3) Positive Symptoms of Paranoid Schizophrenia

Symptoms of schizophrenia are typically divided into three categories: positive, negative and cognitive symptoms. The paranoid subtype of schizophrenia is distinct in the fact that those who suffer from it express a prominence of positive symptoms such as hallucinations, delusions and thought disorder. Hallucinations are prevalent in many psychotic diseases, but every type of hallucination is observed in schizophrenia. Types of hallucinations include auditory verbal, visual and tactile or somatic hallucinations, and less frequently olfactory and gustatory hallucinations.

In addition, the use of techniques such as voxel based morphometry and diffusion tensor imaging, structural abnormalities of hallucinations have also been studied[1]. Neuroimaging studies have shown several differences in the mechanisms and structural and functional abnormalities of hallucinatory experiences for each of these different sensory modalities. Abnormalities in the superior temporal gyrus, the primary auditory cortex and language areas responsible for hearing and speech associated with auditory verbal hallucinations[2]; while abnormalities in the primary visual cortex has been shown to be associated with visual hallucinations[3]. These studies suggest that hallucinations may be sensory-modality specific, with different areas of the brain associated with a different type of hallucination[4].

Studying positive symptoms and hallucinations in schizophrenia can be difficult as the mechanisms for different sensory modalities can be complex. The majority of studies in hallucinations investigate auditory verbal hallucinations since it is the most prevalent out of all the sensory modalities, however other sensory forms are just as fascinating and worth exploring.

1 Auditory Verbal Hallucinations

Auditory verbal hallucinations (AVHs) are the most common type of hallucination experienced in paranoid schizophrenia. AVHs involve the perception of sound that is not associated with reality. In essence, those who experience AVHs often hear third person human voices speaking to them, often in a persecutory nature. Sometimes these voices even drive patients to commit acts of violence, hence the danger of paranoid schizophrenia[5].Neuroimaging studies using novel techniques such as voxel-based morphology and diffusion tensor imaging have revealed several neurological characteristics of patients who experience AVHs. In addition, recent studies have revealed a genetic connection that may be involved in the manifestation of auditory verbal hallucinations.

1.1 Superior Temporal Gyrus Abnormalities

Among the majority of studies of auditory verbal hallucinations that a decrease in grey matter in the superior temporal gyrus is correlated with the presence of AVHs. Abnormalities in Heschl’s gyri are particularly important in correlation to AVHs[16]. It is important to note that speech production areas and language areas are located within or in close proximity to the superior temporal gyrus[1]. In addition, AVH severity is negatively correlated to the amount of grey matter in the superior temporal gyrus[16][6]. Hence, more hallucinations are experienced when there is less grey matter in the superior temporal gyrus. In studies of brain activity during hallucinations, increased activation of the superior temporal gyrus, Broca’s area, the basal ganglia and the anterior cingulate were detected, indicating involvement in the mechanisms of AVHs[7].

1.2 Hyperconnectivity and Hypoconnectivity

The hyperconnectivity hypothesis of AVHs suggest that increases in brain activity result in the display of AVHs. In addition the to superior temporal gyrus, the perisylvian language area is also a region that displays several abnormalities. The perisylvian language area consists of Broca’s area for speech production, Wernicke’s area for speech comprehension, and the primary auditory cortex, Heschl’s convolutions. The arcuate fasciculus is the white matter tract that connects these auditory and language areas. In the analysis of white matter tracts via diffusion tensor imaging, increased fractional anisotropy values were found for the arcuate fasciculus, indicating increased connectivity in this language area. These findings account for the hyperconnectivity hypothesis of auditory verbal hallucinations. However, in addition to this, the hypoconnectivity hypothesis AVHs, suggest that decreases in activity in certain areas are related to the disengagement of a schizophrenia from reality. Disruptions in attentional networks are related to AVHs. An issue with patients who experience AVHs, is their inability to self-monitor and distinguish their hallucinations from reality. Decreased connectivity in the prefrontal cortex, which plays a role in attention, was found, accounting for this difficulty. ([8]; [1]. In addition, disrupted connectivity in the anterior cingulate cortex has also been implicated in AVHs. For patients with AVHs, unusual activation of the anterior cingulate cortex occurs during speech attribution tasks further solidifying their involvement in AVHs and the connection to disruptions in attentional networks. [6].

