have created frameworks around suicide prevention tailored for colleges and universities. Hillary will dramatically increase funding for campus suicide prevention, investing up to $50 million per year to provide a pathway for the country’s nearly 5,000 colleges – whether private or public, two-year or four-year – to implement these frameworks on behalf of students.
Partner with colleges and researchers to ensure that students of color and LGBT students are receiving adequate mental health coverage. Evidence suggests that the psychological needs of students of color are disproportionately unmet, impeding their ability to adapt to college life. LGBT students face added burdens as well, with gay youth being four times more likely than their straight peers to attempt suicide. Hillary will direct the Departments of Education and Health and Human Services to work with universities, researchers and community programs to determine how best to meet and respond to the challenges these students face and to provide specialized counseling.
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] :
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
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
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.
References
Schmitz EB, Robertson MM, Trimble MR. Depression and schizophrenia in epilepsy: social and biological risk factors. Epilepsy Res. May 1999;35(1):5968. [Medline].
Kanner AM, Barry JJ, Gilliam F, et al. Psychiatric Comorbidities in epilepsy: Streamlining Recognition and Diagnosis to Improve Quality of Life. Counselling Points. 2009;1:115.
Sackellares JC, Berent S. Psychological Disturbances in Epilepsy. Neurology. Jan 11 2000;54(1):814. [Medline].
Gibbs FA. Ictal and nonictal psychiatric disorders in temporal lobe epilepsy. 1951. J Neuropsychiatry Clin Neurosci. Spring 1997;9(2):2936. [Medline].
Vuilleumier P, Jallon P. [Epilepsy and psychiatric disorders: epidemiological data]. Rev Neurol (Paris). May 1998;154(4):30517. [Medline].
Tucker GJ. Seizure disorders presenting with psychiatric symptomatology. Psychiatr Clin North Am. sep 1998;21(3):62535. [Medline].
Torta R, Keller R. Behavioral, psychotic, and anxiety disorders in epilepsy: etiology, clinical features, and therapeutic implications. Epilepsia. 1999;40 Suppl 10:S220. [Medline].
TellezZenteno JF, Patten SB, Jetté N, Williams J, Wiebe S. Psychiatric comorbidity in epilepsy: a populationbased analysis. Epilepsia. Dec 2007;48(12):233644. [Medline].
Ettinger A, Reed M, Cramer J. Depression and comorbidity in communitybased patients with epilepsy or asthma. Neurology. Sep 28 2004;63(6):100814. [Medline].
Kobau R, Gilliam F, Thurman DJ. Prevalence of selfreported epilepsy or seizure disorder and its associations with selfreported depression and anxiety: results from the 2004 HealthStyles Survey. Epilepsia. Nov 2006;47(11):191521. [Medline].
Barry J, Lembke A, Gisbert PA, et al. Affective disorders in epilepsy. In: Ettinger AB, Kanner AM. Psychiatric issues in Epilepsy: A Practical Guide to Diagnosis and Treatment. Philadelohia PA: Lippincott Williams & Williams; 2007:203247.
Jobe PC, Dailey JW, Wernicke JF. A noradrenergic and serotonergic hypothesis of the linkage between epilepsy and affective disorders. Crit Rev Neurobiol. 1999;13(4):31756. [Medline].
Jobe PC. Common pathogenic mechanisms between depression and epilepsy: an experimental perspective. Epilepsy Behav. Oct 2003;4 Suppl 3:S1424. [Medline].
Gibbs FA. Ictal and nonictal psychiatric disorders in temporal lobe epilepsy. J Nerv Ment Dis. Jun 1951;113(6):5228. [Medline].
Perez MM, Trimble MR. Epileptic psychosisdiagnostic comparison with process schizophrenia. Br J Psychiatry. 137:2459. [Medline].
Qiu A, Wang L, Younes L, Harms MP, Ratnanather JT, Miller MI, et al. Neuroanatomical asymmetry patterns in individuals with schizophrenia and their non psychotic siblings. Neuroimage. Oct 1 2009;47(4):12219. [Medline]. [Full Text].
Witthaus H, Mendes U, Brüne M, Ozgürdal S, Bohner G, Gudlowski Y, et al. Hippocampal subdivision and amygdalar volumes in patients in an atrisk mental state for schizophrenia. J Psychiatry Neurosci. Jan 2010;35(1):3340. [Medline]. [Full Text].
Kuroki N, Shenton ME, Salisbury DF, Hirayasu Y, Onitsuka T, ErsnerHershfield H, et al. Middle and inferior temporal gyrus gray matter volume abnormalities in first episode schizophrenia: an MRI study. Am J Psychiatry. Dec 2006;163(12):210310. [Medline]. [Full Text].
Suzuki M, Zhou SY, Takahashi T, Hagino H, Kawasaki Y, Niu L, et al. Differential contributions of prefrontal and temporolimbic pathology to mechanisms of psychosis. Brain. Sep 2005;128:210922. [Medline].
van Lutterveld R, Sommer IE, Ford JM. The neurophysiology of auditory hallucinations a historical and contemporary review. Front Psychiatry. May 16 2011;2:28. [Medline]. [Full Text].
Tebartz Van Elst L, Baeumer D, Lemieux L, Woermann FG, Koepp M, Krishnamoorthy S, et al. Amygdala pathology in psychosis of epilepsy: A magnetic resonance imaging study in patients with temporal lobe epilepsy. Brain. Jan 2002;125:1409. [Medline].
Kanner AM. Psychosis of Epilepsy: A Neurologist’s Perspective. Epilepsy Behav. Aug 2000;1(4):219227. [Medline].
So NK, Savard G, Andermann F, Olivier A, Quesney LF. Acute postictal psychosis: a stereo EEG study. Epilepsia. MarApr 1990;31(2):18893. [Medline].
Stagno SJ. Psychiatric aspects of epilepsy. In: Wyllie E. The Treatment of Epilepsy. Baltimore MD: Williams & Wilkins; 1997:11311144.
Logsdail SJ, Toone BK. Postictal psychoses. A clinical and phenomenological description. Br J Psychiatry. Feb 1988;152:24652. [Medline].
Dongier S. Statistical study of clinical and electroencephalographic manifestations of 536 psychotic episodes occurring in 516 epileptics between clinical seizures. Epilepsia. Dec 1959;1:11742. [Medline].
Slater E, Beard AW, Glithero E. The schizophrenialike psychoses of epilepsy. Br J Psychiatry. Jan 1963;109:95150. [Medline].
Onuma T, Adachi N, Ishida S, Katou M, Uesugi S. Prevalence and annual incidence of psychosis in patients with epilepsy. Psychiatry Clin Neurosci. Jun 1995;49(3):S267 8. [Medline].
Adachi N, Matsuura M, Okubo Y, Oana Y, Takei N, Kato M, et al. Predictive variables of interictal psychosis in epilepsy. Neurology. Nov 14 2000;55(9):13104. [Medline].
Fenwick P. Psychiatric disorder and epilepsy. In: Hopkins A, Shorvon S, Cascino G. Epilepsy. London: 1995:453–502.
Schmitz B, Wolf P. Psychoses in epilepsy. In: Epilepsy and behavior. New York: WileyLiss; 1991:97128.
