Detailed info on diagnosis and treatment of panic disorder and phobias in children and adolescents.

Panic attacks can occur in the context of several psychiatric conditions. A panic attack is a time-limited intense episode in which the individual experiences feelings of dread accompanied by physical sensations. Panic attacks usually average a couple of minutes but can last as long as 10 minutes and occasionally longer. Some really feel that they are about to die or have a serious medical problem. Children tend to have less insight than adults. Children may also be less articulate in describing their symptoms.

Common symptoms of a panic attack include:

• Chest pain
• Excessive perspiration
• Heart palpitations
• Dizziness
• Flushing
• Tremor
• Nausea
• Numbness in extremities
• Choking sensation or shortness of breath
• Feeling that one is not entirely in reality
• Extreme anxiety
• Fear that one is going to die
• Fear that one will become insane or lose control.

Panic Disorder is more likely to start in late adolescence or in adulthood. However, it can occur in children. The incidence of panic disorder with or without agoraphobia is lower than the incidence of simple phobia in children and adolescents.

Biederman and colleagues diagnosed panic disorder in 6% and agoraphobia in 15% of children and adolescents referred to a pediatric psychopharmacology clinic. Many of the children with panic disorder also had agoraphobia. The children with panic or agoraphobia had a high rate of co-morbid depression, and other anxiety disorders. However they also had a high incidence of disruptive behavior disorders such as Conduct Disorder and ADHD. The course of the panic disorder and agoraphobia appeared to be chronic.

Studies of adult panic disorder indicate that there is a high incidence of suicidal behavior, especially when it is accompanied by depression. Adults with panic disorder have an increased incidence of substance abuse. Thus one must look closely for the presence of other psychiatric disorders and make sure that the child or adolescent gets treatment. One should also screen for substance abuse.

A child with panic disorder should have a careful medical screening. It may be appropriate to screen for thyroid problems, excessive caffeine intake, diabetes and other conditions. Some sensitive individuals might have a panic-like reaction to certain asthma medications.

Treatment of panic disorder: Both medication and therapy have been used effectively. In children and adolescents with mild or moderate anxiety, it makes sense to start first with psychotherapy. If this is only partially effective, medication may be added. In children with severe anxiety or with co-morbid disorders, one might start therapy and medications simultaneously. Medications are similar to those used for adults. These would include SSRI medications (such as fluoxetine, fluvoxamine, , and paroxetine.) Individuals with panic disorder often respond to much lower doses of SSRIs, and may not do as well if started off with higher doses. Other medications used include beta blockers such as propranolol, the tricyclics (such as Nortriptyline), and occasionally the benzodiazepines (such as clonazepam.)

Psychotherapy: Individuals benefit from regular meals, adequate sleep, regular exercise and a supportive environment. One might teach the individual to use deep abdominal breathing and other relaxation techniques. Once real medical causes have been ruled out, the individual should remind himself that the symptoms are frightening but not dangerous. The person should learn to label the episode as a panic attack and understand it as an exaggeration of a normal reaction to stress. The person should not try to fight the episode, but should simply accept that it is happening and is time limited. Some learn to go outside themselves and rate the symptoms on a scale of 1-10. The individual should be encouraged to stay in the present and notice what is going on in the here and now.

If agoraphobia is present, the child should make up a hierarchy of fear-inducing situations. With help from parents and therapists, the child should move up the hierarchy of feared situations.

Simple Phobias in Children

Simple phobias are fairly common in children. Phobias often begin in childhood. Many do not cause significant life impairment and thus would not meet criteria for a formal psychiatric diagnosis. Milne et al found 2.3% of young adolescents in a community sample met criteria for a clinical phobic disorder. However, a much larger number, 22% had milder phobic symptoms. Girls had a higher rate than boys, and African Americans had a higher rate than Caucasians. Individuals with more severe phobias were more likely to have other psychiatric diagnoses than those with milder phobias.

The therapist should work with a parent or other responsible adult to gradually desensitize the child to the feared object. Relaxation training is helpful here too.

References

• Biederman, J et al, Panic Disorder and Agoraphobia in Consecutively Referred Children and Adolescents, Journal of the American Academy of Child and Adolescent Psychiatry, Vol. 36, No. 2, 1997.
• Clark, D.B. et al, Identifying Anxiety Disorders in Adolescents Hospitalized for Alcohol Abuse or Dependence, Psychiatric Services, Vol. 46, No. 6, 1995.
• Milne, J.M. et al, Frequency of Phobic Disorder in a Community Sample of Young Adolescents, Journal of the American Academy of Child and Adolescent Psychiatry, 34:9-13. 1995.

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By Wayne Lax
Without Restraint
Spring 2000

I spent 25 years in a state of confusion and despair. My brother died and I turned to alcohol. I had 108 admissions, and approximately 80 ECT treatments. They were treating me for an addiction; they did this with ECT treatments; the doctors kept giving me more and more medication (every drug under the sun), up to 17 different pills per day. As a result of the shock treatments, I am missing large portions of my memory and suffer chronic severe back pain from not enough relaxants. My children suffered from the effects of a loss of a parent. My friends didn't know how to respond to my behaviour, the hallucinations and delusions. They (Psychiatrists) would shock me, get me all medicated up and send me home where I would drive a taxi. Finally after 25 years of this hell, I ended up in a bad car crash. I was charged and convicted of impaired driving. It was the best thing that could have happened to me ... It was the beginning of the end. I stopped taking all the meds, refused any more shock, and then a year later - quit drinking. I have not been in a hospital since, except to visit. Still, today when I walk down the halls of Lakehead Psychiatric Hospital (LPH), patients come up to me and say "Hi", they know me, but I have no idea of who they are. They don't even look familiar. They say I spent a lot of time with them, but I have no memory. Part of me is missing forever. They treat us like guinea pigs, trying anything on us with no concern about the damage they do. Why do we give them this power? Why is it that medical doctors, whom are not experts on mental health, can prescribe any psycho tropic agents, even against a psychiatrist's advice? Why aren't they required to learn more about mental illnesses before they go around diagnosing and drugging us? I am not saying there aren't competent professionals, or that you shouldn't listen to your doctor. What I'm saying is that you should make sure you are making an informed decision, and ensure that the communication is there between your psychiatrist and GP. During my 25 years in the mental health system, some "professionals" recommended that I be taken off all the drugs, given no- more shock and receive proper counseling. My GP chose to ignore this advice without even informing me of their recommendations. This is unacceptable. What has personally helped me is counseling and the peer support I receive from the self-help group that I am actively involved with. I am dead against ECT under any circumstances. Even with the people it helps, the results are short-lived and the side effects long term. Why would delivering electricity through a brain be anything less than destructive and damaging?

