PSYU3344 Neuropsychology in Clinical Practice Final Exam Prep

Traumatic brain injury

an acquired brain injury due to damage to the brain as a result of the sudden application of mechanical energy from external physical forces

Penetrating (open) TBI

when a foreign object enters the brain; pathology concentrated around the path of the intruding object

Contact (closed) TBI

when the head suddenly at force comes into contact with a stationary object; brain compresses against the inner surface of the skull; ricocheting movement; lesions all over the surface of the brain from the deceleration; most common form; diffuse/widespread pathology; outcome often poorer

TBI prevalence

very common neurological syndrome; males:females = 2-3:1 (more common among males than females)

Cause of TBI

Fall, transport-related accident, assault, sports injury; falls most common for children and adults older than 45;

Violence and motor vehicle accidents most common form for adolescents and young adults;

Occurs more in lower SES, unemployed, substance abuse, poor academic performance

Sports-related concussion

rates highest for motor sports, equestrian activities, Australian football, rugby and roller sports; in Vic the frequency of hopsitalisation increased by 60.5% over 9 years and accounted for 16.5% of all hospitalisations for concussion

A TBI can occur due to

both contact forces to the head and acceleration/deceleration head movements (brain suddenly starts moving in the skull); linear forces and angular rotation

Inertia

Brain lags behind the skull. The head starts moving but the brain is lagging behind and this is why the brain will start ricocheting off of the inner surface of the skull when acceleration/deceleration forces are applied to the head. This causes bruising and tearing of the external surface of the skull and because the brain is comprised of tissues with different densities, tissues move relative to one another.

Neuropathology of TBI: Immediate (primary effects)

what happens at the actual time of trauma:

- injury to scalp

- fractures to skull

- surface brain contusions (bruising)

- cerebral lacerations (tearing from the bony underside of the skull)

- diffuse axonal injury (rotational forces and different parts of the brain moving relative to one another)

- diffuse vascular injury (not just white matter but the different types of vessels that supply the brain can also be damaged)

Injury to the scalp

- external injuries to the face, scalp: scalp lacerationn, brusing, abrasion

- skull fractures

- contusion

Contusion

bruising. Occurs when the brain comes into contact with bony areas of the skull.

Coup/countercoup injury - occur individually and together

Coup lesion

lesion of the brain under the point of impact (frontal lobes); occur at site of impact/contact

Countercoup lesion

bruising or contusion of the occipital lobes opposite the point of impact; associated with translation (linear) acceleration

3 protective layers of the brain

1) Dura mater

2) Arachnoid

3) Pia mater

Extradural (type of intracranial bleed)

bleed between the skull and dura mater (first protective layer)

Intradural (type of intracranial bleed)

Subdural = underneath the dural, between the dura mater and arachnoid (2nd protective layer)

Subarachnoid = between the arachnoid and the pia mater (3rd protective layer)

Intracerebral haematoma

bleeding within the brain substance itself/hemispheres

White matter tracts

one of the principle sequalae of TBI

Diffuse axonal/vascular injury or traumatic axonal injury (TAI)

extensive white matter lesions and shearing strain/injury; principle pathological substrate producing neurological impairment

- Following severe TBI: tearing of axons

- Following milder TBI: stretching of the axons; temporary disruption of function; good potential to recover

Petechial haemorrhages (TAI)

tearing of the capillaries; like TAI are the result of rapid acceleration/deceleration forces; may coalesce/combine into larger lesions with progressive secondary haemorrhage; patients deteriorate within the first 24-48 hours because of the bleeding in the brain

Mild TBI (TAI)

may produce no permanent damage to cells; axons have a capacity for stretch without axotomy (severing of axons) occurring

Mild to severe TBI (TAI)

Macroscopic haemorrhages in midline structure (including brainstem) which over time shrink to sunken cystic scars;

Microscopic axonal injuries: days (numerous axonal swellings and axonal bulbs in deep); months-years (small healed superficial contusions, extensive white matter degeneration, relatively intact gray matter, enlarged ventricles

Degree of TAI is

proportional to the severity of TBI

TAI 17 month survival in vegetative state

marked symmetrical dilation of the ventricles; absence of surface contusions; loss of definition; brain showing significant (chronic) pathology following very severe TBI

Neuropathology of TBI: Secondary Effects

- Ischaemic (reduced blood supply to brain tissues)

- Hypoxia (lack of oxygen)

- Swelling (oedema)

- Raised intracranial pressure (ICP)

These factors negatively affect outcome in terms of patients prognosis for recovery.

