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B&B Part 2 > B&B Week 9 > Flashcards

B&B Week 9 Flashcards

1
Q

what two areas does the basal ganglia communicate with?

A

there are tracts between the basal ganglia and the thalamus, and the basal ganglia and the cortex

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2
Q

what is the striatum?

A

caudate and putamen

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3
Q

what is the input to the basal ganglia?

A

corticostriatal tracts (striatum is caudate plus putamen)

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4
Q

what are the reciprocal interconnections of the basal ganglia?

A

striato-nigral (between striatum and substantia nigra)

subthalamic nucleus (between STN and globus pallidus)

globus pallidus and striatum

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5
Q

where does the output from the basal ganglia go?

A

thalamic facsiculus (from globus pallidus to thalamus)–> lenticular fasciculus and ansa lenticularis

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6
Q

what is the major NT of the basal ganglia? what is the clinical correlate for this?

A

many of the tracts involving the basal ganglia are dopaminergic (i.e nigrostriatal) and thus have implications in psychosis, since psychosis is linked to dopaminergic dysregulation

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7
Q

how many cerebellar hemispheres are there?

A

2–> there is an ipsilateral and a contralateral side

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8
Q

what is the vermis of the cerebellum?

A

midline, with nodule as most anterior part

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9
Q

where is the flocculus in the cerebellum?

A

in the groove between the superior and inferior surfaces

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10
Q

where is the tonsil of the cerebellum?

A

on the inferior surface –> prominent bulges on hemispheres, adjacent to the vermis

**sit right above the foramen magnum–> can get tonsillar herniation

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11
Q

what are the 3 lobes of the cerebellum?

A
  1. flocculonodular
  2. anterior–> rostral to primary fissure dividing the superior surface in half (quite small compared to posterior lobe)
  3. posterior–> remainder of the cerebellum
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12
Q

what is the largest cerebellar nucleus? what does it do?

A

dentate nucleus

links it to the rest of the brain

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13
Q

other than the dentate nucleus, name three other deep cerebellar nuclei

A

emboliform

globose

fastigial

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14
Q

what neurotransmitter is linked to extra-pyramidal movement disorders?

A

dopamine deficiency

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15
Q

what are extra-pyramidal symptoms?

A

include movement disorders –> pseudoparkinsonism, akathisia, akinesia

linked to dopamine deficiency

do NOT involve the pyramidal tract or lateral corticospinal tract

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16
Q

what would lead to extra-pyramidal symptoms? (EPS)

A

lesions to the cerebellar loops (i.e vestibulocerebellar, spinocerebellar or cerebrocerebellar loops)

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17
Q

what are the two major classifications for the motor system in the brain?

A
  1. pyramidal

2. extra-pyramidal

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18
Q

what is the pyramidal portion of the motor system in the brain?

A

primary motor pathway in the brain, goes via the medullary pyramids

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19
Q

what symptoms does damage to the pyramidal motor system cause?

A

spasticity (increased tone or passive resistance; velocity and direction dependent)

weakness

paralysis (no movement)

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20
Q

what structures are part of the extra-pyramidal motor system?

A 
contains the basal ganglia structures:
caudate and putamen ("striatum")
globus pallidus (internal and external)
substantia nigra (pars reticularis and pars compacta)
subthalamic nucleus
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21
Q

which system is implicated in most movement disorders, extrapyramidal or pyramidal?

A

extra pyramidal

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22
Q

what symptoms would arise from a lesion in the extrapyramidal pathway?

A

rigidity

no overt weakness

insufficient OR excessive/abnormal movements (depending on whether the lesion is in the direct or indirect pathways)

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23
Q

what is the direct pathway of the extrapyramidal system?

A

cortex–> striatum–> GPi/SNr (globus pallidus interna/substantia nigra reticulate)

promotes movement–> “accelerator pedal”

damage to this pathway causes SLOWING of movement

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24
Q

what is the indirect pathway of the extrapyramidal system?

A

cortex–> striatum–> globus pallidus externa–> subthalamic nucleus–> globus pallidus interna/substantia nigra reticularis

inhibits movement–> “Brake pedal”

damage to this pathway causes EXCESSIVE movement

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25
Q

what NT helps control the balance of the direct and indirect pathways?

A

dopamine

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26
Q

list common movement disorders caused by lesions in the extrapyramidal pathway (i.e the basal ganglia)

A
  1. parkinson’s disease
  2. huntington’s disease
  3. tourette’s syndrome
  4. ballism
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27
Q

what is the pathophysiology of parkinson’s disease? what symptoms are associated with it? what is the tx?

A

extrapyramidal/basal ganglia movement disorder

damage to the dopamine secreting neurons in the SUBSTANTIA NIGRA (pars compacta)

difficulty initiating movements, stooped posture, shuffling gate, postural instability

tx–> replace dopamine with levodopa

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28
Q

what is the pathophysiology of huntington’s disease? what symptoms are associated with it? what is the tx?

A

mostly affects the STRIATUM

chorea, dementia

tx for chorea–> dopamine DEPLETING agent (tetrabenzine)

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29
Q

what is the pathophysiology of tourette’s syndrome? what symptoms are associated with it? what is the tx?

A

damage to the thalamus, basal ganglia and frontal cortex

multiple tics, childhood onset, persistent for more than 1 year, coprolalia

tx–> dopamine DEPLETING agents (tetrabenzine)

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30
Q

what is the pathophysiology of ballism? what symptoms are associated with it? what is the tx?

A

damage to the SUBTHALAMIC NUCLEUS

hemiballism is often associated with stroke

can develop into chorea

tx–> sedation, tetrabenzine it develops into chorea

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31
Q

name the first generation typical antipsychotics

A
  1. haloperidol
  2. loxapine
  3. chlorpromazine
  4. fluphenazine
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32
Q

which of the first generation typical antipsychotics has a low affinity for D2 receptors? high affinity?

A

low affinity–> chlorpromazine (need higher dosage)

high affinity–> haloperidol, dimozide, perphenazine (need lower dosage)

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33
Q

what are the receptor effects of first generation antipsychotics that have low affinity for the D2 receptor, like chlorpromazine?

A

related to H1, alpha-1 and M2 receptor antagonism at high intakes

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34
Q

what are the receptor effects of first generation antipsychotics that have high affinity for the D2 receptor, like haloperidol, dimozide, perphenazine?

