week 9/10 Flashcards
how are schizophrenia spectrum and other psychotic disorders defined as
abnormalities in 1+ of the following:
1. delusions (fixed false beliefs)
2. hallucinations (more transient, incorrect perceptions of objects or events involving the senses)
3. disorganized thinking (speech)
4. grossly disorganized or abnormal motor behaviour (including catatonia)
5. negative symptoms
1-4 are positive symptoms
what is schizophrenia
lasts for at least 6 mo and includes at least 1 mo of active-phase symptoms + includes a decline in social or occupational functioning
- affects 1% of the population
schizophreniform disorder
characterized by a symptomatic presentation equivalent to that of schizophrenia except for its duration (less than 6 mo) and the absence of a required for a decline in functioning
schizoaffective disorder
- mood episode and active-phase symptoms of schizophrenia occur together and are followed by at least 2 wks of delusions or hallucination with prominent mood symptoms
what’s the difference between schizophrenia and schizoaffective
the key difference between schizoaffective disorder and schizophrenia is the prominence of the mood disorder. with schizoaffective disorder, the mood disorder is front and center. with schizophrenia, it’s not a dominant part of the disorder
brief psychotic disorder
lasts more than 1 day and remits by 1 mo
schizotypal (personality) disorder
- have odd beliefs or superstitions. have trouble forming close relationships tend to distort reality. can seem like a mild form of schizophrenia
- ppl who have schizotypal personality disorder don’t typically have delusions and hallucinations and they may go on to develop schizophrenia
diagnostic criteria (sympt) of schizophrenia
2+ of the following for present for a significant portion of time during a 1 mo period. as least one must be (1,2,3):
- delusions
- hallucinations
- disorganized speech
- grossly disorganized or catatonic behaviour
- negative symptoms
additional diagnostic criteria for schizophrenia
- for significant portion of the time since the onset of the disturbance, level of functioning in 1 or more major areas like work, self care, etc, is marked below level achieved prior to the onset.
- ** continuous signs of the disturbance persist for at least 6 mo. this 6 mo period must include at least 1 mo of symptoms.
- schizoaffective disorder or depressive or bipolar disorder w psychotic features have been ruled out bc either 1) no major depressive or manic episodes have occurred concurrently w the active-phase symptoms or 2) if mood episodes have… not continued on slides
what are delusions
- false beliefs that are firmly held that are not amenable to change in light of conflicting evi
- deemed bizarre if they are impossible and not understandable to same-culture pers, not derived from ordinary life experiences
what is persecutory delusions
belief that one is going to be harmed, harassed
what are referential delusions
belief that certain gestures, comments, environment cues, are directed at oneself
grandiose delusions
he/she has exceptional abilities, wealth, or fame
erotomanic delusions
believes falsely that another person is in love w him or her
nihilistic delusions
conviction that a major catastrophe will occur
somatic delusions
preoccupation regarding health and organ function
hallucinations
- incorrect perceptions of objects or events involving the senses
- usually transient
- can be very distressing: visual, auditory, sensory, olfactory (smell), gustatory (taste)
disorganized thinking
- typically inferred from individual’s speech
- switching from one topic to another: derailment or loose associations
- answers to questions may be obliquely related or completely unrelated: tangentiality
- can resemble receptive aphasia in its linguistic disorganization: incoherence or “word salad”, circumferential or fixation
- must be severe enough to substantially impair effective communication
grossly disorganized or abnormal behaviour
- problems may be noted in any form of goal-directed behaviour, leading to difficulties in performing activities of daily living
catatonic behaviour is marked decrease in reactivity to the environment
1. catalepsy (i.e. passive induction of posture held against gravity)
2. waxy flexibility (i.e. slight and even resistance to positioning)
