Closing Down

Wagblog is going off-line. Maybe we will return, maybe not. It won’t a great loss to the world in any event. Too many words, too much garbage…

As Lao Tzu was said to have written, “Much talk means much exhaustion, better far it is to keep your thoughts.” Well, I shut up vocally many weeks ago, and it was indeed better for everyone around me…so now maybe if I also cease this incessant blather it will be another improvement for the world.

Sorry for everything. Mea culpa, mea maxima culpa.

 

NEW POEM, OR REWRITTEN POEM, ABOUT BEING MUTE

ON NOT SPEAKING

Over the seasons of my sixties

and unwillingly

suddenly silent

no wonders spark in my visual brain.

But a reason why’s no wonder.

For so many years schooled

into naming everything

words and sounds categorize the world

and wordify my senses.

Precipice, for instance,

with its sliced peaks.

And acrid’s encaustic, that bite on my tongue.

Even blench

somehow leaves me paler

and more livid than before.

But there are descents into being speechless

for reasons besides pathology.

Although these may not seem any reason

or even be

reason enough, to many,

who believe only talking out pain aloud

makes sense.

Sensible or senseless

I know when shutting up is preventive.

or at least is less insane

than trying to be heard

by those inured to hurting

or being hurtful

when they indeed would rather hurt me

than pay heed, having heard me.

But if silence as you claim

overspeaks the chattering air

why do you refuse

to hear all I cannot use

my voice to say.

PASSION AND POETRY ARE LIFE, NOT PATHOLOGY!

Tidal Wave ATC (Artist Trading Card)
Tidal Wave ATC (Artist Trading Card)

 

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!

Praying For Foolishness: A Poem

THE OLD STORY

My father spoke of atheism as if it were a religion,

pounding the points of his argument into the dinner table,

spilling the salt with the seed of his own bad temper.

He raised me to be an atheist, too,

and I learned well the commandments of godlessness.

But at night in bed I suffered for it and was penitent

memorizing prayers buy the pages

glossing the psalms with a litany of pleas

that somehow God would find me, small as I was,

and make me a believer,

and, though a prodigal daughter, much loved, much loved.

How I longed for the sweet blow of grace

coming upon me like a hammer on a nail,

or a beggar on a penny

or raindrops on the parched red clay

turned to rust in the arid fields of my soul.

 

One night – I was under the covers saying the Lord’s Prayer

with a lengthy meditation for each line –

my father, making the rounds, heard me.

What are you doing? he asked, more awful than the God I longed for.

I told him, expecting punishment,

expecting a lecture on the purity of the godless intellect.

He stood a while in silence

while I waited for the one blow I didn’t want.

Then he said, laughing,

you’ll grow out of such foolishness, I hope.

 

I didn’t grow out of it.

Though I never found God and stopped looking for Him

I remember my father’s laughter,

the hard, cold sneer of it,

laughter at his daughter longing for God

and hoping for love

that would come like a thief in the night.

 

Now that I am older I know that belief’

doesn’t fall like a hammer

that the beggar is always penniless

and that rainfall soon evaporates returning to the cloud.

Atheism is a creed I have lived by, learned by,

and have at times been comforted by.

but if God should ever find me

I pray for foolishness.

 

1988

Two Poems

Audobon Field Guide Barred Owl
Audubon Field Guide Barred Owl

TIME-BANK POEM

Dear R, you who have asked me,

via my Service Offer (“I write personal poems”),

to “create” you a poem, can’t know,

when my second late night email

fails to elicit a prompt response,

how my certainty of rejection hammers me

into old penances, and how I tinfoil walls

and barricades against my extruded poisons.

Then when your emails resume the next day

mentioning your little white house,

a she-owl who watches you with soulful eyes

and your growing “sense of despair”

I imagine a woman of mature years,

alone, though perhaps through choices

not always made freely. So to meet you

I navigate unfamiliar and unpaved roads

parking behind a half-built barn

and a muddy old green Subaru.

Younger than I expect, you’ve moved here

to escape precisely what we never discuss.

You reference only the need for peace of mind,

and a relief from startling triggers.

Nevertheless, I understand your need to know

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

feathered unlucky, tarred, locked in golden cage

my voice remains only a memento

of everything

I wanted to say, but could not get out,

I couldn’t get it out, I could not get it out…

Toltec Wisdom (and a Little of My Own!)