If you would like to contact me, please e-mail me at seps@voyageur.ca or fax me at 807-468-2220.

Or write me at:
Wayne Lax
Comp. 4, Site 297, RR#2
Kenora, Ontario
P9N 3W8

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The issue of informed consent for ECT is a hot one. The problem with the informed consent statements that exist today is that they just aren't honest. They gloss over the main points about ECT - that's it is a temporary fix, and that memory/cognitive damage does occur.

In a continuing education course for ECT practitioners, Max Fink tells participants they are legally safe by using the informational pamphlets from the ECT machine manufacturers, plus videotapes (he does go a little bonkers in self-love, envisioning himself a TV star - kind of comical).

If you can write in your chart that the family saw the Mecta booklet, "you're home free" legally, says Fink, in advising these guys on how to protect themselves in case of lawsuit.

That's what's important - protection. Fink goes on to explain how to "save yourself the hassle of consent."

This audio clip requires the Real Player, available for free download at http://www.real.com (you can try and use Windows Media Player, but you do so at your own risk. It may or may not work, and please don't write me telling me it won't work if you're not using the REAL PLAYER!)

Here are some examples of informed consent forms and informational booklets given to patients.

First, read what a doctor who runs informedconsent.org has put together as a model informed consent form. This eye doctor says: "So that I may clearly state the content and conditions of my consent to permit medical and surgical procedures, I write my orders at home and bring them to the treatment facility. My orders override any and every blanket consent form I am asked to sign. Make them a permanent part of my medical record and provide me the following choices:" and then goes on to list everything in detail. I suggest that if you or a loved one is considering ECT, you adapt this kind of language into your own consent form and insist on these measures. This will make YOU a truly INFORMED consumer, and not just a submissive patient at the mercy of the powers that be.

From Dr. Richard Abrams, a sample statement from his book "Electroconvulsive Therapy," the bible for ECT practitioners. Abrams explains how to reduce your risk of litigation. (if you're an ECT doc) Here is a copy of the Somatics (Abrams' company) brochure for patients. Please do NOT take this as serious information about ECT. This is what Somatics (leading manufacturer of ECT machines and accessories) gives/sells to doctors/hospitals who do ECT. What Abrams writes in this brochure to patients and families is not even close to what he tells doctors. If in the brochure, he says 2 plus 2 equals nine, in his book to docs, he says 2 plus 2 equals four. One of these days I'll try and put up a lengthy critique, but you can do it yourself if you read the literature and compare it to what this brochure says.

Outside
Inside (sorry about the coffee stains)

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Timeline of Events

Kathleen Garrett's doctor Ricky Mofsen, DO, says he wants her to have ECT. She says no. He takes her to court.

The judge rules Mofsen may shock her against her will.

Treatments begin, but Kathleen is transferred from Southpointe to Des Peres Hospital (both owned by Tenet) because the shock machine breaks.

Kathleen Garrett repeatedly states she wants no more shock treatments. Complains of paralysis in her legs, but says nurses ignored her.

Son Steve Vance makes contact with activists who begin a public campaign to stop the forced shock!

Des Peres hospital is "deluged" with email, phone calls and faxes demanding that this forced treatment stop immediately.

Hospital appears to concede and calls Steve the next morning to say she'll be released the following day.

Surprise early morning shock outrages the world, after hospital had said it would release her.

Kathleen states numerous times that hospital staff tried to coerce her into signing a statement saying she wanted more shock.

Steve becomes convinced that the early morning shock was extreme because his mother is so much more confused than after the previous shocks.

Staff from Des Peres begin to call Kathleen, forcing Steve to change her number. (The concern is that they will again try to coerce her into saying she wanted more shock)

Kathleen is now being harassed over a $3,200 medical bill, with threats of ruining her credit and taking her to court. Her son says this is adding to her stress and has asked that they leave her alone. He says he has been met with nothing but rudeness and hatred, and that the minute he calls, they "know who I am."

He is becoming so concerned with her safety after learning of Tenet's history that he is now seriously considering moving his mother to nearby Illinois. "I can't believe how they've behaved," says Steve. "These aren't people who care. They only care about my mother's money!"

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Find out how parents can deal with child's anxiety and help their child.

Watching a child struggling with anxiety can be very difficult for parents. Anxiety may begin to color their perception of their child and convince them that he can't do things that he really can. Many parents find it helpful to keep track of the child's accomplishments and abilities so that they don't begin thinking of their child as anxious and fearful. Instead they can recognize what abilities their child has that might be useful in dealing with anxiety.

It is particularly helpful for parents to find out how the anxiety is frightening their child so that they can help develop counter-tactics. Here are some examples of how some parents helped when anxiety threatened sleep:

• When Maureen discovered that anxiety flooded 5-year-old Erica with worries that kept her from sleeping, she gave Erica a set of Mexican worry dolls and suggested that Erica tell each doll a problem at bedtime so that the dolls could solve them while she slept
• When 11-year-old Lisa told Ron and Elaine that fear of "something happening" kept her awake at overnights, they suggested that, in her imagination, she station each of her parents at the foot of her bed. This way they could guard her through the night.

It is also helpful for parents to keep track of times when their child is in charge of his life and the anxiety does not veer him off course. They can remind the child of those times and even celebrate these successes together to give him hope.

Questions for Parents

• Can you identify the tricks anxiety is using against your child? What are counter-tactics that would be appropriate for his age and interests?