1.3 FOXP2 and the Genetics of Auditory Verbal Hallucinations

There is not a lot of information concerning the genetics of hallucinations, but studies have unveiled Forkhead-box P2 (FoxP2) as a gene related specifically to AVHs[9]. FOXP2 is a gene associated with language disorders and considering the language and speech abnormalities exhibited in AVHs, FoxP2 may play a role in susceptibility to experiencing AVHs. In gene expression studies, a connection between several FoxP2 polymorphisms and hallucinations have been discovered. A specific single nucleotide polymorphism (SNP), the rs10447760 variant has been identified in a haplotype in schizophrenics. It is suggested that the rs10447760 variant in schizophrenia patients makes them more vulnerable to experience AVHs[10]. In addition, another SNP, the rs2253478 variant has also been implicated in language disorders in schizophrenia[11].

2 Visual Hallucinations

Visual hallucinations are hallucinations that involve the perception of visual images without the absence of a visual stimulus. Most media portrayals of schizophrenia depict visual hallucinations. Images consist of figures, sometimes religious beings, animals and symbolize something particular. Visual hallucinations rarely occur alone in schizophrenic patients and usually coincide with auditory verbal hallucinations[12].

2.1 Primary Visual Cortex Abnormalities

In line, with the hypothesis that neurological abnormalities associated with hallucinations correspond to the sensory modality, most studies have found that abnormalities in the primary visual cortex are associated with visual hallucinations. Simple hallucinations consist of abnormal activity in the primary visual cortex, which become more complex when abnormal activation arises in visual association areas[13].

2.2 Neurotransmitters and Attentional Networks

There are hypotheses that the detachment from reality is related to dysfunctions in attention, as seen with abnormalities in the PFC[8]. This is the same with visual hallucinations as complex hallucinations are hypothesized as arising from reduced activity in the Dorsal Attention Network[13]. Furthermore, this activity is modulated by neurotransmitter activity. Hallucinations, in general are associated with disruptions in glutaminergic and dopaminergic systems[14][1]. Visual hallucinations as a result of attentional dysfunction can be related to dysfunction of monoaminergic, cholinergic and serotonergic systems. Dopamine is a modulatory neurotransmitter that modulates pathways between attentional networks, in particular networks in the striatum and midbrain[13]. Among the different sensory modalities, disruptions in attention seems to play a role in the manifestation of hallucinations.

2.3 Visual Hallucinations and Emotion

Visual hallucinations may also be the result of hyperconnectivity. In addition to attentional disruption, visual hallucinations may also be related to emotions. A recent study has uncovered a new connection between visual hallucinations and the limbic system. In patients with schizophrenia experiencing visual hallucinations, hyperconnectivity is found between the primary visual cortex and the amygdala. This could account for the emotional reaction experienced by patients who visualize threatening hallucinations (Ford et al., 2014). This hyperconnectivity facilitates the emotional experience of viewing visual hallucinations.

3 Somatic Hallucinations

Somatic (or tactile) hallucinations occur when a person experiences sensory touch in the absence of the stimulus[17]. Generally somatic hallucinations in paranoid schizophrenia are not very common. Once again they coincide with other types of hallucinations, most common gustatory and olfactory hallucinations. In fact it is reported that only up to 17% of schizophrenic patients endure somatic hallucinations, while only 11% experience either olfactory or gustatory hallucinations[18]. Similarly to AVHs and visual hallucinations, somatic hallucinations are also connected to several brain region abnormalities.

3.1 Somatosensory Cortex Abnormalities

Similarly to AVHs and visual hallucinations, somatic hallucinations are also connected to brain regions specific to somatosensory modality. Therefore, increased activation of the primary somatosensory, posterior parietal cortex and the thalamus are associated with somatic hallucinations. In addition, findings of increased activity in the insula and bilateral posterior cingulate gyri suggest that these areas also contribute to the pathology of somatic hallucinations[17].

3.2 Grey Matter Volume in the Right Thalamus

Along with the primary somatosensory cortex, recent work has discovered the involvement of the right thalamus in somatic hallucinations. Using voxel-based morphometry and diffusion tensor imaging, a sample of healthy people were compared to schizophrenia patients with hallucinations versus those without hallucinations. Reductions in grey matter in the right thalamus were identified, as well as a decrease in grey matter in the pars triangularis. This is suggested to be a correlation to the prevalence of somatic or tactile hallucinations[19].