Despair on Park Bench
Despair on Park Bench

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?

Hartford COurant Article (that won’t be) about Michael E Balkunas, MD, Chief of psychiatry at HOCC

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.

– See more at: http://www.apna.org/i4a/pages/index.cfm?pageid=3730#Release

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.

– See more at: http://www.apna.org/i4a/pages/index.cfm?pageid=3730#Release

The Marionette and the Golden Pot: Does Art Mean Anything?

Maybe this is meaningful, since I was thinking about con-artists, and maybe not…but I did not know what I was drawing or why until hours later…

Does Art Mean Something and if so, What?
Does Art Mean Something and if so, What? (unfinished drawing)

JULIEMADBLOGGER on BINGE EATING AND THE TRUTH ABOUT EDs

Pamela Spiro Wagner:

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.

Originally posted on This Hunger Is Secret:

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…

View original 1,733 more words

SCHIZOPHRENIA and TEMPORAL LOBE EPILEPSY: MORE INFORMATION From MEDSCAPE

Psychiatric Disorders Associated With Epilepsy

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

Updated: Oct 28, 2013

Overview

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

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

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

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

Factors in the relationship between epilepsy and behavioral disorders

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

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

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

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

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

epilepsy

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

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

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

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

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

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

of seizures.”[3]

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

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

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

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

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

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

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

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

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

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

Atypical for the psychiatric disorder Episodic
Pleomorphic

Psychotic Disorders

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

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

diagnosed with schizophrenia.[15]

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

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

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

Psychiatric Disorder

Controls

Patients With Epilepsy

Major depressive disorder

10.7%

17.4%

Anxiety disorder

11.2%

22.8%

Mood/anxiety disorder

19.6%

34.2%

Suicidal Ideation

13.3%

25.0%

Others

20.7%

35.5%

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

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

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

distinct nosologic entity differing from schizophrenia.[21]

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

drugs.[22]

Ictal events

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

Postictal events

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

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

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

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

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

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

intoxication, complex partial status epilepticus, metabolic disturbance).

Interictal events

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

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

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

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

Factors in the development of psychosis

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

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

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

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

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

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

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

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

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

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

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

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

Schizophrenia

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

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

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

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

Delusions of reference
More benign and variable course

Treatment

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

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

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

Forced normalization

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

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

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

Bipolar Affective Disorders

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

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

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

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

other disorders.[47]

Depression

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

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

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

of the epilepsy.

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

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

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

studies have found this difference.[50]

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

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

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

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

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

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

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

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

Physiologic factors associated with epilepsy and depression

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

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

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

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

confirmed by a few other investigators.[56]

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

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

Other authors report no laterality differences in depression rates.

Other factors associated with depression in epilepsy

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

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

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

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

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

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

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

Phenobarbital Primidone Vigabatrin Levetiracetam Felbamate Topiramate

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

Frequency of depression in epilepsy

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

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

that depression was the most common psychiatric diagnosis.

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

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

Characteristics of depression in patients with epilepsy

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

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

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

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

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

Depressed mood Anergia
Pain
Insomnia

Fear
Anxiety
Paroxysmal irritability Euphoric moods

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

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

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

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

manifested by the following[71] :

Irritability Oppositionality Aggression Anger

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

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

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

Preictal symptoms of depression

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

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

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

Ictal symptoms of depression

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

anhedonia, guilt, and suicidal ideation.[74]

Postictal symptoms of depression

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

Interictal symptoms of depression

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

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

III­R criteria.

Treatment

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

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

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

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

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

increased incidence of psychiatric problems.[80]

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

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

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

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

needed.[81]

Mania

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

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

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

Suicidal Behaviors

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

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

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

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

epilepsy and suicidality is complex and multifactorial.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Symptoms of anxiety in epilepsy

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

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

of primary anxiety disorder.[85]

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

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

and autonomous phenomena.[1, 86]

Anxiety in association with type of epilepsy and frequency of seizures

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

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

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

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

Anxiety can also be seen in frontal lobe epilepsy.

Ictal and interictal anxiety

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

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

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

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

Treatment

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

Research

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

Personality Disorders

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

Geschwind syndrome.[89]

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

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

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

myoclonic epilepsy.[91]

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

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

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

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

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

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

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

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

Psychotropic Effects of Antiepileptic Drugs

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

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

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

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

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

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

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

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

disorders and mesial temporal lobe surgery.