The greater the number of pathological factors occurring

the greater the permanent damage resulting from TBI

Neuropathology of TBI: Delayed effects

- Ongoing atrophy (degeneration) of white matter, appearing more marked over time

- Hydrocephalus = due to problems of reabsorption of CSF (e.g. from subarachnoid haemorrhage, oedema)

- Meningitis and brain abscess - most common following depressed or based of skull fractures, surgery

- Post-traumatic epilepsy (incidence approx 5%)

Two parameters measured when measuring severity of TBI

1. Level of coma/impaired consciousness (degree to which consciousness is being disturbed)

2. Post-traumatic amnesia

Coma/impaired consciousness

Glasgow Coma Scale (GCS)

Glasgow Coma Scale (GCS)

Presence, duration and depth of impaired consciousness and coma; used to describe altered consciousness from a mild confusional state to deep coma; confused = consciousness disturbed

3 aspects measured:

1) verbal responses

2) motor responses

3) eye opening

GSC: Verbal responses

Highest level of responsiveness; mild disturbance = GCS of 14/15; orientation

GCS: Motor responses

Can they touch your nose? can you wave to me?

Level of responsiveness can reduce to the point that there is no motor response indicated

Commands; how to they respond to pain?

GCS: Eye opening

The more severe the impairment, the less likely they are to be able to open their eyes

Spontaneous speech; pain (opens eyes under pressure/does not open eyes)

GCS: Full orientation

What is your name? Where are you? Why are you here? What month are we in? What year are we in?

GCS: Total coma score

Eye opening + Motor responses + Verbal responses = 15 (range is 3-15)

Score of 15 - no disturbance of consciousness

Person with a score of 15 can still be in PTA

Score if 14-9 indicates that there is some disturbance of consciousness

A lower GCS

more severe TBI; the longer the amnesia; and the more probable death/mortality

Coma

not opening eyes, not obeying commands, not uttering understandable words; 90% of people with a GCS of equal to or lower than 8 will be in a coma; score of 3 = deepest level of coma

GCS score of 8

critical score

Mild TBI injury GCS

13-15; up to 24 hours

Moderate TBI injury GCS

9-12; >1 and <7 days

Severe TBI injury GCS

3-8; >7 days

Post-traumatic amnesia (PTA)

- Length of PTA is used as an index of TBI severity

- An acute but temporary period following coma/impairment consciousness during which the patient is confused, disoriented

- Hallmark = amnesia (starts time of injury)

- Period of connected recall - remembering most of what is going on

- Characterised by intellectual and behavioural disturbances

- Correlates most strongly with outcome following TBI

- The longer the period of PTA the more likely a patient is going to demonstrate residual cognitive and behavioural change

-

Standardised prospective measurement of moderate to severe PTA

Westmead PTA Scale

Standardised prospective measurement of mild TBI/concussion

Abbreviated-Westmeead PTA Scale

Test begins when patient communicates intelligibly and is able to follow commands (i.e. GCS motor score = 6+)

Test stops when person is out of PTA (i.e. achieve a perfect GCS score of 12/12 for 3 consecutive days)

Westmead PTA Scale (WPTAS)

7 orientation questions e.g. DOB, month, time of day, year, place

5 memory questions e.g. examiners name and face, 3 picture cards

Westmead PTA Scale (WPTAS) contains

Administered hourly for up to 4 hours

Can be administered at any time within 24hours of injury

Combines the GCS score with the picture items from the WPTAS

Patient is out of PTA on the first score of 18/18 - no longer amnesic

If unable to meet criteria and obtain a score of 18 when give 4 opportunities then they move on to thee WPTAS