• What does your child do that is helpful when anxiety is becoming present? Can you help create more contexts where this could happen or find ways to help him notice these times?

• If you believe that your child is experiencing pressure, can you speak to her about being satisfied with her accomplishments, without letting perfectionism, competition, or stress take over?

• Are there ways that your family can focus more on fun and less on performance?

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Strategies to guide parents in helping your child deal with his fears and anxieties.

Parents can help children develop the skills and confidence to overcome fears so that they don't evolve into phobic reactions. The following steps will guide you in helping your child deal with his fears and anxieties.

Recognize that the fear is real. As trivial as a fear may seem, it feels real to the child and it is causing him to feel anxious and afraid. "Being able to talk about fears can help," says Katharina Manassis, MD, author of Keys to Parenting Your Anxious Child. "Words often take some of the power out of emotion; if you can give the fear a name it becomes more manageable. As with any negative feeling, the more you talk about it, the more it becomes less powerful."

Never belittle the fear as a way of forcing the child to overcome it. Telling a child, "Don't be ridiculous! There are no monsters in your closet!" may get him to go to bed, but it won't make the fear go away.

However, don't cater to fears. If your child doesn't like dogs, don't cross the street deliberately to avoid one. This will reinforce that dogs should be feared and avoided.

Teach the child how to rate fear. If your child can visualize the intensity of the fear on a scale of 1 to 10, with 10 being the strongest, he may be able to "see" the fear as less intense than first imagined. Younger children can think about how "full of fear" they are, with being full "up to my knees" as not so scared, "up to my stomach" as more frightened, and "up to my head" as truly petrified.

Teach coping strategies. Try these easy-to-implement techniques. Using you as "home base," the child can venture out toward the feared object, and then return to you for safety before venturing out again. The child can also learn some positive self-statements, such as "I can do this" and "I will be OK," which he can say to himself when he feels anxious. Relaxation techniques are helpful as well, including visualization (of floating on a cloud or lying on a beach, for example) and deep breathing (imagining that the lungs are balloons and letting them slowly deflate).

The key to resolving fears and anxieties is to overcome them. Using these suggestions, you can help your child better cope with life's situations.

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Donald I. Templer and David M. Veleber
Clinical Neuropsychology (1982) 4(2): 62-66

Literature relevant to the question of whether ECT permanently injures the brain was reviewed. Similar histological findings of epileptics and patients who had received ECT were discussed. Experimental research with animals seems to have demonstrated both reversible and nonreversible pathology. Psychological test findings, even when attempting to control for possible pre-ECT differences, seem to suggest some permanent cognitive deficit. Reports of spontaneous seizures long after ECT would appear to point to permanent brain changes. Human brain autopsies sometimes indicate and sometimes do not indicate lasting effects. It was concluded that vast individual differences are salient, that massive damage in the typical ECT patient is unlikely, and that irreversible changes probably do occur in some patients.

This review centers around five areas germane to the question of whether electroconvulsive therapy (ECT) causes permanent brain pathology. Relatively indirect evidence is provided by two of these areas, the brain condition of epileptics and the examination of animal brains after experimental ECT. The other three areas are psychological testing findings with history of many ECTs, spontaneous seizures, and autopsy findings. The review does not concern the extensive literature that shows that ECT temporarily impairs cognitive functioning. Such literature eventually shows impairment beginning with the first ECT and becoming progressively worse with succeeding treatments. Improvement occurs following the course of ECT, sometimes with the tested functioning actually being higher than the pretreatment level, which is presumed to have been impaired by psychopathology such as thought disorder and depression. Reviews of this literature can be found elsewhere (American Psychiatric Association, 1978; Campbell, 1961; Dornbush, 1972; Dornbush and Williams, 1974; Harper and Wiens, 1975), as can reviews indicating that the unilateral ECT (applied to the right side) in increasing usage in recent years causes less impairment than bilateral ECT (American Psychiatric Association, 1978; d'Elia, 1974; Hurwitz, 1974; Zamora and Kaelbing, 1965). This literature is really not very relevant to the central issue of our review. It has never been disputed that cognitive impairment occurs after ECT. Even the most fervent and excathedra defenders acknowledge that "temporary" impairment occurs. It is the issue of permanency that has been controversial.

THE BRAINS OF EPILEPTICS

It would seem that if an epileptic grand mal seizure produces permanent brain changes, then an electrically induced convulsion should also do so. In fact, inspecting the evidence with respect to epileptics may provide us with a conservative perspective in regard to ECT since the latter could produce damage from the externally applied electrical current as well as from the seizure. Experimental research with animals has shown that the electric shocks (not to the head) produce more deleterious effects in the central nervous system than any other locality or system of the body. More pertinent are the studies of Small (1974) and of Laurell (1970) that found less memory impairment after inhalant induced convulsions than ECT. And, Levy, Serota and Grinker (1942) reported less EEG abnormality and intellectual impairment with pharmacologically induced convulsions. Further argument provided by Friedberg (1977) is the case (Larsen and Vraa-Jensen, l953) of a man who had been given four ECTs, but did not convulse. When he died three days later, a subarachnoid hemorrhage was found in the upper part of the left motor region at the site where an electrode had been applied.

A number of post-mortem reports on epileptics, as reviewed by Meldrum, Horton, and Brierley (1974) have indicated neuronal loss and gliosis, especially in the hippocampus and temporal lobe. However, as Meldrum et al. pointed out, on the basis of these post-mortem reports, one does not know whether the damage was caused by the seizures or whether both were caused by a third factor intrinsic to the epilepsy. To clarify this issue, Meldrum et al. pharmacologically induced seizures in baboons and found cell changes that corresponded to those in human epileptics.

Gastaut and Gastaut (1976) demonstrated through brain scans that in seven of 20 cases status epilepticus produced brain atrophy. They reasoned that "Since the edema and the atrophy were unilateral or bilateral and related to the localization of the convulsions (unilateral or bilateral chronic seizures), the conclusion can be drawn that the atrophic process depends upon the epileptic process and not on the cause of the status."