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

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

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

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

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

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

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

Conclusion

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

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

Contributor Information and Disclosures

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

Disclosure: Nothing to disclose.

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

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

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

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

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

Disclosure: Nothing to disclose.

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

Disclosure: Medscape Salary Employment

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

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

Disclosure: LGCH, Inc Ownership interest Consulting

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

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

Disclosure: Nothing to disclose.

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This Post is Dedicated to TakingTheMaskOff.Com and Cortland Pfeffer, With Love

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.

http://www.takingthemaskoff.com

pam w.

Here are the Lyrics to HUMAN BEINGS, in English followed by the Italian (just in case anyone wants to sing along –as I did!)

HUMAN BEINGS/Esseri Humani

Nowadays, people judge you

Because of your appearance

They see only masks

They don’t even know who you are

You must show yourself invincible

Collecting trophies

But when silently you cry

You find out who you really are

I believe in human beings

I believe in human beings

I believe in human beings

The courageous ones

The courage of being human

I believe in human beings

I believe in human beings

I believe in human beings

The courageous ones

The courage of being human

Take my hand and stand up

You can trust me

I am an ordinary man

One out of many just like you

But what a splendor there is in you

In your fragility

And I remind you that we are not alone

Fighting this reality

I believe in human beings

I believe in human beings

I believe in human beings

The courageous ones

The courage of being human

I believe in human beings

I believe in human beings

I believe in human beings

The courageous ones

The courage of being human

Love, love, love

Won, wins and will always win

Love, love, love

Won, wins and will always win

Love, love, love

Won, wins and will always win

Love, love, love

Won, wins and will always win

I believe in human beings

I believe in human beings

I believe in human beings

The courageous ones

The 
courage of being human

I believe in human beings

I believe in human beings

I believe in human beings

The courageous ones

The courage of being human

Human beings

Human beings

Esseri umani

Oggi la gente ti giudica,
per quale immagine hai.
Vede soltanto le maschere,
non sa nemmeno chi sei.

Devi mostrarti invincibile,
collezionare trofei.
Ma quando piangi in silenzio,
scopri davvero chi sei.

Credo negli esseri umani.
Credo negli esseri umani.
Credo negli esseri umani
che hanno coraggio,
coraggio di essere umani

Credo negli esseri umani.
Credo negli esseri umani.
credo negli esseri umani
che hanno coraggio,
coraggio di essere umani.

Prendi la mano e rialzati,
tu puoi fidarti di me.
Io sono uno qualunque,
uno dei tanti, uguale a te.

Ma che splendore che sei,
nella tua fragilità.
E ti ricordo che non siamo soli
a combattere questa realtà.

Credo negli esseri umani.
Credo negli esseri umani.
Credo negli esseri umani che hanno coraggio,
coraggio di essere umani.

Credo negli esseri umani.
Credo negli esseri umani.
Credo negli esseri umani che hanno coraggio,
coraggio di essere umani.

Essere umani.

L’amore, amore, amore
ha vinto, vince, vincerà.
L’amore, amore, amore
ha vinto, vince, vincerà.

L’amore, amore, amore
ha vinto, vince, vincerà.
L’amore, amore, amore,
ha vinto, vince, vincerà.

Credo negli esseri umani.
Credo negli esseri umani.
Credo negli esseri umani che
hanno coraggio,
coraggio di essere umani.

Credo negli esseri umani.
Credo negli esseri umani.
Cedo negli esseri umani che hanno coraggio,
coraggio di essere umani.

Essere umani.
Essere umani.

So You Thought Your Genes or Drugs Cause Drug Addiction? Read This and Think Again

 
Johann Hari Headshot

FROM THE HUFFINGTON POST:

The Likely Cause of Addiction Has Been Discovered, and It Is Not What You Think

By Johann Hari

It is now one hundred years since drugs were first banned — and all through this long century of waging war on drugs, we have been told a story about addiction by our teachers and by our governments. This story is so deeply ingrained in our minds that we take it for granted. It seems obvious. It seems manifestly true. Until I set off three and a half years ago on a 30,000-mile journey for my new book, Chasing The Scream: The First And Last Days of the War on Drugs, to figure out what is really driving the drug war, I believed it too. But what I learned on the road is that almost everything we have been told about addiction is wrong — and there is a very different story waiting for us, if only we are ready to hear it.