3. stupor (no psychomotor activity; not actively relating to the environment)
4. agitation not influenced by external stimuli
5. mutism (i.e. no or little, verbal response but this is not applicable if there is established aphasia)
6. negativism (i.e. opposing or not responding to external stimuli)
7. posturing (i.e. spontaneous and active maintenance of a posture against gravity)
8. mannerisms (i.e. odd caricature of normal actions)
9. stereotypes (i.e. repetitive, abnormally frequent, non-goal-directed movements)
10. grimacing
11. echolalia (i.e. mimicking another’s speech)
12. echopraxia (i.e. mimicking another’s movements)
what 2 negative symptoms are particularly prominent in schizophrenia
- diminished emotional and facial expression (flat affect)
- reduction of eye contact, intonation of speech, and movements of the hand, head, and face that normally give an emotional emphasis - diminished speech
others include:
alogia
anhedonia
avolition
asociality
what is alogia
diminished speech output
what is anhedonia
decreased ability to experience pleasure from positive stim
what is avolition
decrease in motivation to perform self directed activities
what is asociality
lack of interest in social interaction
how much of the population has schizophrenia
1%
when is the disorder usually diagnosed
late adolescence or early adulthood
when are men vs women diagnosed w schizophrenia
men - early 20s
women - late 20s
is schizophrenia more common in men or women
makes + people who grew up in urban areas
describe phase 1 of schizophrenia
phase 1 - prodromal
- s/s that precede the characteristic manifestations of an acute, fully developed illness (withdrawn). characterized by some form of maladjustment
- appearance of symptoms may be subtle and gradual
describe phase 2 of schizophrenia
acute phase
- active phase of the disorder (negative, positive, cognitive symptoms)
describe phase 3 of schizophrenia
recovery
symptoms of acute stage are either absent or no longer prominent. negative symptoms may remain
(establishing a diagnosis of schizophreniform/schizophrenia)
medication regimens are established
describe schizophrenia exacerbations
- “relapses” do occur (in part bc of the chronic nature of the illness)
- w each relapse, there is no longer a recovery time (importance in early diagnosis and treatment)
- medication and psychosocial therapy greatly diminish the severity and frequency of relapses
- major reasons for relapse is non-adherence to medications
describe schizophrenia prodrome
early warning signs or early stage of schizophrenia. like a “prelude” before the full-blown symptoms of schizophrenia appear. a person might start to experience subtle changes in their thoughts, feelings, or behaviour, but not a full diagnosis yet.
what are the 3 types of non-diagnostic types of schizophrenia
- paranoid type
- disorganized type
- catatonic type
what is the paranoid type of schizophrenia
preoccupied w delusions or auditory hallucinations
what is the disorganized type of schizophrenia
disorganized speech, disorganized behaviour, and flat or inappropriate affect
what is the catatonic type of schizophrenia
(at least 1 of these characteristics)
- motor immobility, excessive or purposeless motor activity, extreme negativism, posturing, prominent grimacing, echolalia (repetition of someone else’s words) or echopraxia
what neurodevelopment etiology causes schizophrenia
- abnormal development of brain during prenatal life (where neurons fail to migrate correctly, make inappropriate connections, and lead to apoptosis later in life)
- attempt to explain how genes and events in life, such as infections, cause schizophrenia (ex: early prenatal exposure to infection, obstetric complications)
- neurodevelopment models remain dominant and are fuelling advances in epidemiology, imaging, and genetics
what neurotransmitters, pathways, and receptors etiology causes schizophrenia
- the dopamine hypothesis
- too much dopamine in the mesolimbic pathway cause positive symptoms
- too little dopamine in the prefrontal cortex causes the negative and cognitive symptoms
2 other drugs supported this theory. notably cocaine causes behavioural symptoms that are similar to paranoid schizophrenia - does not result from dysfunction of a single neurotransmitter
what are some other possible etiology of schizophrenia
estrogen?
cannabis?
autoimmune disorders?
