Venlafaxine for Autistic Disorders in Young Persons /4 Abstracts

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SCIENCE AND MEDICINE

Also: Four New Autism Research Abstracts

Venlafaxine for Autistic Disorders in Young Persons

[Associated FEAT Daily Newsletter editor offers her

comments and a research abstract on the drug Venlafaxine (Effexor).]

http://www.alertpubs.com/april2000csa.htm

This report of Effexor's usefulness in autism is good news, but I

wanted to add that two psychiatrists have told me that it's very difficult

to for patients to withdraw from Effexor. Both of these physicians had had

patients become psychotic during their withdrawals. My understanding is that

these patients were adults with depression, none of whom had experienced

psychosis in the past (although I haven't fact-checked this).

I haven't heard of autistic children becoming psychotic when

withdrawing from Effexor, but on the other hand I've only known one child

with autism who was taking it.

I was also told, by a 3rd psychiatrist, that a general principle

concerning side effects is that the more problems your brain has to begin

with, the more likely you are to suffer all the possible untoward effects of

a medication and then some.

In other words, the more problems you have to begin with, the more

problems you're going to have with the medications that treat your problems.

Another one of life's little ironies.

This psychiatrist, who has a specialty in autism, was responding to an

audience question concerning whether people with autism are more likely to

develop tardive dyskinesia while taking antipsychotics than other patient

populations. This idea floats through the psychiatric community.

His answer was yes; and he said that the reason for autistic people's

added vulnerability to side effects like tardive dyskinesia is that autistic

people are suffering more serious neurological differences than other

patients in the first place.

Important: these are the informal statements of 3 physicians . . . and

I for one am not convinced that the neurological differences of autism are

worse than those of schizophrenia. (I have no idea whether autistic brain

differences are or are not " worse " than schizophrenic differences; I'm just

saying I'm not sure anyone else knows this, either. I could be wrong.)

I've veered off-topic here because I don't want to be terrifying

parents who are giving their children Risperdal, the atypical neuroleptic

that has pretty much been a miracle drug for a lot of us. I believe there's

an entire generation of children who, just 10 years ago, would have been

placed out of home if it weren't for Risperdal--so, to those of you whose

children have had their lives given back to them by Risperdal, don't panic!

Recently a speaker at the Seaver conference addressed the issue of

tardive dyskinesia and Risperdal, saying that of all the many children she's

treated or known of taking long-term Risperdal, only one may be showing

signs of tardive dyskinesia. This was a girl who was taking an extremely

high dose, and had been for years.

Back to Effexor: assuming it's true that autistic children are more

likely to experience severe side effects than other children, it's possible

that autistic children are more likely to have severe withdrawals from

Effexor than others. (The psychiatrists I mentioned above did say that very,

very slow withdrawals from Effexor help . . . )

Again, I have no idea!

Just brightening up your day!

Venlafaxine for Autistic Disorders in Young Persons

http://www.alertpubs.com/april2000csa.htm

Both selective serotonin reuptake inhibitors and dopamine antagonists

are useful in treating autism. Although norepinephrine reuptake inhibitors

do not affect core autistic symptoms, they can reduce accompanying

hyperactivity. Venlafaxine (Effexor), a novel antidepressant, inhibits

reuptake of serotonin and dopamine and to a lesser extent norepinephrine.

Methods: A treatment review was undertaken in 10 patients (mean age 10

years, range 3–21 years, 9 males) with autism spectrum disorders (5 Asperger

’s syndrome, 4 autism, 1 pervasive developmental disorder, NOS) and various

comorbid disorders. All patients had been started on 12.5 mg venlafaxine

once daily and increased as tolerated. Two patients received concomitant

drugs during the study. The primary outcome measure for response was a

Clinical Global Impressions (CGI) score of very much or much improved.

Results: The mean length of treatment was 5 months, and the mean

dosage of venlafaxine was 25 mg/day (range 6–50 mg/day). Six of the 10

patients had CGI scores of " much improved " or " very much improved. " Some

improvements were noted in all 3 core areas of autistic spectrum disorders

(social deficits, communication and language impairments, and restricted

interests and repetitive behaviors), and in symptoms of associated features

such as ADHD. Five patients (responders and non-responders) experienced

behavioral activation which was transient in 3 and caused 2 patients to

discontinue medication.

