Dreams in Psychology

Dreams in Psychology

Why are dreams so important in analysis. Patients are often haunted by recurring dreams of their traumas and awaken in terror. As long as they remain ill, these dreams don't change their basic structure. The neural network that represents the trauma – such as Mr. L's dream that he was missing something – is persistently reactivated, without being retranscribed. Should these traumatized patients get better, these nightmares gradually become less frightening, until ultimately the patient dreams something like At first I think the trauma is recurring, but it isn't; it's over now, I've survived . This kind of progressive dream series shows the mind and brain slowly changing, as the patient learns that he is safe now. For this to happen, neural networks must unlearn certain associations – as Mr. L. unlearned his association between separation and death – and change existing synaptic connections to make way for new learning.

What physical evidence exists that dreams show our brains in the process of plastic change, altering hitherto buried, emotionally meaningful memories, as in Mr. L.'s case?

The newest brain scans show that when we dream, that part of the brain that processes emotion, and our sexual, survival, and aggressive instincts, is quite active. At the same time the prefrontal cortex system, which is responsible for inhibiting our emotions and instincts, shows lower activity. With instincts turned up and inhibitions turned down, the dreaming brain can reveal impulses that are normally blocked from awareness.

Scores of studies show that sleep affects plastic change by allowing us to consolidate learning and memory. When we learn a skill during the day, we will be better at it the next day if we have a good night's sleep. “Sleeping on a problem” often does make sense.

A team led by Marcos Frank has also shown that sleep enhances neuroplasticity during the critical period when most plastic change takes place. Huben and Wiesel blocked one eye of a kitten in the critical period and showed that the brain map for the blocked eye was taken over by the good eye – a case of use it or lose it. Frank's team did the same experiment with two groups of kittens, one group that it deprived of sleep, and another group that got a full amount of it. They found that the more sleep the kittens got, the greater the plastic change in their brain map.

Scientists blocked one eye of a kitten and showed that the brain map for the blocked eye was taken over by the good eye. Photo by Elena.

The dream state also facilitates plastic change. Sleep is divided into two stages, and most of our dreaming occurs during one of them, called rapid-eye-movement sleep, or REM sleep. Infants spend many more hours in REM sleep than adults, and it is during infancy that neuroplastic change occurs most rapidly. In fact, REM sleep is required for the plastic development of the brain infancy. A team led by Dr. Gerald Marks did a study similar to Frank's that looked at the effects of REM sleep on kittens and on their brain structure. Marks found that in kittens deprived of REM sleep, the neurons in their visual cortex were actually smaller, so REM sleep seems necessary for neurons to grow normally. REM sleep has also been shown to be particularly important for enhancing our ability to retain emotional memories and for allowing the hippocampus to turn short-term memories of the day before into long-term ones (i.e., it helps make memories more permanent, leading to structural change in the brain).

Each day, in analysis, Mr. L, worked on his core conflicts, memories, and traumas, and at night there was dream evidence not only of his buried emotions but of his brain reinforcing the learning and unlearning he had done.

We understand why Mr. L. at the outset of his analysis, had no conscious memories of the first four years of his life: most of his memories of the period were unconscious procedural memories – automatic sequences of emotional interactions – and the few explicit memories he had were so painful, they were repressed. In treatment he gained access to both procedural and explicit memories from his first four years. But why was he unable to recall his adolescent memories? One possibility is that he repressed some of his adolescence; often when we repress one thing, such as a catastrophic early loss, we repress other events loosely associated with it, to block access to the original.

But there is another possible cause. It has recently been discovered that early childhood trauma causes massive plastic change in the hippocampus, shrinking it so that new, long-term explicit memories cannot form. Animals removed from their mothers let out desperate cries, then enter a turned-off state – as Spitz's infants did – and release a stress hormone called “glucocorticoid.” Glucocorticoids kill cells in the hippocampus so that it cannot make the synaptic connections in neural networks that make learning and explicit long-term memory possible. These early stresses predispose these motherless animals to stress-related illness for the rest of their lives. When they undergo long separations, the gene to initiate production of glucocorticoids gets turned on and stays on for extended periods. Trauma in infancy appears to lead to a supersensitization – a plastic alteration – of the brain neurons that regulate glucocorticoids. Recent research in humans shows that adult survivors or childhood abuse also show signs of glucocorticoid supersensitivity lasting into adulthood.

That the hippocampus shrinks is an important discovery. Depression, high stress, childhood trauma all release glucocorticoids and kill cells in the hippocampus, leading to memory loss. The longer people are depressed, the smaller their hippocampus gets. The hippocampus of depressed adults who suffered prepubertal childhood trauma is 18 percent smaller than that of depressed adults withous childhood trauma – a downside of the plastic brain : we literally lose essential cortical real estate in response to illness.

If the stress is brief, this decrease in size is temporary. If it is too prolonged, the damage is permanent. As people recover from depression, their memories return, and research suggests their hippocampi can grow back. In fact, the hippocampus is one of two areas where new neurons are created from our own stem cells as part of normal functioning.

Antidepressant medications increase the number of stem cells that become new neurons in the hippocampus. Rats given Prozac for three weeks had a 70 percent increase in the number of cells in their hippocampi. It usually takes three to six weeks for antidepressants to work in humans – perhaps coincidentally, the same amount of time it takes for newly born neurons in the hippocampus to mature, extend their projections, and connect with other neurons. So we may, without knowing it, have been helping people get out of depression by using medications that foester brain plasticity. Since people who improve in psychotherapy also find that their memories improve, it may be that it also stimulates neural growth in their hippocampi.

(Turning Our Ghosts into Ancestors. The Brain That Changes Itself by Norman Doidge, M.D., excerpt).

We are often haunted by important relationships from the past that influence us unconsciously in the present. Photo by Elena.