genetics - twin studies
what are possible genes involved in schizophrenia
- disruptedin-Schizophrenia I (DISCI)
- neuregulin I (NRG I)
- Dystrobrevin binding protein/dysbindin (DTNBPI)
- catechol-O-methyltransferase (COMT)
- metabotropic glutamate receptor 3 (GRM3)
- brain derived neurotrophic factor (BDNF)
overall for etiology of schizophrenia what is believed
that it is a biological disease influenced by environmental factors
MULTIFACTORIAL
for PTSD what is the must have’s for exposure
- directly experiencing the traumatic event
- witnessing, in person, the event(s) as it occurred to others
- learning that the traumatic event(s) occurred to a close family member or close friend
- experiencing repeated or extreme exposure to aversive details of the traumatic event(s)
what are the 4 criteria to meet diagnostic threshold for PTSD
- intrusion symptoms
- avoidance of stim
- negative alterations in cognitions and mood
- alterations in arousal and reactivity
*duration of disturbance is more than 1 month
describe intrusion symptom criteria for PTSD
- recurrent, involuntary, and intrusive distressing memories of the traumatic event(s)
- recurrent distressing dreams in which the content and/or affect of the dream are related to the traumatic event (s)
- dissociative reactions (e.g. flashbacks) in which the individual feels or acts as if the traumatic event (s) were recurring
- intense or prolonged psychological distress at exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event(s)
- marked physiological reactions to internal or external cues that symbolize or resemble an aspect of the traumatic event(s)
describe avoidance of stimuli and mood criteria for PTSD
- avoidance of or efforts to avoid distressing memories, thoughts, or feelings
- avoidance of or efforts to avoid external reminders that arouse distressing memories, thoughts or feelings
describe negative alterations in cognitions criteria for PTSD
- inability to remember an important aspect of the traumatic event(s)
- persistent and exaggerated negative beliefs or expectations about oneself, others, or the world
- persistent, distorted cognitions about the cause or consequences of the traumatic event(s) that lead the individual to blame herself/himself or others
- persistent negative emotional state (ex: fear, horror, anger, guilt, or shame)
- markedly diminished interest or participation in significant activities
- feelings of detachment or estrangement from others
- persistent inability to experience positive emotions
describe alterations in arousal and reactivity criteria for PTSD
- irritable behaviour and angry outbursts (with little or no provocation) typically expressed as verbal or physical aggression toward people or objects
- reckless or self-destructive behaviour
- hypervigilance
- exaggerated startle response
- problems with concentration
- sleep disturbance (ex: difficulty falling or staying asleep or restless sleep
describe PTSD and dissociative symptoms
person meets criteria for PTSD and in response to stressor experiences either of:
1. depersonalization
- persistent or recurrent experiences of feeling detached from, as if one were an outside observer of, one’s mental processes or body (ex: feeling as though one were in a dream; feeling a sense of unreality of self or body or of time moving slowly)
2. derealization
- persistent or recurrent experiences of unreality of surroundings (ex: the world around the individual is experienced as unreal, dreamlike, distant, or distorted). note: to use this subtype, the dissociative symptoms must not be attributable to the physiological effects of a substance or another medical condition.
treatments for PTSD
- CBT
- COT
- PET
- MDR
- Medicine - SSRI’s
PSTD signs
- acoidance of thinking of trauma
- avoidance of talking abuot it
- easily frightened
- negative mood
- negative thinking
- always on guard
- avoiding places
- avoiding activities
- flashbacks
- cannot concentrate
- aggressive behaviour
- loss of interest
- feeling guilt or shame
- substance abuse
- sleeping difficulty
- bad dreams
why do cognitive disorders result plus there range
- result from changes in the brain
- marked by disturbances in orientation, memory, judgement, and affect - range from minor to major impairment
2 main cognitive disorders
- delirium
- dementia (DSM5 “major or mild cognitive disorders)
- term dementia (meaning ‘without mind’) has been retired due to stigma
what is delirium cognitive disturbance characterized by
- acute onset
- inattention
- disorganized thinking
- disturbance of consciousness
what causes delirium
- always secondary to another physiological condition and transient (determine cause to reverse symptoms)
- can be caused by UTIs, new meds, drug toxicity, alcohol, drug withdrawal, metabolic imbalances, terminal illness, fever in children,, malnutrition, sleep deprivations, pain, surgery
onset of delirium
abrupt
even tho this delirium is a short term condition, what are some long term consequences
- disorientation to person, place, time
- medical emergency
- accelerates cognitive decline
- associated w post-delirium depression
what are predisposing factors of delirium
- existing cognitive impairment
- low functional autonomy
- polypharmacy
- illness severity
what is CAM
confusion assessment method
diagnosis required BOTH A and B, and either C or D
A (acute onset and fluctuating course):
is there evidence of acute change in mental status from baseline?