Trimble M. Psychoses in epilepsy. New York: 1991.
Tarulli A, Devinsky O, Alper K. Progression of postictal to interictal psychosis.
Epilepsia. Nov 2001;42(11):146871. [Medline].
Kristensen O, Sindrup EH. Psychomotor epilepsy and psychosis. I. Physical aspects.
Acta Neurol Scand. May 1978;57(5):3619. [Medline].
Jensen I, Larsen JK. Mental aspects of temporal lobe epilepsy. Followup of 74 patients after resection of a temporal lobe. J Neurol Neurosurg Psychiatry. Mar 1979;42(3):25665. [Medline]. [Full Text].
Reid AH. Psychoses in adult mental defectives. II. Schizophrenic and paranoid psychoses. Br J Psychiatry. Feb 1972;120(555):2138. [Medline].
Gillberg C, Persson E, Grufman M, Themner U. Psychiatric disorders in mildly and severely mentally retarded urban children and adolescents: epidemiological aspects. Br J Psychiatry. Jul 1986;149:6874. [Medline].
Harris JC. Assessment. diagnosis, and treatment of developmental disorders. In: McConnell HW, Snyder PJ, eds. Developmental neuropsychiatry. 2. New York NY: Oxford University Press; 1998:169186.
Mellers JD, Adachi N, Takei N, Cluckie A, Toone BK, Lishman WA. SPET study of verbal fluency in schizophrenia and epilepsy. Br J Psychiatry. Jul 1998;173:6974. [Medline].
Onuma T. Limbic lobe epilepsy with paranoid symptoms: analysis of clinical features and psychological tests. Folia Psychiatr Neurol Jpn. 1983;37(3):2537. [Medline].
Trimble MR, Schmitz B. The psychoses of epilepsy: a neurobiological perspective. In: McConnell HW, Snyder PJ. Psychiatric Comorbidity in Epilepsy. 43(8). Washington DC and London: American Psychiatric Press; 1998:169186.
Tandon R, DeQuardo JR. Psychoses and epilepsy. In: Sackellares JC Berent S. Psychological Disturbances in Epilepsy. Boston: ButterworthHeinemann; 1996:171 189.
Kanner AM. Psychosis of Epilepsy: A Neurologist’s Perspective. Epilepsy Behav. Aug 2000;1(4):219227. [Medline].
Mazza M, Di Nicola M, Della Marca G, Janiri L, Bria P, Mazza S. Bipolar disorder and epilepsy: a bidirectional relation? Neurobiological underpinnings, current hypotheses, and future research directions. Neuroscientist. Aug 2007;13(4):392404. [Medline].
Chang HJ, Liao CC, Hu CJ, Shen WW, Chen TL. Psychiatric disorders after epilepsy diagnosis: a populationbased retrospective cohort study. PLoS One. 2013;8(4):e59999. [Medline]. [Full Text].
Ettinger AB, Reed ML, Goldberg JF, Hirschfeld RM. Prevalence of bipolar symptoms in epilepsy vs other chronic health disorders. Neurology. Aug 23 2005;65(4):53540. [Medline].
Kanner AM, Balabanov A. Depression and epilepsy: how closely related are they?. Neurology. Apr 23 2002;58(8 Suppl 5):S2739. [Medline].
Mendez MF, Cummings JL, Benson DF. Depression in epilepsy. Significance and phenomenology. Arch Neurol. Aug 1986;43(8):76670. [Medline].
Perrine K, Hermann BP, Meador KJ, Vickrey BG, Cramer JA, Hays RD, et al. The relationship of neuropsychological functioning to quality of life in epilepsy. Arch Neurol. Oct 1995;52(10):9971003. [Medline].
Robertson MM, Trimble MR, Townsend HR. Phenomenology of depression in epilepsy. Epilepsia. JulAug 1987;28(4):36472. [Medline].
Boylan LS, Flint LA, Labovitz DL, Jackson SC, Starner K, Devinsky O. Depression but not seizure frequency predicts quality of life in treatmentresistant epilepsy. Neurology. Jan 27 2004;62(2):25861. [Medline].
Kanner AM, Balabanov A. Depression and epilepsy: how closely related are they?. Neurology. Apr 23 2002;58(8 Suppl 5):S2739. [Medline].
Baker GA. Depression and suicide in adolescents with epilepsy. Neurology. Mar 28 2006;66(6 Suppl 3):S512. [Medline].
Schildkraut JJ. The catecholamine hypothesis of affective disorders: a review of supporting evidence. Am J Psychiatry. Nov 1965;122(5):50922. [Medline].
Jobe PC, Dailey JW, Wernicke JF. A noradrenergic and serotonergic hypothesis of the linkage between epilepsy and affective disorders. Crit Rev Neurobiol. 1999;13(4):31756. [Medline].
FlorHenry P. Psychosis and temporal lobe epilepsy. A controlled investigation. Epilepsia. Sep 1969;10(3):36395. [Medline].
LopezRodriguez F, Altshuler L, Kay J. Depression and laterality of epileptogenic region in patients with medically refractory temporal lobe seizures. Epilepsia. 1999;40(suppl7):60.
Kanner AM, Balabanov A. Depression and epilepsy: how closely related are they?. Neurology. Apr 23 2002;58(8 Suppl 5):S2739. [Medline].
Harden CL, Goldstein MA. Mood disorders in patients with epilepsy: epidemiology and management. CNS Drugs. 2002;16(5):291302. [Medline].
Baker GA, Smith DF, Dewey M, Jacoby A, Chadwick DW. The initial development of a healthrelated quality of life model as an outcome measure in epilepsy. Epilepsy Res. Sep 1993;16(1):6581. [Medline].
Hermann BP. Quality of life in epilepsy. J Epilepsy. 1992;5:153165.
Perrine K, Hermann BP, Meador KJ, Vickrey BG, Cramer JA, Hays RD, et al. The relationship of neuropsychological functioning to quality of life in epilepsy. Arch Neurol. Oct 1995;52(10):9971003. [Medline].
Harden CL, Goldstein MA. Mood disorders in patients with epilepsy: epidemiology and management. CNS Drugs. 2002;16(5):291302. [Medline].
Hermann BP. Psychopathology in epilepsy and learned helplessness. Med Hypotheses. Jun 1979;5(6):7239. [Medline].
McConnell H, Duncan, D. . Treatment of psychiatric comorbidity in epilepsy. In: McConnell H, Snyder P. Psychiatric Comorbidity in Epilepsy. 245. Washington, DC:
American Psychiatric Press; 1998.
Hermann BP, Jones JE. Depression in Epilepsy: What is the Extent of the Current Problem?. In: Mood Disorders in Epilepsy: Bridging the Gap Between Psychiatry and Neurology. American Epilepsy Society and IntraMed Scientific Solutions. 2005;311.
Williams D. The structure of emotions reflected in epileptic experiences. Brain. Mar 1956;79(1):2967. [Medline].
Blumer D. Epilepsy and disorders of mood. In: Smith D, Treiman D, Trimble D. Advances in Neurology. 55. New York: Raven Press; 185195.
