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85 Cards in this Set
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In the MSE, what do you see in the appearance of pts with schizo?
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-Motor disturbances
Catatonia Stereotypy Mannerisms -Behavioral problems Hygiene Social functioning Substance abuse |
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Discuss the ways catatonia can look:
What could it be confused with? |
Patients are immobile, mute, yet conscious. They exhibit waxy flexibility, or assumption of bizarre postures as the most dramatic example.
Catatonic excitement is uncontrolled and aimless motor activity. It is important to differentiate from substance-induced movement disorders, such as extrapyramidal symptoms and tardive dyskinesia. |
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stereotypy:
mannerisms: |
-Stereotypy: repetitive or ritualistic movement, posture, or utterance
-Mannerisms: A habitual gesture or way of speaking or behaving; an idiosyncrasy. |
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In the MSE, what do you see in the Mood and Affect of pts with schizo?
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-Affective flattening
-Anhedonia -Inappropriate Affect -Possibly depression |
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In the MSE, what do you see in the Thought Process of pts with schizo?
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Associative disorders/loosening
Circumstantial Thinking Tangential thinking Lack of ability to think abstractly |
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In the MSE, what do you see in the Thought Content of pts with schizo?
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-Hallucinations
-Delusions (is the TV sending you messages?) |
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formication:
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Tactile hallucination--the feeling of bugs crawling on your skin.
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In the MSE, what do you see in the Cognition of pts with schizo?
How critical are the cognitive deficits in schizo? |
-Subtle impairments
-Frontal lobe function declines -Associative thinking decreases -Lack of insight -The level of these deficits may be the best predictor of functioning. |
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What are the positive symptoms of schizo?
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Hallucinations
Delusions Formal thought disorder Movement Disorders *Disorders of commission |
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What are the negative symptoms of schizo?
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Alogia [poverty of speech, or poverty of content]
Affective flattening Anhedonia Avolition/apathy Attention *Disorders of omission |
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Which present earlier? positive or negative symptoms?
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In general patients exhibit more positive symptoms earlier on and as their disease progress the negative symptoms become more prominent.
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When does schizo start in people?
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Late adolescence/early adulthood.
Men get it earlier. And more severely. If it looks like it's occurring in an old person, it's probably something else! |
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How is schizo diagnosed?
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-“A” Criteria = Psychosis
-Duration = acute symptoms for 1 month; overall duration 6 months -Global Criteria |
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What are the schizo A criteria?
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Must have 2 or more:
Delusions Hallucinations Disorganized speech Grossly abnormal behavior Negative symptoms |
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Schizophreniform disorder:
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Like Schizophrenia except the duration is between 1 and 6 months (prodrome + episode + residual).
Impaired psychosocial functioning is not required for the diagnosis; probably about 2/3 go on to become Schizophrenics. If a person presents with psychotic symptoms for less than 6 months, however they are still psychotic, we would add the qualifier "provisional" to the diagnosis. Also we would note whether they had a good or poor prognosis. |
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Brief Psychotic Disorder:
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Brief Psychotic Disorder is different in that the psychotic symptoms last for less than a month and there is full remission by one month.
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Schizoaffective Disorder:
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Has symptoms of both Schizophrenia and of a Mood Episode. It fulfills symptoms of "Criterion A" of Schizophrenia. For diagnosis, at some point, psychotic symptoms have to be independent of mood (for at least 2 weeks).
Symptoms of a Mood Episode may include either manic, depressed or mixed symptoms. These have to occur for a "substantial" amount of time; otherwise you would be more likely to just give the patient 2 diagnoses (schizophrenia and major depressive disorder). |
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Delusional Disorders:
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Patients present with persistent delusions. Delusions are usually nonbizarre, thus differentiating this from schizophrenia. Hallucinations are not prominent.
Psychosocial functioning is okay, except for the direct impact of delusion (ex. Might not go on bus, because thinks people talking about them). |
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Shared Psychoses:
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Folie á Deux: this is when two people share the same delusion. Has two components, an inducer and a secondary. The inducer is a person who already has some psychotic disorder (usually schizophrenia). A second person, in a close relationship with the inducer, comes to share the delusion. This second person is usually in a dependent relationship with the inducer.