If we truly absorb this new story, we will have to change a lot more than the drug war. We will have to change ourselves.

I learned it from an extraordinary mixture of people I met on my travels. From the surviving friends of Billie Holiday, who helped me to learn how the founder of the war on drugs stalked and helped to kill her. From a Jewish doctor who was smuggled out of the Budapest ghetto as a baby, only to unlock the secrets of addiction as a grown man. From a transsexual crack dealer in Brooklyn who was conceived when his mother, a crack-addict, was raped by his father, an NYPD officer. From a man who was kept at the bottom of a well for two years by a torturing dictatorship, only to emerge to be elected President of Uruguay and to begin the last days of the war on drugs.

I had a quite personal reason to set out for these answers. One of my earliest memories as a kid is trying to wake up one of my relatives, and not being able to. Ever since then, I have been turning over the essential mystery of addiction in my mind — what causes some people to become fixated on a drug or a behavior until they can’t stop? How do we help those people to come back to us? As I got older, another of my close relatives developed a cocaine addiction, and I fell into a relationship with a heroin addict. I guess addiction felt like home to me.

If you had asked me what causes drug addiction at the start, I would have looked at you as if you were an idiot, and said: “Drugs. Duh.” It’s not difficult to grasp. I thought I had seen it in my own life. We can all explain it. Imagine if you and I and the next twenty people to pass us on the street take a really potent drug for twenty days. There are strong chemical hooks in these drugs, so if we stopped on day twenty-one, our bodies would need the chemical. We would have a ferocious craving. We would be addicted. That’s what addiction means.

One of the ways this theory was first established is through rat experiments — ones that were injected into the American psyche in the 1980s, in a famous advert by the Partnership for a Drug-Free America. You may remember it. The experiment is simple. Put a rat in a cage, alone, with two water bottles. One is just water. The other is water laced with heroin or cocaine. Almost every time you run this experiment, the rat will become obsessed with the drugged water, and keep coming back for more and more, until it kills itself.

The advert explains: “Only one drug is so addictive, nine out of ten laboratory rats will use it. And use it. And use it. Until dead. It’s called cocaine. And it can do the same thing to you.”

But in the 1970s, a professor of Psychology in Vancouver called Bruce Alexandernoticed something odd about this experiment. The rat is put in the cage all alone. It has nothing to do but take the drugs. What would happen, he wondered, if we tried this differently? So Professor Alexander built Rat Park. It is a lush cage where the rats would have colored balls and the best rat-food and tunnels to scamper down and plenty of friends: everything a rat about town could want. What, Alexander wanted to know, will happen then?

In Rat Park, all the rats obviously tried both water bottles, because they didn’t know what was in them. But what happened next was startling.

The rats with good lives didn’t like the drugged water. They mostly shunned it, consuming less than a quarter of the drugs the isolated rats used. None of them died. While all the rats who were alone and unhappy became heavy users, none of the rats who had a happy environment did.

At first, I thought this was merely a quirk of rats, until I discovered that there was — at the same time as the Rat Park experiment — a helpful human equivalent taking place. It was called the Vietnam War. Time magazine reported using heroin was “as common as chewing gum” among U.S. soldiers, and there is solid evidence to back this up: some 20 percent of U.S. soldiers had become addicted to heroin there, according to a study published in the Archives of General Psychiatry. Many people were understandably terrified; they believed a huge number of addicts were about to head home when the war ended.

But in fact some 95 percent of the addicted soldiers — according to the same study — simply stopped. Very few had rehab. They shifted from a terrifying cage back to a pleasant one, so didn’t want the drug any more.

Professor Alexander argues this discovery is a profound challenge both to the right-wing view that addiction is a moral failing caused by too much hedonistic partying, and the liberal view that addiction is a disease taking place in a chemically hijacked brain. In fact, he argues, addiction is an adaptation. It’s not you. It’s your cage.

After the first phase of Rat Park, Professor Alexander then took this test further. He reran the early experiments, where the rats were left alone, and became compulsive users of the drug. He let them use for fifty-seven days — if anything can hook you, it’s that. Then he took them out of isolation, and placed them in Rat Park. He wanted to know, if you fall into that state of addiction, is your brain hijacked, so you can’t recover? Do the drugs take you over? What happened is — again — striking. The rats seemed to have a few twitches of withdrawal, but they soon stopped their heavy use, and went back to having a normal life. The good cage saved them. (The full references to all the studies I am discussing are in the book.)

