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Management of Neuropsychiatric Disorders > Brain injury > Flashcards

Brain injury Flashcards

(60 cards)

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1
Q

what is a TBI

A

Caused by trauma to the head from an external mechanical force

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2
Q

what is an ABI?

A

Any non-congenital, non-degenerative injury to the brain inc. TBI but also others e.g. cerebral infections

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3
Q

TBI risk factors

A

male
young/ old
alcohol
risk taking behaviour
lower socioeconomic status
psychiatric hx

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4
Q

contusions

A

Mix of cortical necrosis and haemorrhage, typically orbital & medial prefrontal cortex, temporal pole & inferior temporal surface with contrecoup occipital pole injuries

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5
Q

cerebral anoxia

A

lesions depths cortical sulci, basal ganglia, loss of Purkinje cells in the cerebellum (‘watershed’ areas)

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6
Q

neuroimaging of anoxic brain injury

A

Scan may look normal initially but in severe hypoxic brain injuries there is atrophy over time and loss of grey-white differentiation

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7
Q

GCS

A

eye opening
best verbal response
best motor response
out of 15

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8
Q

GCS - mild

A

13-15

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9
Q

GCS - moderate

A

9-12

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10
Q

GCS - severe

A

3-8

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11
Q

mayo classification

A

definite moderate to severe
probable mild
possible TBI

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12
Q

psychiatric consequences of acute stage tbi

A

delirium - hypo or hyper active

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13
Q

delirium

A

acute disturbances of attention, orientation, and at least one other aspect of cognitive function, in the absence of another plausible medical or substance-related cause

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14
Q

hyperactive delirium

A

commoner in males

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15
Q

hypoactive delirium

A

commoner in females
Easily missed BUT associated with poorer long-term outcomes
Management is primarily non-pharmacological
limited role of stimulants or melatonin

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16
Q

what is pta

A

Amnestic gap from moment of injury to time of resumption of normal continuous memory

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17
Q

true or false PTA can occur without loss of consciousness

A

True

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18
Q

what is the duration of pta

A

minutes to weeks

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19
Q

what is retrograde amnesia

A

time between moment of injury and last clear memory from before the injury

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20
Q

what is anterograde amnesia

A

Deficit in forming new memories after injury

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21
Q

what are good indicators of tbi severity

A

GCS
Duration of LOC
Duration of PTA
Evidence of delirium immediately after injury
Neurological sx and signs
Skull fracture or other abnormalities on imaging
Blood in CSF

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22
Q

what are poor indicators of tbi severity

A

duration of retrograde amnesia
abnormalities on eeg

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23
Q

what % experience depression post tbi

A

20-40%

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24
Q

what % experience anxiety post tbi

A

10-15%

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25
what % experience ptsd post tbi
10-30%
26
prevalence of psychosis
less common mostly in pt predisposed to psychosis psychosis interacts with cognitive deficits limited to one or two psychotic sx vs schizophreniform picture
27
prevalence of suicide
3-4x more common in tbi compared to general population
28
risk factors for suicide post tbi
alcohol substance misuse shared risk factors
29
tx of post-concussional syndrome
difficult to tx potentially antidepressants or mood stabilisers modified cbt approach
30
frontal lobe syndromes
personality change
31
syndromes of damage to orbitofrontal region
disinhibition euphoria emotional lability poor judgement environmental dependency
32
syndromes of damage to dorsolateral and medial brain regions
apathy loss of initiative slowing of thought and action - Inattention, distractibility, poor planning and judgement - Motor programming impairments - Reduced verbal fluency
33
damage to the dominant hemisphere premotor cortex causes
Broca;s dysphasia
34
what does damage to the anterior cingulate cortex cause?
impaired motivation akinetic mutism apathy
35
what are some parietal lobe syndromes
Cortical sensory loss Astereognosis Disorders of body schema Anosognosia Gerstmann syndrome (dominant parietal lobe)
36
what is Gerstmann syndrome
Dyscalculia Dysgraphia Finger agnosia R-L disorientation
37
temporal lobe syndromes
Auditory deficits Sensory dysphasia Visual, esp. prosopagnosia Memory impairments Personality change/psychosis
38
occipital lobe syndromes
Cortical blindness (bilateral) Homonymous hemianopia (unilateral) Scotomata Visual agnosia Alexia without agraphia
39
what are risk factors for post tbi personality change
moderate to severe injury PTA longer terms emotional/ behavioural changes frontal/ temporal damage premorbid cognition and psychiatric illness substance misuse
40
which post injury factors increase risk for post tbi personality change
care/ support specialist neurorehab legal proceedings
41
what % of pt are affected by personality change post tbi
30-60%
42
what are anatomical correlates of frontal lobe syndrome
frontal lobe damage particularly orbitofrontal cortex
43
principles of pharmacological interventions
start low and go slow titrate cautiously monitor for adverse effects sedating drugs can compromise cognitive/ physical gains over time wean meds as pt improves
44
what are early pharmacological interventions for agitation
Good evidence for Propranolol Some evidence for Amantadine, Valproate, Carbamazepine, antipsychotics Negative evidence for benzodiazepines, opiates, psychostimulants, phenytoin
45
what are long term pharmacological interventions for agitation/ aggression/ impulsivity
Good evidence for Anticonvulsants: Valproate, Carbemazepine, (Lamotrigine) Propranolol (range of doses: slow titration and weaning, ECG monitoring) Amantadine
46
when is the best use of olanzapine to manage agitation etc (antipsychotic)
acute vs long term
47
antidepressants
Some evidence for antidepressants (Sertraline, Amitriptyline) even without overt mood disturbance
48
what guides the choice of long term medication
Presence of mood symptoms Presence of psychotic symptoms Other medical problems, other medications Tolerability in the individual case
49
what characterises severe apathy post tbi
akinetic mutism
50
post tbi apathy is associated with damage to which area
anterior cingulate cortex (ACC) medial prefrontal cortex insula thalamus basal ganglia
51
pharmacological interventions for apathy
Dopamine agonists e.g. Pramipexole Psychostimulants (Methylphenidate) Amantadine Cholinesterase inhibitors Antidepressants (but unclear that they help in non-depressed patients – some recent evidence for Agomelatine, Atomoxetine)
52
ethical considerations for prescribing stimulants
Prescribing stimulants/controlled drugs may present an ethical dilemma in patients with history of substance misuse
53
tx
multidisciplinary
54
two main principles of tx and rehabilitation
what are the aims/ goals what is realistic/ achievable
55
what is the role of psychology in tx
neuropsychological ax CBT cognitive training relaxation mindfullness anger mx social skills training
56
what is the role of occupational therapy in tx
‘Real world’ skills Self-care Shopping, cooking, household Planning and managing demands of life
57
what is the role of speech and language therapists in tx
Dysphasia Dysphagia Dysarthria Communication problems e.g. conversational style
58
what is cerebellar cognitive-affective syndrome
Associated with damage to posterior lobes of cerebellum
59
what deficits are characteristic of cerebellar cognitive-affective syndrome
Emotional regulation Use of language Executive function Visuospatial function clinically similar to presentations post prefrontal cortex damage
60
what explains the overlap between cerebellar cognitive-affective syndrome and frontal damage
Reciprocal connections between cerebellum and cortical regions

Management of Neuropsychiatric Disorders (25 decks)

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