Schizophrenia

Schizophrenia

A term coined by Eugen Bleuler (1908) to refer to a break from reality.

Syndrome

A collection of signs and symptoms of unknown etiology.

Positive Symptoms

Symptoms that make themselves known by their presence (excess), including thought disorders, delusions, and hallucinations.

Thought disorder

Disorganized, irrational thinking and difficulty arranging thoughts logically.

Delusions

Beliefs that are contrary to fact, such as persecution, grandeur, or control.

Hallucinations

Perceptions of stimuli that are not actually present, most commonly auditory.

Negative Symptoms

Symptoms known by the absence or diminution of normal behaviors, such as flattened emotional response, poverty of speech, or social withdrawal.

Cognitive Symptoms

Difficulty in sustaining attention, low psychomotor speed, deficits in learning and memory, poor abstract thinking, and poor problem-solving.

Hypofrontality

Decreased activity of the frontal lobes, particularly the dlPFC.

Sensory-motor gating deficits

Difficulties screening out irrelevant stimuli and focusing on salient ones.

Structural Differences in Schizophrenia

The relative ventricle size of schizophrenic patients was more than twice as big as that of normal control subjects.

Schizophrenia (Genetics)

A heritable trait, although it is not due to a single dominant or recessive gene.

Paternal Age (Schizophrenia)

Mutations in the spermatocytes due to cell division.

Dichorionic

Occurs before day 4, the two organisms develop independently, each forming their own placenta

Monochorionic

Occurs after day 4, the two organisms become monochorionic - share a single placenta.

Early Neurodevelopmental Model

Events in early life (prenatally) cause deviations from normal neurodevelopment and these lie dormant until the brain matures sufficiently to call into operation the affected systems.

Late Neurodevelopmental Model

Schizophrenia may result from an abnormality or deviation in adolescence, when synaptic pruning takes place.

Dopamine (DA) Hypothesis

Proposes that schizophrenia is caused by abnormalities in DA functioning in the brain.

Mesolimbic Pathway

Overactivity of DA in the mesolimbic system results in the positive symptoms of schizophrenia.

Mesocortical Pathway

Underactivity of DA in the mesocortical system results in the negative and cognitive symptoms of schizophrenia

DA agonists

Drugs that produce symptoms that resemble the positive symptoms of schizophrenia.

Typical Antipsychotics

Drugs that eliminate, or at least diminish the positive symptoms in most of the patients.

Tardive dyskinesia

Patients with tardive dyskinesia are unable to stop moving.

Atypical Antipsychotics

Antipsychotics that improve both positive and negative symptoms of schizophrenia and improve performance in neuropsychological tests.

Glutamate Hypo-functioning Hypothesis

Suggests schizophrenia is due to NMDA receptor hypofunction.

Microglial activation and schizophrenia

The brain’s immune cells are hyperactive in people who are at risk of developing schizophrenia.

Amoeboid

Activating state of Microglia in the CNS

Oestrogen Hypothesis of Schizophrenia

Estrogen seems to play a protective role against the development of schizophrenia