Discussion: In this open-label study of children, adolescents, and

young adults with autism spectrum disorders, venlafaxine appeared to be an

effective agent for treating both core symptoms and associated symptoms,

such as ADHD. The positive findings of this trial suggest that a

prospective, double-blind, placebo-controlled trial is warranted. Hollander

E, Kaplan A, Cartwright C, Reichman D: Venlafaxine in children, adolescents,

and young adults with autism spectrum disorders: an open retrospective

clinical report. Journal of Child Neurology 2000;15 (February):132–135. From

Mount Sinai School of Medicine, New York, NY. Funded in part by the Seaver

Foundation.

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Clinico-Neurobiological Features and Therapy in Autism

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_ui

ds=11391966 & dopt=Abstract

1: No To Hattatsu 2001 May;33(3):238-40

[Article in Japanese]

Hashimoto T, Koeda T.

PMID: 11391966 [PubMed - in process]

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Sleep In Infantile Autism

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_ui

ds=11391493 & dopt=Abstract

1: Rev Neurol 2001 Apr 16;32(7):641-644

Abril Villalba B, Mendez M, Sans Capdevila O, Valdizan Uson JR.

Servicio de Neurofisiologia Clinica; Hospital Servet, Zaragoza,50009,

Espana.

INTRODUCTION. Analysis of nocturnal sleep in infantile autism has been

presented in various studies. However, there has been no systematization

including the different structural and paroxystic alterations at the same

time as permitting the development of a general theory of the effect of

sleep on prognosis and treatment, particularly in a spectrum in which there

is currently no definite solution.

DEVELOPMENT. A systematic review was made of the literature obtained

from publications included in MEDLINE and web pages of the last 25?years

using the key words: autism, Asperger s disorder, sleep, childhood and Rett

s syndrome. Altogether 21?papers fulfilled criteria for inclusion. Disorders

of sleep in infantile autism were classified into three types: immaturity of

sleep, showing a destructured polysomnographic recording and negative

correlation with the level of development; functional alterations of sleep

with early waking and difficulty in going to sleep being the disorders most

frequently seen; and paroxystic alterations with epileptiform discharges

being the commonest, without necessarily occurring together with seizures.

The opinions stated on questionnaires and the data observed on the

polysomnography were not in agreement.

CONCLUSIONS. Analysis of the literature has permitted us to make an

initial classification of sleep disorders in autistic children, and has

shown a marked presence of these disorders in the evolution of autistic

children. It is necessary that further studies being done, polysomnographic

rather than by means of questionnaires, for two reasons: clinical and in

order to obtain more precise classification.

PMID: 11391493 [PubMed - as supplied by publisher]

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Causes And Consequences Of Imitation

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_ui

ds=11390296 & dopt=Abstract

1: Trends Cogn Sci 2001 Jun 1;5(6):253-261

Heyes C.

Department of Psychology, University College London, Gower Street, WC1E 6BT,

London, UK

Recent behavioural and neuroscientific research concerning imitation

has revealed evidence of experience-dependent imitation in chimpanzees and

birds, wide ranging imitation deficits in autism, and unintentional

imitation in adult humans.

This review examines these findings and also evaluates evidence of

neonatal imitation and intentional imitation in infancy, and evidence

suggesting that the left inferior frontal gyrus is specialized for

imitation.

At the theoretical level, the empirical findings support the view that

the perceptual-motor translation that is a unique and defining property of

imitation depends primarily on direct links between sensory and motor

representations established through correlated experience of observing

movements and carrying them out.

PMID: 11390296 [PubMed - as supplied by publisher]

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Receptive And Expressive Communication Development Of Young Males With

Fragile X Syndrome

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_ui

ds=11389664 & dopt=Abstract

1: Am J Ment Retard 2001 May;106(3):216-30

JE, Mirrett P, Burchinal M.

Porter Graham Child Development Center, University of North Carolina

at Chapel Hill, 27599-8180, USA. joanne_roberts@...

We prospectively examined the developmental trajectories of receptive

and expressive communication skills of 39 young males, 20 to 86 months of

age, with fragile X syndrome. Eight showed features characteristic of

autism.

Children were tested one to three times using a standardized language

test. They showed marked delays in language development, but substantial

individual variability. Participants acquired expressive language skills

more slowly than receptive language over time, gaining receptive language at

about half the rate expected for typically developing children and

expressive language at one third the rate.

Both cognitive skills and autistic characteristics of the young males

with fragile X syndrome related to receptive and expressive communication

development, but neither predicted the discrepancies between expressive and

receptive language acquisition over time.

PMID: 11389664 [PubMed - in process]

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Reader’s Posts

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