does the abnorm behaviour:
- come and go
- fluctuate during the day
- increase/decrease in severity
B (inattention):
does the pt:
- have diff focusing attention
- become easily distracted
- have difficulty keeping track of what is said
C (disorganized thinking):
is the pt thinking:
- disorganized
- incoherent
for ex does pt have:
- rambling speech/irrelevant conversation?
- unpredictable switching of subjects
- unclear or illogical flow of ideas
D (altered level of consciousness)
overall what is the pt level of consciousness:
- alert (norm)
- vigilant (hyper-alert)
- lethargic (drowsy but easily roused)
- stuporous (difficult to rouse)
- comatose (unrousable)
treatment for delirium
treat the cause!
- drug reactions
- vit def
- lyte imbalance
- anemia
- thyroid dysfunction
- infection
what is dementia
- progressive deterioration of cognitive functioning and global impairment of intellect with no change in consciousness (progressive degeneration of brain cells that is irreversible)
- manifests as difficulty with memory, problem solving (executive functioning) and comprehension
greatest risk factor for dementia
- greatest risk factor is advancing age
- genetics, lifestyle, environment
types of dementia (9) dont say what they are just state them
- alzheimer’s type
- vascular dementia
- lewy body disease
- frontotemporal dementia or Pick’s disease
- alc-related dementia
- creutzfelldt-jakob disease
- wenicke-korsakoff
- stroke related dementia
- parkinson’s disease dementia
what is alzheimer’s type
most prevalent type. abnormal developments of proteins (amyloid) in and around brain cell deposits of which form plaques around brain cells. other protein is called tau, deposits of which form tangles within brain cells.
what is vascular dementia
caused by reduced blood supply to the brain due to disease blood vessels
lewy-body disease
tiny deposits of a protein (alpha-synuclein) that cause low levels of acetylcholine and dopamine. characterized by dementia, psychosis, and features of parkinsonism
frontotemporal dementia or pick’s disease
occurs when nerve cells in the frontal and/or temporal lobes of the brain die, and the pathways that connect the lobes change
alcohol-related dementia
alcohol related brain damage
creutzfelldt-jakob disease
caused by an abnormal isoform of a cellular glycoprotein known as the prion protein
wernicke-korsakoff
lack of thiamine (vit B1). it may result from alcohol abuse, dietary deficiencies, prolonged vomiting, eating disorders, or the effects of chemotherapy
what is alzheimers
progressive brain disorder affecting memory, thinking, and behaviour. most common cause of dementia, a term for serious memory loss and other cognitive abilities that interfere with daily life.
s/s of alzheimers
early signs: forgetfulness, confusion, diff speaking, trouble w daily tasks
as it progresses: ppl struggle w recognizing family members, becoming disoriented, losing ability to communicate
mechanisms of alzheimer’s + cause
Brain Changes: Alzheimer’s disease causes abnormal changes in the brain, including the buildup of two types of harmful substances: amyloid plaques (clumps of protein that disrupt brain cells) and tau tangles (twisted proteins inside brain cells that affect their function).
Cell Death: These plaques and tangles damage brain cells, leading to loss of connections between cells and eventually brain cell death, particularly in areas that control memory and thinking.
