Genetic Although environmental factors likely play an important role in the onset of the disorder, people who have relatives with
schizotypy,
mood disorders, or other disorders on the
schizophrenia spectrum are at a higher likelihood of developing StPD. The
COMT Val158Met polymorphism and its Val or Met
allele are suspected to be associated with Schizotypal personality disorder. These genes affect
dopamine production in the brain, a
neurochemical thought to be associated with schizotypal traits. The gene may also contribute to decreased levels of gray matter in the
prefrontal cortex. This may lead to impaired capacities for decision-making, speech,
cognitive flexibility, and altered perceptual experiences. The rs1006737
polymorphism of the
CACNA1C gene is also believed to have a part in schizotypal symptoms. It may lead to a significantly increased
physiological response to
stress through the
cortisol awakening response in the brain. It may also negatively affect reward processing in the brain and lead to
anhedonia or
depression in patients. These factors possibly lead to the development of Schizotypal traits. The
zinc-finger protein ZNF804A likely affects the levels of
paranoia,
anxiety, and
ideas of reference in StPD. This gene is also thought to negatively impact
attention in people with StPD. It may lead to an increased level of
white matter volume in the
frontal lobe. Another gene, the
NOTCH4 is thought to relate to schizophrenia spectrum disorders. It can lead to disruptions in the
occipital cortex, and therefore symptoms of schizotypy. The
GLRA1 and the
p250GAP genes are also potentially associated with StPD. It may lead to abnormally low levels of
Glutamic acids in the
NMDA receptors, which impairs memory and learning. StPD may stem from abnormalities in
Chromosome 22.
Neurological Exposure to influenza during week 23 of
gestation is associated with a higher likelihood of developing StPD. Poor
nutrition in childhood may also contribute to the onset of StPD by altering the course of brain development. Numerous areas of the brain are thought to be associated with StPD. Higher levels of dopamine in the brain, possibly specifically the
D1 receptor, might contribute to the development of StPD. StPD is associated with heightened dopaminergic activity in the
striatum. Their symptoms may also stem from higher
presynaptic dopamine release. People with StPD may also have decreased volumes of
grey or
white matter in their
caudate nucleus, which leads to difficulties in speech. People with StPD likely have a reduced volume in their temporal lobes, possibly specifically the left hemisphere. The reduced levels of
gray matter in these areas may be linked to their negative symptoms. Reduced volume of gray or
white matter in the
superior temporal gyrus or the
transverse temporal gyrus are thought to lead to issues with speech, memory, and
hallucinations. Deficits in the gray matter volume of the
temporal lobe and
prefrontal cortex are likely associated with impairments in
cognitive function,
sensory processing,
speech,
executive function,
decision-making, and
emotional processing present in people with StPD. StPD symptoms may also be influenced by reduced
internal capsule, which carries information to the
cerebral cortex. People with StPD can also have impairments in the
uncinate fasciculus, which connects parts of the
limbic system. People with StPD have reduced levels of gray matter in their
middle frontal gyrus and
Brodmann area 10, although not as reduced as patients with schizophrenia, Increased
gyrification in
gyri by the
cerebellum may lead to
dysconnectivity in the brain, and therefore, schizotypal symptoms. They may also have a hyporeactive or hyperreactive
amygdala as well as hyperactive
pituitary glands and
putamens. It is also possible that lower capacities for
prepulse inhibition plays a role in StPD. Research has suggested that people with StPD can have higher concentrations of
Homovanillic acids. Abnormalities in the
cave of septum pellucidum may also be present. In people predisposed to schizophrenia spectrum disorders, the consumption of
cannabis can induce the onset of StPD or other disorders with psychotic symptoms.
Environmental Unique environmental factors, which differ from shared sibling experiences, have been found to play a role in the development of StPD and its dimensions. There is evidence to suggest that
parenting styles, early separation,
childhood trauma, and childhood neglect can lead to the development of schizotypal traits. Neglect, abuse, stress, trauma, or family dysfunction during childhood may increase the risk of developing schizotypal personality disorder. People with the most severe cases of StPD usually have a combination of childhood trauma and a genetic basis for their condition. During childhood, people with StPD may have seen little
emotional expression from their parents. Another possibility is that they were excessively criticized or felt like they were constantly under threat, potentially resulting in the onset of social anxiety, strange thinking patterns, and blunted affect present in StPD. Over time, children learn to interpret social cues and respond appropriately but for unknown reasons this process does not work well for people with this disorder. Their difficulties in social situations might eventually cause the individual to withdraw from most social interactions, thus leading to
asociality. and are more anxious, socially isolated, and sensitive to criticism. There is also evidence indicating that disruptions in brain development during the prenatal period could affect the development of StPD. == Diagnosis ==