Kanner AM. How to recognize depression in epilepsy. In: Mood Disorders in Epilepsy: Bridging the Gap Between Psychiatry and Neurology. American Epilepsy Society and IntraMed Scientific Solutions. 2005;1321.
Jones JE, Hermann BP, Barry JJ, Gilliam FG, Kanner AM, Meador KJ. Rates and risk factors for suicide, suicidal ideation, and suicide attempts in chronic epilepsy. Epilepsy Behav. Oct 2003;4 Suppl 3:S318. [Medline].
ThomeSouza S, Kuczynski E, Assumpção F Jr, Rzezak P, Fuentes D, Fiore L, et al. Which factors may play a pivotal role on determining the type of psychiatric disorder in children and adolescents with epilepsy?. Epilepsy Behav. Dec 2004;5(6):98894. [Medline].
Rafnsson V, Olafsson E, Hauser WA, Gudmundsson G. Causespecific mortality in adults with unprovoked seizures. A populationbased incidence cohort study. Neuroepidemiology. Oct 2001;20(4):2326. [Medline].
Kanner AM. Depression in epilepsy: prevalence, clinical semiology, pathogenic mechanisms, and treatment. Biol Psychiatry. Aug 1 2003;54(3):38898. [Medline].
Kanner AM, Soto A, GrossKanner H. Prevalence and clinical characteristics of postictal psychiatric symptoms in partial epilepsy. Neurology. Mar 9 2004;62(5):708 13. [Medline].
Kanner AM, Barry JJ, Gilliam F. Psychiatric Comorbidities in epilepsy: Streamlining Recognition and Diagnosis to Improve Quality of Life. Counseling Points. 2009;1:115.
Kraepelin E. Leipzig. Psychiatrie. 3. Germany: Johann Ambrosius Barth; 1923.
Bleuler E. Lehrbuch der. Psychiatrie. 8. Berlin Germany: Springer; 1949:7046.
Schmitz B. Psychiatric syndromes related to antiepileptic drugs. Epilepsia. 1999;40 Suppl 10:S6570. [Medline].
McConnell H, Duncan D. Behavioral effects of antiepileptic drugs. In: McConnell H, Duncan D. Psychiatric Comorbidity in Epilepsy. Washington DC and London: American Psychiatric Press; 1998b:205244.
Harden CL. The comorbidity of depression and epilepsy: epidemiology, etiology, and treatment. Neurology. Sep 24 2002;59(6 Suppl 4):S4855. [Medline].
Harden CL, Pulver MC, Ravdin LD, Nikolov B, Halper JP, Labar DR. A Pilot Study of Mood in Epilepsy Patients Treated with Vagus Nerve Stimulation. Epilepsy Behav. Apr 2000;1(2):9399. [Medline].
Williams D. The structure of emotions reflected in epileptic experiences. Brain. Mar 1956;79(1):2967.
Vazquez B, Devinsky O. Epilepsy and anxiety. Epilepsy Behav. 2003;4 (Suppl 4):520 525.
Goldstein MA, Harden CL. Epilepsy and Anxiety. Epilepsy Behav. Aug 2000;1(4):228 234. [Medline].
Beyenburg S, Mitchell AJ, Schmidt D, Elger CE, Reuber M. Anxiety in patients with epilepsy: systematic review and suggestions for clinical management. Epilepsy Behav. Sep 2005;7(2):16171. [Medline].
Marsh L, Rao V. Psychiatric complications in patients with epilepsy: a review. Epilepsy Res. Mar 2002;49(1):1133. [Medline].
Goldstein MA, Harden CL, Radvin LD. Does anxiety in epilepsy patients decrease with increasing seizure frequency?. Epilepsia. 1999;40(Suppl8):6061.
Waxman SG, Geschwind N. The interictal behavior syndrome of temporal lobe epilepsy. Arch Gen Psychiatry. Dec 1975;32(12):15806. [Medline].
Benson DF, Hermann B. Personality disorders. In: Engel J, Pedley TA, eds. Epilepsy:
A Comprehensive Textbook. Philadelphia: LippincottRaven; 20652070.
Trinka E, Kienpointner G, Unterberger I, Luef G, Bauer G, Doering LB, et al. Psychiatric comorbidity in juvenile myoclonic epilepsy. Epilepsia. Dec 2006;47(12):208691. [Medline].
Trimble M. Treatment issues for personality disorders in epilepsy. Epilepsia. Mar 2013;54 Suppl 1:415. [Medline].
Chou IC, Chang YT, Chin ZN, Muo CH, Sung FC, Kuo HT, et al. Correlation between epilepsy and attention deficit hyperactivity disorder: a populationbased cohort study. PLoS One. 2013;8(3):e57926. [Medline]. [Full Text].
Kaufmann R, GoldbergStern H, Shuper A. Attentiondeficit disorders and epilepsy in childhood: incidence, causative relations and treatment possibilities. J Child Neurol. Jun 2009;24(6):72733. [Medline].
Ettinger AB. Psychotropic effects of antiepileptic drugs. Neurology. Dec 12 2006;67(11):191625. [Medline].
Hamid H, Devinsky O, Vickrey BG, Berg AT, Bazil CW, Langfitt JT. Suicide outcomes after resective epilepsy surgery. Epilepsy Behav. Mar 2011;20(3):4624. [Medline].
Quigg M, Broshek DK, Barbaro NM, Ward MM, Laxer KD, Yan G, et al. Neuropsychological outcomes after Gamma Knife radiosurgery for mesial temporal lobe epilepsy: a prospective multicenter study. Epilepsia. May 2011;52(5):90916. [Medline]. [Full Text].
Christmas D, Steele JD, Tolomeo S, Eljamel MS, Matthews K. Vagus nerve stimulation for chronic major depressive disorder: 12month outcomes in highly treatmentrefractory patients. J Affect Disord. Jun 28 2013;[Medline].
Rong PJ, Fang JL, Wang LP, Meng H, Liu J, Ma YG, et al. Transcutaneous vagus nerve stimulation for the treatment of depression: a study protocol for a double blinded randomized clinical trial. BMC Complement Altern Med. Dec 14 2012;12:255. [Medline]. [Full Text].
Elger G, Hoppe C, Falkai P, Rush AJ, Elger CE. Vagus nerve stimulation is associated with mood improvements in epilepsy patients. Epilepsy Res. Dec 2000;42(23):20310. [Medline].
I have a confession to make. I don’t think what I do each day makes any sense.
Perhaps I should explain myself. Six months ago, I started my own private psychiatry practice. I made this decision after working for several years in various community clinics, county mental health systems, and three academic institutions. I figured that an independent practice would permit me to be a more effective psychiatrist, as I wouldn’t be encumbered by the restrictions and regulations of most of today’s practice settings.
My experience has strengthened my long-held belief that people are far more complicated than diagnoses or “chemical imbalances”—something I’ve written about on this blog and with which most psychiatrists would agree. But I’ve also made an observation that seems incompatible with one of the central dogmas of psychiatry. To put it bluntly, I’m not sure that psychiatric medications work.
