Low Latent Inhibition and Delusions: A Model for the Formation of Delusional Thinking

Have you ever experienced a moment when reality seemed to slip away? I've had two such experiences that left me questioning my very existence. The first occurred after unknowingly consuming a potent "special" brownie, which sent me spiraling into a world of paranoia and delusions. The second was during a psychotic episode as I was falling asleep, convinced that the government had drugged me and my brain was disintegrating. While these events seem vastly different, they share a common thread: an overwhelming flood of information from my surroundings, as if my mind had lost its ability to filter out irrelevant stimuli.

Understanding Latent Inhibition

To make sense of these experiences, we need to explore the concept of latent inhibition. In classical conditioning, latent inhibition refers to the phenomenon where a familiar stimulus takes longer to acquire meaning than an unfamiliar one (Baruch, Hemsley, & Gray, 1988). It's an evolutionary advantage that helps us learn significant associations faster by filtering out previously irrelevant connections. In essence, latent inhibition is our brain's way of saying, "We've seen this before, and it wasn't important then, so let's focus on something else."

Latent inhibition is closely tied to attention. Right now, as you're reading this article, you've probably tuned out the low hum of your heating system or the feeling of your socks on your feet. These are unimportant stimuli, and there's no reason to pay attention to them. However, now that I've mentioned them, you might suddenly become aware of these sensations. This ability to assess salience and switch our attention accordingly is a crucial aspect of latent inhibition.

But what happens when this filter malfunctions? That's where low latent inhibition comes into play, and it might just be the key to understanding how delusions form.

The Schizophrenia Connection

Schizophrenia, a severe psychiatric disorder that distorts a person's thoughts, behaviors, and feelings, provides an interesting window into the relationship between latent inhibition and delusions (Picchioni & Murray, 2007). Schizophrenic patients often experience attention deficits, which fall into two categories:

1. The "jumping" attention: Seen in acute patients with positive symptoms (like hallucinations and delusions).
2. The fixated attention: Observed in chronic patients with negative symptoms (such as reduced motivation and social withdrawal).

Research has shown that acute schizophrenic patients tend to have lower levels of latent inhibition, while chronic patients exhibit enhanced latent inhibition (Rascle et al., 2001). This correlation suggests that latent inhibition might play a crucial role in preventing the formation of delusions and helping us maintain a sensible view of reality.

An experiment by Rascle et al. (2001) investigated this relationship between latent inhibition and schizophrenia. They found that acute schizophrenic patients with positive symptoms quickly attended to stimuli whether they were relevant or irrelevant, indicating lower latent inhibition. In contrast, chronic patients showed enhanced latent inhibition, taking much longer to recognize when a previously irrelevant stimulus became relevant.

From Low Latent Inhibition to Delusions: A Possible Model

So, how might low latent inhibition lead to delusions? Let's break it down:

1. Sensory Overload: Individuals with low latent inhibition struggle to filter out irrelevant perceptual information. Imagine trying to focus on a conversation in a noisy, crowded party – that's what their brain experiences constantly (Maher, 2005).

2. Perceptual Flooding: This overwhelming influx of sensory information often results in confusion and distraction. Interestingly, while perceptual flooding is common in acute schizophrenics, it's only seen in chronic schizophrenics when they're experiencing delusions (Kapur, 2003).

3. Flawed Plausibility Reasoning: When our brains are overloaded and confused, our ability to judge what's plausible becomes compromised. We start making erroneous connections that healthy individuals typically wouldn't (Nelson, Whitford, Lavoie, and Sass, 2014).

4. Mixing Relevant and Irrelevant Evidence: In forming beliefs, people with low latent inhibition may incorporate both relevant and irrelevant information as supporting evidence. This is where the concept of plausibility reasoning comes into play. Normally, multiple nodes of relevant evidence converging on a conclusion make a belief more plausible. However, for individuals with low latent inhibition, these nodes of evidence may include irrelevant information, leading to unusual or delusional beliefs.

5. Delusional Beliefs: The combination of these factors can lead to the formation of beliefs that seem highly improbable to others but feel entirely plausible to the individual experiencing them. Delusions typically manifest as beliefs that are highly improbable but not impossible, suggesting problems with inferential logic (Roberts, 1992).

The Bigger Picture

It's important to note that low latent inhibition is likely not the sole factor in delusion formation. The human mind is complex, and mental health issues rarely have a single, simple cause. Abnormal levels of dopamine, for instance, have been attributed to causing both positive and negative symptoms in schizophrenia (Howes, Mccutcheon, & Stone, 2015).

However, understanding the role of latent inhibition in logical thinking and belief formation is crucial for developing better treatments and support for those experiencing delusions. The fact that low latent inhibition often occurs before the appearance of delusions (Maher, 2005) suggests it could be a potential cause or at least a significant contributing factor.

In conclusion, our ability to filter information – to decide what's relevant and what's not – plays a vital role in how we perceive and interpret the world around us. When this filter malfunctions, as in cases of low latent inhibition, it can open the door to a reality that looks very different from what others experience. By studying these mechanisms, we inch closer to unraveling the mysteries of the human mind and finding ways to help those who see the world through a different lens.

References

Baruch, I., Hemsley, D. R., & Gray, J. A. (1988). Latent inhibition and "psychotic proneness" in normal subjects. Personality and Individual Differences, 9(4), 777-783.

Carson, S. H., Peterson, J. B., & Higgins, D. M. (2003). Decreased Latent Inhibition Is Associated With Increased Creative Achievement in High-Functioning Individuals. Journal of Personality and Social Psychology, 85(3), 499-506.

Elvevag, B., & Goldberg, T. E. (2000). Cognitive Impairment in Schizophrenia Is the Core of the Disorder. Critical Reviews™ in Neurobiology, 14(1), 21.

Howes, O., Mccutcheon, R., & Stone, J. (2015). Glutamate and dopamine in schizophrenia: An update for the 21st century. Journal of Psychopharmacology, 29(2), 97-115.

Kapur, S. (2003). Psychosis as a State of Aberrant Salience: A Framework Linking Biology, Phenomenology, and Pharmacology in Schizophrenia. American Journal of Psychiatry, 160(1), 13-23.

Maher, B. (2005). Delusional thinking and cognitive disorder. Integrative Physiological & Behavioral Science, 40(3), 136-146.

Nelson, B., Whitford, T., Lavoie, S., & Sass, L. (2014). What are the neurocognitive correlates of basic self-disturbance in schizophrenia?: Integrating phenomenology and neurocognition. Schizophrenia Research, 152(1), 20-27.

Picchioni, M. M., & Murray, R. M. (2007). Schizophrenia. BMJ, 335(7610), 91-95.

Rascle, C., Mazas, O., Vaiva, G., Tournant, M., Raybois, O., Goudemand, M., & Thomas, P. (2001). Clinical features of latent inhibition in schizophrenia. Schizophrenia Research, 51(2-3), 149-161.

Roberts, G. (1992). The Origins of Delusion. British Journal of Psychiatry, 161(03), 298-308.

Todd, A. (2018). COG250 Lectures, University of Toronto. Toronto, Ontario, Canada.