From traumatic birth to death in a group home

Working papers Viewpoint on the brain disorder(2003) (View in 2000)
and notes: The auditory system The inferior colliculus Hemoglobin & the brain
Concepts of autism Autism spectrum Social responsibility


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Conrad Simon Memorial Research Initiative
http://conradsimon.org /inc/docinfo.shtml
Date posted:  April 24, 2000 08:01 PM
Website links updated:  January 20, 2023 06:44 PM
© Copyright 1999-2000
Eileen/Nicole Simon

Conrad and Gammy
Conrad Simon
Conrad with his grandmother, Evalyn Brodie Higginbottom

Conrad was born December 20, 1963. He was born pale and limp, and I remember the anxiety I felt; his brother, Ralf, born 15 months earlier cried before I could be told his sex. However, Ralf's birth had been traumatic (a brow presentation) and he had a cephalhematoma that was noticeable over the right half of his head until he was almost two; he still has a scar from forceps under his right eye. I was told Conrad was a "face presentation" - born face first, which was why forceps were needed for his delivery too.

Conrad's motor development was normal, unlike Ralf whose delay in learning to roll over, sit up, crawl, and walk had been worrisome. Conrad used words and phrases on time, but everything he said was a verbatim recitation of something he had heard. He recited nursery rhymes and sang songs in perfect pitch, and we thought this might have come about from Ralf's coaching him to speak. Ralf had been late learning to speak but could read at the age of two. Ralf may represent a case of high functioning autism, or Asperger syndrome, but he is a thoughtful and sensitive human being; he does not deserve any labels.


Conrad was a classic example of an autistic child, by all current definitions of the syndrome. He was in special education programs until age 22 and made great strides in communication, but sadly it was clear he would not become an independent self-supporting adult. When special education funding ended he was placed in a community group home where he lived until his death at age 31.
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Investigation of Conrad's Death

We were shocked to learn that cause of death was due to chlorpromazine (Thorazine) intoxication. Investigations by the Massachusetts Department of Mental Retardation and the Disabled Persons' Protection Commission included a review of the data by an independent toxicologist, who concluded that death may have resulted from a phenothiazine induced cardiac conduction block or dysrhythmia.

The medication administration record was carefully reviewed and no discrepancy in drug inventory was found. No indication of accidental overdose was indicated. Physician orders were:

  • Haldol (haloperidol) 6 mg/day 3 mg at 8am and 3:30pm
  • Thorazine (chlorpromazine) 1500 mg/day 500 mg at 3:30pm, 7pm, and 8:30pm
  • Depakote (valproate) 2000 mg/day 500 mg at 8am and 3:30pm, 1000mg at 7pm
  • Mylicon (simethicone) 80 mg at 8am, 3:30pm, and 7pm
  • Chloral Hydrate 2 grams at 8:30pm

The most recent orders were written by a psychiatrist who had taken on care of the group home residents only recently, and who expressed concern to the investigators about the use of two phenothiazine compounds. Staff of the group home had been reluctant to accept a change in medications, claiming that it was this combination that brought clinical stability to this client over the past four years.

Conrad's physical health was excellent; he was not overweight, he exercised, and ate well. There was no family history of cardiovascular causes. At his annual physical exam, liver enzymes and other laboratory studies were all within normal limits. According to the autopsy report, there were no significant atherosclerotic changes in blood vessels of the heart.

I reported this case to the Food and Drug Administration, and submitted a 500-word letter-to-the editor for publication. I received a form letter from the FDA and a rejection from the journal to which I submitted a letter. We investigated filing a lawsuit, but abandoned this when it appeared to be turning into a long, complicated, and futile effort. I am sure Conrad's is not the only death so neatly swept under the rug.

I don't understand legal proceedings, but I have now spent much of my life investigating all that is known about autism. The legal route did not appear to offer any solutions for better treatment of people with autism; science should. So I decided my efforts would be better spent in trying to promote wider understanding of autism based on multi-disciplinary viewpoints such as the findings from research on cerebral circulation and metabolism.

Chlorpromazine was introduced nearly half a century ago as a treatment for intractable psychotic illnesses. It is not a cure and it is clearly toxic. Its use for treatment of autism would appear to be utterly unwarranted, and based on totally out-of-date thinking about therapeutic approaches to working with people with autism spectrum disorders.

Bibliography
(on deaths related to use of anti-psychotic medications):

Hollister LE, Kosek JC: Sudden death during treatment with phenothiazine derivatives. JAMA 1965; 192:1035-1038

Moore MT, Book H: Sudden death in phenothiazine therapy (a clinicopathologic study of 12 cases). Psychiatric Quarterly 1970; 44:389-402

Cancro R, Wilder R: A mechanism of sudden death in chlorpromazine therapy. Am J Psychiatry 1970; 127:368-371

Girdwood RH: Death after taking medicaments. British Medical Journal 1974; 1(906):501-504

Evans DL, Rogers JF, Peiper SC: Intestinal dilation associated with phenothiazine therapy: a case report and literature review. Am J Psychiatry 1979; 136:970-972

Wakasugi C, Nishi K, Yamada M: Sudden death in a patient taking neuroleptics. American Journal of Forensic Medicine and Pathology 1986; 7:165-166

Jusic M, Lader M: Post-mortem antipsychotic drug concentrations and unexplained deaths. British Journal of Psychiatry 1994; 165:787-791


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