Before you jump to the conclusion that I’m just another disgruntled, anti-medication psychiatrist who thinks we’ve all been bought and misled by the pharmaceutical industry, please wait. The issue here is, to me, a deeper one than saying that we drug people who request a pill for every ill. In fact, it might even be a stretch to say that medications never work. I’ve seen antidepressants, antipsychotics, mood stabilizers, and even interventions like ECT give results that are actually quite miraculous.
But here’s my concern: For the vast majority of my patients, when a medication “works,” there are numerous other potential explanations, and a simple discussion may reveal multiple other hypotheses for the clinical response. And when you consider the fact that no two people “benefit” in quite the same way from the same drug, it becomes even harder to say what’s really going on. There’s nothing scientific about this process whatsoever.
And then, of course, there are the patients who just don’t respond at all. This happens so frequently I sometimes wonder whether I’m practicing psychiatry wrong, or whether my patients are playing a joke on me. But no, as far as I can tell, I’m doing things right: I prescribe appropriately, I use proper doses, and I wait long enough to see a response. My training is up-to-date; I’ve even been invited to lecture at national conferences about psychiatric meds. I can’t be that bad at psychiatry, can I?
Probably not. So if I assume that I’m not a complete nitwit, and that I’m using my tools correctly, I’m left to ask a question I never thought I’d ask: Is psychopharmacology just one big charade?
Maybe I feel this way because I’m not necessarily looking for medications to have an effect in the first place. I want my patients to get better, no matter what that entails. I believe that treatment is a process, one in which the patient (not just his or her chemistry) is central. When drugs “work,” several factors might explain why, and by the same token, when drugs don’t work, it might mean that something else needs to be treated instead—rather than simply switching to a different drug or changing the dose. Indeed, over the course of several sessions with a patient, many details inevitably emerge: persistent anxiety, secretive substance abuse, a history of trauma, an ongoing conflict with a spouse, or a medical illness. These often deserve just as much attention as the initial concern, if not more.
Although our understanding of the pathophysiology of mental illness is pure conjecture, prescribing a medication (at least at present) is an acceptable intervention. What happens next is much more important. I believe that prescribers should continue to collect evidence and adjust their hypotheses accordingly. Unfortunately, most psychopharmacologists rarely take the time to discuss issues that can’t be explained by neurochemistry (even worse, they often try to explain all issues in terms of unproven neurochemistry), and dwindling appointment times mean that those who actually want to explore other causes don’t have the chance to do so.
So what’s a solution? This may sound extreme, but maybe psychiatry should reject the “biochemical model” until it’s truly “biochemical”—i.e., until we have ways of diagnosing, treating, and following illnesses as we do in most of the rest of medicine. In psychiatry, the use of medications and other “somatic” treatments is based on interview, gut feeling, and guesswork—not biology. That doesn’t mean we can’t treat people, but we shouldn’t profess to offer a biological solution when we don’t know the nature of the problem. We should admit our ignorance.
It would also help to allow (if not require) more time with psychiatric patients. This is important. If I only have 15-20 minutes with a patient, I don’t have time to ask about her persistent back pain, her intrusive brother-in-law, or her cocaine habit. Instead, I must restrict my questions to those that pertain to the drug(s) I prescribed at the last visit. This, of course, creates the perfect opportunity for confirmation bias—where I see what I expect to see.
We should also make an effort to educate doctors and patients alike about how little we actually know. The subjects in trials to obtain FDA approval do NOT resemble real-world patients and are not evaluated or treated like real-world patients (and this is unlikely to change anytime soon because it works so well for the drug companies). Patients should know this. They should also know that the reliability of psychiatric diagnosis is poor in the first place, and that psychiatric illnesses have no established biochemical basis with which to guide treatment.
Finally, I should say that even though I call myself a psychiatrist and I prescribe drugs, I do not believe I’m taking advantage of my patients by doing so. All of my patients are suffering, and they deserve treatment. For some, drugs may play a key role in their care. But when I see my entire profession move towards a biochemical approach—without any good evidence for such a strategy, and without a fair assessment of alternative explanations for behavior—and see, in my own practice, how medications provide no real benefit (or, frequently, harm) compared with other treatments, I have to wonder whether we’ve gone WAY beyond what psychopharmacology can truly offer, and whether there’s any way to put some logic back into what we call psychiatric treatment.
I fell in love with this next song, maybe it was the beat, the lyrics, or just the fact that I think Ingrid Michaelson is the cat’s meow, right up there with Mraz and, yes, Bruno Mars (!). Yes, I know, the lyrics can seem depressing, but if you are the “You” in this song, you will never fall and never be alone…Anyhow, I love this next song, depressing or not…
I’ll bet if you felt down before Mraz’s “I’M YOURS,” you felt or will feel better for hearing it. It is surely better than any benzo and if ADs work for you, well, all I can say is a jolt of Jason Mraz and Michaelson’s “EVERYBODY” (see at bottom) would be a quicker and whole lot safer than messing with your serotonin and norepinephrine levels just because Big Pharma wants your money and claims the AD’s work as they say they do. Trust me. (No, why would you trust me???? You shouldn’t trust me, I know nothing except what I read, and I don’t read all that much, due to my vision problems…)
Still, I can’t help but wonder if music played a bigger role in treatment of depression and even of schizophrenia, whether people wouldn’t get better a lot faster, or at least learn to calm themselves reliably and find a way to talk about what is going on rather than taking pills to render them oblivious. Music alone might be enough to put things back together again…Music and sleep, which knits up the raveled sleeve of many a care in this world, “balm of hurt minds” and as Shakespeare knew well, the lack of which can spell danger even for the hardiest soul.
But if we get our sleep via benzos or some other drug that knocks us out, are we really getting brain rest, or just body rest? Moreover, will we regret listening to the docs who prescribed nightly benzodiazapines after we find out we have developed either acute amnesia or its much more tragic cousin, Alzheimer’s Disease? I wonder. I wonder…How much will we choose to blame ourselves for not knowing better, and how much will we dare blame any doctor, who after all and after “primum non nocere” (First do no harm…) right? just how much will we dare to blame the doctors who told us the stuff was okay, not dangerous, and certainly better than suffering from insomnia.
Listen, insomnia is a drag, and I have suffered enough of it for, well, I won’t say “for a lifetime” because that would mean I’d had enough, and I haven’t. But I don’t like not sleeping, not one bit. Sometimes I take Benadryl to sleep at night because i’ve been sold that same bill of goods that says, “Okay, it is OTC and therefore must be essentially harmless.” It helps me to get to sleep yes, and sometimes even to stay asleep, though with narcolepsy it is hard to know whether or not any sleep will be properly restorative, natural or “unnatural”.
That said, Benadryl, as I am reminded every time I feel like pigging out after a night when I took 50mg…is an antihistamine, and anti-histaminic drugs (like Zyprexa) have this unfortunate side effect of inducing weight gain. So I won’t take Benadryl very often. Otherwise my appetite goes way overboard and I feel that same “eat! eat! eat!” anxiety that has nothing to do with food per se, and everything to do with yet another drug’s untoward side effects.
So what do I do in order to sleep? Well, first, I try not to worry about it…because that way disaster lies. If I can’t fall asleep easily, and with narcolepsy I should be out like a light within 4 minutes, but if that 4 minutes drags on into 7 or 10 minutes or more, I have learned to get up and do something else. I try mightily not to worry about not sleeping because it won’t do me any good. It will only make me more anxious.
