Lori Carlson over at her WordPress blog, one of several, AS THE FATES WOULD HAVE IT, http://asthefateswouldhaveit.wordpress.com wrote this lovely passage about why she has to write:
“I enjoy reading poetry and prose that inspires me, that wrenches at my heart, and that puts me in the grip of Knowing — that silent moment when what someone else has written rings so true with you, that you are in complete awe. That is the way I write, or at the very least, I strive to write that way. And so I have made it my life’s goal to write poetry and short fiction, to give back to others the passion that fuels my soul.”
My response to Lori was this: “Passion pushes life to its purest pitch. A passionate enthusiasm is not pathological, as some might have us believe when we are caught up in its grip…Never believe them. Without passion, poetry is just a dim simulacrum of itself, veiled but without mystery, deaf not just to the world but to itself as well.”
Best wishes, Lori, and every one of you writers out there who might have been told to “cool it” or to stop dreaming and “get real.” Best wishes for all the dreams and all the passion your life can encompass, brim over with and then more! more! YES! MORE!
that spirit-familiar, the barred she-owl, Strix varia,
roosting on a white pine bough
outside your window all winter,
less guardian than too starving to move away
or predate the small animals atop the ice layer
between her and proper voles held in safety beneath.
Only when deep-freeze breaks in early March
and a shadow swoops silently across your pane,
do you know who’s won the battle,
and cheer for a raptor’s kill that saves her life.
The world, after all, is all about killing or being eaten,
which is true even in the human world
where your neighbors stalk you with barking dogs,
and talk nights, beneath your bedroom window
of that woman next door, who is not like them,
with her window salad garden and that owl.
Fearful, blind, they believe that hoot owls
harbinger death. Instead you try to see
the way a mythical Owl might see,
through cold and black of night
for clarity, for lucency, for whatever it is
that warms the living embers
and rem-embers your mind to peace.
——————————————————
This next poem describes the present situation, which continues…with the following explanations.
In the Greek myth, Philomela is raped and has her tongue cut out by Tereus, the husband of her sister Procne. Rendered mute, Philomela weaves a tapestry detailing the crime to inform her sister, who, enraged, takes revenge on Tereus. At the end of the story, both Procne and Philomela are transformed into birds. In some versions of this story, Philomela turns into a female nightingale, while in others she becomes a swallow. However, neither of these birds can sing.
Jerry Mahoney and Charlie McCarthy are two famous American ventriloquists’ dummies
PHILOMELA
I haven’t spoken out loud for many weeks,
bullied by “voices” to a frightened into myself silence.
Still, what does “speechless” mean
in these days of text-to-speech software,
with its choice of Vikki or Samantha or Victoria voices,
especially when I’m possessed of a blog and writing fluency
enough to speak my mind to my heart’s content?
Even so, being mute is not a manner of speaking.
Yet I tell you I can talk. Nothing physical impedes
my tongue, or locks my lips
except my brain’s hallucinated snarls,
Jerry Mahoney and Charlie McCarthy thrown
into surrounding shadows
ordering up this stoppage, blockage, blockade.
Now, like Stevens’ fire-fangled bird at the end of the mind
Sometimes you never know who it is that has a disabling mental “illness,” not even when they are right in front of you. Not every person who has been diagnosed with schizophrenia, for instance, looks like it or pushes a shopping cart laden with household “extranea” down the street, homeless, filthy, and laughing wildly to themselves…Not that this is so terrible either, frankly. We should all not be so quick to judge. And no, we should not judge even this notion of the homeless-shopping-cart-person as “bad” or “wrong” — not until we know the person and understand what he or she wants from life and his or her history. I am not saying that anyone should freeze to death from exposure, or suffer from hunger or from any unwanted basic deprivation, only that no one understands the life conditions of another until you talk with them and come to know that person…
Too many people make assumptions that are wrong and/or erroneous based only on what they want and are comfortable with, not on what the other person needs and wants. Believe me, I know, having been there way more often than I wish and experienced it from that “other side.” Far too many times have people claimed to be “helping me” and have only hurt me! It is not that I think they were badly intentioned, so much as that they were only thinking about how they felt or would feel. They were not being truly empathic, not giving an inch or a nanosecond to trying to think about how I, personally, did feel nor for that matter asking me what I might want or need at that moment.