A common finding in epileptics and ECT patients is noteworthy. Norman (1964) stated that it is not uncommon to find at autopsy both old and recent lesions in the brains of epileptics. Alpers and Hughes (1942) reported old and recent brain lesions associated with different series of ECT.

ANIMAL BRAINS

There are a number of articles concerning the application of ECT and subsequent brain examination in animals. In the 15 study review of Hartelius (1952), 13 of the 15 reported pathological findings that were vascular, glial or neurocytological, or (as was generally the case) in two or three of these domains. However, as Hartelius pointed out, inferences of these studies tended to be conflicting because of different methods used and because of deficient controls. The research that Hartelius himself carried out was unquestionably the outstanding study in the area with respect to methodological sophistication and rigor. Hartelius employed 47 cats; 31 receiving ECT, and 16 being control animals. To prevent artifacts associated with the sacrificing of the animals, the cerebrums were removed under anesthesia while the animals were still alive. Brain examinations were conducted blindly with respect to ECT vs. control of subject. On a number of different vascular, glial, and neuronal variables, the ECT animals were significantly differentiated from the controls. The animals that had 11-16 ECTs had significantly greater pathology than the animals that had received four ECTs. Most of the significant differences with respect to reversible type changes. However, some of the significant differences pertained to clearly irreversible changes such as shadow cells and neuronophagia.

PSYCHOLOGICAL TEST FINDINGS WITH HISTORY OF MANY ECTS

There have been several studies regarding the administration of psychological tests to patients with a history of many ECTs. Unfortunately, all were not well controlled. Rabin (1948) administered the Rorschach to six chronic schizophrenics with a history of from 110 to 234 ECTs. Three patients had 6, two had 4, and one had 2 Piotrowski signs. (Piotrowski regards five or more as indicating organicity.) However, control subjects were not employed. Perlson (1945) reported the case of a 27-year-old schizophrenic with a history of 152 ECTs and 94 Metrozol convulsions. At age 12 he received an IQ of 130 on the Stanford Achievement Test; at age 14 an IQ of 110 on an unspecified general intelligence test. At the time of the case study, he scored at the 71st percentile on the Otis, at the 65th percentile on the American Council on Educational Psychological Examination, at the 77th percentile on the Ohio State Psychological Examination, at the 95th percentile for engineering freshman on the Bennett Test of Mechanical Comprehension, at the 20th percentile on engineering senior norms and at the 55th percentile on liberal arts students' norm on a special perception test. These facts led Perlson to conclude that convulsive therapy does not lead to intellectual deterioration. A more appropriate inference would be that, because of the different tests of different types and levels and norms given at different ages in one patient, no inference whatsoever is justified.

There are two studies that provide more methodological sophistication than the above described articles. Goldman, Gomer, and Templer (1972) administered the Bender-Gestalt and the Benton Visual Retention Test to schizophrenics in a VA hospital. Twenty had a past history of from 50 to 219 ECTs and 20 had no history of ECT. The ECT patients did significantly worse on both instruments. Furthermore, within the ECT groups there were significant inverse correlations between performance on these tests and number of ECTs received. However, the authors acknowledged that ECT-caused brain damage could not be conclusively inferred because of the possibility that the ECT patients were more psychiatrically disturbed and for this reason received the treatment. (Schizophrenics tend to do poorly on tests of organicity.) In a subsequent study aimed at ruling out this possibility, Templer, Ruff, and Armstrong (1973) administered the Bender-Gestalt, the Benton, and the Wechsler Adult Intelligence Scale to 22 state hospital schizophrenics who had a past history of from 40 to 263 ECTs and to 22 control schizophrenics. The ECT patients were significantly inferior on all three tests. However, the ECT patients were found to be more psychotic. Nevertheless, with degree of psychosis controlled for, the performance of the ECT patients was still significantly inferior on the Bender-Gestalt, although not significantly so on the other two tests.

SPONTANEOUS SEIZURES

It would appear that if seizures that were not previously evidenced appeared after ECT and persisted, permanent brain pathology must be inferred. There have been numerous cases of post-ECT spontaneous seizures reported in the literature and briefly reviewed by Blumenthal (1955, Pacella and Barrera (1945), and Karliner (1956). It appears that in the majority of cases the seizures do not persist indefinitely, although an exact perspective is difficult to obtain because of anticonvulsant medication employed and the limited follow-up information. another difficulty is, in all cases, definitively tracing the etiology to the ECT, since spontaneous seizures develop in only a very small proportion of patients given this treatment. Nevertheless, the composite of relevant literature does indicate that, at least in some patients, no evidence of seizure potential existed before treatment and post-ECT seizures persist for years.

An article that is one of the most systematic and representative in terms of findings is that of Blumenthal (1955) who reported on 12 schizophrenic patients in one hospital who developed post-ECT convulsions. Six of the patients had previous EEGs with four of them being normal, one clearly abnormal, and one mildly abnormal. The patients averaged 72 ECTs and 12 spontaneous seizures. The time from last treatment to first spontaneous seizure ranged from 12 hours to 11 months with an average of 2 and 1/2 months. The total duration of spontaneous seizures in the study period ranged from 1 day to 3 and 1/2 years with an average of 1 year. Following the onset of seizures, 8 of the 12 patients were found to have a clearly abnormal, and 1 a mildly abnormal EEG.

Mosovich and Katzenelbogen (1948) reported that 20 of their 82 patients had convulsive pattern cerebral dysrhythmia 10 months post ECT. None had such in their pre-treatment EEG. Nine (15%) of the 60 patients who had 3 to 15 treatments, and 11(50%) of the 22 patients who had from 16 to 42 treatments had this 10 month posttreatment dysrhythmia.