So sometimes I get up and do art for a couple of hours. Or write, which in my case is far from a soporific activity. If I really am desperate to sleep, as I sometimes feel (though in my life, on disability, really everything can wait, and be postponed, if I can’t drive the next day due to lack of sleep. No one is going to need me for anything that can’t bide its time. ) Really are any of us indispensible? Maybe as a mother or parent you feel you are. But if you get snappy and do things you wouldn’t ordinarily because you force yourself to perform on too little sleep, who are you serving — say it honestly? Wouldn’t your family be better served by your deciding to take care of yourself and sleep in, or take a nap instead of doing whatever it was you promised them you would do?
Well, enough for the evening. I am sick of lecturing and indeed I should be, because NO ONE listens to lectures, and diatribes. No one. So instead, I’ll shut up. Why not listen to “Everybody” by Ingrid Michaelson instead!
PHYSICIAN ABILIFY SAMPLES – DO NOT ADD TO ANYTHING! THIS IS NOT AN ANTIDEPRESSANT. THIS IS AN ANTIPSYCHOTIC AND A DANGEROUS DRUG.
I know, I know, you have probably seen the commercials, but I am new to television and I only just started to watch them…and I just saw one that has been running probably for years now with the sad little pill that gets people to “add Abilify” to their so-called “anti-depressant” in order to boost its effectiveness. I learned about this advertisement recently from a friend of mine who innocently enough told me, told me, that Abilify is “just another antidepressant”.
Excuse me? I said to her. Abilify is NOT an antidepressant.
“Yes it is,” she insisted. “I saw it on TV.”
“No, Abilify is an atypical antipsychotic drug, not unlike Zyprexa or Risperdal. I don’t know what you are talking about, calling it an antidepressant.”
That’s when she told me about the sad little pill commerical. Well, okay, so the pill isn’t sad, the woman in the commercial supposedly is, and when the nice doctor she sees, adds the nice little Abilify pill to her so-called anti-depressant, she perks right up like an obedient child and, wow, the two pills work like magic to make the world right again. WOWEE!
So again the public is sold two lies, or maybe three or maybe half a dozen. First we are sold the lie that antidepressants do something in the first place. WAIT A MINUTE. Okay, they do do something, I admit it. They change the levels of neurotransmitters in the brain, yes, they do that. They alter something. Yes, and doing something, making a difference, altering anything makes people feel DIFFERENT and doing anything to change people’s feelings about ANYTHING when they are depressed can lead them to feel that it is better than doing nothing. ‘
But you have to understand that taking a mind altering substance to do something, anything at all, just to feel different, is not at all the same thing as actually treating a pre-existing chemical imbalance. And they know now that there is no such thing as a serotonin imbalance in the brains of depressed people. NO SUCH THING. In fact, they cannot figure out why people become depressed at all, but they do know that serotonin levels are not involved in any such simplified ways that the SSRI drugs purport to “treat.” Even Prozac researchers have admitted as much. Prozac researchers knew that their drug did not work way back in the 80s when Prozac first came out. They knew it induced suicidality in a large number of people, but they rushed it onto the market because Lilly needed a blockbuster drug, period to pad their pockets.
But that aside, the researchers to this day know that antidepressants do nothing to actually treat depression, because they have admitted that they do not understand what causes depression.
That said, does anyone who takes an anti-depressant understand what they are doing when their friendly psychiatrist or family doctor “ADDS ABILIFY” to their nice little psychoactive cocktail? Well, in addition to experiencing some or all the terrible but COMMON side effects of, say, Zoloft or Prozac (these are just those for Zoloft):
Inability to have an Erection
Severe
Sexual Problems
Severe
Altered Interest in Having Sexual Intercourse
Severe
Drowsiness
Less Severe
Dizzy
Less Severe
Chronic Trouble Sleeping
Less Severe
Low Energy
Less Severe
Excessive Sweating
Less Severe
Involuntary Quivering
Less Severe
Loss of Appetite
Less Severe
Weight Loss
Less Severe
Head Pain
Less Severe
Feel Like Throwing Up
Less Severe
Gas
Less Severe
Diarrhea
Less Severe
Stomach Cramps
Less Severe
Feeling Weak
Less Severe
they might well experience these COMMON side effect of Abilify:
A Feeling of Restlessness with Inability to Sit Still
Severe
Feeling Restless
Less Severe
Indigestion
Less Severe
Incomplete or Infrequent Bowel Movements
Less Severe
Drowsiness
Less Severe
Dizzy
Less Severe
Chronic Trouble Sleeping
Less Severe
Increased Hunger
Less Severe
Head Pain
Less Severe
Feel Like Throwing Up
Less Severe
Throwing Up
Less Severe
High Amount of Triglyceride in the Blood
Less Severe
Anxious
Less Severe
These are the commonly reported side effects from common antidepressants Celexa and Lexapro: in terms of Psychiatric Disorders, to which one might be told to “add Abilfy”:
Now, I ask you, everyone, DOES THIS SOUND LIKE A RECIPE FOR CURING DEPRESSION? Any fool would look just at the list of side effects and say, uh, I would be more depressed if I experienced even two of these….But doctors think that people will feel better if they take drugs like these two together, and put up with these side effects, just because they are told that “by adding abilify” and their depression will go away.
The point is, the doctors are IN THE DARK. They read mostly what you do, and they see the same commericals you do. Most of them have no more idea whether the drugs work than you do, and they only know what they are told by the drug reps and the drug companies….DO NOT BELIEVE THEM when they tell you that you have a chemical imbalance. They are either lying to you, or believing a lie they were told by someone else. ASK THEM questions, investigate. Ask precisely what is the correct balance, what are the correct numbers…Do not be sheep. What were the studies showing any proof? Who did the studies and who paid for them? Changes are you won’t get good answers, or if you do, your answers won’t make you any more secure than I am. Because drug companies pay for most of their own studies and they only pay for the results they want, ie what they want to hear…They do not want to hear that Abilify hurts patients, or doesn’t actually work, or that Abilify does not boost Zoloft’s anti-depressant IN-efficacy. No, they want to lie and “prove” a lie or else not prove it by not actually doing the study to prove anything. They want to market the drug and advertise things that have NOT BEEN SHOWN TO BE TRUE AT ALL. They want to market a lie, sell a drug and make money, without doing any research to prove anything, and pick up the pieces billions of dollars later, if at all.
I say, BULL SHIT
My advice? Don’t add Abilify. Add only Sunlight and Truth to everything.
It has always been about Dopamine, but they never told us that impeding our dopamine receptors would impair our ability to feel pleasure and the high of “reward” — No wonder our “negative symptoms of “not wanting to do” so many things! The drugs blocked our native dopamine flow! (Decades ago they knew that it has NOTHING whatsoever to do with schizophrenia, but they persisted in the lie nevertheless…
To explain the picture/letters above, I was practicing some lettering, briefly, and did not know what I was writing until later…which makes what I wrote all the more interesting a message from my subconscious. Clearly I agree with almost everyone else I have ever heard from: Haldol is the drug from hell! About the rest of it, well, Psychiatrie macht frie derives from the sign that was posted above Auschwitz and other concentration camps during WWII, Arbeit macht frei, or Work makes (you) free. So this transposition is meant to suggest (sardonically) that psychiatry will free you in just the same way… NOT!