A

related to D2 receptor antagonism (very strong D2 receptor blockers)

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35
Q

what are side effects of chlorpromazine (low affinity for D2 receptor)?

A

sedation

weight gain

orthostatic hypotension

urinary retention

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36
Q

what are side effects of haloperidol, dimozide, perphenazine (high affinity for D2 receptor)?

A

extrapyramidal symptoms–> dystonia, and pseudoparkinsonism

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37
Q

what is the MOA of first generation typical antipsychotics?

A

dopamine antagonist in the brain

goal is to antagonize the dopamine receptors in the mesolimbic system in the brain

specifically, the mesolimbic system is responsible for positive symptoms, therefore blocking DA receptors will reduce positive symptoms

side effects arise from dopamine antagonism in other pathways in the brain, and effects on other receptors

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38
Q

in addition to the mesolimbic pathway (memory and emotional behaviors), what other pathways in the brain use dopamine as a major NT (and thus can be affected by first generation typical antipsychotics)?

A

mesocortical pathway

tuberoinfundibular pathway

nigrostriatal pathway

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39
Q

what is the function of the mesolimbic pathway?

A

associated with memory and emotional behaviors

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40
Q

what is the function of the mesocortical pathway?

A

associated with cognition and motivation

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41
Q

what is the function of the nigrostriatal pathway?

A

controls motor movement and extrapyramidal signs

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42
Q

what is the function of the tuberoinfundibular pathway?

A

controls prolactin secretion

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43
Q

what side effects result from typical antipsychotics due to the following action:
dopamine antagonist in the mesocortical pathway?

A

neuroleptic induced deficit syndrome–> makes negative symptoms worse

i.e alogia (inability to speak), affective flattening, avolition (lack of motivation, drive)

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44
Q

what side effects result from typical antipsychotics due to the following action:
dopamine antagonism in the nigrostriatal pathway?

A

extrapyramidal symptoms

i.e dyskinesias (repetitive, involuntary and purposeless movements), akathisia (extreme internal or external restlessness), dystonia (very strong uncontrollable muscle contractions)

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45
Q

what side effects result from typical antipsychotics due to the following action:
dopamine antagonism in the tuberoinfundibular pathway?

A

hyperprolactinemia

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46
Q

what side effects result from typical antipsychotics due to the following action:
H1 antagonism?

A

sedation, weight gain

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47
Q

what side effects result from typical antipsychotics due to the following action:
alpha-1 antagonism?

A

decreased BP, dizziness, drowsiness

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48
Q

what side effects result from typical antipsychotics due to the following action:
M1 antagonism?

A

dry mouth

urinary retention

blurred vision

constipation

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49
Q

how does the MOA of typical and atypical antipsychotics differ?

A

typical–> D2 antagonsim

atypical–> D2 and 5HT2a receptor antagonism

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50
Q

how do the side effect profiles of typical and atypical antopsychotics differ?

A

typical–> neuroleptic induced deficit syndrome, extrapyramidal signs, increase in prolactin

atypical–> reduced neuroleptic induced deficit syndrome (better), reduced EPS (better), reduced prolactin liability (better) BUT have metabolic side effects

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51
Q

is there a clear and consistent difference between typical and atypical antipsychotics when it comes to positive symptoms treatment?

A

no

***exception!!–> CLOZAPINE
clozapine works in resistant patients

*atypical agents have better treatment response to negative symptoms (i.e do not induce negative symptoms)

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52
Q

what antipsychotic is known to work in resistant patients?

A

clozapine (atypical)

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53
Q

what are the metabolic side effects associated with atypical antipsychotics?

A

weight gain

T2D

dyslipidemia

metabolic syndrome

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54
Q

name 4 atypical antipsychotics

A

clozapine

olanzapine

quetianine

risperidone

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55
Q

what is the MOA of atypical antipsychotics?

A

specific dopamine antagonist in the MESOLIMBIC pathway ONLY

5HT2a antagonism results in increased DA release in other brain pathways to reduce SEs–> normally, 5HT binds to 5HT2a receptors on dopamine neurons–> results in decreased dopamine release–> with atypical antipsychotics you stop this 5HT/dopamine neuron interaction and thus there is less inhibition of dopamine release and you get increased dopamine release–> for some weird reason this does not affect the positive pathway

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56
Q

what are side effects of atypical antipsychotics?

A

can be classified by on/off rates–> i.e time that drug is engaged with the receptor

rapid on/off–> clozapine, quetiapine (seconds)

  • side effects related to H1, M1 receptor antagonism
  • sedation, weight gain, orthostatic hypotension, urinary retention

slower on/off–> risperidone, olanzapine

  • side effects related to D2 receptor antagonism
  • EPS (dose related)–> due to decreased DA transmission and increased ACh transmission
  • treat with anticholinergics
  • *some antipsychotics have potent anticholinergic action, which provides some inherent anti-EPS mechanism
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57
Q

what is the “treatment guide” or progression for the use of atypical antipsychotics?

A

trial of atypical agent 1–> substitute for atypical agent 2–> substitute clozapine–> augmentation of clozapine with other class of drugs (lithium, anticonvulsants, antidepressants, benzos)–> combination of atypical and/or conventional agents (same class, antipsychotics)

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58
Q

what factors may prompt you to decide to change antipsychotics?

A

persistent positive symptoms more than mild

persistent negative symptoms

side effects

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59
Q

how do you treat EPS when it is a side effect of antipsychotic use?

A

anticholinergic and/or decrease dose of antipsychotic

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60
Q

how do you treat akathisia when it is a side effect of antipsychotic use?

A

beta blocker and/or decrease dose of antipsychotic–> benzodiazepine and/or decrease dose of antipsychotic

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61
Q

how do you treat neuroleptic malignant syndrome when it is a side effect of antipsychotic use?

A

discontinue antipsychotic use

agonists such as dantrolene, bromocriptine or amantadine may improve symptoms

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62
Q

what is neuroleptic malignant syndrome?