HUMAN BRAIN AUTOPSY REPORTS

In the 1940s and 1950s there were a large number of reports concerning the examination of brains of persons who had died following ECT. Madow (1956) reviewed 38 such cases. In 31 of the 38 cases there was vascular pathology. However, much of this could have been of a potentially reversible nature. Such reversibility was much less with the 12 patients who had neuronal and/or glial pathology. The following are the comments pertaining to the neuronal and glial pathology and the amount of time between last treatment and death: "Gliosis and fibrosis" (5 months); "Small areas of cortical devastation, diffuse degeneration of nerve cells", "Astrocytic proliferation" (1 hour, 35 minutes); "Small areas of recent necrosis in cortex, hippocampus and medulla", "Astrocytic proliferation" (immediate); "Central chromatolysis, pyknosis, shadow cells (15 to 20 minutes); "Shrinking and swelling. ghost cells", "Satellitosis and neuronophagia" (7 days); "Chromatolysis, cell shrinkage''. "Diffuse gliosis, glial nodules beneath the ependyma of the third ventricle" (15 days); "Increased Astrocytes" (13 days); "Schemic and pyknotic ganglion cells" (48 hours); "Pigmentation and fatty degeneration, sclerotic and ghost cells", "Perivascular and pericellular gliosis" (10 minutes); "Decrease in ganglion cells in frontal lobes, lipoid pigment in globus pallidus and medical nucleus of thalamus", "Moderate glial proliferation" (36 hours); "Glial fibrosis in marginal layer of cortex, gliosis around ventricles and in marginal areas of brain stem, perivascular gliosis in white matter" (immediate); "Marginal proliferation of astrocytes, glial fibrosis around blood vessels of white matter, gliosis of thalamus, brain stem and medulla" (immediate). In one case the author (Riese, 1948), in addition to giving the neuronal and glial changes, reported numerous slits and rents similar to that seen after execution. Needless to say, patients who died following ECT are not representative of patients receiving ECT. They tended to be in inferior physical health. Madow concluded, on the basis of these 38 cases and 5 of his own, "If the individual being treated is well physically, most of the neuropathological changes are reversible. If, on the other hand, the patient has cardiac, vascular, or renal disease, the cerebral changes, chiefly vascular, may be permanent."

CONCLUSION

A wide array of research and clinical based facts that provide suggestive to impressive evidence in isolation, provide compelling evidence when viewed in a composite fashion. Some human and animal autopsies reveal permanent brain pathology. Some patients have persisting spontaneous seizures after having received ECT. Patients having received many ECTs score lower than control patients on psychological tests of organicity, even when degree of psychosis is controlled for.

A convergence of evidence indicates the importance of number of ECTs. We have previously referred to the significant inverse correlations between number of ECTs and scores on psychological tests. It is conceivable that this could be a function of the more disturbed patients receiving more ECTs and doing more poorly on tests. However, it would be much more difficult to explain away the relationship between number of ECTs received and EEG convulsive pattern dysrhythmia (Mosovich and Katzenelbogen, 1948). No patients had dysrhythmia prior to ECTs. Also difficult to explain away is that in Table I of Meldrum, Horton and Brierley (1974), the nine baboons who suffered brain damage from experimentally administrated convulsions tended to have received more convulsions than the five that did not incur damage. (According to our calculations, U=9, p < .05 ) And, as already stated, Hartelius found greater damage, both reversible and irreversible, in cats that were given 11 to l6 than in those given 4 ECTs.

Throughout this review the vast individual differences are striking. In the animal and human autopsy studies there is typically a range of findings from no lasting effect to considerable lasting damage with the latter being more of the exception. Most ECT patients don't have spontaneous seizures but some do. The subjective reports of patients likewise differ from those of no lasting effect to appreciable, although usually not devastating impairment. The fact that many patients and subjects suffer no demonstrable permanent effects has provided rationale for some authorities to commit the non-sequitur that ECT causes no permanent harm.

There is evidence to suggest that pre-ECT physical condition accounts in part for the vast individual differences. Jacobs (1944) determined the cerebrospinal fluid protein and cell content before, during, and after a course of ECT with 21 patients. The one person who developed abnormal protein and cell elevations was a 57-year-old diabetic, hypertensive, arteriosclerotic woman. Jacobs recommended that CSF protein and cell counts be ascertained before and after ECT in patients with significant degree of arteriosclerotic or hypertensive disease. Alpers (1946) reported, "Autopsied cases suggest that brain damage is likely to occur in conditions with pre-existing brain damage, as in cerebral arteriosclerosis." Wilcox (1944) offered the clinical impression that, in older patients, ECT memory changes continue for a longer time than for younger patients. Hartelius (1952) found significantly more reversible and irreversible brain changes following ECT in older cats than younger cats. Mosovich and Katzenelbogen (1948) found that patients with pretreatment EEG abnormalities are more likely to show marked post-ECT cerebral dysrhythmia and to generally show EEGs more adversely affected by treatment.

In spite of the abundance of evidence that ECT sometimes causes brain damage, the Report of The Task Force on Electroconvulsive Therapy of the American Psychiatric Association (1978) makes a legitimate point in stating that the preponderance of human and animal autopsy studies were carried out prior to the modern era of ECT administration that included anesthesia, muscle relaxants, and hyperoxygenation. In fact, animals which were paralyzed and artificially ventilated on oxygen had brain damage of somewhat lesser magnitude than, although similar patterns as, animals not convulsed without special measures. (Meldrum and Brierley, 1973; Meldrum, Vigourocex, Brierley, 1973). And it could further be maintained that the vast individual differences stressed above argue for the possibility of making ECT very safe for the brain through refinement of procedures and selection of patients. Regardless of such optimistic possibilities, our position remains that ECT has caused and can cause permanent pathology.

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Are panic attacks biological or mental? What causes anxiety and stress and creates a panic attack? Find out here.

Many people who have problems with anxiety and stress seem to have a heightened sensitivity to the environment and react more strongly to the stimuli around them. In some people, there may exist what's called a "deficit in their stimulus barrier," in other words, noises, action, movement, smells and sights in their surroundings may be more difficult for them to shut out than it is for most people.

Well, this would seem to suggest that panic attacks are biological in nature. Yet everything we've discussed so far has pointed to environmental and developmental causes of panic attacks. Could it be a combination of the two?

