Schizophrenia example #43812

-Disorder characterized by psychotic symptoms which are usually persistent (>6 mos.) or at least recurrent -significant impairment in functioning -major cause of inpatient care episodes

-"split personality" -major source of violence, danger to others

*A*. Characteristic symptoms: *2 or more of the following*, each *present for a significant portion of time* during a 1 month period: • Delusions • Hallucinations • Disorganized speech • Grossly disorganized or catatonic behavior • Negative symptoms -*Only one* of these symptoms is required *if* delusions are bizarre or hallucinations consist of a voice keeping a running commentary *B*. Sufficient to *cause social/occupational dysfunction* *C*. Duration: Continuous signs of disturbance for at least *6 months* which may include a prodromal period or residual period *D*. Exclusion of schizoaffective and mood disorders, substance-induced psychosis, or psychosis due to a medical condition

-Thought disorder *+* Mood disorder -An uninterrupted period of illness during which, at some time, there is a Major Depressive, Manic, or Mixed Episode *concurrent with symptoms that meet Criterion A for Schizophrenia*

-Meets most criteria for schizophrenia but episode lasts *less than 6 months* -Impaired social & occupational functioning are *not* required Note: If symptoms persist beyond a six month period, the diagnosis is changed to schizophrenia

Catatonic—dominant symptoms relate to decreased or increased motor activity

-A psychomotor *symptom of catatonic schizophrenia* -Leads to a decreased response to stimuli and a *tendency to remain in an immobile posture*.

Disorganized—speech and behavior are disorganized; flat or inappropriate affect

Paranoid—delusions are especially prominent; paranoid ideation; auditory hallucinations

Residual—has history of schizophrenia, *but* no longer meets criteria; typically, mostly negative symptoms remain

Undifferentiated: Criteria for sub-types *not* met

-Paranoid

-One must always rule out physical causes for what might appear to be mental illness; this is esp. true if the onset is acute (over hours or days) and/or there is no prior history of mental illness. -Head Injury -Low sodium (hyponatremia) -Liver disease -Pancreatitis -Acute Intermittent Porphyria Infection (mimics it). -Heavy Metal Poisoning (Mercury in tuna) -Hyperthyroidism —mimics mania, anxiety, lability; look for increased pulse, tremor, sweating, weight loss, visual disturbances. -Digitalis toxicity may present with unusually well-formed visual hallucinations of "small people". -Anticholinergic toxicity Many OTC and psychotropic meds have ACh activity. -Other drug reactions (bath salts) -Drug abuse/intoxication .

*Delusional disorder*—prominent delusions, usually *non-bizarre*, without other features of psychosis (look normal, speak normally, & behave normally). *Capgras Syndrome*—belief that others have been replaced with imposters; or may be unable to recognize self in mirror. *Brief/reactive psychosis*—acute onset of apparent schizophrenia, brief duration. *Shared psychosis* (Folie a Deux)—SO's "acquire" schizophrenic-like features. Schizotypal and schizoid personality disorders

-Many major mental illnesses tend to begin in childhood -Childhood MI's usually go undetected and untreated for 7-9 years (there may be a prodromal phase where "soft" or early signs are present but unrecognized) -Earlier recognition leads to earlier treatment -Earlier treatment is believed to limit the amount of neurological damage that accrues, improving the long-term prognosis -Early treatment reduces maladaptive coping and provides for interventions to reduce developmental deficits that otherwise tend to occur -Staff may mislabel symptoms as resistance or other negative, volitional (chosen) behavior and respond non-therapeutically

An abnormality or excess in normal functioning or the presence of abnormal functioning, typically including: -hallucinations -delusions -thought disorder -disorganized and sometimes bizarre speech, and behavior

-Have a relatively more *acute onset* (weeks to months), and typically have *exacerbations & remissions* (with residual symptoms) rather than an unremitting course. -They usually *do not have a family history* of psychosis, and typically *lack structural brain abnormalities*. -Such patients also tend to *experience a better prognosis* and often return closer to their premorbid functioning than persons with predominately negative symptoms.

A decrease in or loss of normal function; examples: -Affective flattening (constriction, blunting) -Apathy—hygiene deficits -Anhedonia (unable to experience pleasure) -Asociality (social withdrawal) -Alogia (absence or poverty of speech) -Avolition (reduced spontaneous movement) -Attentional impairment—distractibility -Reduced goal-directed behavior or task completion NOTE—the above are sometimes assumed to be "choices" about how to behave made by the pt, but they are not—they are part of the illness.

-Tend to have experienced a more *insidious/chronic onset* (months to years). They often experienced significant behavioral problems and *high levels of anxiety and worry during childhood*. -Typically they tend to have a *poorer prognosis*, with a pattern of *chronic deterioration* and sometimes extended institutional placements. -They often *have a family history* of schizophrenia, and *demonstrate structural brain abnormalities*.