I want to remind people to remember that “ASSUME makes an ASS out of U and Me..” so instead of assuming anything about another person, especially someone who has an apparent mental “illness” or someone who at any rate seems somehow “different” from the people who are familiar to you, ask them questions…Find out what they want and what makes them comfortable!
As Toltec spiritual advisor Don Miguel Ruiz tells us in THE FOUR AGREEMENTS, which is the best book of its sort I have ever read, you can and should ask any question you want to, so long as you are honestly prepared to accept the answer.
By the way, the Second Agreement, in his book, an Agreement I find so fundamentally important, is Do Not Take Anything Personally. By taking things personally — that way danger and disappointment and all distress lies. Truly this is so. People are all in their own little bubbles, taking their own lives personally and frankly, think about that! We are only on the periphery of everyone else’s thinking and living, and in a very real way they cannot ever know us as we know ourselves, they can only know us through the lens of their own lives, their own bubbles. This revelation can be freeing if you let it…
That is why we should not take anything personally — because other people are too busy doing the same thing and not seeing us as we are, but only as adjuncts to their lives and thinking. If we truly knew and accepted this, we would be free from a great deal of angst and upset. But of course this is a very difficult thing to do…to free ourselves of the notion that we are as important in others lives as we are in our own. No, they are the important actors on their own stage, we are not. We really need to get over thinking that we are prima donnas in everyone’s drama as well as our own…Is not our own life enough? I should think so. Who would want to star in more than one drama at a time?
Patients placed in Seclusion or Restraints are to be debriefed afterwards. To see standards of care, see below this reprint article.
I moved to Brattleboro Vermont on February 4, 2015, leaving my home state of Connecticut where I’ve lived for nearly 60 years. l had to move because of the horrific psychiatric abuses I experienced in Connecticut hospitals and my fear that if ever I were hospitalized again I would be killed.
I feel guilty, however, just getting out without accomplishing something to stop what continues to happen in Connecticut psychiatric units and hospitals.
The experience of mechanical four-point restraints – leather cuffs that are tightened around the wrists and ankles to immobilize a patient to a bed – or being isolated by force in an often freezing seclusion cell is almost universally terrifying. Nevertheless, both cell and/or restraints are routinely employed to curb loudness and undesirable behaviors at the Hospital of Central Connecticut on Grand Street in New Britain. I know this because I was subjected to both seclusion and restraints multiple times in the spring of 2014, despite a diagnosis of chronic paranoid schizophrenia, as well as PTSD that was triggered by precisely this sort of thing.
Bizarrely, the hospital psychiatrist, Dr Michael E Balkunas, treating me at HOCC challenged my PTSD diagnosis. “Patient misperceives her treatment as traumatic,” he wrote in my chart. Well, maybe so, but I don’t know how I can be accused of misperceiving three entire days callously abandoned alone, tied to the four posts of a metal bedstead at U-Conn’s Dempsey Hospital (for trying to escape the locked unit) as anything but brutality, even if it was in the 1990s. I also think it is nearly by definition traumatic to be forced to defecate in one’s own clothing while tied to a bed which is what they did at Hartford Hospital’s Institute of Living in the winter of 2013. This was after I was told to lie down and place my own limbs in the leather cuffs (“as a consequence but not a punishment”) for walking away from the very same “Side Room” that I had just been assured was “not a seclusion room unless you call it a seclusion room.”
Again, maybe I misperceived being grabbed and held face-down and nearly suffocated numerous times by staff at Yale Psychiatric Hospital in August 2013, who injected 10-20 milligrams of Haldol, a known drug of torture. Maybe this was just kindliness that I misunderstood as traumatic, maybe it was merely a “psychotic misperception” on my part? Maybe, and maybe not.