Are Panic Attacks Biological or Mental?

There are those who would make the argument that panic disorder is solely a biological phenomenon, whereas others would take the opposite stance and contend that panic is related solely to environment and developed personality traits.Most practicing psychotherapists tend to view a problem like panic disorder as being related to both human anatomy and human psychology. The interplay between inherited genetic trends, brain chemistry and a given character style in a given environment is what creates a panic attack. For further evidence to support the biochemistry side of the argument, let's look at the crucial anatomical components.

The Brain:
The brain is one of mankind's most perplexing puzzles. Despite being shrouded in mystery, the brain is slowly beginning to reveal important facts about itself. Scientists are making advances daily in the study of the human brain and the role that biochemical factors play in contributing to the development of psychiatric disorders. The two parts of the brain that scientists have concentrated on the most so far in this respect are the neurotransmitters and the amygdala.

Neurotransmitters:
Neurotransmitters are basically chemical messengers in the brain. Just like the various instant messaging systems on our computers, the neurotransmitters transfer information from one part of the brain to the other.

One biochemical explanation for panic is that there is an over-activity in what's called the locus ceruleus. The locus ceruleus is the part of the brain that triggers a response to danger. It's like our brain's alarm system. People who get panic attacks can be thought of as unwittingly sending alarms to this part of the brain. A trigger-happy locus ceruleus could wreak havoc with a person's perspective. We discussed "catastrophizing" in This is Not a Catastrophe in the context of behavioral choices. Faulty neurotransmitters would be a physical manifestation of "catastrophizing." The cause is different; the result is much the same.

What Happens After the Locus Ceruleus Sounds the Alarm?

Amygdala:
The amygdala is the part of the brain that holds old memories, feelings, sensations and emotions and then transmits this information to the rest of our bodies. It is in the amygdala that we store, among myriad other things, all of our primal memories of powerlessness and helplessness that we experienced during infancy and early childhood.

Well, when the neurotransmitters pick up over-activity in the locus ceruleus, the part of the brain that instructs us to run from danger, the amygdala hears the alarm, and instantly calls up the memories of past events that were dangerous and terrifying. The present danger may be, and most likely is, nothing compared to earlier dangers we've experienced, particularly the way we experienced danger as infants. But we nevertheless experience the fear as viscerally and as primally as we would if our very lives were at stake.

Many child development experts believe that early infancy can be a very scary time. Just imagine a 3-year-old playing in a sandbox, weighing about 40 pounds. He looks up and, instead of seeing his mother, can only -- even for a moment -- see other children and frightening adults all around him. Translate the weight difference into adult terms: for a tantamount experience you would have to be surrounded by a throng of beings who weighed 700 pounds each and stood 4 times as tall as you. That's exactly how minor dangers are perceived during a panic attack.

So, the amygdala goes into action, warning the heart to beat faster, instructing our breathing to become rapid, heightening all the biological components of the fight/flight response. Outcome: Full Blown Panic Attack.

Genetics of Panic:

There is some evidence of genetic pre-disposition to panic. About 20 to 25 percent of people with panic have close relatives with panic disorder. Often there is a deficit in the protein that transports serotonin, an important neurotransmitter in the regulation of mood and the ability to tolerate and process anxiety.

Another genetic defect that some people have is one which affects dopamine, another important neurotransmitter.

Other genetic mutations that affect other neurotransmitters are speculated about, but are not yet understood by medical science.

About the author: Mark Sichel is a Licensed Clinical Social Worker who has been practicing psychotherapy in New York City since 1980. He is also the author of the popular self-help book, Healing from Family Rifts.

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Clinical neuropsychology is a specialized field of endeavor which seeks to apply the knowledge of human brain-behavior relationships to clinical problems. Human brain-behavior relationships refer to the study of research-derived associations between an individual's behavior, both normal and abnormal, and the functioning of his or her brain. The clinical neuropsychologist takes extensive measurements of a variety of kinds of human behavior, including receptive and expressive language, problem-solving skills, reasoning and conceptualization abilities, learning, memory, perceptual-motor skills, etc. From this complex and detailed set of behavioral measurements, a variety of inferences can be drawn relating directly to the functioning of an individual's brain. In clinical neuropsychology, the operation and condition of an individual's brain is assessed by taking measures of his or her intellectual, emotional and sensory-motor functioning.

In studying brain functioning by measuring behavior, the clinical neuropsychologist makes use of a specialized set of tools which is appropriately labeled the clinical neuropsychological evaluation. This instrument is generally composed of numerous psychological and neuropsychological procedures which measure various abilities and skills. Some of these procedures are drawn from psychology (WAIS-R, Form Board in TPT) and others have been developed specifically from neuropsychological research (Category Test, Speech Sounds Perception Test, etc.). These strictly neuropsychological procedures compose the greater part of the evaluation, especially since they were developed specifically to assess brain functioning by measuring higher mental abilities. Still other procedures in the evaluation were borrowed directly from neurology (certain items on Aphasia Screening; Sensory Perceptual Examination) and were standardized in their administration. Some of the procedures in the evaluation are rather homogeneous in that they depend on mainly one ability or skill for success or failure (Finger Oscillation Test primarily relies on motor tapping speed). Other procedures are more heterogeneous and depend on the organized and complex interaction of several distinct skills or abilities for success (Tactual Performance Test - tactile perceptual ability; appreciation of two-dimensional space; planning and sequencing ability; etc.). In all, the clinical neuropsychological evaluation gives the practitioner in this field a wealth of information about an individual's unique pattern of skills and abilities.

The clinical neuropsychological evaluation has essentially two main purposes: one involving diagnosis and the other involving behavioral description. The diagnostic power of a neuropsychological instrument, such as the Halstead-Reitan Battery, has been well documented and need not be discussed in detail (Vega and Parsons, 1967; Filskov and Goldstein, 1974; Reitan and Davison, 1974). In neuropsychological diagnosis, the presence or absence of impairments in brain functioning can be determined along with other important factors, such as lateralization, localization, severity, acuteness, chronicity or progressivity, and type of impairment suspected of being present (tumor, stroke, closed head injury, etc.). Four primary methods of inference are utilized in making these determinations, namely, level of performance, pathognomonic sign, comparison of the two sides of the body and specific patterns of test scores.

