Image Unavailable

Characterized by hallucination and delusions, schizophrenia is a debilitating mental disorder affecting 0.5-1.5% of the world’s population. Symptoms first begin to present themselves in the late teens to mid thirties. Based on the presence of certain symptoms, patients are classified into one of five subtypes: paranoid, catatonic, disorganized, residual, or undifferentiated[1]. Though there have been documented cases dating from 1809, there is still much to discover in regards to the neuroscience of schizophrenia[2]. Even with the great amount of current literature, modern techniques are just now beginning to shed light on the affect of schizophrenia on the brain. The early onset, severe prognosis, and high co-morbidity rates emphasize the importance of further research. These all contribute to the high costs associated with the disorder which is a reason for additional studies in itself. Hence, this neurowiki will examine a variety of subtopics which include molecular mechanisms, risk factors, and associated brain abnormalities within schizophrenia and its subtypes.

2. Heinrichs, R.W. Historical origins of schizophrenia: two early madmen and their illness. J Hist Behav Sci. 39 (4), 349-363 (2003).

Brain Morphology and Schizophrenia

main article: Brain Morphology and Schizophrenia
author: Kamalpreet Mann

Image Unavailable

Neuroimaging is a nascent research tool in neuroscience that allows studying the brain structurally and functionally. Since the development of this technique there has been increased amount of research done to suggest that schizophrenia patients have alterations in brain connectivity[1]. There are two forms of schizophrenia: acute and chronic. In acute onset outbreak takes place rapidly, usually triggered by some sort of event. On the other hand, chronic schizophrenia takes place over time, where the signs start to accumulate over years and finally leading to being diagnosed as schizophrenic. This difference between two forms is important to point out because brain abnormalities are associated with the chronic onset.

1. Lewis, D. Distributed disturbances in brains Structure and function in schizophrenia. The American Journal of Psychiatry 157, 1-2 (2000).
2. Schmitt, A. et al. Schizophrenia: brain morphology and treatment aspects. Eur Arch Psychiatry Clin Neurosci 263, 1-2 (2013).
3. Üçok, A. et al. Duration of untreated psychosis may predict acute treatment response in first –episode schizophrenia. Journal of Psychiatric Research 38, 163-1683 (2004).

Drug Use and Schizophrenia

main article: Drug Use and Schizophrenia
author: Pratheep Thavarajah

Image Unavailable
Cannabis is a popular street drug in the youth population

The relationship between recreational drug and psychosis is one that has been long investigated. Of this, the similarities and correlations between recreational drugs and symptoms resembling Schizophrenia have garnered attention and research. Of the associations studied, the one between Cannabis use and Schizophrenia has accumulated the most amount of research and publications but relatively recent studies have explored the association between the well-known anesthetic drug Ketamine and the presence of schizophrenic like symptoms[1]. While there are inherent differences in the demographic and numbers of the population using Cannabis compared to Ketamine, an important similarity is that both are known to produce symptoms similar to some of the ones characteristic to schizophrenia and both having negative effects on individuals function as well as society in term of productivity, resources, and healthcare/therapy costs. Much of the currently existing research has examined the types of schizotypal symptoms that recreational use of these drugs produces[1], the pathways these drugs target which gives rise to these symptoms, as well as the effects these drugs have in terms of onset and prognosis for these disorders[2].

1. Ebert, A., Haussleiter, I. S., Juckel, G., Brune, M. & Roser, P., Impaired facial emotion recognition in a ketamine model of psychosis. Psychiatry Research (200), 724-727 (2012).
2. Linzen, D. H., Dingemans, P. M. & Lenior, M. E., Cannabis Abuse and the Course of Recent-Onsey Schizophrenic Disorders. Arch General Psychiatry 51, 273-279 (1994).
3. Nolen-Hoeksema, S. & Rector, N. A., in Abnormal Psychology, edited by Hunter, D. (McGraw-Hill Ryerson, Toronto, 2011), Vol. II, pp. 376-414.

Molecular Mechanisms of Schizophrenia

main article: Molecular Mechanisms of Schizophrenia
author: Anuradha Kamath

Image Unavailable
A picture drawn by a Schizophrenic patient illustrating his hallucination.
He hallucinated about being wheeled past a scene of mass execution and
described hearing the cries and groans of the people who were being beheaded.

Schizophrenia is a debilitating and complex mental disorder that affects a huge number of people around the world. Although the term schizophrenia was coined decades ago, with the first antipsychotic drugs discovered in the 1950s and its effect on monoamine receptors in the 1960s [1], mechanisms underlying the disorder is still relatively unknown. Genetic studies have established that the disorder has high heritability, increasing susceptibility to the illness but is not solely responsible for its development in a person. Other triggers and environmental factors such as pregnancy and birth complications, drug abuse, improper child development, etc., also play a role. This has led to the understanding that the disorder is dynamic and involves the dysregulation of multiple pathways, which includes abnormalities in several neurotransmitter systems and signal transduction pathways. However, it remains unknown whether these abnormalities are causal in nature or not.
In an attempt to understand the cellular and molecular mechanisms of the disorder, researchers have postulated a number of hypotheses. These hypotheses not only attempt to account for the symptoms but also attempt to provide potential therapeutic strategies in order to reduce its severe prognosis.
Schizophrenia shares co-morbidity with numerous disorder which include anxiety disorders, depression, substance abuse, etc. These disorders also show neurotransmitter dysfunctions. There are many other mental disorders such as Autism (see Autism), Bipolar Disorder (see Bipolar Neuroscience), and Parkinson's disease (see Parkinson's Disease) that have also shown abnormal neurotransmission.

1. Seeman, P. (1987). Dopamine receptors and the dopamine hypothesis of schizophrenia. Synapse, 1(2), 133-152.

Neural Substrates of Hallucinations

main article: Neural Substrates of Hallucinations
author: hillsar1

Image Unavailable

Hallucinations are the perception of sensory information that is not present in reality. They can occur in any of the senses or even co-occur simultaneously. This phenomenon is most associated with a diagnosis of paranoid schizophrenia. The current view on the neural basis of hallucinations is that of a modality-specific model, meaning that abnormal connectivity in certain sensory brain regions result in corresponding sensory hallucinations[1]. For example, it has been shown that auditory hallucinations result from abnormal connectivity between Heschl’s gyrus and other brain regions[2]. For the most part research has focused on auditory hallucinations due to their high prevalence[1]. However, other sensory hallucinations are now being examined. By looking at the abnormalities in sensory networks, we can garner insight into how these systems work in normal cases. This research is also important due to the fact that hallucinations greatly decrease a person’s quality of life; for example, difficulty interacting in social situations. By understanding the neural basis of hallucinations, improved treatments can be developed to help those affected.

1. Pavlović, D.M., Pavlović, A.M., & Lačkovć, M. The neuropsychology of hallucinations. Arch Biol Sci.63 (1), 43-48 (2011).
2. Shinn, A.K., et al. Functional connectivity of left Heschl’s gyrus in vulnerability to auditory hallucinations in schizophrenia. Schizophr Res. 143, 260-268 (2013).

Add a New Comment