Schizophrenia Daily News Blog

Biological Basis of Hallucinations

Hallucinations are a common symptom of schizophrenia. The paper reviewed here discusses a relatively new theory, which proposes that hallucinations and psychotic behavior are the result of the uncoupling of sensory input from perception. Information about the world around us is collected by different kinds of sensory receptors (visual, auditory, tactile, olfactory, and taste) and travels to different parts of the brain specialized for processing a specific kind of sensory information. For example visual information travels to the visual cortex in the occipital lobe of the brain and auditory information travels to auditory cortex in the temporal lobe. From these specialized areas, information travels to the parts of the brain responsible for movement and conscious thought. However, before any of this processing occurs, sensory information is filtered through an area of the brain called the thalamus. The thalamus weeds out irrelevant stimuli so that the brain is not overloaded with information. In addition to receiving information directly from sensory neurons, the thalamus gets input back from other areas of the brain such as the visual and auditory cortices and areas of the brain responsible for attention and motivation. This feedback helps prioritize information and decide how stimuli will be filtered through the thalamus. These complex processes transform abstract sensory information such as sound and light waves into a complete and useful picture of the world around us.

Neurons in the thalamus are organized into circuits, which tend to synchronize into a specific rhythm of activity and form the basis for perception. When you are awake, the activity is normally constrained by sensory input. When you are asleep, the sensitivity of the neurons increases and they tend to fire randomly, which may be the basis for dreaming. Hallucinations may also be the result of increased sensitivity in these neuronal circuits. In this state, sensory information is not transferred effectively. It becomes uncoupled from perception and the normally minimal feedback from other areas of the brain takes over. The hypothesis proposed in this paper is that people with schizophrenia have chronically oversensitive neurons and thus are biologically prone to misperceptions and hallucinations. In any individual, there is a certain amount of background noise in neuronal circuits; however, people with schizophrenia have more background noise in their neuronal circuits so it takes a stronger stimulus to get through. Previous research showing that sensory perception is less acute in people with schizophrenia, and often their relatives as well, would seem to support this hypothesis.

The exact molecular mechanism of over-sensitization is still not clear. There are several different neurotransmitters (molecules that carry information between neurons) that mediate the activity of neurons in the thalamus. Some neurotransmitters excite activity in the cells receiving their signal, while others inhibit activity. Two culprits, dopamine and serotonin, have been previously implicated in several disorders of the brain. Dopamine in the thalamus is an excitatory neurotransmitter, so the authors of this paper propose that dopamine hyperactivity may be one cause of oversensitivity. Serotonin, on the other hand normally plays an inhibitory role, so it is the reduced activity of serotonin that may lead to oversensitivity. Similarly, the reduced activity of the neurotransmitter GABA may also be part of the problem. Malfunction of the receptors that pick up neurotransmitters is another possible explanation for the oversensitivity of neuronal circuits. People with schizophrenia have been shown to have fewer NMDA and nicotine receptors compared to people without schizophrenia. Both of these receptors play an important role in regulating neuronal activity.

None of these defects alone would cause schizophrenia or trigger a psychotic episode; however, they do confer a predisposition for developing schizophrenia. In most sufferers, it is likely that several of these neurotransmitter and receptor networks are malfunctioning simultaneously to make a person more susceptible to misperception and hallucination. Onset of the disease or a psychotic episode is likely to be triggered by environmental or social stress.

Source: Behrendt, Ralf-Peter. “Dysregulation of thalamic sensory ‘transmission’ in schizophrenia neurochemical vulnerability to hallucinations”. Journal of Psychopharmacology. 2005. http://jop.sagepub.com

For more information about the biology of schizophrenia, try Schizophrenia Biology and Genetics on the main page.

For more information about the structure and function of the brain:
The first two links have interactive maps of the brain.
http://www.pbs.org
http://www.bbc.co.uk
http://www.waiting.com