The level of performance approach primarily involves determining how well or how poorly an individual performs on a certain task, usually by means of a numerical score. Cut-off scores are generally developed for such a task, which allow the practitioner to classify an individual as either impaired or unimpaired with respect to brain functioning, depending upon whether his score falls above or below the cut-off value in use. The Halstead Category Test provides an example of this level of performance approach. On this procedure, a score of 51 errors or above places an individual in the impaired range. Likewise, a score of 50 errors or below places the individual in the normal range generally characteristic of individuals with unimpaired brain functioning. The primary danger of using level of performance measures alone to diagnose brain dysfunction is that of classification errors. In most cases, the cut-off score will not completely separate individuals with brain dysfunction from those without. Therefore, both false-positive and false-negative errors can be expected, depending upon the particular cut-off score established. Such a procedure in fact used in isolation is tantamount to employing single tests to diagnose "brain damage, and this approach has been justly criticized in previous work (Reitan and Davison, 1974). Additional methods of inference are used in neuropsychological assessment in order to sharpen diagnosis and minimize errors.

The pathognomonic sign approach essentially involves identifying certain signs (or specific types of deficient performance) which are always associated with brain dysfunction whenever they occur. An example of such a pathognomonic sign would be an instance of dysnomia on Aphasia Screening made by an individual with a college degree and normal IQ values. Such an individual would not be expected to say "spoon" when shown a picture of a fork and asked to name this object. The appearance of a true pathognomonic sign in a neuropsychological evaluation can always be associated with some sort of impairment in brain functioning. However, the converse is not true. That is, the absence of various pathognomonic signs in a particular individual's record does not mean that this individual is free of brain dysfunction. Thus, using, the pathognomonic sign approach alone, one runs a considerable risk of making a false-negative error or discounting the presence of brain dysfunction when it in fact does exist. If other methods of inference are employed with this approach, however, then the likelihood is increased that any brain dysfunction present will be identified even in the absence of pathognomonic signs. Therefore, one may again see the value of and necessity for multiple and complimentary methods of inference in clinical neuropsychology.

The third method of inference involves a comparison of the performances of the two sides of the body. This method was borrowed in principle almost directly from clinical neurology but involves measurement of a variety of sensory, motor and perceptual-motor performances on the two sides of the body and comparing these measures with respect to their relative efficiency. Since each cerebral hemisphere governs (more or less) the contralateral side of the body, some idea of the functional condition of each hemisphere relative to the other can be gleaned from measuring the performance efficiency of each side of the body. An example here is the Finger Oscillation Test. Here, tapping speed in the dominant hand is compared with tapping speed in the non-dominant hand. If certain expected relationships are not obtained, then inferences with respect to the functional efficiency of one hemisphere or the other can be made. This inferential approach provides important corroborative and complementary information, especially with respect to lateralization and localization of brain dysfunction.

The final, method of inference to be discussed is that of specific patterns of performance. Certain scores and results may combine into particular patterns of performance which carry important inferential meaning for the clinician. For example, the relative absence of constructional dyspraxia, sensory-perceptual deficits, and aphasic disturbances, together with significant deficits on grip - strength, Finger Oscillation and the Tactual Performance Test, may possibly be associated with brain dysfunction which is more anterior in location than posterior. As another example, severe constructional dyspraxia with an absence of aphasic disturbances, together with severe sensory and motor losses in the left upper extremity, is likely associated with dysfunction in the right hemisphere rather than in the left.

Clinical neuropsychological diagnosis of brain dysfunction is carried out utilizing four primary methods of inference in a complex yet integrated fashion. Each of these methods is dependent upon and complementary to the others. The strength of neuropsychological diagnosis lies in the simultaneous utilization of these four methods of inference. Thus, some particular impairment in brain functioning may yield relatively normal levels of performance but, at the same time, may produce certain pathognomonic signs or yield patterns of performance which are clearly associated with brain dysfunction. The cross-checks and multiple avenues of gaining information, made possible by the simultaneous use of these four methods of inference, allow sound and accurate diagnosis of brain dysfunction by the experienced clinical neuropsychologist.

The second major purpose of clinical neuropsychology, as mentioned above, is behavioral description and delineation of behavioral strengths and weaknesses. This type of formulation can be most essential in making recommendations for an individual's treatment, disposition and management. This, in fact, is considered by some practitioners to be the most important function of the clinical neuropsychological evaluation. Behavioral description is the clinical neuropsychologist's unique input into a patient's total medical workup. Other specialists, notably the neurologist and neurosurgeon, are excellent neurological diagnosticians, and it is not the purpose of clinical neuropsychology to compete with these individuals or attempt to take their place. Thus, neuropsychological diagnosis can be considered an additional avenue of diagnostic input into a patient's workup. Behavioral description, on the other hand, is the clinical neuropsychologist's unique domain. Here, this practitioner can provide input into a patient's total medical picture which is not available from any other source.

Behavioral descriptions should start out with a thorough understanding of the patient's background, his educational level, his occupation, his age, his likes, dislikes, future plans, etc. This information is usually brought into play subsequent to a blind analysis of the patient's neuropsychological evaluation and a preliminary diagnosis and behavioral description based on this analysis. Before the final behavioral description and recommendations are given, however, the patient's background information is integrated into the formulation. Here, the clinical neuropsychologist can look at the particular patient's pattern of intellectual and adaptive strengths and weaknesses shown on the neuropsychological evaluation and integrate these findings with the patient's individual situation. This can be considered to be a very important process in terms of formulating specific, meaningful and directly applicable recommendations for the particular individual under study.