A

Neuroleptic malignant syndrome (NMS) is a rare, but life-threatening, idiosyncratic reaction to neuroleptic medications that is characterized by fever, muscular rigidity, altered mental status, and autonomic dysfunction

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63
Q

what are common co-existing symptoms in someone with a psychotic disorder/getting treated for a psychotic disorder (i.e either comorbid or as a result of antipsychotic tx)? how do you treat them?

A
  1. agitation/excitement–> benzos, conventional antipsychotics, olanzapine, risperidone PRN
  2. insomnia–> benzos, trazodone, zopiclone PRN//switch agents
  3. persistent symptoms of aggression/hostility and mood lability–> mood stabilizer (valproic acid, lithium, carbamazepine)
  4. depression (common together)–> SSRI, switch antipsychotic
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64
Q

can someone smoke when they are on treatment for schizophrenia?

A

nicotine is okay, but smoking can interfere with schizophrenia tx due to the effects of hydrocarbons on CYP 1A2 as an INDUCER

this can effect treatment by affecting medication levels

be aware that if patients are not allowed to smoke in hospital, when they leave hospital and smoke their levels of drug will decrease

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65
Q

what NT do the axons leaving the striatum and globus pallidus use? what effect does this have? why do we care clinically?

A

axons leaving the striatum and globus pallidus use GABA as their NT–> thus they make INHIBITORY synapses on their targets

the neurons from the internal globus pallidus projecting to the thalamus is TONICALLY ACTIVE and thus inhibits parts of the thalamus

this is important because modulations of basal ganglia activity are achieved via altering this output because thalamocortical connections are excitatory

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66
Q

are thalamocortical connections inhibitory or excitatory?

A

excitatory

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67
Q

what are the two pathways from the striatum to the internal globus pallidus? are these inhibitory or excitatory?

A

there are TWO pathways from the striatum (caudate and putamen) to the internal globus pallidus

  1. direct pathway–> theres a single INHIBITORY neuron that uses GABA when it synapses of the pallidothalamic fibre
  2. indirect pathway–> consists of a chain of TWO INHIBITORY neurons that synapse on an EXCITATORY neuron in the subthalamic nucleus rather than the internal globus pallidus

**the big picture here is that activation of the direct pathway leads to increased activity from the thalamus to the cortex and theremore more movement (target specific)

**activation of the indirect pathway results in decreased activity from the thalamus to the cortex and therefore decreased movement (less superfluous movement)

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68
Q

what pathway is stimulated by dopaminergic neurons from the substantia nigra?

A

dopaminergic neurons from the substantia nigra will stimulate the direct pathway (D1 receptors) and inhibit the indirect pathway (D2 receptors)

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69
Q

what effect does dopamine have on movement when it acts in the basal ganglia?

A

bottom line is dopamine activity in the basal ganglia means increased movement

its important to note the way that dopamine neurons from the substantia nigra inhibit the indirect pathway by inhibiting an excitatory cholinergic interneuron

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70
Q

what effect does ACh have on movement when it acts in the basal ganglia?

A

decreased movement

*note that elsewhere in the body, liek in the neuromuscular junction, ACh is essential for movement–> its just in the basal ganglia it acts to decrease movement whereas dopamine increases movement (because the basal ganglia projections are inhibitory)

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71
Q

what is the pathophysiology of ballismus? specifically, what NT is involved? what is the tx?

A

ballismus is uncontrolled, big time movement/flinging of the limbs (on one side only it is called hemiballismus)

problem is in the SUBTHALAMIC nucleus, usually due to a vascular lesion (stroke)

the excitatory neurotransmitter GLUTAMATE that normally stimulates inhibition of the thalamus is gone, therefore there is uncontrolled thalamus activity to the cortex and those crazy movements

tx–> dopamine blocking drugs (i.e perphenazine, haloperidol)

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72
Q

what is the pathophysiology of huntington’s chorea? specifically, what NT is involved? what is the tx?

A

repetitive, rapid “dance like” movements of limbs and often face and tongue

problem is degeneration of the STRIATUM, specifically the CAUDATE NUCLEUS

it appears that there is increased movement because of the loss of the FIRST INHIBITORY synapse in the INDIRECT pathway resulting in increased activity in the second inhibitory neuron in the indirect pathway and therefore inhibition of the excitatory neuron from the subthalamic nucleus–> this means the inhibition from the internal globus pallidus to the thalamus is decreased and the thalamus is “set free” to be overly active–> increased movement results

ACh and GABA are implicated

tx–> supportive (tx for other types of chorea is to treat the underlying cause)

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73
Q

what is the pathophysiology of parkinson’s? specifically, what NT is involved? what is the tx?

A

difficulty moving (hypokinesis, akinesia), bradykinesia, resting tremor and rigidity

there is degeneration of the DOPAMINE-containing neurons of the SUBSTANTIA NIGRA

since dopamine always means go, loss of dopamine will result in a no go

tx–> methods of increasing or replacing dopamine and anticholinergic drugs

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74
Q

what is the etiology of schizophrenia?

A

psychotic disorders are caused by both genes and environment

the genetic differences that contribute to psychotic disorders are best referred to as “conferring susceptibility”, vulnerability or predisposition–> NOT causation

in general, psychotic disorders are NOT inherited, but one can inherit a vulnerability to it–> i.e DiGeorges Syndrome

environmental factors include: obstetric complications, drug use (esp. marijuana), winter births, immigration, urban upbringing, head injury, stress

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75
Q

what is DiGeorges syndrome?

A

22q11 deletion syndrome

a rare genetic cause of psychosis

30% of patients will have at least one incident of psychosis

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76
Q

what is the pathyphysiology of schizphrenia?