What particularly sickens me personally is the damage the fiction called the Dopamine Hypothesis — how an excess of dopamine causes schizophrenia — may have done to the millions of people like me who have taken antipsychotic drugs for decades, unknowingly buying into the medical model and this notion that we somehow had too much dopamine coursing around in our brains.
Life is ALL about dopamine, LIFE has always been about dopamine. Here are some of the human functions to which dopamine is essential
movement
memory
pleasurable reward
behavior and cognition
attention
inhibition of prolactin production
sleep
mood
learning
Why on earth would anyone deprive another human being of the one neurotransmitter that allows us to feel good about things? It would seem to be a diabolical plot, if anyone actually did such a thing, right? And yet, for decades right on through today, that is what doctors want us to do, block the transmission of dopamine to the brains of those of us diagnosed with schizophrenia. They know, of course, that it is impossible, that the brain up-regulates the flow of dopamine in such a way as to thwart at least in part the antipsychotic receptor blockade. Homeostasis will be re-established eventually, even if at abnormal levels due to the drug’s presence.*
No one can live without dopamine, after all. But to understand the necessity of dopamine, and that they have known for years that an imbalance of dopamine metabolism is NOT implicated in schizophrenia, and finally to “grok” that they have nonetheless perpetuated the lie that is the “dopamine hypothesis” just boggles the mind with its enormity. How can we believe anything they tell us about negative symptoms, now, when as one website informs us:
“Low D2 receptor-binding is found in people with social anxiety or social phobia. Some features of negative schizophrenia (social withdrawal, apathy, anhedonia) are thought to be related to a low dopaminergic state in certain areas of the brain.”
The atypical AP drugs induce a D2 receptor blockade as a matter of course. After all, if you don’t feel any reward-sense from your life and living, your normal dopamine being in an antipsychotic blockade, why would you want to change your clothes, or take care of yourself, much less bother to go to work or even think? But we have been led to believe that such negative symptoms are part of schizophrenia and NOT part of the drug treatments for it! No one told us they were taking away all our incentive to do anything, to even move or think. They told us they were helping us, not hurting us, not destroying our lives!
Even more diabolical, to my way of thinking is the idea that some doctors actually add an atypical antipsychotic onto the treatment of mere depression. Can you imagine how you would feel if you were taking an SSRI (which is ineffective) and which already deprived you of sexual satisfaction or any sexual feelings at all, and then you are given an adjunctive antipsychotic that subsequently deprives you of dopamine? It might add twenty to forty pounds or even more in no time, up your cholesterol and blood sugar, and then deprive you of any feelings of reward or pleasure…Ah but it will boost your antidepressant’s antidepressant activity? J’en doute fortement… I doubt it highly!
What do the doctors care? Either they bought into the drug company’s literature and haven’t read anything independently since med school…or they are on the take themselves from Big Pharma in some fashion and don’t give a damn.
We need to be on the look out for ourselves, because god knows the doctors are not on our sides, most of them. They cannot be. This is their bread and butter, folks esp the psychiatrists and if they cannot prescribe pills, what will they do? They won’t be “real doctors” any more and their prestige will plummet yet again…OH NO! The fact is, they need to learn to do psychotherapy again, or get out of medicine because they cannot prescribe pills that do not work, and there are none that do! None that do reliably and well or better than placebo. In fact, except for the occasional use of a benzodiazepine, and the judicious use of cognitive enhancers for the proper people, and meds for sleep, I am convinced that precious few drugs in the psychoactive armamentarium are worthy of anything but the dustbin.
I think most are ONLY placebos, if they do anything at all. Frankly. And I say this despite having once written testimonials in praise of Zyprexa and other drugs…I dunno, I dunno. How could Zyprexa be anything except a placebo? It is a dirty drug that hits nearly every known neurotransmitter of importance…And yet we do not know how it does what it does…and it has horrendous side effects. That much we know. Since we do not have any reason to think it is the action on dopamine or serotonin that is the “antipsychotic” activity, in essence we cannot say why or if it does anything at all. ALL the AAPs drugs work on the neurotransmitters in a more or less dirty fashion. In fact the OLDER drugs were less dirty, being more specific to just dopamine!
I reiterate, there is no “chemical imbalance” in schizophrenia, or bipolar “illness’ or in depression. No one has ever proven or shown any such animal ever. Only after patients have taken a drug to “treat” such conditions is there ever an “imbalance” and this imbalance is a direct result of having taken the drug. PLEASE remember this and question your doctors next time they warn you that if you stop your meds your “chemical imbalance” will reassert itself and make you sick again. Ask, “What chemical imbalance and where did it come from? What chemicals and what is the normal level I should have?” I know I know, the doctor will say, dopamine, if you “have” schizophrenia, or “serotonin” if you “have” depression. Lord knows what she will claim if you “have” bipolar tendencies of one sort or another, as so many millions upon millions of Americans these days have been told they now do…But it isn’t true. Not even if they claim it is. There has never been any proof of altered neurotransmitter levels and in fact it is the opposite: drug-naive people with schizophrenia and depression, that is to say, those who have never taken any medication, have been shown to have the exact same dopamine and serotonin levels as anyone else!
As for those who suffer from the condition called “bipolar” — You know, it used to be a very rare condition, manic-depression. Now, you see “bipolars” coming out of the woodwork everywhere. One used to have to have been crazy-manic at least once, to the extent of having been hospitalized to qualify for the diagnosis, and this made sense as it was restrictive and not a broad umbrella. Given that the illness was considered a very serious one, no one wanted to bring too many within the definition. Now, with so many drugs used to “treat” (ha ha ha) the condition, and with the help of DSM IV and 5 to bring patients to the drug companies’ financial assistance, you need only complain of a garden variety “depression” to be counted as bipolar…
But remember: 1) the drug companies treating bipolar etc only want to make money, 2) the drugs treat something — a neurotransmitter imbalance that doesn’t exist 3) bipolarity is a fiction that keeps lengthening, like Pinocchio’s nose, with every newly expanded definition…
Think about malaria, a real illness. It doesn’t make more people ill just because it gets redefined. Malaria is caused by a protozoan (injected through the bite of a mosquito), and it sickens people who are vulnerable to the ravages of that organism inside the body…in the same way each time. You don’t “get” malaria more because a financially- interconnected organization of doctors/drug companies decides to change the definition of what constitutes malaria. No, you get malaria the way people always gotten malaria, largely through not using mosquito nets and other preventive measures…i.e. via a mosquito bite.
Ay, this is NUTS! It should not be so fricking easy to fit everyone into a diagnostic category of mental illness. Emotions are NOT illnesses by definition, they are normal and necessary, even excessive emotional reactions are quite normal; they happen every day to everyday normal people. Some cultures define themselves by their emotionality! It behooves us to remember this and not pathologize it.