The couple rarely seek treatment and the secondary almost never does - shared psychotic disorder usually becomes evident when the inducer is treated. The primary intervention is to separate the second person from the inducer. |
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Psychosis due to something else:
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Psychotic Disorder Due to a General Medical Condition includes hallucinations or delusions that are directly secondary to a medical disorder. One must differentiate this from Delirium, in which delusions or hallucinations can occur, but are part of the delirium.
Substance-Induced Psychotic Disorder has the same story as Psychotic Disorder Due to a General Condition, including the Delirium rule out. You’ll often see psychiatrics use something called Psychotic Disorder NOS. This is usually a provisional diagnosis, used when we don’t know enough yet to make a real diagnosis. It can also be used to diagnosis someone who truly has a unique psychotic disorder that doesn’t fit into any of the other categories, but that is rare. |
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Differential diagnosis for Schizo:
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Delirium
Dementia Other Medical, neurological Medication-induced Other Psychiatric Illnesses |
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Delirium:
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Delirium is an acute confusional state, with multiple possible etiologies that can cause delusions and hallucinations. Usually delusional hallucinations are poorly formed, and not very elaborate, and they occur in a setting of "clouding of consciousness."
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Dementia:
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Typically are persecutory delusions: after losing wallet, might accuse loved one of stealing it. These also tend to be poorly formed, not elaborate, and they wouldn't justify a second diagnosis of a psychotic disorder.
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What neurological disorders may be confused with schizo?
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Temporal Lobe Epilepsy, tumor, stoke, and brain trauma.
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What general medical disorders may be confused with schizo?
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Endocrine and metabolic disorders (like Porphyria), vitamin deficiency, infections, autoimmune disorders (like Systemic Lupus Erythematosus) or toxins (like heavy metal poisoning).
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What medications might cause schizo-like symptoms?
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Stimulants (amphetamines, cocaine) hallucinogens (PCP), anticholinergic medications, Alcohol Withdrawal (Delirium Tremens), and barbiturate withdrawal.
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What other psych disorders may be confused with schizo?
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-Major Depression with psychotic features (which only occurs during depressive episodes)
-Panic Disorder (Patients may report they feel they are "going crazy") -Depersonalization Disorder -OCD, obsessions may reach point where they seem like delusions. -Personality Disorders, especially Cluster B (Borderline Personality Disorder, for example), can show elements of psychosis. -Must consider factitious disorder and malingering. Fortunately, these disorders are difficult to fake. |
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Schizo comorbidities. How common are these?
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Substance Abuse (esp etoh)
Depression Medical disorders Extremely common |
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What are the 3 stages of schizo?
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prodromal phase, active phase and residual phase.
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prodromal phase:
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Prodromal phase may precede the active phase of illness by many years. It is characterized by social withdrawal and other subtle changes in behavior and emotional responsiveness.
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active phase
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Has psychotic symptoms ("Criterion A"), which predominate.
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residual phase:
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Similar to the prodromal phase, although affective flattening and role impairment may be worse. Psychotic symptoms may persist, but at a lower level of intensity, and they may not be as troublesome to the patient.
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What are outcomes like in schizo patients?
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1/4 good outcome (defined as no hospital readmission during follow-up)
1/4 bad outcome (defined as continuous hospitalization during follow-up, or moderate to severe intellectual or social impairment) ½ intermediate outcome. Schizophrenia has a high mortality rate: perhaps 10% commit suicide. |
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What are positive prognostic predictors in schizo? 7
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Acute onset
Short duration Good premorbid functioning Normal affect/Affective symptoms Confused while psychotic Good social functioning High social class |
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What are negative prognostic predictors in schizo? 9
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Insidious onset
Long duration Family hx of psych illness Obsessions/Compulsions Flattened affect Assaultive Behavior Poor premorbid functioning Neurologic/anatomic abn. Low social class |
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Schizo is increasingly thought to be a _____ disorder.
Dysregulation in the _____ and ____ modulation of ____ may play a role in the manifestation of symptoms. |
neurodevelopmental
glutamatergic GABAergic dopamine |
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What are some of the risk factors for schizo involving pregnancy?
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Obstetric and perinatal complications
Maternal nutritional status Influenza infection in the first trimester Winter-spring birth excess |
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What are some environmental factors that put someone at risk for schizo?
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-Urban residence
-Migration -Childhood adversity parental loss/separation child abuse bullying -Stressful life events |
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How genetic is the transmission for schizo?