Bibliography
1. Fenelon, G & Hamdani, N. (2010). “Hallucinations in Neuropsychiatry and Drug Abuse: From Phenomenology to Pathophysiology.”
2. Kompus et al. (2013). "The role of the primary auditory cortex in neural mechanisms of auditory verbal hallucinations." Frontiers in Human Neuroscience, 7(144): 1-13.
3. Shine, J. M., O’Callaghan, C., Halliday, G. M. & Lewis, S. J. G. (2014). “Tricks of the mind: Visual hallucinations as disorders of attention.” Progress in Neurobiology.
4. Allen, P., Laroi, F., McGuire, P. K. & Aleman, A. (2008). “The hallucinating brain: A review of structural and functional neuroimaging studies of hallucinations.” Neuroscience and Behevioral Reviews, 32: 175-191.
5. Wong, A. H. C. & Van Tol, H. H. M. (2003). "Schizophrenia: from phenomenology to neurobiology". Neuroscience and Biobehavioural Reviews, 27: 269-306.
6. Wolf, N. D. et al. (2011). "Dysconnectivity of multiple resting-state networks in patients with schizophrenia who have persistent auditory verbal hallcucinations". J Psychiatry Neurosci, 36(6):366-374.
7. Aguilar, E. J., Sanjuan, J., Garcia-Marti, G., Lull, J. J. & Robles, M. (2008). “MR and genetics in schizophrenia: Focus on auditory hallucinations”. European Journal of Radiology, 67: 434-439.
8. Rotarska-Jagiela et el. (2009). “Anatomical brain connectivity and positive symptoms of schizophrenia: tensor imaging study”. Psychiatry Research: Neuroimaging, 174: 9-16.
9. Li et al. (2013). "FoxP2 is significantly associated with schizophrenia and major depression in the Chinese Han Population". The World Journal of Biological Psychiatry, 14: 146-150.
10. Sanjuan J., Tolosa A., Gonzalez J. C., Aguilar E. J., Perez-Tur J., Najera C., et al. 2006. "Association between FOXP2 polymorphisms and schizophrenia with auditory hallucinations." Psychiatr Genet, 16(2):67–72.
11. Tolosa et al. (2010). " FOXP2 gene and language impairment in schizophrenia:association and epigenetic studies". BMC Medical Genetics, 11:114.
12. Manford, M. & Andermann, F. (1998). “Complex visual hallucinations: Clinical and neurobiological insights”. Brain, 121: 1819-1840.
13. Shine, J. M., O’Callaghan, C., Halliday, G. M. & Lewis, S. J. G. (2014). “Tricks of the mind: Visual hallucinations as disorders of attention”. Progress in Neurobiology.
14. Anticevic et al. (2013). “Connectivity, pharmacology, and computation: toward and a mechanistic understanding of neural system dysfunction in schizophrenia”. Frontiers in Psychiatry, 4(169): 1-21.
15. Ford et al. (2014). “Visual Hallucinations Are Associated With Hyperconnectivity Between the Amygdala and Visual Cortex in People With a Diagnosis of Schizophrenia”. Schizophrenia Bulletin.
16. Modinos et al. (2012). "Neuroanatomy of verbal hallucinations in schizophrenia: a quantitative meta-analysis of voxel-based morphometry studies". Cortex, 49(4): 1046-1055.
17. Shergill et al. (2001). “Modality specific neural correlates of auditory and somatic hallucinations”. J Neurol Neurosurg Psychiatry, 71: 688-690.
18. Lewandowski, K. E., DePaola, J., Camsari, G. B., Cohen, B. M. & Ongur, D. (2009). “Tactile, Olfactory and Gustatory Hallucinations in Psychotic Disorders: A Descriptive Study”. Ann Acad Med Singapore, 38(5): 383-387.
19. Spalletta, G., Piras, F., Rubino, I. A., Caltagirone, C. & Fagioli, S (2013). “Fronto-thalamic volumetry markers of somatic delusions and hallucinations in schizophrenia.”Psychiatry Research: Neuroimaging 212:54-64.

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