Orientation items:

If patients response incorrect, immediately presented with the correct answer. If they respond with "I don't know" or doesn't respond spontaneously, provided with multiple choice

Picture cards:

If one or more pictures cards not recalled spontaneously, a choice is given from the 3 target pictures and 6 distractor items

PTA status:

A patient is considered to be out of PTA on the first score of 18/18

Abbreviated Westmead PTA Scale (A-WPTAS)

Retrograde Amnesia (RA) in the context of PTA

- Loss of memory for the period prior to onset of the brain injury

- Temporal gradient: the more distal the memory the more likely it is to bee retained

- Failure to recall events prior to the TBI

- RA usually shorter duration than PTA

- RA may shrink overtime as the individual recovers from PTA (PTA won't shrink)

- Length of RA associated with TBI severity (e.g. in mild TBI, RA may be minutes to seconds); the more severe the brain injury, the longer the period of retrograde amnesia

Neuropscyhological Screening of PTA in the Acute Phase

Orientation questions: (Mini-mental state examination; brief cognitive examination)

Memory: (Westmead Selective Reminding Test)

Processing speed: Symbol Digit Modalities test (oral and written)

Executive function/processing speed: (FAS - Controlled Oral Word Association Test

Psychological tests to screen for acute stress disorder, depression and anxiety

Postconcussion symptom reporting (PCS checklist, neurobehavioural symptom inventory)

Differential diagnosis to exclude a degenerative disorder (Addenbrooke's Cognitive Examination)

Other neuropsychological screening tests in the acute phase of PTA

Postconcussive syndrome checklist

Physical, cognitive and behavioural changes that are very often endorsed post TBI

Depression anxiety stress scales (DASS)

7 items measuring depression

7 items measuring anxiety

7 items measuring stress

Can gauge the severity of those psychological factors

If the patient is endorsing high levels of postconcussive symptoms, very high levels of depression, anxiety and stress...

the cognitive impairments that you are seeing on testing are due to psychological disorder rather than underlying brain injury

Neuropscyhological Screening of PTA in the Chronic Phase

Usually takes 3-4hours in a face-to-face assessment to evaluate:

- Intllifence

- Memory (typically anterograde)

- Executive/Adaptive Function

- Motivation/Effort

- Psychological measures: PTSD Checklist for DSM-5, DASS, post-concussion checklist or neurobehavioural symptom inventory

Comparing patients with PTA's current cognitive functioning to their premorbid functioning occurs when

neuropscyhological screening PTA in the chronic phase

Mild Traumatic Brain Injury/Concussion

GCS of 13-15, PTA <24 hours

Neuropsychological impairment: attention, learning and memory, speed of information processing - these deficits resolve quickly within the first few weeks

Neuropsychological impairment: Mild Traumatic Brain Injury/Concussion

Overall neuropsychological recovery occurs most quickly during the first two weeks; return of baseline at 1-3 months

Neuropsychological recovery: Mild Traumatic Brain Injury/Concussion

Moderate to Severe Traumatic Brain Injury

GCS of equal to or less than 12, PTA >1 day

More likely to see ongoing and permanent impairment

- memory impairment - difficulty in learning (encoding) particularly when material needs to be organised or strategies developed, in retrieval and storage problems

- adaptive or executive abilities - an inability to adapt, regulate and control responses in accord with novel and unusual task demands

- attention and speed of information processing deficits

- dose-response relationship between TBI severity and neuropsychological impairment

Neuropsychological impairment: Moderate to Severe Traumatic Brain Injury

- Rapid recovery in the first 3-6 months

- continued, slower recovery over 1-2 years and then a plateau

- reduction in learning and processing speed at 1-year predict long-term disability and the degree of functional independence

- behavioural changes e.g. aggressive behaviour: orbito-frontal syndrome associated with behavioural excess - impulsivity, disinhibition, hyperactivity, distractability and mood lability

- adverse effects on functioning include effects on employment, independent, social, leisure activities and quality of life

Neuropsychological recovery: Moderate to Severe Traumatic Brain Injury

Preinjury history of mood or anxiety disorder significantly more frequent in patients who develop post-TBI major depression, post-traumatic stress and other psychological disorders.