A
  1. enlarged ventricles and smaller brain volume occur in some, but not all, patients with schizophrenia–> changes are not specific and cannot be used to make a diagnosis
  2. symptoms are likely due to aberrant functional connectivity (between temporal, frontal and subcortical regions)
    - white matter tracts that connect frontal, temporal and subcortical brain regions are smaller or disorganized
    - electrophysiological parameters are altered
    - pre-pulse inhibition (stimulus that attenuates the startle reflex) is reduced (so more startle reflex)
  3. atrophy of neutropil (regions between cell bodies; includes axons, dendrites and other processes)
    - decreased size and complexity of neuronal dendrites
    - neurons are slightly smaller–> smaller cell body, therefore, smaller processes
    - decreased number of dendritic spines
    - decreased levels of synaptic proteins
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77
Q

neurotransmission is thought to be altered in schizophrenia… how is the following neurotransmitter implicated in this?

dopamine

A

INCREASED dopamine activity in SUBCORTICAL regions, in particular the mesolimbic pathway–> results in POSITIVE symptoms

DECREASED dopamine activity in the FRONTAL cortex, in particular the mesocortex pathway–> results in NEGATIVE symptoms and cognitive deficits

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78
Q

neurotransmission is thought to be altered in schizophrenia… how is the following neurotransmitter implicated in this?

serotonin

A

psychotic symptoms result from INCREASED 5HT transmission

LSD acts on the 5HT2a receptor

many atypical antipsychotics are 5HT2a antagonists

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79
Q

neurotransmission is thought to be altered in schizophrenia… how is the following neurotransmitter implicated in this?

glutamate

A

psychotic symptoms result from DECREASED glutamate transmission

phencyclidine (PCP) and ketamine are NMDA (glutamate) receptor antagonists–> binding of these drugs to the receptor can mimic both positive and negative symptoms of schizophrenia

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3
4
5
Perfectly
80
Q

neurotransmission is thought to be altered in schizophrenia… how is the following neurotransmitter implicated in this?

GABA

A

major inhibitory neurotransmitter in the brain

post mortem studies report abnormalities in GABA-ergic interneurons in schizophrenia

81
Q

neurotransmission is thought to be altered in schizophrenia… how is the following neurotransmitter implicated in this?

Ach

A

nicotine causes the release of Ach

the rate of smoking in individuals with schizophrenia exceeds that seen in the general population

82
Q

neurotransmission is thought to be altered in schizophrenia… how is the following neurotransmitter implicated in this?

neuroendocrine system

A

stress is commonly associated with the onset of psychotic episodes

changes in the HPA axis function have been reported in schizophrenia

83
Q

how is brain development related to schizophrenia?

A

deficits in brain development could occur at several stages (fetal development and phases of synaptic pruning or myelination) and could lead to altered brain structure and thereby increase susceptibility to schizophrenia

alterations in positions of cells in the brain observed in patients with schizophrenia –> reflects an abnormality of cell migration during early brain development

84
Q

how do you treat schizophrenia?

A

tx is not solely based on decreased hallucinations and delusions

atypical antipsychotics are the first line tx because of more benign side effect profile as well as their efficacy in treating negative symptoms compared to typical antipsychotics

effective tx requires a combination of medications, psychotherapy and appropriate psychosocial measures

85
Q

what is the first line tx for schizophrenia?

A

atypical antipsychotics

86
Q

what happens when a psychotic patient exhibits behaviour that is violent or so disorganized and uncooperative that clinical evaluation is impossible?

A

the temporary use of restraints is indicated while rapid tranquilization is initiated

rapid tranquilization involves serial doses of high-potency antipsychotic

oral (preferred), IM or IV doses can be given

haloperidol is widely used

**benzodiazepines are effective in managing agitation in patients who have alcohol or sedative-hypnotic withdrawal, cocaine intoxication or a contraindication to neuroleptic use

87
Q

what is a major risk with the atypical antipsychotic clozapine?

A

seizures and agranulocytosis

only recommended when typical and other atypical antipsychotics have proven ineffective

88
Q

what are the mainstay of tx in psychosis/schizophrenia?

A

antipsychotic meds

atypical antipsychotics are used a first line tx and are all safe and effective in both acute and mainstay phases –> more effective against negative sx compared to typical and reduced risk of EPS and tardive dyskinesia

typical antipsychotics are safe and effective in treating acute symptoms and preventing relapse but have a relatively high risk of adverse effects (tardive dyskinesia and parkinsonism, especially in older patients)–> mainly effective against positive symptoms

89
Q

what do you do if there has been no response to acute phase meds for schizophrenia/psychosis after 4-6 weeks? how long do you continue maintenance tx?

A

change of meds should be considered

maintenance should continue for 1-2 years after the initial episode and at least 5 years following multiple episodes

thereafter, reduction in meds should be spaced over several months

90
Q

what are the core components of non-pharmacological tx for schizophrenia that should be used in all patients?

A

case manager

psycho-education

stress management skills

family intervention–> reduction of expressed emotion

91
Q

what are some other components of non-pharmacological behavior that may be initiated in some patients?

A
  1. CBT–> thoughts and behaviours influence emotions and psychosis
  2. vocational interventions–> “place then train” approach is more effective
  3. cognitive remediation–> computer based program aimed at restoring normal function or to compensate for congitive deficits
92
Q

using the agent/host/environment model, what role do each of these play in substance abuse disorders?

A
  1. agent–> addictive qualities of substances (drugs, alcohol) such as dopamine release
  2. host–> family history of substance abuse disorder, genetic predisposition, poor coping skills, mental health problem (i.e 47% of those with substance abuse have mental health problems)
  3. environment–> exposure to stress, PTSD, neglect, lack of social support, behaviour of peers
93
Q

using the agent/host/environment model, what role do each of these play in psychotic disorders?

A
  1. agent–> often there is no specific agent or exposure which is why cases are so complicated to treat; some psychotic disorders may be related to a past traumatic event; indirect evidence of prenatal virus exposure and schizophrenia
  2. host–> family history, genetic predisposition (i.e 50% concordance os schizophrenia in MZ twins), gender, race, age
  3. environment–> lack of social support, social stigmas can have negative consequences on the condition progression, geographical variance and winter season of birth have been implicated in schizophrenia
94
Q

using the agent/host/environment model, what role do each of these play in movement disorders?

A
  1. agent–> parkinson’s is a combination of oxidative stress to dopaminergic neurons, environmental toxins (i.e pesticides)
  2. host–> gene mutation in familial parkinsons disease, and huntingtin gene n huntington’s disease
  3. environment–>?
95
Q

what is the narrowest definition for psychotic disorders? what is a broader definition?

A

narrowest definition–> restricted to delusions and/or hallucinations (essentially person is not in touch with reality)

broader definition–> includes positive symptoms of schizophrenia

  • disorganized speech
  • disorganized behaviour
  • functional impairment
  • impaired reality testing
  • duration
96
Q

list the forms of psychotic disorder

A
  1. schizophrenia
  2. schizophrenie form psychosis
  3. schizoaffective disorder
  4. delusional disorder
  5. brief psychotic disorder
  6. shared psychotic disorder
  7. psychotic disorder due to general medical condition
  8. substance induced psychotic disorders
97
Q

what are the characteristic symptoms of schizophrenia?