Specific issues which often warrant coverage in neuropsychological behavior description involve a variety of areas. From the clinical neuropsychological evaluation, specific areas in need of rehabilitation can be identified, as well as areas of behavioral strength which warrant the individual's awareness. Advice on coping with environmental demands in the face of particular behavioral deficits is often necessary, as well as some realistic prediction of future change in neuropsychological status. The degree of behavioral deficit in various areas can often be specified and questions with respect to a patient's ability to manage himself and behave adaptively in society can be answered directly. Forensic issues can often be dealt with in terms of providing direct, clear information with respect to a patient's judgment, competence, degree of intellectual and adaptive loss following brain disease or trauma, etc. Other specific areas in which the clinical neuropsychological evaluation can provide input include educational potential, occupational potential, the effects of brain dysfunction on social adjustment, etc. The importance of the behavioral picture of a patient obtained from the neuropsychological evaluation is immense.

As mentioned above, the clinical neuropsychological evaluation is not meant to compete with or take the place of more traditional medical procedures. In fact, certain important differences exist between the clinical neuropsychological evaluation and these procedures. First of all, the neuropsychological evaluation is primarily concerned with higher mental abilities, such as language, reasoning, judgment, etc. Traditional neurology, on the other hand, emphasizes assessment of sensory and motor functions and reflexes. Thus, although the neurologist and neuropsychologist study the same general phenomenon, that is, nervous system function and dysfunction, these practitioners nevertheless emphasize different aspects of this phenomenon. The clinical neuropsychologist takes precise and specific measurements of a variety of aspects of higher cortical functioning. The neurologist, on the other hand, primarily concentrates on lower-level phenomena of nervous system functioning. The results of these two types of evaluation may not always agree, given the different aspects of the central nervous system emphasized and the different methods and procedures used by each of these practitioners. Logically, the clinical neuropsychological assessment and the neurological evaluation should be considered complementary to each other. Certainly, neither one is a substitute for the other. Where possible, both of these procedures should be employed in order to obtain a full and detailed picture of an individual's central nervous system functioning.

Traditional psychological assessment procedures and the clinical neuropsychological evaluation also have a number of differences worth noting. In traditional psychological assessment, for example, an individual's average or modal performance is usually desired. On the neuropsychological evaluation, however, the examiner strives to obtain an individual's best or optimal performance. Considerable encouragement and positive support is given to the patient during a neuropsychological evaluation to perform as well as possible. Such encouragement is generally not given under traditional psychological assessment conditions. Additionally, psychological procedures, such as the Rorschach, MMPI, Wechsler Intelligence Scales, Draw-A-Person, etc., have traditionally been used by psychologists who diagnose brain damage and disease. Although each of these procedures may contribute significant information about a person's behavior, their validity in detecting the presence or absence of brain dysfunction and determining the nature and location of the dysfunction is rather limited. These assessment procedures have not been developed specifically for the purpose of identifying and describing brain damage and disease. The clinical neuropsychological evaluation, on the other hand, has been developed specifically for this purpose and has been validated against stringent medical criteria, such as surgical findings and autopsy reports. In addition, traditional psychological assessment procedures generally do not make use of the multiple inferential methods employed by the clinical neuropsychological evaluation. Oftentimes, only one or at most two inferential methods are used with traditional psychological assessment procedures in making determinations of the presence or absence of brain dysfunction. Thus, the comprehensive approach to making inferences and drawing conclusions used by the clinical neuropsychologist is felt to be superior to more traditional psychological methods in the diagnosis and description of brain dysfunction.

References

Filskov, S. & Goldstein, 5. (1974). Diagnostic validity of the Halstead-Reitan Neuropsychological Battery. Journal of Consulting and Clinical Psychology, 42(3), 382-388.

Lezak, M.D. (1983). Neuropsychological Assessment. New York: Oxford University Press.

Reitan, R.M. & Davidson, L..A. (1974). Clinical Neuropsychology: Current Status and Applications Washington: VJ-I. Winston & Sons.

Vega, A., & Parsons, 0. (1967). Cross-validation of the Halstead-Reitan Tests for brain damage. Journal of Consulting Psychology, 3 1(6), 6 19-625.

Dr. Alan E. Brooker is a clinical neuropsychologist with the Department of Mental Health at the David Grant USAF Medical Center. Travis Air Force Base, CA. 94535.

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From Linda Andre

On Friday, May 18th, the New York State Assembly held public hearings on electroshock. Among those testifying was psychologist Harold Sackeim. Sackeim, dubbed the nation's "electroshock czar", receives tens of millions of dollars in federal funding to research electroshock. He has an exclusive grant to investigate the adverse effects of ECT, which he has held for 20 years. (He has also "consulted" for the shock machine manufacturers continuously over these years.) He's known as the foremost proponent of electroshock in the world.

Sackeim claimed that in his 20 years of shocking people he has never seen even one case in which ECT has had a permanent effect on memory function (anterograde memory).

He stated:

"I invite anyone in the country who believes ECT's had a deleterious effect on their cognition to come to us for an evaluation."

In the interests of science, let's take him on up on this offer---made before a large audience, recorded on tape and in official transcripts! Please write, call, fax or email Harold Sackeim. Tell him you had ECT, and you are responding to his request to evaluate people who experienced adverse cognitive effects.Ask for an appointment for an evaluation. (Don't worry about paying for it---he's got plenty of grant money to study ECT survivors.)

It is important to make a record of your request. If you email, send a copy to Committee for Truth in Psychiatry at ctip@erols.com. You may mail a copy to CTIP at P.O. Box 1214, New York, NY 10003. If possible, it's a good idea to send your request for an evaluation by certified mail.

Harold Sackeim, PhD
Chief, Dept. of Biological Psychiatry
New York State Psychiatric Institute
1051 Riverside Drive
New York, NY 10032-2965

Telephone: (212) 543-5855 (it can be difficult to reach him on this number sometimes) or (914) 238-8613
Fax: (212) 543-5854

email: has1@columbia.edu

Harold has repeatedly said that he would never even try to study persons who experienced permanent adverse memory effects from ECT because such persons are so "rare" he could never find enough of us for a study. Let's show him he's wrong.

Linda Andre
CTIP Director

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