Where's the schizo gene? |
80%
But...identical twins only get it half the time, suggesting environmental influence. There's no one gene. Candidates are involved in neurodevelopment, plasticity, and transmission. |
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How might the environment interact with genes in teenage years?
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One example is pot. If you have the Val/Val allele of COMT and smoke pot, you're more likely to develop psychotic symptoms.
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What brain structural abnormalities do we see in schizo pts?
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-Enlarged lateral and third ventricles
-Reduced cortical gray matter volume in: Cortex Association neocortex (Prefrontal & Superior temporal) Hippocampus Thalamus -But magnitude of change is small, overlaps with comparison groups and is not specific -Remember it's a neurodevelopmental disorder. NOT degenerative. |
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Is schizo a disorder of early brain development or late?
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BOTH.
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What happens with pyramidal neurons in the PFC in schizo?
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-Increased density of pyramidal neurons in the dorsolateral PFC.
-It is thought that the increased density is due to a decrease in axon terminals and dendritic spines that occupy the space in between neurons. -Shorter dendrite length. -There have been a number of studies, in addition, that have shown that the neuronal cell bodies themselves are smaller in areas of the PFC and the hippocampus. |
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What does fMRI show in the prefrontal cortex in schizo pts?
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Hypofrontality, a phenomenon in which patients cannot activate prefrontal cortex
This may explain the cognitive insufficiency and deficits in attention, alerting, memory, learning and shifting sets that schizophrenic patients display even before their first psychotic episode. |
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In schizo, what's going on with the medial temporal lobe?
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Mild cortical atrophy has been reported in the medial temporal lobe along with cortical neuronal disarray.
Focal abnormalities indicating abnormal alignment of neurons have been observed in medial temporal lobe structures such as the amygdala, entorhinal cortex, and especially the Hc --> poor memory |
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In schizo, what's going on with the thalamus?
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Probable thalamic dysfunction.
PET shows significantly decreased relative glucose metabolic rate primarily located bilaterally in the region of the mediodorsal nucleus (MD) in patients with schizophrenia. The worse the schizo is, the lower the glucose metabolic rate is. |
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What pathways significant to schizo is dopamine involved in?
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a.)Nigrostriatal- Involved in movement
b.) Mesolimbic- emotional behaviors [Increased activity in this pathway is thought to cause positive symptoms of schizophrenia] c.) Mesocortical- cognition/behavior [Decreased activity in this pathway is thought to contribute to negative and cognitive symptoms of scz] d.) Tuberinfundibular-Maintains prolactin regulation |
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What evidence supports dopamine's role in schizo?
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-All antipsychotics block D2 receptors
-Dopamine agonists can cause psychosis (i.e. amphetamine...smaller doses needed to make schizo patients go psycho) |
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What does the hypofrontality theory change about the dopamine theory?
What specifically is happening? |
It adds to it. Says that in addition to an excess of DA activity in the basal ganglia, there is a decrease of DA activity in the PFC--> loss of executive function.
In the DLPFC, there's a decrease in tyrosine hydroxylase--> decreased DA synthesis. There may be upregulation of D1 receptors in the PFC due to lack of DA. |
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Why are we studying glutamate and GABA now, and moving forward from the DA/hypofrontal theories?
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Dysfunction of Glutamate receptors leads to decreased activity in the mesocortical pathway-->
And increased activity in the mesolimbic pathway--> |
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What's going on with chandelier neurons in schizo?
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Chandelier neurons are a subset of GABA neurons. They connect with other neurons through cartridges which are dilitations off the axon. Patients with schizophrenia have a reduction in the amount of cartridges per chandelier neuron. This may interfere with fine-tuning of prefrontal cortical networks.
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-Good evidence for hyperactivity of dopamine at the D2 receptors in the ____ ____ leading to psychotic symptoms (in a majority of patients)
-Some evidence for altered neurotransmitter activity (____, ____, ____) in the prefrontal cortex as well as deficits in neuronal structure/blood flow that may lead to negative and cognitive symptoms -Glutamate/GABA dysregulation may be contribute to ____ dysregulation -Schizophrenia is likely a heterogeneous disorder with a very complicated underlying pathophysiology that is not yet well understood. |
basal ganglia
DA, GABA, GLU DA |
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Typical antipsychotics are ____ receptor antagonists that exert their therapeutic benefit primarily by blocking ____ transmission in the ____ tract.