When I first learned about this, I was puzzled. How can this be? This new theory is such a radical assault on what we have been told that it felt like it could not be true. But the more scientists I interviewed, and the more I looked at their studies, the more I discovered things that don’t seem to make sense — unless you take account of this new approach.

Here’s one example of an experiment that is happening all around you, and may well happen to you one day. If you get run over today and you break your hip, you will probably be given diamorphine, the medical name for heroin. In the hospital around you, there will be plenty of people also given heroin for long periods, for pain relief. The heroin you will get from the doctor will have a much higher purity and potency than the heroin being used by street-addicts, who have to buy from criminals who adulterate it. So if the old theory of addiction is right — it’s the drugs that cause it; they make your body need them — then it’s obvious what should happen. Loads of people should leave the hospital and try to score smack on the streets to meet their habit.

But here’s the strange thing: It virtually never happens. As the Canadian doctor Gabor Mate was the first to explain to me, medical users just stop, despite months of use. The same drug, used for the same length of time, turns street-users into desperate addicts and leaves medical patients unaffected.

If you still believe — as I used to — that addiction is caused by chemical hooks, this makes no sense. But if you believe Bruce Alexander’s theory, the picture falls into place. The street-addict is like the rats in the first cage, isolated, alone, with only one source of solace to turn to. The medical patient is like the rats in the second cage. She is going home to a life where she is surrounded by the people she loves. The drug is the same, but the environment is different.

This gives us an insight that goes much deeper than the need to understand addicts. Professor Peter Cohen argues that human beings have a deep need to bond and form connections. It’s how we get our satisfaction. If we can’t connect with each other, we will connect with anything we can find — the whirr of a roulette wheel or the prick of a syringe. He says we should stop talking about ‘addiction’ altogether, and instead call it ‘bonding.’ A heroin addict has bonded with heroin because she couldn’t bond as fully with anything else.

So the opposite of addiction is not sobriety. It is human connection.

When I learned all this, I found it slowly persuading me, but I still couldn’t shake off a nagging doubt. Are these scientists saying chemical hooks make no difference? It was explained to me — you can become addicted to gambling, and nobody thinks you inject a pack of cards into your veins. You can have all the addiction, and none of the chemical hooks. I went to a Gamblers’ Anonymous meeting in Las Vegas (with the permission of everyone present, who knew I was there to observe) and they were as plainly addicted as the cocaine and heroin addicts I have known in my life. Yet there are no chemical hooks on a craps table.

But still, surely, I asked, there is some role for the chemicals? It turns out there is an experiment which gives us the answer to this in quite precise terms, which I learned about in Richard DeGrandpre’s book The Cult of Pharmacology.

Everyone agrees cigarette smoking is one of the most addictive processes around. The chemical hooks in tobacco come from a drug inside it called nicotine. So when nicotine patches were developed in the early 1990s, there was a huge surge of optimism — cigarette smokers could get all of their chemical hooks, without the other filthy (and deadly) effects of cigarette smoking. They would be freed.

But the Office of the Surgeon General has found that just 17.7 percent of cigarette smokers are able to stop using nicotine patches. That’s not nothing. If the chemicals drive 17.7 percent of addiction, as this shows, that’s still millions of lives ruined globally. But what it reveals again is that the story we have been taught about The Cause of Addiction lying with chemical hooks is, in fact, real, but only a minor part of a much bigger picture.

This has huge implications for the one-hundred-year-old war on drugs. This massive war — which, as I saw, kills people from the malls of Mexico to the streets of Liverpool — is based on the claim that we need to physically eradicate a whole array of chemicals because they hijack people’s brains and cause addiction. But if drugs aren’t the driver of addiction — if, in fact, it is disconnection that drives addiction — then this makes no sense.

Ironically, the war on drugs actually increases all those larger drivers of addiction. For example, I went to a prison in Arizona — ‘Tent City’ — where inmates are detained in tiny stone isolation cages (‘The Hole’) for weeks and weeks on end to punish them for drug use. It is as close to a human recreation of the cages that guaranteed deadly addiction in rats as I can imagine. And when those prisoners get out, they will be unemployable because of their criminal record — guaranteeing they with be cut off even more. I watched this playing out in the human stories I met across the world.