A 
two for at least one month:
delusions
hallucinations
disorganized speech
disorganized behavior
negative symptoms

social/occupational dysfunction

duration six months (one month of characteristic symptoms)

98
Q

what is the major age group affected by schizophrenia?

A

ages 15-30

schizophrenia–> “catastrophic illness”

99
Q

what is the suicide rate among those with schizophrenia?

A

10%

100
Q

how common is schizophrenia in the general population?

A

0.5-1%

“the cancer of mental illness”

101
Q

does schizophrenia affect only one system?

A

no–> it is like syphilis and MS in that it is multisystem

symptoms from multiple domaines: emotion, personality, cognition, motor activity

102
Q

what do you mean by “positive” symptoms of schizophrenia? “negative”?

A

positive–> distortions or exaggerations of normal functions

  • hallucinations–> perception is distorted
  • delusions–> inferetial thinking is distorted
  • disorganized speech–> thought/language is distorted
  • bizarre behavior (bizarre meaning doesnt follow the laws of physics… can have bizarre and nonbizarre delusions)–> behavioral monitoring is distorted

negative–> diminution of normal function

  • alogia–> fluency of thought/speech is distorted
  • affective blunting–> emotional expression is distorted
  • avolition–> volition and drive are distorted
  • anhedonia–> hedonic capacity is distorted (enjoyment)
103
Q

what are the types of hallucinations?

A

auditory
visual
tactile
olfactory

104
Q

what are the types of delusions?

A 
persecutory
grandiose
religious
jealous
somatic
105
Q

what are the subtypes of schizophrenia?

A

paranoid

disorganized

catatonic

undifferentiated

residual

**the DSM V has taken away these subtypes because they did not change treatment (but some docs or patients may still use them)–> instead they added course specifiers (i.e episodes, severity, marked stressors etc..)

106
Q

how has the definition of schizoaffective disorders changed in the new DSMV?

A

now based on lifetime (rather than episodic) duration of illness in which the mood and psychotic symptoms described in criterion A occur

107
Q

how is catatonia treated in the new DSMV?

A

now exists as a specifier for neurodevelopmental, psychotic, mood and other medical disorders (as represented in the DSMIV, it was under recognized, particularly in psychiatric disorders and in other medical disorders)

108
Q

what are the proposed criteria for Attenuated Psychosis Syndrome (APP)? (recently added to the DSM)

A
  1. at least 1/3 core psychosis symptoms with relatively intact reality testing, and warrants clinical attention
  2. symptoms more than one week in past month
  3. symptoms began or worsened in past year
  4. not better explained by another mental disorder
  5. criteria for another psychotic disorder never met
109
Q

what is schizophreniform disorder?

A

characteristic symptoms of schizophrenia

duration of at least one month but less than 6 months

with or without good prognostic features (acute onset)

confusion or perlexity

good premorbid functioning

absence of blunted affect

110
Q

what is schizoaffective disorder?

A

characteristic symptoms of schizophrenia plus depressed, manic or mixed episode of mood

presence of delusions or hallucinations for at least two weeks in the presence of mood symptoms

specifiers: bipolar type or depressive type

  • combination of schizophrenia and mood disorder
  • better prognosis than schizophrenia but not as good as mood disorder
  • tx usually requires antipsychotics
111
Q

what is delusional disorder?

A

i.e stalkers of celebrities

non-bizarre delusions (paranoia, infection, deception or having a disease) at least one month

characteristic symptoms of schizophrenia NOT present (tactile and olfactory hallucinations may be present if related to delusion)

functioning NOT impaired

subtypes (erotomanic, grandiose, jealous, persecutory, somatic, mixed)

  • *note the lack of functional impairment
  • *often poor response to tx
112
Q

what is brief psychotic disorder?

A

presence of one or more:

  • delusions
  • hallucinations
  • disorganized speech
  • disorganized behavior

duration of at least one day but less than one month –> eventual return to premorbid functioning

specifiers with marked stressors, without marked stressors, or post partum onset (within 4 weeks)

post partum psychosis is a brief psychotic disorder

**generally has a good outlook

113
Q

what is shared psychotic disorder?

A

delusion develops in the context of a close relationship with another person who already has an established delusion

delusion has similar content

114
Q

what is a psychotic disorder due to a general medical condition?

A

subtypes with delusions or with hallucinations

prominent hallucinations or delusions

evidence of dire physiological consequence of general medical condition

not accounted for by another mental disorder

disturbance not exclusively during course of delirium

115
Q

what are some medical conditions that may present with psychosis?

A
  1. temporal lobe epilepsy
  2. tumor
  3. stroke
  4. trauma
  5. endocrine/metabolic abnormalities
  6. infections
  7. MS
  8. autoimmune diseases
116
Q

what is substance abuse psychotic disorder?

A

specifiers are onset during intoxication, or onset during withdrawal

prominent hallucinations or delusions (without insight)

evidence of symptoms develop during or within a month of sunstance intoxiation or withdrawal

substance use etiology clearly related to the disturbance

117
Q

what are some drugs that may induce psychosis?

A

amphetamines

marijuana

hallucinogens

cocaine

118
Q

why might antipsychotics precipitate movement disorders?

A

due to “oversuppression” or “overcorrection” of neurotransmitter levels that are important in movement

i.e most commonly seen extra-pyramidal sx are precipitated by haloperidol

119
Q

how does alcohol affect neurotransmitter function?

A

classed as a sedative-hypnotic

GABAa and glycine agonist, NMDAr antagonist–> leads to increased inhibition

decrease in glutamate (from NMDA blocking)

increased opiate, dopaine, serotonin, GABA

withdrawal results in an decrease in inhibitory neurotransmitters, increase in excitatory neurotransmitters and thus sx of insomnia, irritation, tremor, risk of seizure

120
Q

how does cannabis affect neurotransmitter function?