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D2
DA mesolimbic |
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Typical antipsychotics can worsen negative symptoms and cause EPS including: 4
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akathesia, parkinsonism, dystonia and tardive dyskinesia
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Atypical antipsychotics block both ____ and ____ neurotransmission. They have fewer EPS but can cause ____ ____.
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5HT
DA metabolic syndrome |
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What receptors do typical antypsychotics block?
Why is this wide effect significant? |
D2, M1, H1, alpha-1
Significant for side effects. |
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List the 4 principal DA pathways in the brain:
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-Nigrostriatal pathway connects the substantia nigra and the basal ganglia.
-Mesolimbic pathway travels from the midbrain (ventral tegmental area) to the nucleus accumbens which is part of the limbic system. -Mesocortical pathway travels from the midbrain (ventral tegmental area) to the prefrontal cortex. -Tuberoinfundibular pathway travels from the hypothalamus to the pituitary gland. |
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What are the effects of a typical antipsychotic in each of the DA pathways?
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a.)Nigrostriatal: D2 blockade in this pathway leads to extra-pyramidal side effects; if >80% blocked
b.) Mesolimbic: D2 blockade in this pathway leads to decreased positive symptoms; 60-70% block reqd. c.) Mesocortical: D2 blockade in this pathway can increase the negative and cognitive symptoms, worsening of cortical symptoms d.) Tuberoinfundibular: D2 blockade in this pathway leads to hyperprolactinemia, sexual dysfunction; galactorrhea in women; decreased bone density. |
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List the early onset and Tardive syndrome EPSs that can result from typical antipsychotics. 3 of each
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Early onset: Dystonia, Parkinsonism, Akathisia
Tardive syndromes: Dyskinesia, Akathisia, Dystonia |
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Describe dystonia that may result from typical antipsychotics.
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-Can be acute or tardive
-Occurs within hours or days of starting the medication -Terrifying -Spasms involving neck, back, tongue, muscles that control lateral eye movement, larynx. |
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Describe akathesia that may result from typical antipsychotics.
What second drug can help these effects? |
-Subjective feeling of restlessness in the lower extremities--> inability to sit still
-Occurs shortly after starting the medication -Occurs in a high percentage of pts -Can be mistaken for an exacerbation of psychosis, anxiety, depression -Beta blockers can sometimes help in treating this effect. |
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Why might typical antipsychotics cause Parkinsonism?
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-Ach> DA in basal ganglia
-Gradual effect, may not appear for weeks |
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Describe Tardive syndromes that may result from typical antipsychotics.
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-Tardive just means late onset
Tardive dyskinesia: -Involuntary choreoathetoid movements of the face, trunk or extremities -5% per year in young adults -30% per year in the elderly |
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What non-psych med can cause tardive dyskinesia?
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metoclopramide
prochlorperazine |
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What is Neuroleptic Malignant Syndrome, what causes it, and how do you treat it?
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-Associated with high potency conventional antipsychotics but can be seen with atypicals
Muscle rigidity (more so with typicals) Fever Autonomic instability Elevated WBC (> 15,000) Elevated CPK Treatment: stop antipsychotic, supportive treatment |
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What are the side effects of typical antipsychotics dealing with M, H, and alpha receptors?
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M1: blurred vision, dry mouth, constipation, urine retention
H1: Sedation, weight gain alpha-1: Orthostatic hypotension |
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List two examples of high potency typical anti-psychotics. What is unique about these?
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-Haloperidol and Fluphenazine:
-Bind more tightly to D2 receptors -Associated with more EPS -Often need to give anti-cholinergic medication with it for to treat side effects. -Less anti-cholinergic; often need to give anti-cholinergic medication with it to treat side effects. |
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List one example of low potency typical anti-psychotics. What is unique about these?
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-Chlorpromazine
-Binds less tightly to the D2 receptors -Associated with less EPS than high potency but more than atypicals. -More anti-cholinergic; causes sedation and hypotension |
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What's an advantage of atypicals?
A disadvantage? |
-Much less EPS.
-agranulocytosis; was actually withdrawn because of this. -reintroduced because it works when other treatments don't |
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Why is clozapine "dirty"?