There is an alternative. You can build a system that is designed to help drug addicts to reconnect with the world — and so leave behind their addictions.

This isn’t theoretical. It is happening. I have seen it. Nearly fifteen years ago, Portugal had one of the worst drug problems in Europe, with 1 percent of the population addicted to heroin. They had tried a drug war, and the problem just kept getting worse. So they decided to do something radically different. They resolved to decriminalize all drugs, and transfer all the money they used to spend on arresting and jailing drug addicts, and spend it instead on reconnecting them — to their own feelings, and to the wider society. The most crucial step is to get them secure housing, and subsidized jobs so they have a purpose in life, and something to get out of bed for. I watched as they are helped, in warm and welcoming clinics, to learn how to reconnect with their feelings, after years of trauma and stunning them into silence with drugs.

One example I learned about was a group of addicts who were given a loan to set up a removals firm. Suddenly, they were a group, all bonded to each other, and to the society, and responsible for each other’s care.

The results of all this are now in. An independent study by the British Journal of Criminology found that since total decriminalization, addiction has fallen, and injecting drug use is down by 50 percent. I’ll repeat that: injecting drug use is down by 50 percent. Decriminalization has been such a manifest success that very few people in Portugal want to go back to the old system. The main campaigner against the decriminalization back in 2000 was Joao Figueira, the country’s top drug cop. He offered all the dire warnings that we would expect from the Daily Mail or Fox News. But when we sat together in Lisbon, he told me that everything he predicted had not come to pass — and he now hopes the whole world will follow Portugal’s example.

This isn’t only relevant to the addicts I love. It is relevant to all of us, because it forces us to think differently about ourselves. Human beings are bonding animals. We need to connect and love. The wisest sentence of the twentieth century was E.M. Forster’s — “only connect.” But we have created an environment and a culture that cut us off from connection, or offer only the parody of it offered by the Internet. The rise of addiction is a symptom of a deeper sickness in the way we live — constantly directing our gaze towards the next shiny object we should buy, rather than the human beings all around us.

The writer George Monbiot has called this “the age of loneliness.” We have created human societies where it is easier for people to become cut off from all human connections than ever before. Bruce Alexander — the creator of Rat Park — told me that for too long, we have talked exclusively about individual recovery from addiction. We need now to talk about social recovery — how we all recover, together, from the sickness of isolation that is sinking on us like a thick fog.

But this new evidence isn’t just a challenge to us politically. It doesn’t just force us to change our minds. It forces us to change our hearts.

Loving an addict is really hard. When I looked at the addicts I love, it was always tempting to follow the tough love advice doled out by reality shows like Intervention — tell the addict to shape up, or cut them off. Their message is that an addict who won’t stop should be shunned. It’s the logic of the drug war, imported into our private lives. But in fact, I learned, that will only deepen their addiction — and you may lose them altogether. I came home determined to tie the addicts in my life closer to me than ever — to let them know I love them unconditionally, whether they stop, or whether they can’t.

When I returned from my long journey, I looked at my ex-boyfriend, in withdrawal, trembling on my spare bed, and I thought about him differently. For a century now, we have been singing war songs about addicts. It occurred to me as I wiped his brow, we should have been singing love songs to them all along.

 

 

The full story of Johann Hari’s journey — told through the stories of the people he met — can be read in Chasing The Scream: The First and Last Days of the War on Drugs, published by Bloomsbury. The book has been praised by everyone from Elton John to Glenn Greenwald to Naomi Klein. You can buy it at all good bookstores and read more at www.chasingthescream.com.

Johann Hari will be talking about his book at 7pm at Politics and Prose in Washington DC on the 29th of January, at lunchtime at the 92nd Street Y in New York City on the 30th January, and in the evening at Red Emma’s in Baltimore on the 4th February.

The full references and sources for all the information cited in this article can be found in the book’s extensive end-notes.

If you would like more updates on the book and this issue, you can like the Facebook page: https://www.facebook.com/chasingthescream

What Makes you Healthy?? Conventional vs Natural Medicine

GOTTA SEE THIS SHORT VIDEO about Naturopathic medicine, no mention of God by the way, at “God made dirt”…Really terrific!

What Makes you Healthy?? Conventional vs Natural Medicine.

"While I breathe, I hope"– Surviving Schizophrenia

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