So too, think of this: depression frequently is just sadness, folks. We used to know the truth of the saying, “This too will pass…” There are problems in living that are just problems in living, and I think that some people for whatever reason are simply miserable, without having a mental illness. They would not do better being labeled with an illness or being treated for one. In fact, I have seen people in states of abject misery do a great deal worse under the burden of a label…
I have had it. I do not trust a drug company or a prescription at all, none of them. The foxes are in charge of the chickens and they are up to no good, no good at all. So this weekend I am OFF all Abilify. HURRAY! After that I start cutting out the Geodon…(I have already halved the Ritalin simultaneously with the decrease of Abilify. I had to, I simply don’t need the Ritalin as much, as I am not as sleepy. After Geodon, there is only the Topamax, which I take for seizures and migraines.. Have to decide about that one. I want to be off it, I really do. But can i?**
*Note that although some of these conclusions are my own, I drew most of the research I have based them on from my readings in Robert Whitaker’s fine books MAD IN AMERICA and ANATOMY OF AN EPIDEMIC. I highly recommend reading both of them, which can be accessed through the link I provide at the top of the page in my blogroll. The link goes directly to ANATOMY but MAD can be found easily through there. Good reading! And please do let me know what you think at any time. (Adding this note at a later time, very much the same information can be found in Dr Joanne Moncrieff’s books — a British psychiatrist who came to similar conclusions as Whitaker. Her book on antipsyhcotics is THE BITTEREST PILLS, and her book on psychtherapeutic drugs in general is THE MYTH OF THE CHEMICAL CURE.
**writing in Dec 2017 i have never been able to get off the Geodon or the Abilify, nor the other drugs, though i have cut the Geodon in half somewhat successfully. (I am unable to speak at present, but i do not believe the two are linked, as i dropped the Geodon/ziprasidone dose more than a month ago and the muteness started less than a week ago). That said, i still do not believe they help me. I just maintain that once you have been on these drugs for literally decades as i have been, more or less by force, then your brain changes in response and ends up “imbalanced” and in that sense alone does need the drugs.
I feel like screaming, I am a human being, you effers, treat me like one! But of course, that is what I would say only to one group of people, the hospital personnel who so tortured me, and not everyone does that. Though I get this sense that a lot of people treat me like I am my diagnosis and not a real HB…if you know what I mean. As soon as they know you carry some sort of MI Dx, and I do not blab about that, but they find out, esp if they know the meds I take, then they suddenly do not trust me any longer, trust that I live a life that even remotely resembles theirs. Suddenly they seem to believe that I am not like them in anything that they could possibly begin to believe in. Or worse that they cannot “get into my mind” and therefore they assume that I live in some world that they cannot possibly comprehend either…
Weirdly enough, I live assuming the precise opposite, that our worlds are pretty much the same, that what I think, they pretty much think. I assume that whatever differences there may be, they are very small when it comes right down to it, and that they are miniscule in the larger plan. So it hauls me up short when I realize that they believe they cannot understand me. And are afraid of me and do not want to try to get to know me, because of that fear. And it makes me feel VERY MUCH ALONE.
You who are married or have relationships or have had them in the past, you do not know how lucky you are. I never have. I have never loved anyone, nor felt that I was safe with someone and not going to be abused or taken advantage or or simply that I was with a person I loved and was loved by and was their first priority. Not someone who was my peer. Yes, for 7 years I was, I think, my father’s priority, maybe his first priority, I dunno. I felt cared about and loved. But he was my father and he owed that to me. I ought to have felt that way all my life. All children should feel loved and cared for by their parents…no matter what.
I feel so alone, so alone. I do not know who to turn to or who to talk to. I do not know what to do or how to stop this juggernaut from sliding down into the abyss, taking me with it . It started with the headache all week, which went away yesterday but came back with a vengeance again today! I feel like no one in my family cares about me or even likes me except perhaps my brother, and he may do so on sufferance, I dunno. I do not trust anyone…
How can I? I have been so broken by people who said they cared about me and wanted to help me and then tortured me (hospitals) or abandoned me (my father) that I have no reason to trust or love…I do love my family, mind you. I even like them all. But it doesn’t even matter to them whether I love or like them, my like and love are meaningless to them, worse they are burdensome to them.
I sense that this is often the case, and it is why I have never bestowed my love on anyone: people do not want my love, not my real undying love. They would fear it and hate it. It would be a huge burden on them. So I haven’t burdened anyone in the world with my love ever. Because I would never do anything so evil to anyone, not even my worst enemy…though I do try to practice love thy enemy, as I have said, and I try to make my enemies my best friends. Nevertheless, I would not in fact give my enemy the worst burden of all, the loathsomeness of my heart. Who could stand it, who could tolerate it? I would rather die than think that I had so oppressed any person with something so intolerable.
But oh, how I cry to think that I am so loathsome, and why is it? Who and what am I that I am so disgusting? Why did I turn out this way? I always tried to do good, and to do it secretly so no one would be embarrassed or have to thank me…and now what am I but a disgusting turd who only oppresses the world with her presence. Whose love and heart would only horrify the person to whom she gave it…Not that I would dare do so, but that is because I understand the horror of such a gift-curse.
How did this happen? What happened? It will never change, I know that. It is a fact of my existence, of Existence itself. My father cared about me, but he also know how burdensome I was…He was glad to die and leave me, I think. Or perhaps he could handle my loathsomeness because he didn’t have to deal with me much…Who knows. All I know is that I am alone, alone, alone…and I will never be anything but alone. How can I go on, knowing that? Oh, I will. I will go on. But how do you? Faking it, always, pretending to people that all is fine and dandy, because no one wants to know how awful things are, NO ONE. If they did, it would only be another intolerable burden…
So you fake it and smile and go on…That is all anyone can do, right? Stiff lower lip and square your shoulders and pretend it is okay. Because you have to have people like you, or smile at you…or you will die. And unless you want to die and you do not, you need those fake smiles back at you for food to relieve the loneliness that nothing and no one will ever fill.
____________________________________
Sorry about this post, but i had to write it. I had to get it off my chest or I would have cried all evening. I promise I am working on the Liebster Aware, slowly but surely. I still need to get all the 11 blogs in order, and the questions written, but I plan to do that on the train to NC on Wed. Perhaps I will have it all done by the time i am back on the 17th. My apologies for the self-pity in this post. I try not to sit there, but I cannot always keep my head above water, or my arse off that pot. I’ll try to do better. But if I cannot be honest here, then I won’t continue to write. It isn’t worth it to lie here and have to lie about how I feel everywhere else as well. Okay?
Thank you for listening, if you did. Thank you from the bottom of my impoverished, dried up, lonely old heart.
Pam W
I wanted to add certain comments that were particularly to the point. Here is one or two from Lady Quixote:Dear Pam,
I liked this post, although I hate that you are in such pain, I like the honesty, I applaud the bravery, very very much. And oh yes I do understand, I relate with all my being, to virtually every word you wrote in this post, and in these your comments, too. Both comments.
As I’ve told you, I am writing a memoir about my similar history. I’ve changed the working title on my book a few times: From Here To Insanity, Healing From Broken, Growing Up Crazy, and some others. The working title I have now is my favorite. I’m now calling my book GOING CRAZY, a memoir of horror, hope, and healing.