-Formal thought disorder (cognitive thought process impairment) -Looseness of associations (i.e., LOA... fragmented, poorly constructed associations) -Flight of ideas (FOI) -Disorganized thoughts—incoherence -Speech—Tangentiality, circumstantiality, word salad, neologisms, clanging, echolalia, pressured speech -Referentiality, magical thinking, -Impaired stimulus processing -Memory impairment -Thought blocking; thought broadcasting

-Impaired ability to "read" others' -Impaired judgment and problem-solving -Decreased impulse control -Unintended criminal or rule-breaking behavior -Impaired awareness of illness (ANOSOGNOSIA--50% of patients do not believe they have the Dx) -Neurological deficits—object recognition, pain perception, perception of the passage of time, etc -Compulsive behavior (water intoxication) -Grimacing, posturing, echopraxia -Affective instability (lability, inappropriateness) -Anxiety and/or frustration intolerance -Dysphoria and depression -Maladaptive coping (substance abuse, etc) -Suicidality (10% kill themselves) -Rarely, violence

-*Symptom* of Schizophrenia -It is the *difficulty evident* in cognitive processes and thought content, along with *impaired* executive functioning (information processing, decision making, planning tasks, problem solving, ability to abstract [i.e. overly concrete thinking]).

-Hallucinations originate with an inability to correctly attribute one's perceptions to external sources, or to perceiving sensations *which do not exist* in reality. -They *can be* caused by physical illnesses (delirium, withdrawal). Types of hallucinations include: 1) Auditory—most common form; often accusatory or derogatory; assess COMMAND FORM; r/o dissociative disorder (must distinguish from dissociative "voices") 2) Visual—second most common form; r/o "flashbacks" 3) Olfactory—more common in neuro disorders 4) Tactile—more common in neuro disorders and withdrawal states 5) Gustatory—rare

-Delusions represent irrational and illogical interpretations or explanations of one's experiences, held despite evidence to the contrary. -In some cases, delusions develop as the person attempts to understand his hallucinations. Includes: -Grandiose -Paranoid -Religious -Somatic (Feel like have a disease when they don't) -Nihilistic -Erotomanic (feelings of love for somebody who doesn't even know they exist)

-Genetic abnormalities and inheritance patterns suggest the possibility of genetic causation. -However, the inheritance patterns and other data are inconclusive and do not present as high a degree of predictability as might be expected otherwise. -Genetic mutation would, however, be consistent with such irregular patterns. Chromosome 6 is one suspected location. -A gene for the enzyme catecho-O-methyltransferase (COMT), which chemically breaks down dopamine, comes in three varieties, one of which seems to shift the dopamine balance between the prefrontal cortex and the mid-brain (NIMH, 2005).

-A variety of scanning technologies have shown variances in brain structure in schizophrenics vs. non-schizophrenics. Some of these abnormalities exist before birth. Their causes could range from genetics to viruses/prions to environmental toxins. -Affected structures include the prefrontal cortex, the hippocampus, and the ventricles (*ventricular enlargement*). -Again, however, the patterns are irregular; not all patients with schizophrenia present these changes. And it's not clear whether such changes represent causes of the disorder, or are themselves consequences of the disorder. -One theory holds that certain parts of the brain fail to fully develop. -Another suggests that certain portions of the brain somehow atrophy. -Still another suggests that the normal "pruning" phenomena, wherein certain neurons are eliminated as the brain's organization progresses during adolescence, somehow goes awry, resulting in excessive pruning and neuron loss.

-An early and ongoing theory involves dysregulation of neurotrans-mitter function; one or more homeostatic mechanisms that normally assure the proper amount of various neurotrans-mitters, and/or the activity and availability of receptor sites, is defective, resulting in over- or underactivity of the affected neurotransmitters. -*Dopamine* is involved in many of the brain centers that regulate many of the functions that affected in schizo-phrenia. Many antipsychotic medications affect dopamine levels, distribution, receptor sites, or activity (are antidopiminergic, block receptors, etc). -*Serotonin* and glutamate are also implicated. PCP, which produces a drug-induced psychosis, interferes with glutamate dynamics. Serotonin modulates dopamine. Atypical antipsychotic meds tend to impact both serotonin and dopamine pathways.

-Early theories suggested that stressors such as double-bind messages or pathological parenting (the so-called "schizophrenegenic mother") caused the disorder. Such theories have been largely discarded in favor of biological-based theories. -However, stressors of a social or biological nature sometimes seem to be associated with the onset of the disorder. It could be that, in persons with a biological predisposition to develop schizophrenia, certain stressors may trigger the disorder (stress diathesis theory). The absence of these stressors in other such persons might help explain the unexpected variances observed in this disorder (e.g. a monozygotic twin concordance rate of only 50%). -Some of the stressors implicated to date include: drug abuse, CNS infections or trauma, hostile social (e.g. high EE [expressed emotion] families) or physical environments, abuse, inadequate coping or social skills, poverty, medical illnesses, inadequate nutrition or sleep, and isolation.

-Approximately 20% of persons with a functional psychosis such as schizophrenia seem to recover essentially to their premorbid state. -Approximately 60% appear to have a course of exacerbations and remissions, with varying degrees of residual symptoms in-between periods of decompensation. -Approximately 20% tend to experience a devastating course that is deteriorating in nature & overwhelming in consequence; they are sometimes called the "back ward patients" because they are often institutionalized for many, many years. -Some theorize that the different outcomes may represent different, but similar-appearing, disorders; or they could represent varying degrees of severity in the same disorder. -Recent research suggests that more frequent exacerbations and longer periods of time without treatment may worsen the prognosis. Earlier onset is also associated with a poorer prognosis.