How Everyone Became Depressed

The rise and fall of the nervous breakdown

Classic Treatment for a Classic Condition

Bring back the Benzos!

In a recent issue of the Australian and New Zealand Journal of Psychiatry, Dr David Healy, professor of psychiatry at Bangor University in the United Kingdom, tells the story of “Cora,” a beautiful young 18-year-old who turned up at Healy’s hospital one day mute (Healy, 2013).

They couldn’t get a word out of her. Bad trip? Boyfriend took off? She refused to answer.

Then she did start to talk, but began to alternate episodes of volatility with lying in bed “almost completely unresponsive.”

Now, I’ve told you enough already to give you the diagnosis. Mute? Alternating stupor and agitation?

These are the symptoms of catatonia, a diagnosis that goes back to the 1870s and that US psychiatrist Max Fink has recently revived (Fink, 2012). The treatments of choice for catatonia are benzodiazepines (Valium-style drugs) and shock therapy (electroconvulsive therapy, ECT).

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But before Healy could begin the appropriate treatment, she checked out and went off with her parents. She was then readmitted a year later to another hospital, this time overactive. Doctors at this hospital diagnosed schizophrenia (!) and put her on antipsychotics. She had just given birth and they took her baby away from her.

“Some months later,” Healy says, “having told her parents she was going out for a walk, she laid her neck on the track in the face of an oncoming express train.”

Cora’s death was completely pointless, because her clinicians failed to recognize the symptoms of catatonia and to put her on the standard anticatatonic treatments, which are highly effective.

There are many Cora’s on this side of the pond too, patients whose catatonia is unrecognized and who are treated inappropriately: antipsychotics worsen the symptoms of catatonia and are counter-indicated.

There are two problems here. One is the under-diagnosis of catatonia. This is about to be corrected because the new DSM-5 includes catatonia outside the context of schizophrenia (for a hundred years it had been considered a subtype of schizophrenia, and if your patient wasn’t schizophrenic, catatonia would not occur to you as a diagnosis). This is one of the few good things one can say about DSM-5, that it will make clinicians more familiar with the stereotypical movements, the negativism, the posturing, the “waxy rigidity” of the limbs, the alternation of stupor and agitation, the mutism, the food refusal . . . the symptoms of catatonia are quite extensive.

The other problem, however, is not about to be corrected, and that is medicine’s horror of a drug class that was once a therapeutic mainstay: the benzodiazepines. Younger clinicians today have almost all learned in their training that benzos are “highly addictive” and must never be prescribed, except possibly for the short-acting variety that serve as hypnotics. But the benzos with longer half-lives, such as Valium – one of the single most useful drugs in psychiatry – hey, no way, man!

This benzo refusal is a perfect example of a time-honored principle in medicine: Why react when you can overreact? In the 1970s benzos were widely prescribed for “anxiety,” much as the stimulants became widely prescribed in the 1950s and -60s for weight loss. And like the stimulants, some patients took the benzos at high doses for long periods and experienced symptoms of withdrawal when they tried to get off them. Withdrawal is not really a problem at lower doses for short periods. (Katz et al., 1990).

But what convinced physicians as a whole that the benzos were as deadly as rat poison was not the experience of a few patients abusing them; it was the advertising of the makers of the competing Prozac-style drugs, flogging their wares for “depression.” Prozac and its cousins were hyped as “non-addictive.” The whole anxiety diagnosis became associated with the now stigmatized benzos, and medicine moved on from a highly effective drug class to the SSRI (Prozac-style) drug class that senior clinicians see as almost inert, at least in the treatment of depression (Shorter, 2008).

The catatonia diagnosis means the return of the benzodiazepines, the only effective treatment for the disorder outside of ECT. For once, science will be driving psychiatry.

References

Fink, M. (2013). Rediscovering catatonia: the biography of a treatable syndrome. Acta Psychiatr Scand Suppl (441), 1-47. doi:10.1111/acps.12038.

Healy, D. (2013). Catatonia from Kahlbaum to DSM-5. Aust N Z J Psychiatry, 47(5), 412-416. doi:10.1177/0004867413486584

JL Katz et al., (1990) “Abuse Liability of Benzodiazepines, “ In I Hindmarch et al. (eds.) Benzodiazepines: Current Concepts: Biological, Clinical and Social Perspectives. (pp. 181-198) Chichester: Wiley.

Shorter, E. (2008). Before Prozac: The Troubled History of Mood Disorders in Psychiatry. Oxford: Oxford University Press.

Edward Shorter, Ph.D., is the Jason A. Hannah Professor in the History of Medicine at the University of Toronto.

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