The pain, the loneliness, the “shame” and isolation of having a been labeled Mentally Ill…. the label is a curse that hurts as much, if not more, than the disorder itself.
Here are the words I have on the cover of my memoir-in-progress, words that echo this post to the marrow of my bones. I have this on the front cover:
Mental illness seems to run in my family. (So does Protestantism and the tendency to vote Republican.) What causes mental illness: nature, nurture, or a combination of things? After a series of traumatic events, I had a “breakdown” at age 14 and was put in an insane asylum for 2 years. For the past 4 decades I have tried to forget my allegedly schizophrenic episode. But when I learned—in the midst of a family crises—that my first great-grandchild was on the way, I embarked on a Madness Marathon in search of answers.
And this is on my back cover:
Was I Cured of Schizophrenia? Do I Have “Complex” Post-Traumatic Stress Disorder?
MY MIND WAS BROKEN—DOES THE “LABEL” MATTER?
The extreme childhood trauma that caused my mind to shatter was painful. Being diagnosed with schizophrenia at age fourteen and placed in a state insane asylum for almost two years was even more painful.
But my most damaging experience by far has been the shame and isolation I’ve lived with for over forty years, caused by the demoralizing stigma of having been labeled “mentally ill.”
For most of my life I’ve tried to hide my history. Now I’m telling my story to help transform the hurtful prejudice borne of ignorance, into the healing mindset of understanding and compassion. Having recently become a great-grandmother, I feel compelled to write my memoir as a legacy of truth and enlightenment for my adult children and grandchildren, who have suffered so unfairly as a result of my emotional wounds. I am also sharing my story for anyone with a background similar to mine, to let you know you’re not alone.
………………………..
I’m sending you love and hugs and compassion in my heart and mind right now. I hear you. Loud and clear. I have stopped communicating with a sister who refused to honor my request to please stop passing messages on the me from our mother, particularly the “tell Lynda I love her” messages. NO, my mother does not love me. Her actions have proven it over and over and over again. I told my youngest sister: “I’m not asking you to agree with me or believe me, I’m not asking you to take sides. We can agree to disagree about whether or not our mother loves me, that’s OK with me. All I ask is that you please stop telling me that she does.” My sister said nothing, no response of any kind to my request. Then a few weeks later she posted right on my Facebook wall, on Christmas Eve of 2012: “Merry Christmas Big Sis, and Mom says to tell you how much she loves you.” I deleted that message off my wall, and my sister then deleted her account… so I deleted my account, for over a year, only coming back to FB a couple of months ago to keep up with my grandchildren.
I think we know when we are not loved, when we are not wanted, considered an embarrassment and a burden. I have grown nieces who do not know me, but they would post rude things on Facebook about me because I was locked up in an institution and diagnosed with schizophrenia 46 years ago. I was released from that place 44 years ago. I have had numerous doctors and therapists over the years tell me that I was misdiagnosed, I had PTSD or something else. But in my family of origin’s eyes, all but a couple of my relatives still treat me like the embarrassing crazy lady…. it HURTS. Yes it does. It EFFING HURTS. Worse than the pain and horror of “going crazy” in the first place. You SEE it in their eyes, you HEAR it in their words, their tone of voice, you DISCERN it in their body language, that “jumpiness” that 99% of the people get when you tell them, or they otherwise find out, about your MI Dx. It’s like a mask comes down over their face…. and you feel that ARCTIC CHILL, the deep-freeze of being frozen out.
Also, Pam, in a marriage the loneliness and the judgments, the raised eyebrows, the rolled eyes, the heavy sighs, the thoughtless comments, such as my now EX husband made to the intake nurse at Johns Hopkins University Hospital Psychiatric unit, where I had gone voluntarily hoping for HELP with my then-intractable depression. In describing the harrowing traffic in the streets of Baltimore as he had driven me to the hospital that day, my now EX quipped: “The traffic was so bad, I thought *I* was going to go crazy, HAHAHA.”
NOW I am lucky, NOW I am married to a man with severe chronic PTSD from Vietnam combat, a man who has spent time as a patient on a psych ward, so he UNDERSTANDS and does not hold himself above me or apart from me.
I’ve said it before, I’ll say it again and again and again until I die: The CURE for all types of mental illness labels must begin with CARE: Compassion, Acceptance, Respect, and Encouragement. Everything that is the opposite of the shunning, the subtle cold shoulder, the jumpiness that we can SEE and FEEL and HEAR because, yes, dammit, we may have a screw loose here or there, but we are not stupid, deaf, or blind.
And this:
Oh no, I just went back and reread my comment, and it’s full of typos. So sorry, I was writing in my emotional part of my brain, not in the editing part. Also I put that the message that made me go off FB for over a year was posted Christmas Eve of 2012. Obviously that’s wrong, it was 2011.
Brenda, I wanted to tell you that I appreciate the things you wrote, too, particularly the part about our need to be kind and loving to ourselves. So true. It’s also very true, what you said about hospitals being an unnatural setting, and that we cannot read minds, and there may be times when we are mistaken in thinking that certain people do not really like or love us. I do believe that is also true. However, that jumpy feeling you so honestly said you feel when you discover that someone has an MI Dx,,,, thank you for being so honest, and yes, that is an all-too-typical response, and it is THAT RESPONSE, that involuntary attitude of the general public toward people with certain mental illness diagnosis, that jumpy reaction is very easy to discern. And it may be involuntary and unintentional and even understandable, thanks in large part to how the media portrays people with serious MI labels, BUT.IT.HURTS, when YOU are the one being looked at and talked to like you are a freak, the boogie man, a strange and unpredictable creature from another dimension.
I am lucky to finally have my “certifiable” husband, whom I did not meet and marry until we were both in our 50s, and our sweet fur-baby Cattle Dog, who doesn’t know a thing about Mental Illnesses and couldn’t care less, so long as we feed and water and walk her and give her lots of back rubs. I worry about you, Pam, feeling so alone. Loneliness is a soul killer. I know, for I have spent the vast majority of my life feelings just as alone as you describe in this post, yes, even when I was married. In my experience, there is nothing more lonely than being married to someone who talks down to you and treats you like the worst of the personnel in the psych hospitals treated you. I don’t know why a man who looks down on the mentally ill would even want to marry me in the first place, when I had not ever hidden that part of my history from a potential husband. I can only surmise, based on how I was treated, that a man like that is looking for a woman he can control and verbally and even sometimes physically abuse, cheat on her and do whatever the heck he wants when he wants, and feel all justified about it and superior to her because, after all, his wife is “crazy.” I would rather live all alone under a bridge and eat out of garbage cans, to ever be in a marriage like that again!
Note to Lynda from pam: i looked and looked but just could not find any typos to correct for you…sorry. The date part i let you correct in your note, but the spelling typos just do not exist so far as i know or even that spellcheck can see. I know that there could be homonyms that were misspelled, but i did not detect any of those either. So there! 8) thanks for your brilliant addendum!
“In India when we meet and part we Often say, ‘Namaste’, which means: I honor the place in you where the entire universe resides; I honor the place in you of love, of light, of truth, of peace. I honor the place within you where if you are in that place in you and I am in that place in me, there is only one of us." ~~Ram Dass~~
WAGblog: Dum Spiro Spero 