SCHIZOPHRENIA
Skhizein (to split or scatter) + Phren (the mind)
Schizophrenia is the quintessential psychotic condition. Psychosis is the loss of reality. It’s a weird condition with an equally weird name.
Epidemiology?
It usually onsets around the time kids go off to college. The negative symptoms usually start first, begin to escalate, then the patient suddenly gets worse in what’s called a “psychotic break” or “post-mortem decline.” There is a genetic component to schizophrenia. You have an 80% chance of getting Schizo if your identical twin has it. 35% for fraternal twins, 35% for two parents, 10% for one parent and 3% for one 2nd-degree relative. In women, Schizo is less common, onsets later in life and has less severe symptoms (Estrogen is believed to play a protective role).
Pathophysiology?
Essentially, Schizophrenia is believed to be a Dopamine problem. It’s believed to result from too much Dopamine in the mesolimbic path, and too little Dopamine in the mesocortical path. Nobody knows why (update - more recent evidence suggests that schizophrenia isn’t a neurotransmitter-based disease, but rather an abnormality in structural brain development).
The mesolimbic path is the reward center of the brain. It gets activated when Dopamine binds to D2. Continual overactivation of it results in the positive symptoms of Schizophrenia. They’re constantly getting reward signals!
The mesocortical path is involved in motivation, emotion and cognition. It gets activated when Dopamine binds to D1 and when Serotonin binds to 5-HT2A. Underactivation results in the negative symptoms of Schizophrenia. They basically have no emotions!
Keep in mind that Serotonin (5-HT2A) plays a big role in this path. That’s why Typical Antipsychotics (which only block D2 receptors) don’t treat the negative symptoms, but Atypical Antipsychotics (which block Dopamine AND Serotonin) help!
