Global Health Asia-Pacific July 2020 July 2020 | Page 48
Cover Story
The Thorazine Shuffle: from the short film, The Dandelion King
The advent
of a new drug
accelerated
the demise of
lobotomies by
offering a better
alternative
apathetic and slow, while losing their ability for
creativity and initiative. Rosemary Kennedy, a
lobotomy patient and sister of the late US President
John F. Kennedy, was left with reduced intellectual
abilities after the operation and had to undergo
months of therapy to talk and walk again.
By the 1950s, however, the surgical technique
started to fall out of favour and not only because of its
less than impeccable track record.
“It remained unclear what lobotomy actually
did to the individual, and the issue of a scientific
validation could no longer be evaded. At a time when
the standards for clinical research became stricter
in general, follow-up studies produced discouraging
results,” Thomas Schlich wrote in The Lancet.
At the same time, the advent of a new drug
accelerated the demise of lobotomies by offering a
better alternative. In 1954, the US Food and Drug
Administration (FDA) greenlighted chlorpromazine,
also known as thorazine, the first medication approved
to treat schizophrenia and other mental disorders.
Originally developed to treat a condition affecting
the cardiovascular system, the compound was hailed
as a sort of “chemical lobotomy” by both clinicians
and pharmaceutical companies because it produced
similar effects to those achieved by surgery but with
less serious risks.
While thorazine often reduced delusional thinking
and hallucinations, many sufferers didn’t take it for
long because of its side effects, which �ranged from
chronic nausea to a sense of restlessness that some
described as wanting to crawl out of one’s skin,”
wrote Professor Harrington. “Many also gained a lot
of weight, and a significant number also developed
tardive dyskinesia, a neurological disorder that causes
abnormal limb movements, disabling facial twitches,
and tongue protrusion…even more developed a
(usually reversible) �arkinson’s-like side effect of the
drugs: a strange shu�ing way of walking that was so
common that it became known among patients as the
�Thorazine shu�e.�
At first, however, thorazine wasn’t considered a
treatment that acted on the underlying causes of
schizophrenia, but a substance that simply gave
people some respite from their symptoms while
making them easier to handle. In fact, it was referred
to as a major tranquilliser.
Further studies, however, shifted the way of
thinking about thorazine and led to the development of
new drugs.
The observation that substances like
amphetamines and LSD could cause hallucinations
and delusions suggested that a similar brain chemical
could alter normal biological processes and lead
people to develop the symptoms of schizophrenia.
After other compounds were investigated as
potential actors in the development of the condition,
the one rising to prominence was dopamine.
This particular brain chemical caught the attention
of schizophrenia researchers when they saw that
depleting dopamine levels in lab mice led the animals
to develop motor symptoms similar to those of
individuals on long-term chlorpromazine treatment for
schizophrenia.
This offered an indirect link between the
administration of chlorpromazine and decreased
dopamine levels � a connection that was finally
established in the 1970s when chlorpromazine and
similar schizophrenia drugs were shown to reduce
dopamine levels in the brain.
Coupled with experiments proving that
amphetamines didn’t lead to schizophrenia-like
symptoms in mice that previously received drugs
to block dopamine activity, this series of studies
contributed to the notion that schizophrenia was
caused by abnormal dopamine increases and to the
reframing and renaming of schizophrenia drugs, from
major tranquillisers to antipsychotics, substances
that aim to counteract psychosis (loss of contact with
reality) by acting on its supposed biological triggers.
Over the years, the framing of schizophrenia as a
chemical disorder gained such a powerful traction
that it was successfully employed as an argument in
favour of the legalisation of compulsory schizophrenia
treatment in the U.S.
“Serious mental illnesses like schizophrenia are
brain diseases in which parts of the brain are not
functioning properly,” Dr E. Fuller Torrey, a psychiatrist
and a prominent supporter of compulsory treatment,
wrote in his 1988 book Nowhere To Go: The Tragic
Odyssey of The Homeless Mentally Ill. “Since the
organ is impaired, it makes little sense to insist that
only those persons should be treated who want help
and ask for it.”
Despite the currency it has enjoyed since the
46 JULY 2020 GlobalHealthAndTravel.com