A

CB1 receptors are central
CB2 receptors are peripheral

9-tetrahydrocannabinol (THC)–> binds to CB1 and CB2 receptors

increases (dis-regulates) dopamine–> stimulant and depressant

increased appetite, decreased nausea, decreased pain

121
Q

how does cocaine affect neurotransmitter function?

A

increased dopamine, serotonin and NE

cocaine and crack are reuptake inhibitors of all 3

methamphetamines increase the release of all 3

use–> alert, powerful, insomnia, anorexia

122
Q

how does alcohol effect psychomotor symptoms, tremor?

A

alcohol intoxication–> leads to impaired motor control and altered reality and judgement

in withdrawal:

  • you get hallucinations (visual, tactile, and/or auditory)
  • tremor–> seizures–> if severe, status epilepticus (due to low GABA and high glutamate)
  • late withdrawal you can get delirium tremens
123
Q

how does cannabis affect psychomotor symptoms, tremor?

A

heavy users (more than 50X) by age 18 were 6X more likely to have a schizophrenia diagnosis than non-users

usage doubles the risk of developing future psychotic disorders

psychotic symptoms are more likely in marijuana with high THC, low CBD, in a person with VV alleles on COMT gene

may not cause schizophrenia but bring out expression of latent psychotic disorder

124
Q

how do stimulant drugs affect psychomotor symptoms, tremor?

A

symptoms come on after drug use and may persist for hours, days, or rarely weks

largely caused by dopamine dysregulation

if symptoms persist for weeks or months, then an underlying psychotic disorder is at play ot the drug damaged dopaminergic pathways (see following slides for specifics)

125
Q

by what mechanisms do amphetamines increase postsynaptic dopamine activity?

A
  1. increased presynaptic NT release
  2. inhibition of presynaptic dopamine reuptake
  3. inhibition of dopamine breakdown (by inhibiting MAO)

these mechanisms cause increased dopamine transmission and can lead to psychosis

126
Q

by what mechanisms does cocaine increase postsynaptic dopamine activity?

A

via inhibition of presynaptic dopamine reuptake

causes increased dopamine transmission that can lead to psychosis

127
Q

how does alcohol affect movement disorders?

A

wernicke-korsakoff syndrome–> EtOH blocks NMDA

in withdrawal, glutamate slams away at the NMDA receptor (get ataxia, tremor)

long term–> get cerebellar cell destruction (ataxia, tremor), peripheral neuropathy (stocking glove anesthesia or burning)

128
Q

how do stimulants affect movement disorders?

A

acute use–> abnormal picking, tremor/seizures (from NOR), myoclonic jerking (from 5HT)

full blown SEROTONIN SYNDROME–> rigidity, myoclonic jerking, hyper reflexia, vasomotor instability, confusion disorientation –> if writhing (choreaform) movements persist, then there is damage to dopaminergic pathways

129
Q

what % of people with a sibling with schizophrenia also have it?

A

10%

130
Q

what % of people with two schizophrenia parents go on to have schizophrenia?

A

40%

131
Q

what % of MZ twins both have schizophrenia?

A

50%

132
Q

what is the dopamine hypothesis theory of schizophrenia etiology?

A

excess activity in the mesolimbic dopamine pathway may mediate positive symptoms of psychosis

decreased activity in mesocortical pathway or abnormalities in NMDA receptors which regulate glutamate release may be responsible for negative symptoms

other neurotransmitters have been implicated

133
Q

what are specific risk factors related to alcohol use?

A

strong genetic component–> male, novelty seeking, increase beta-endorphin rise

family history positive males tend to report less intoxication from alcohol –> early lack of intoxication increases risk of later alcohol abuse or dependence–> these patients have a hard time realizing the effect of EtOH and stopping

little acetaldehyde build up due to a fast acting acetaldehyde dehydrogenase enzyme polymorphism leads to a higher risk for alcoholism

134
Q

what are specific risk factors related to cannabis?

A

THC is the active ingredient in cannabis–> increases risk of developing schizophrenia with heavy use during youth

cannabidiol (CBD) is a natural plant product in cannabis–> protective of psychosis

as the THC content increases in a plant, the CBD content decreases

potent marijuana therefore is more likely to cause psychosis

135
Q

what are specific risk factors related to cocaine and amphetamine use? (stimulants)

A

similar genetic and shared environmental factors account for dependence as any other substance

endogenous opioids are protective of cocaine dependence

stimulants can induce movement disorders

  • acute–> abnormal picking (formication), tremors/seizure, myoclonic jerking
  • serotonin syndrome
  • choreaform movements–> can cause damage to dopaminergic pathways is sustained
136
Q

what are some protective factors against substance abuse?

A
  1. role modeling–> drinking, drugging vs. sober
  2. family disruption–> abuse/neglect vs. stable and supportive
  3. coping strategy–> bury trauma, pain and mental health versus healthy ways to self-sooth and cope
  4. economic–> poverty-hopelessness-addiction cycle, industry pressures (EtOH) vs. stable employment with a chance for a future
  5. other protective factors–> social skills, family and social support, personal coping skills, and self-esteem, stress management and medication

**kids who dont know how to self-soothe have a harder time and higher incidence of self soothing with substances

137
Q

what qualifiers does the DSM V use to describe substance abuse disorders?

A
  1. severity
    - mild–> 2-3 symptoms
    - moderate–> 4-5 symptoms
    - severe–> 6 or more symptoms
  2. remission
    - early–> 3-12 months (only criteria left may be craving)
    - sustained–> 12 months or longer (craving may remain)
    - in a controlled environment (access restricted)
  3. on maintenance therapy
    - agonist, agonist/antagonist, full antagonist
138
Q

what is the prevalence of alcohol use in the past year (2011)?

A

78% general population

youth aged 15-24 –> 70.8% consumed

lifetime harms–> 21.4% males and 11.2% females

139
Q

what is the prevalence of marijuana use in the past year (2011)?

A

9.1% general population

  1. 6% of youth
  2. 7% of adults over 25
140
Q

what is the prevalence of other drug use in the past year (2011)?

A
  1. 8% for youth

1. 1% for adults

141
Q

what are ways to try and distinguish a primary mental health versus primary substance abuse problem in co-occuring disorders?

A
  1. use a timeline–> any mental health symptoms prior to substance initiation? during periods of prolonged abstinence? under acute stress?
  2. take a family history–> any first or second degree relatives with mental health issues?
142
Q

what is the hallmark of an addicting substance?

