In his latest book, titled Rediscovering catatonia: the biography of a treatable syndrome,
Professor Emeritus Max Fink argues for the recognition of catatonia as
an independent diagnostic category by tracing the syndrome from its
first description in 1874 through its current status in the proposed
DSM-5. 
The
“biography” of catatonia takes the reader back to a nineteenth century
asylum filled with “the cacophony of cries and the pungent odors of
urine, sweat, and the medicine paraldehyde” where the director, Karl
Kahlbaum, first identified catatonia. “The patients were immobile and
posturing, remaining in one position for hours; or moving continuously,
pacing or hitting a wall or themselves… repeating words or phrases over
and over again.” Because Kahlbaum lacked an effective treatment, he was
able to observe the entire syndrome: its sudden onset, progressive
course and debilitating outcome. Catatonia looked to Kahlbaum like “an
immobility induced by severe mental shock.”
While Kahlbaum’s description won early acceptance by many clinicians worldwide, catatonia became submerged as a type of dementia praecox
in the textbooks of the influential German psychiatrist Emil Kraepelin
and later as a subtype of schizophrenia in the diagnostic scheme of Paul
Eugen Bleuler. It has remained hidden there ever since, despite the
publication throughout the 20th century of articles identifying
catatonia in patients with diseases other than schizophrenia. Interest
in catatonia waned once it could be quickly relieved by an injection of
sodium amobarbital (Amytal).
When neuroleptic drugs were
introduced in the 1950’s the association between catatonia and
schizophrenia led psychiatrists to prescribe them to people with
catatonia, often with disastrous results. A review article in 1980
identified the life-threatening "neuroleptic malignant syndrome", the
acute onset of catatonic symptoms accompanied by high fever and
cardiovascular changes. The severity of the syndrome, together with the
discovery that it could be relieved by the administration of lorazepam
or with ECT, led to a renewed interest in catatonia and a growing
recognition of its independence from schizophrenia.
In its
rediscovered state, catatonia came to be recognized in patients
diagnosed with delirious mania, autism spectrum disorders and mental
retardation. Dr. Fink lists additional syndromes that warrant
consideration as variations of catatonia, including Tourette’s syndrome,
anti-NMDAR encephalitis, obsessive-compulsive disorder and akinetic
mutism.
Although it has been known for more than 50 years that
catatonic patients respond well to barbiturates and to ECT while
schizophrenic patients do not, the official diagnostic manual of the
American Psychiatric Association continued to include catatonia only as a
type of schizophrenia. The inclusion of ‘catatonia secondary to a
medical disorder’ in the 1994 DSM-IV was a victory of sorts, but it had
little influence on clinical practice.
When the APA began to
plan for the DSM-5, a group of scholars and clinicians familiar with
catatonia successfully advocated for the deletion of catatonia as a type
of schizophrenia and the addition of a new independent class. They
argued that the traditional scheme increased the risk of inducing
neuroleptic malignant syndrome and obscured the fact that catatonia is
easily treatable. The APA DSM-5 Work Group eliminated the catatonia
type of schizophrenia and added a new class of ‘catatonia not elsewhere
classified’ with an independent numeric code. The main issue now is how
the new classifications will be treated in psychiatric textbooks and
official treatment guidelines. The fact that 80% of patients with
catatonia respond well to benzodiazepines is positive, but the fact that
the remaining 20% are best treated with ECT is limited by the prejudice
against its application.
Dr. Fink next considers the possible
origins of catatonia in the fear response described by psychologists as
"tonic immobility." If catatonia is a relic of an epoch when humans
froze in fear to escape the notice of aggressive animals, it should be
regarded as an exaggeration of the normal biological state and attention
should be paid to the stress aspects of the patient's history.
A
concluding discussion examines parallels between catatonia and
melancholia in the diagnostic manuals. Despite its long history,
melancholia is not given a separate category in the DSM classification,
but treated as a specifier of mood disorders. The fact that both
catatonia and melancholia are rapidly resolved by ECT and are marked by
similar hormone abnormalities suggests that there may be a connection
between them.
The book was published as Volume 127, Supplement 441 to the journal Acta Psychiatrica Scandinavica in January 2013.
