The Man Who Couldn’t Stop (20 page)

Before SSRI drugs became available in the 1980s and 1990s, OCD was treated with clomipramine, a brute of an antidepressant drug with nasty side effects that carried the risk of a fatal overdose. The risks were considered worth it because clomipramine gave hope to people with OCD. Hope that was discovered only thanks to random chance and a little cross-border narcotics smuggling.

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Clomipramine is a little different from the SSRI drugs, but it's similar to an antidepressant called imipramine, which was launched by the Swiss drug company Ciba in the 1950s. Both are tricyclic compounds – they have three joined carbon rings at their heart. On a trip to Switzerland in the 1960s, where imipramine was widely available, a French psychoanalyst called Jean Guyotat stuffed some into his pockets and took the pills back to his private practice in Lyon, where he started to give them to his obsessional patients. ‘This was somewhat illegal maybe now but it was possible at the time,' he later recalled.

Guyotat wanted to try the new drug because he believed that some obsessions were masked forms of depression. He treated fifteen obsessional or phobic patients, either with the Swiss imipramine or stocks of clomipramine that his clinic already gave as liquid infusions for severe depression. One patient was a male teacher who turned anger at a colleague who played Wagner records a little too loud into rituals to cope with obsessional thoughts of noise. Another was a woman who for the previous seven years had felt compelled to speak her thoughts out loud. The excitement of extramarital affairs eased the compulsion but, as Guyotat explained, this method of self-treatment had to stop when her husband found out. The drugs transformed some of his patients, Guyotat said, sometimes within a few days. In 1967 he published his results and announced to the world imipramine and clomipramine as the first chemical treatments for OCD.

Some six hundred miles to the southwest, psychiatrists at a hospital in Madrid learned of the work in France. They had plenty of intravenous clomipramine so they decided to try it on their own severely obsessional patients. Just like the French, the Spanish team reported rapid improvements. Juan Lopez-Ibor, a psychiatrist who worked at the hospital with his father, saw this change in the way one OCD patient on the ward played table tennis. The first sign of recovery came when the man, whose fear of germs had previously left him unable to touch things, was able to hold a communal bat, as long as he went to wash his hands immediately after he finished. When Lopez-Ibor saw the man complete his own game and then, without washing, choose to stay and watch other patients play, he knew they had stumbled onto something special.

In northwest England, George Beaumont noted keenly the success with OCD the Spanish doctors reported for clomipramine. Beaumont had worked as a GP in Stockport, near Manchester, but then took a job as medical adviser on psychiatrics with Geigy, a pharmaceutical company. Geigy owned clomipramine and Beaumont saw OCD as a potential new market for it − a big one.

Beaumont suggested to UK psychiatrists that they treat OCD with clomipramine. He arranged for them to visit Lopez-Ibor in Madrid and set up some basic clinical trials of the drug. Beaumont worked closely with staff at the Warrington mental hospital that had treated the claustrophobic American woman we met earlier, who compulsively checked to avoid being buried alive. Just like in France and Spain, some British patients seemed to show rapid improvement.

Encouraged by colleagues in Geigy's marketing department, Beaumont applied for an official licence that would allow doctors to prescribe the drug for obsessions and compulsions. He wrote the 2,000-page application himself – it took three months – and in 1975 clomipramine was approved to treat OCD in the UK, and later other places too. ‘Everyone at that time thought that OCD was an unusual, bizarre and rare condition,' Beaumont said later. ‘But as soon as you have a treatment for a condition you discover that it is more common than everybody supposed it to be.'
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For years, OCD sufferers in the United States were denied the drug. The licensing body there, the Food and Drug Administration, was wary of what it saw as a copycat antidepressant that offered no benefit beyond those drugs already available. In response, a frustrated Judith Rapoport described in
The Boy Who Couldn't Stop Washing
how − just like Guyotat twenty years earlier – she had helped to bring the unlicensed drug into the country. The FDA relented and approved clomipramine – known in the US as Anafranil – for OCD in 1990.