A

increased dopamine in the nucleus accumbens

*dopamine and serotonin excess when using stimulants/hallucinogens/alcohol can cause psychosis (“too much meaning”); dopamine depletion through lowered set point ot damaged neurons can produce movement disorder and low mood

143
Q

what is the function of serotoninergic pathways?

A

mood

memory processing

sleep

cognition

144
Q

what is the function of dopamine pathways?

A

reward/motivation

pleasure, euphoria

motor function (fine tuning)

compulsion

perseveration

145
Q

how are dopamine D2 receptors affected in addiction?

A

repetitive high dose or episodic use causes depletion of D2 receptors in the brain

it can take up to a year for those receptors to come back to normal

146
Q

what is a genetic component of alcoholism?

A

polymorphism at the dopamine receptor D4 site has been associated with novelty seeking

genetically high risk individuals get a bigger beta-endorphin rise with drinking which in turn causes increased dopamine

people with AG (vs. AA) allele of A118G site of the mu opioid receptor get a bigger euphoria to alcohol

novelty seeking plus getting a lot of euphoria but little impairment with alcohol –> major risk factor

147
Q

how is alcohol metabolized?

A

EtOH–via alcohol dehydrogenase–> acetaldehyde–via acetaldehyde dehydrogenase–> acetate

*it is acetaldehyde that causes the negative symptoms associated with drinking–> flushing, tachycardia, HTN, nausea, vomiting

148
Q

if you have both a fast alcohol dehydrogenase, and a slow acetaldehyde dehydrogenase (genetically), what is your risk of alcoholism?

what about if you have a slow alcohol dehydrogenase and a fast acetaldehyde dehydrogenase?

A

this genotype (ADH1B2 and ALDH22) would result in lots of acetaldehyde building with drinking

slow ADH and fast ALDH (ADH1B1/1 and ALDH2*1/2) leads to high risk for alcoholism because you get very little acetaldehyde build up

149
Q

what is the function of the endogenous cannabinoid system?

A

infant bonding

regulates dopamine

sleep

150
Q

how does cannabis affect IQ?

A

if initiation started as a youth prior to age 18 then IQ does not recover when detoxed

if adult onset of initial use then can recover IQ after 1+ months

151
Q

what kind of cannabis is recommended for medicinal purposes?

A

inhaled cannabis is NOT recommended for medicinal purposes

buccal spray (THC plus CBD) might be a third or fourth line tx for neuropathic pain

152
Q

how does your risk for schizophrenia change when cannabis use is started before age 16? how do genetics affect this?

A

being age 16 or under when cannabis use is started is associated with a 4X increased risk of later developing schizophrenia (by age 26 for example)

depends on genetics at COMT gene:
alleles MM have NO increased risk (but based on other studies, no genotype is completely protective)
alleles MV have double the risk
alleles VV have 10X the risk of psychosis when using cannabis

153
Q

what are the two primary risk factors for developing cocaine addiction?

A

making more endogenous opioids may protect you from cocaine dependence

if slow to break down dopamine after cocaine use, you can get paranoid

154
Q

what type of gait is associated with dopamine overstimulation (like with stimulant use)?

A

excessive movements like CHORIEFORM gait

155
Q

what type of gait is associated with dopamine hypofunction (like after burning out the dopamine system with severe stimulant use)?

A

decreased movements like a PARKINSONIAN gait

156
Q

what type of movements can be brought on by acutely dropping dopamine levels?

A

akathisia–> restless legs

157
Q

what is the key neurotransmitter involved in addiction, psychosis and movement disorders?

A

DOPAMINE

5HT and NE too

158
Q

what are the main functions of the basal ganglia?

A
  1. modulation of VOLUNTARY motor activity
  2. balance of inhibitory and excitatory pathways gives input to the thalamus and from there to the cortex
  3. three parallel circuits:
    - motor circuit controls body and eye movement
    - associative circuit involved in higher level cognitive function
    - limbic circuit involved in emotional and motivational processing
159
Q

what types of activity are encoded in the basal ganglia?

A
  1. the decision to move
  2. the direction of movement
  3. the amplitude of movement
  4. the motor expression of emotions
  5. making movements and behaviours more efficient (proceduralization)
160
Q

what is the state of the thalamus when we are not moving?

A

the thalamus is under chronic inhibition when we are not moving

less input to the motor cortex

–> when we do want to move, a balance of inhibitory and excitatory circuits to the thalamus result in measured input to the motor cortex and measured movement

161
Q

what is the role of the direct pathway of the basal ganglia?

A

releases the tonic inhibition of the thalamus, leading to more excitation of the motor cortex–> more motor output

it disinhibits the thalamus, so it can signal the cortex

162
Q

what is the role of the indirect pathway of the basal ganglia?

A

counter player to the direct pathway

increases inhibition to the thalamus

inhibits output from the thalamus, leading to less excitation of the motor cortex–> less motor output

163
Q

what is the result if you increase inhibition of the thalamus?

A

less output to the cortex and thus less output from the cortex

164
Q

what is the result if you decrease the inhibition (inhibit the inhibition) of the thalamus?

A

more output to cortex, more output from cortex

165
Q

what is the underlying cause of hemiballism?

A

a lesions (i.e stroke) of the CONTRALATERAL subthalamus nucleus

166
Q

what is the treatment for parkinsons?

A

L-dopa

also deep brain stimulation of the subthalamic nucleus (STN) restores tonic firing pattern from STN to GPi which leads to less inhibition of the thalamus and to more motor output

167
Q

what is the role of the basal ganglia’s associative circuit?

A

participates in planning complex motor activity

when a novel task has been practiced and well learned, activity in the associative circuit decreases and the motor circuit becomes more active

NUCLEUS ACCUMBENS is involved

168
Q

why do you get “mask face” in parkinson’s disease?

A

because the basal ganglia’s limbic circuit is involved in the motor expression of emotion (postures, gestures, facial expressions related to emotion)–> it is rich in dopaminergic neurons

when this circuit is damaged you get mask face

input from amygdala and hippocampus and anterior cingulate/orbitofrontal lobe and frontal association areas to nucleus accumbens feeding thru basal ganglia circuitry back to frontal association areas and orbitofrontal lobe via thalamus

169
Q

what are the three major types of movement disorders?