Nevertheless, the fact remains that in the ED of New Britain’s HOCC, a security guard in May 2014, grabbed me by my left shoulder immediately after he was warned by the nurse that it was my left shoulder that had a rotator cuff tear.
My New Britain chart records that I was admitted to that hospital, and to the IOL and others with a detailed Psychiatric Advance Directive, the first page of which states that seclusion, four-point restraints and forced medication invariably result in regression to “primitive states and severe worsening of symptoms.” It also makes several concrete suggestions how better to deal with me when I am upset. Even though I spent many hours on this document, Psychiatric Advance Directives have no legal clout in Connecticut and doctors can and do ignore them freely.
Perhaps because of this, HOCC staff literally forced me (“escorted me”) to seclusion and/or restrained me again and again. They took to stripping me “for safety’s sake,” and even though I put up no resistance, they had the male guards spread-eagle my limbs while still naked and put restraint cuffs on without even covering me.
Is it any wonder that what resulted was someone who would wash her hair in her own urine, defecate on the floor of her room and smear feces on the wall? Yet Dr Balkunas, the director of W-1, the general psychiatry unit at HOCC claimed that my trauma was imaginary. Why? Because treatment cannot be traumatic. He simply never got the connection between my horrendous decompensation and his so-called “therapy.” Maybe he never appreciated that he was torturing me, like a person who ripped the wings off butterflies as a child. Someone like that would not have understood how those creatures suffer either.
——————–
These are the NURSING De-Briefing standards for after restraints and/or seclusion:
APNA STANDARDS
DEBRIEFING AFTER RESTRAINTS/SECLUSION
Standard: As soon as possible, following the release from seclusion or restraint, the nurse, the person and others as appropriate should participate in a debriefing.
Intent: A debriefing is done with persons who have been secluded or placed in restraints to:
Discuss and clarify any possible misperceptions the person may have concerning the incident.
Ascertain the person’s willingness to involve family or other caregivers in a debriefing to discuss and clarify their perceptions as well as identify additional alternatives or treatment plan modifications.
Support the person’s re-entry into the milieu.
Identify alternative interventions to reduce the potential for additional episodes.
Hear and record the person’s perspective on the episode.
Ascertain that the person’s rights and physical well-being were addressed during the episode and advise the person of processes to address perceived rights grievances.
Address any trauma that may have occurred as a result of the incident.
Modify the treatment plan as needed.
NONE of this was EVER done, ANYWHERE, in any hospital I have ever been in. Why? Because they all knew perfectly well what they had done to me and WHY…Not because I was dangerous to anyone, but as punishment…Naturally they did not want me to have a chance to tell anyone.
My comment to JulieMadBlogger who wrote this was: This is the single most ALIVE, VIBRANT, MOST TRUTH-TELLING piece on the consequences of hospitalization and treatment for EDs (but not for binge eating,) that I have ever read. Read on and you will see why.
Hello! Wow, I have heard this question so frequently. I can’t necessarily say why this happens to every single person who has asked this question. However, I can suggest a few possible explanations as to why this happens so frequently.
Does eating disorders “care” really address binge eating?
I haven’t run the circuit of treatment centers, but from what I have seen, these places address two thing: 1. They restore weight by forceful means. 2. They try to stop you from throwing up by invading your privacy. That doesn’t exactly sound helpful to me. In fact, it sounds downright awful!
Maybe the whole time you were in there, you wondered if you would go back to binge eating upon leaving. This fear may have loomed in your mind the whole time. Since all discussion of binge eating is discouraged, you keep that fear to yourself. If this is your very…
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.
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Read the English Lyrics below first if you need to as this song is in Italian.
HUMAN BEINGS/ESSERI UMANI or go to this link: https://youtu.be/U-4OrzSBfm8
Thank you, TTMO’s Cortland Pfeffer, you are a man of true courage. I thank you for your blog and for everything you have done and are doing in the world and for people who are or were where I have been.
WAGblog: Dum Spiro Spero 