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Sertraline is a powerful drug, especially at the high daily doses given for OCD, but I only notice its impact when I don't take it. Just a day or so without it and, in apparent withdrawal symptoms, my dreams lift from monochrome Kansas to Technicolor Oz. They become so vivid and intense that the emotions they carry linger for most of the day; I can wake myself shouting, once with my eyes wet with tears. And the smells – forget to take my pills and I have smelly dreams. I can wake to the aroma of pungent wood smoke or sweet caramel.

On the drugs, it's harder to describe the effect. It's not like the mood lift reported by people given them for depression. It doesn't feel like anything is fixed or restored, though the medication does take the edge off the anxiety that weird thoughts cause. The thoughts still come – no surprise there, as we've seen, they are common and normal – but they seem less sticky. How long will I take the sertraline for? I'm afraid to stop; rapid relapse among those who do is common apparently. I don't see a downside. What gets you well keeps you well, my psychiatrist says.

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The impact on OCD of the SSRI and some tricyclic drugs has led scientists who work on the causes and nature of obsession to focus on the chemical that the medicines work on: serotonin.

The brain needs serotonin because, as complex and marvellous as it is, most of its neurons can't communicate directly with each other. At the business end of these neurons there lies a tiny gap that separates them from their neighbours. For neuron A to pass a signal to neuron B it needs serotonin. Specifically, the electrical signal, when activated, releases serotonin molecules into the gap between A and B, some of which bump into B. When that happens, B electrically activates and releases its own chemical messages to pass the signal to C, and so on right through the alphabet. Spare serotonin sloshing around in the gaps is reclaimed (taken up) by the neurons for when they will need it again.

That is about all we know for sure about how serotonin works in the OCD brain. Much of the rest of the so-called serotonin hypothesis for OCD is based on some reverse engineering. The logic goes like this: The SSRI drugs keep levels of serotonin in the free space between the cells higher than they would be otherwise. The drugs inhibit the uptake. This seems to relieve OCD symptoms, at least in some people. Therefore, the reverse engineering says, OCD must be caused by abnormally low serotonin levels.

It's notoriously difficult to track and measure neurotransmitter activity, so there's no direct evidence to support this hypothesis. It's certainly possible that the extra serotonin might help to ease OCD because it frees the jammed brake in the basal ganglia, and so allows the thalamus to recognize the stand-down signals sent by the orbitofrontal cortex. But it's equally possible that the change is due to something else.

It could be down to dopamine, another neurotransmitter, which tends to cancel out the effects of serotonin. Drugs that boost dopamine levels in the basal ganglia seem to trigger the sudden onsets of compulsive gambling and theft sometimes seen in Parkinson's patients. A failure to produce enough serotonin might allow dopamine levels to rise to the point where they have a stronger influence on the striatum, which plays a key role in the model of the OCD brain. PET brain scans of people with OCD show reduced serotonin transmission and increased dopamine release in the right areas.

Very recently, neuroscientists have fingered a third neurotransmitter, glutamate, for possible conspiracy to cause OCD. Or there could be a role for oxytocin, labelled as the hug hormone by some because of its role in pair-bonding and maternal behaviour. Oxytocin action is linked to serotonin and can bring on repetitive grooming behaviour in rats. In the mid-1990s scientists at Yale University tried to test its effect on humans. Sadly, regular squirts of oxytocin up the noses of seven OCD patients failed to lift their obsessions with contamination and cleaning.

Although the majority of people with OCD are helped by the SSRIs, a significant number – perhaps up to 40 per cent − see no benefit, even after they have tried four or five different drugs. This has led some scientists to look for obsession elsewhere in the brain, beyond the neurotransmitter systems of the basal ganglia. In 2008, neuroscientists in Turkey reported how they used MRI scans to measure the size of the amygdala and hippocampus in the brains of fourteen OCD patients who had not responded to drug treatment, and compared them to the brains of fourteen normal people. They found both structures were smaller in the OCD group, and the smallest were found in those who had suffered from the condition the longest.