A

pyramidal syndromes

basal ganglia disorders

cerebellar disorders

170
Q

how do you distinguish the three types of movement disorders?

A

pyramidal syndromes–> SPASTICITY (velocity and direction dependent), weakness, paralysis

basal ganglia disorders–> parkinsonian syndromes, dyskinesias, stereotyped movements

cerebellar disorders–> ATAXIA (extrapyramidal–rigidity, no overt weakness, insufficient/excessive/abnormal movements)

171
Q

what is the general approach to patients with movement disorders?

A
  1. identify pattern of abnormal movement (syndrome)
  2. find out underlying cause, if any
  3. treat underlying cause or give symptomatic therapy
172
Q

define dyskinesia

A

abnormal movement of voluntary muscles

173
Q

define bradykinesia

A

slowness of movement

174
Q

define choreoathetosis

A

dance like movements

175
Q

define myocloncus

A

NOT a disease of the basal ganglia

shock like movements

176
Q

define ataxia

A

cerebellar

177
Q

what is a tremor?

A

regular

repetitive

sinusoidal cycles

alternating contractions of antagonistic pairs of muscles

178
Q

how do you clinically assess a tremor?

A

TAF

Topography of tremor (head, chin, jaw, vocal cords, upper/lower extremity, body etc)

Activation condition of tremor (rest, posture, non-goal directed movements, goal oriented movements)

Frequency of tremor (low is less than 4 Hz, medium is 4-7 Hz and high is more than 7Hz)

179
Q

what are some common causes of tremor?

A

enhanced physiological tremor

  • anxiety worsens ALL types of tremor
  • drugs (caffeine, valproate etc)
  • hyperthyroidism

essential tremor

parkinson’s disease

cerebellar disease

180
Q

how can the activation condition of a tremor be associated with the cause?

A
  1. intention tremor–> cerebellar disease
  2. postural tremor–> essential tremor
  3. resting temor–> parkinson’s disease
181
Q

how do essential tremors compare to the tremors seen in parkinsons disease?

A

essential:

  • head/voice may be affected
  • relatively symmetric
  • cogwheeling may be present
  • writing is large and tremulous**
  • typically better while walking
  • often IMPROVES with alcohol

parkinsonian:

  • head tremor is uncommon (but can see lip, chin tremor)
  • asymmetric
  • rigidity
  • writing is small and tremor is not pronounced
  • typically worse while walking
  • alcohol has NO effect
182
Q

what is a mnemonic to remember the major sx of parkinsons?

A

TRAP

Tremor
Rigidity
Akinesia/bradykinesia
Postural instability

183
Q

what is an EARLY sign of parkinson’s?

A

anosmia–> lose sense of smell!!

plus depression/anxiety, sleep disturbances, REM sleep behaviour disorder, mask face, micrographia, stiffness and neck pain, constipation, decreased arm swing

*risk of parkinsons is increased if you have less than 1 bowel movement a day at middle age –> lewy bodies are not just seen in the brain but also in the nervous system of the gut –> surprising relationship between genetic risks for parkinson’s and for crohn’s

184
Q

what symptoms are most predictive of parkinson’s (rather than atypical parkinsonism)?

A

ASYMMETRIC onset of tremor/rigidity/bradykinesia

L-dopa responsiveness

**30% of PD patients do NOT have tremor

185
Q

what is parkinsonism?

A

doesnt respond significantly to meds

symptomatic tx only

186
Q

does L-dopa prolong survival in patients with PD?

A

yes–still gold standard despite long term complications

187
Q

what % of PD patients on dopamine agonists develop impulse control disorders (ICDs)?

A

6-18% (probably higher)

i.e pathological gambling, hypersexuality, compulsive shopping, compulsive eating

188
Q

describe chorea type movements

A

irregular

non-repetitive

non-purposeful

unpredictable

smooth, flowing, fast/slow

not suppressible

189
Q

in addition to huntington’s, waht else can cause chorea?

A

levodopa induced dyskinesia in PD

neuroleptic drugs (dopamine receptor blocking agents)

190
Q

how would you describe the movement associated with tics?

A

irregular

non-purposeful

predictable in pattern but not in time

stereotypic

suppressible

191
Q

how do you treat tourettes?

A

anti-dopaminergic drugs

dopamine depleting agents (i.e tetrabenazine) are preferred rather than receptor blockers (i.e haloperidol)

192
Q

how would you describe the movements associated with ballism?

A

irregular

non repetitive

non purposeful

unpredictable

violent, proximal

not suppressible

193
Q

what structure is normally damaged in ballism?

A

subthalamic nucleus

194
Q

what is dystonia?

A

involuntary muscle contractions

co-contraction of antagonists

abnormal postures

may be worse with specific actions

DISAPPEARS DURING SLEEP

can get focal dystonias (i.e eyelids, face, neck, voice, upper limbs, task specific–writer’s cramp, musician’s cramp, lower limb) or generalized dystonia

195
Q

what is used as symptomatic treatment for dystonia?

A

botulinum toxin (mainly for focal dystonia)

196
Q

list some drug induced movement disorders

A
  1. acute dystonic reactions–> occur within 96 hours of therapy
  2. parkinsonism–> especially metoclopramide (an antiemetic) and flunarizine (a Ca channel blocker)
  3. akathisia–> “inability to remain seated”, often seen in neuroleptic use
  4. neuroleptic malignant syndrome–> uncommon but can be FATAL
  5. tardive dyskinesia –> dyskinesia, dystonia, tic, akathisia, myoclonus, tremor
197
Q

what two drugs in particular are known to cause parkinsonism?

A

metoclopramide–> antiemetic

flunarizine–> calcium channel blocker

198
Q

what is neuroleptic malignant syndrome?

A

can be fatal, but uncommon

agitation, lethargy, confusion, delerium, stupor, coma

hyperthermia, tachypnea, BP changes

rigidity, akinesia, tremor, dystonia, chorea

seizures

elevated creatinine kinase

myoglobinuria

*may occur with first exposure to neuroleptics or when re-instating therapy after a long time, or in acute withdrawal of dopaminergic drugs i.e suddenly stopping treatment in PD

B&B Part 2 (5 decks)

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