Cause: The exact cause is still not fully understood, but age, genetics, and environmental factors seem to play a role. There is also a link with inflammation and reduced blood flow in the brain.
describe to me the extracellular amyloid plaques in alzheimer’s disease
- amyloid-β peptides
- proteolytic fragments of transmembrane amyloid precursor protein (APP), a type of membrane glycoprotein that is involved in neuronal development, signaling, intracellular transport, and neuronal homeostasis
describe to me the intraneuronal neurofibrillary tangles of alzheimer’s disease
- Tau tangles
- brain specific, axon-enriched microtubules-associated protein. role is to stabilize neuronal microtubules under normal conditions.
what does the behavioural symptoms of alzheimer’s correlate w
accumulation of plaques and tangles, and they are a direct consequence of the damage and destruction of synapses that mediate memory and cognition
5 steps on the alzheimers timline
- early brain changes
- subtle decline in thinking
- memory changes, confusion
- inability to bathe, dress, or eat w/o help
- loss of ability to communicate and recognize loved ones
give me the overview of vascular dementia
1. how does is result
2. what do the risk factors lead too
- from brain ischemia or hemorrhage
- vascular risk factors lead to cerebrovascular disease -> brain injury -> disruption of cognitive networks
4 pathophysiology of vascular dementia
- atherosclerosis of large feeding arteries cause infarcts via cerebrovascular occlusion or thromboembolism
- atherosclerosis linked to HTN can cause occlusive disease of small arteries leading to infarcts, hemorrhage and microbleeds
- microvascular disease, closely associated with diabetes, disrupts metabolic function at the capillary level
- APOE ε4 genotype and cerebral amyloid angiopathy in pial and cortical arteries and capillaries
describe what lewy body disease is and how it is characterized
- progressive degenerative brain disorder
- characterized by dementia, psychosis, and features of parkinsonism
describe the acetylcholine deficiency in Lewy Body Disease + what is also diminished
- decreased levels of acetylcholine in the temporal and parietal cortex that can result in visual hallucinations
- upregulation of muscarinic receptors in temporal lobe results in delusions
- dopamine is also diminished
early stage of progression of lewy body dementia
delusions, restlessness, REM sleep disorder, movement difficulties, urinary issues
middle stages of progression of lewy body dementia
motor impairment, speech difficulty, decreased attention, paranoia, significant confusion
later stages of progression of Lewy Body Dementia
extreme muscle rigidity and speech difficulties, sensitivity to touch, susceptibility to infecitons
how does frontotemporal dementia result
from damage to neurons in the frontal and temporal lobes of the brain
when does frontotemporal dementia tend to occur
tends to occur at a younger age than other forms of dementia. roughly 60% of ppl with FTD are 45-64 yrs old.
how is frontotemporal dementia characterized
by intracellular deposition of abnormal protein aggregates in the frontal and temporal lobes resulting in:
1. degeneration of neurons
2. micro vacuole formation
3. astrocytosis
what are the 3 types of frontotemporal dementia (just state dont describe)
- behavioural variant frontotemporal dementia (bvFTD)
- primary progressive aphasia (PPA)
- movement disorders
describe FTD: behavioural variant frontotemporal dementia (bvFTD)
- most common FTD
- changes to personality, behaviour, judgement
- problems planning and sequencing, difficulties prioritizing tasks or activities, repeating the same activity over and over, acting impulsively, or saying and doing inappropriate things
describe FTD: primary progressive aphasia (PPA)
- involves changes in ability to communicate - to use language to speak, read, write, and understand what others are saying.
- includes aphasia and difficulty speaking.
A. Semantic PPA - loses ability to understand single words and sometimes to recognize the faces of familiar people and common objects
B. Agrammatic PPA - more and more trouble speaking and may omit words that link nouns to verbs (such as to, from, the)
C. Logopenic PPA - trouble finding the right words during a conversation but can understand words and sentences
describe FTD: movement disorders
A. corticobasal syndrome - results from corticobasal degeneration, gradual atrophy and loss of nerve cells. progressive loss of the ability to control movement. apraxia most common, inability to use the hands or arms to perform movement despite normal strength
B. progressive supranuclear palsy - causes problems with balance and walking. typically walk slow, experience unexplained falls, loss of facial expression, and have body stiffness. hallmark sign is trouble with eye movements, looking down.