When would you use it? |
Targets lots of 5-HT and DA receptors. It's effective.
Only use it if patient fails to have success with two other drugs. |
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Discuss 5HT-2A receptors. Where are they located? 3
What different functions do they have? |
Cortex, Hc, GABAergic interneurons.
-On GABAergic cells they stimulate GABA release -On pyramidal neurons they can weaken GABA effects -Involved in modulating DA activity |
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Besides clozapine, name 4 other atypical antipsychotics. What receptors do they block?
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Risperidone
Olanzapine Quetiapine Ziprasidone Block both 5HT2A and D2. 5HT2A>D2 |
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What effect does LSD have on 5HT2A receptors?
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It's an agonist.
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Serotonin via the 5HT2A receptor modulates ____ release. In the normal state it serves to ____ the release of ____.
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dopamine
attenuate dopamine |
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There are 5HT2A receptors both on the axon and dendrites of ____ neurons. Serotonin agonism ____ the release of dopamine.
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DA
decreases |
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List the effects of atypical antipsychotics in the mesocortical, nigrostriatal, tuberoinfundibular, and mesolimbic pathways.
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-In the mesocortical, nigrostriatal and tuberoinfundibular pathways the end result is less DA blockade than with the typicals--> less EPS, less negative symptoms, less hyperprolactinemia.
-There continues to be sufficient D2 blockade in the mesolimbic pathway for continued antipsychotic effect. The effect of D2 antagonism is more robust than 5HT antagonism in the mesolimbic pathway. |
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Why do atypicals lead to less DA blockade in the mesocortical pathway?
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In the mesocortical pathway there is a decrease in DA activity in the prefrontal cortex at baseline in patients with schizophrenia.
The action of serotonin at the 5HT2A receptor further decreases dopamine activity. If the 5HT2A receptor is blocked (by an atypical) this inhibition does not occur and the effect of dopamine blockade is attenuated in the prefrontal cortex. INHIBITION OF AN INHIBITOR |
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Why do atypicals lead to less DA blockade in the nigrostriatal pathway?
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In the nigrostriatal pathway, dopamine blockade leads to extrapyramidal symptoms.
With serotonin blockade (by an atypical), the D2 blockade is decreased and so are the extrapyramidal symptoms. INHIBITION OF AN INHIBITOR |
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Side effects of atypicals:
Which drugs are worst, which are in the middle, and which are the least severe in terms of side effects? |
Metabolic syndrome: Hypercholesterolemia, Diabetes, Weight gain
clozapine + olanzapine > risperidone + quetiapine > aripiprazole + ziprasidone |
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What three markers would you check when rxing atypicals and how often?
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Weight, fasting glucose, cholesterol.
Before starting, at 3 months, then yearly. Check weight every month for first year; then every 3 months. |
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So how effective are antipsychotics really? How many pts quit using their meds and why?
What two meds might be most effective? |
-We got some work to do.
-75% of pts quit their meds due to ineffectiveness or side effects. -Clozapine is the only one that is more effective for sure. -Olanzapine may be better, too. |
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Why is psychosocial treatment important in schizo?
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-20-45% of patients with schizophrenia continue to have symptoms that interfere with their functioning despite adequate medication trials
-5-10 % show no benefit with medication -Combined pharmacological and psychosocial treatment is more effective than pharmacotherapy alone |
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What's the goal of psychosocial approaches in treating schizo. What are some examples of approaches?
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Goal: strengthen coping skills and social support system to protect against stressors.
-Family education/therapy -Cognitive Behavioral Therapy -Supported employment -Assertive community treatment -Social skills training |
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Why family therapy in treating schizo? Benefits and goals?
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High expressed emotion (EE) predicts relapse in schizophrenia
EE= high levels of family distress Benefits of ongoing family contact for patients Better work and overall role performance Increase ability to decrease substance use Goals of treatment Educating participants re: illness Improve communication and problem solving skills |
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Why CBT in treating schizo? Benefits? How does it work?
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Can be effective with regard to:
-Positive and negative symptoms -Depression -Adherence to treatment Based on a cognitive model of schizophrenia -Deficit in ability to correctly assess significance or lack of significance of sensory stimuli -Therapy involves identifying affective and behavioral factors that maintain psychotic symptoms -Promote active participation of the patient |