Other studies have found structural differences in the OCD brain, but not consistently enough to build up a clear picture of what they might mean. Bits of the orbitofrontal cortex and basal ganglia have been measured as smaller in OCD and bits of the thalamus larger (more so in patients with more severe forms of the disease). Some scans find differences in the ratio of grey (functional) to white (supporting) brain tissue. Some of these differences go away when the OCD is treated. But scientists are a long way from making sense of these often contradictory findings.

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The conceptual division of the mind and the brain is like the academic separation of neurology, psychology and psychiatry – it seems to make sense until they have a disagreement, at which point it starts to look like a very bad idea indeed.

Can the mind truly develop faults independent of the brain? Or must every shift of mood and change in perception anchor to a chemical and electrical pulse? If so, then can that physical change in the brain be detected? Could it be measured? Could it be treated, as any other physical ailment can be? If it can, should that reassure someone with OCD, or indeed someone with any mental illness? Should it come as a relief that cognitive anguish has a physical root? Or does that just make it more permanent, more of a feature?

Some people with mental illness like to blame the brain, not the mind, as it implies that their problem lies beyond their consciousness and so beyond their control. It's not their fault. I prefer the opposite explanation. That my brain is normal, thanks. The drugs help to keep its complicated and volatile chemistry on track, but it's my mind, the brain's lodger, which has the OCD. My brain is mine to keep and I would like it to be of sound structure. My mind is transient anyway. My mind today is different from what it was yesterday; I have learned new things and forgotten others. The ephemeral mind is flexible in a way that the material brain is not. And, surely, that makes a broken mind easier to fix than a broken brain? I was on my way to the hospital to find out.

 

TWELVE

The helicopter view

When I reported to the hospital for my group therapy sessions in the late summer of 2010, if you were to have peered through the window you would not have spotted anything unusual. You would not have seen people wash their hands, or try not to wash their hands. You would have noticed only a group of half a dozen middle-aged people who sat in a circle of chairs and clutched photocopied handouts, while a much younger, much better dressed man with dreadlocks and a ready smile moved between them. We could have been learning to speak Spanish.

My fellow OCD patients signed up for therapy, as I did, in the full and fair expectation that their involvement would remain confidential. So, I'll be vague. There were two other men and three women. I was the youngest by a good ten years. We were all classed as serious cases (in fact the clinic only treated serious cases). Between us, we ticked most of the big OCD boxes – contamination and checking fears, long-standing symptoms, distress and reduced quality of life. Two of the others had obsessions and compulsions linked to Aids.

We swapped stories and we tried not to swap irrational fears. We agreed to support each other, but, being British, when somebody else told of their darkest moments we mostly shuffled in our seats and looked awkward. And we laughed. We laughed a lot. We laughed at each other and we laughed at ourselves. We had all long passed the time when we feared our OCD, which had announced itself as a mysterious curse on our lives. It was now a hand on our shoulder, a monkey on our back, an irritating shadow. We were fed up with it. We wanted rid of it. But we would probably miss it too. It was simply a part of us.

There was no psychiatrist's couch and no psychoanalysis. We did not talk about our childhoods. The various causes of our obsessions were irrelevant to the treatment, because they would all anyway have been different. The symptoms were what mattered, and to find a way to reduce them. That was what we had in common.

We saw, through wobbly and badly drawn schematic diagrams, how an OCD mind is thought to work. We learned how the compulsions are a shortcut that helps relieve anxiety, but only for a while. We started to identify dysfunctional beliefs and cognitive errors in ourselves. We started to diagnose them in each other. And we smiled nervously as we did so. This was cognitive behavioural therapy (CBT) but it didn't feel like the type of treatment we expected. It was mild. We suspected worse was to come. We were right. I was told to smear my daughter in my own blood.

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The psychologist Richard Solomon worked for the US military through the Second World War. Among other things, he used his expertise on perception and hand-eye coordination to improve the defences of the B-29 Superfortress, the aircraft that would go on to drop atomic bombs on the Japanese cities of Hiroshima and Nagasaki. But it was in the early 1950s, with experiments on a pack of mongrel dogs at Harvard University, that Solomon would make his name.