for alzheimer’s disease give
1. % of dementia cases
2. history
3. s/s
4. pathology/imaging
- 50-80%
- gradual, progressive onset
- memory loss especially names and recent events
- language deficits
- rapid forgetting
- impaired visuospatial skills
- normal gait and neuro exam early
- later affective disturbances; behavioural symptoms such as aggression
- generalized atrophy (esp. medial temporal)
- beta amyloid plaques
- neurofibrillary tangles
for vascular dementia
1. % of dementia cases
2. history
3. s/s
4. pathology/imaging
- 20-30%
- abrupt or gradual onset
- focal neuro signs
- signs of vascular disease
- strokes
- lacunar infarcts
- white matter lesions
- vulnerable to cerebrovascular events
for lewy body dementia
1. % of dementia cases
2. history
3. s/s
4. pathology/imaging
- 10-25%
- insidious onset, progressive w fluctuations
- fluctuating cognition
- visual hallucinations
- neuroleptic sensitivity
- shuffling gait
- increased tone
- tremors
- falls
- generalized atrophy
- lewy bodies in cortex and midbrain
for frontotemporal dementia
1. % of dementia cases
2. history
3. s/s
4. pathology/imaging
- 10-15%
- insidious onset, typically in 50s-60s; rapid progression
3.
- disinhibition
- socially inappropriate behaviour
- poor judgement
- apathy, decreased motivation
- poor executive function
4.
- frontal and temporal atrophy
- pick cells and pick bodies in cortex
common s/s of demtentia
- aphasia
- apraxia
- agnosia
- disturbances in executive functioning
- sexual disinhibition
- preservation
- confabulation
- sundowning
what is aphasia
impairment of language
what is apraxia
diff w motor movements
what is agnosia
inability to process sensory info
confabulation
production of fabricated, distorted, or misinterpreted memories about oneself or the world, without the conscious intention to deceive. made up stories to full gaps in memories.
preservation in dementia
repetition of particular response (such as a word, phrase, gesture)
what is sundowning
symptom of alzheimer’s and other forms of dementia. also known as “late-day confusion.” confusion and agitation may get worse in the late aft/evening
how do we treat alzheimer’s + the medications
no cure :(
3 cholinesterase inhibitors are commonly prescribed:
1. donepezil (aricept)
- treats all stages of the disease. it is taken once a day as a pill.
2. galantamine (razadyne)
- treats mild to moderate alzheimer’s. taken as a pill once a day or as an extended release capsule twice a day.
3. rivastigmine (exelon)
- treats mild to moderate alzheimer’s disease. also taken as a pill. a skin patch is available that can treat severe alzheimer’s.
4. memantine (exixa)
- treats moderate to severe alzheimers
what are cholinesterase inhibitors
- boost the amount of acetylcholine avaliable to nerve cells by preventing its breakdown in the brain
- cannot reverse the disease or stop destruction of nerve cells
- eventually lose effectiveness bc dwindling brain cells produce less acetylcholine as the disease progresses
what are common side effects of cholinesterase inhibitors
n/v, diarrhea
- starting low and working up helps reduce side effects + taking the meds with food.
4 cholinergic inhibitors
- donepezil
- galantamine
- memantine
- rivastigmine
how does memantine work + what for
treatment of moderate to severe alzheimer’s
- regulates activity of glutamate which is a chemical widely involved in brain function (learning + memory)
- glutamate excitotoxicity resulting from excessive glutamate signalling process. results in damaging and killing nerve cells, slowly evolving neurodegeneration
- acts as a antagonist for N-methyl-D-aspartae (NMDA) receptor subtype of the glutamate receptor
- often used in combo w acetylcholinesterase inhibitors
side effects of memantine
headache, dizziness, nausea, diarrhea
MMSE
mini mental status exam
- widely used to test and assess a person’s cognitive function
- screens for dementia and monitor changes over time
- max score is 30
- score of 24 or higher is typically normal
MoCA
montreal cognitive assessment
score /30 w that being the max score
26 or higher is considered normal
19-25 is mild cognitive impairment
11-18 is mild dementia