Post-traumatic stress disorder present in mild TBI and severe TBI

Neuropsychiatric disorders associated with TBI

Dementia

term used to describe the symptoms of a large group of illnesses (unbrella term) which cause a progreesive decline in a person's functioning.

broad term to describe a loss of memory, intellect, rationality, social skills and physical functioning

when the cognitive impairments do not have a functional impact, the person is said to have

Mild Neurocognitive Disorder (NCD) or Mild Cognitive Impairment (MCI)

if the cognitive impairments are impacting on a person's ability to work, undertake activities of self-care, functional things like paying bills/driving, then they satisfy the criteria of

Major Neurocognitive Disorder (NCD)

Second leading cause of death in Australians

Dementia

Which type of dementia is the most common?

Alzheimer's disease (AD)

Which type of dementia is the second most common?

Vascular dementia

Cortical dementia

types of dementia caused by disorders that affect the brain's cerebral cortex (brain's outermost layer)

includes AD, FTD (bv-FTA and Primary Progressive Aphasia)

Subcortical dementia

those diseases which predominantly affects the basal ganglia along with features of cognitive decline - where we process primitive functions (e.g. emotion processed in amygdala)

includes vascular dementia, Parkinson's dementia and huntington's dementia

Early onset AD (< 65)

more rapid progression

AD

Prevalence increases with age

Slow and insidious progression (often lasting 10+ years) - gradual

Amyloid plagues (hard, insoluble accumulation of beta amyloid proteins that clump together between nerve cells (neurons)

Neurofibrillary tangles (within the cell bodies)

Hallmark lesions of AD

Begin in medial temporal lobes (hippocamppi; entorrhinal cortex)

Progresses to slowly involve the parietal and frontal lobes

AD pathology

loss of acetylcholine and nicotinic receptors

70% loss of choline acetyltransferase (precursor to acetylcholine) in temporal and parietal lobes

loss of acetylcholine receptors correlates with number of amyloid plaques and severity of cognitive dysfunction on testing

AD neurochemistry

Get general (global) atrophy; cell death throughout the cortex; greater impairment of the hippocampus and language areas of temporal lobe; appearance of enlarged ventricles (brain isn't filling the space)

Brain changes in AD

Typically memory problems; word finding; spatial issues; impaired reasoning abilities

Early symptoms of AD

Poor insight, difficulty coping with complexity, new situations, changed environments

AD symptoms

Repetitive in conversation

Forget recent conversations

Insidious onset of symptoms (hard to pin-point when the difficulties started)

Deny or minimise deficits

Difficulty with activities of daily living (shopping, managing finances i.e. paying bills, driving)

AD presentation

- typical stage when diagnosed

- wandering and getting lost

- trouble handling money and paying bills

- repeating questions

- taking longer to complete normal daily tasks

- losing things or misplacing them in odd places

- personality and behavioural changes (esp if affecting frontal lobe)

Mild AD

- damage to (surrounding) brain areas controlling language, reasoning, sensory processing

- increased memory loss and confusion

- difficulties recognising family and friends: starts will less familiar people then progresses to those closest

- inability to learn new things

- self-care/dressing problems

- hallucinations, delusions, paranoia

- impulsive behaviour - particularly if they are managing their own finances it can be important to keep track of that - check they are not overspending

Moderate AD

- become entirely dependent on others for care; ability to communicate is lost - global brain atrophy

- inability to communicate

- weight loss

- seizures

- skin infections

- difficulty swallowing

- groaning/grunting

- increased sleeping

- incontinence

Severe AD

age

family history

vascular disorder

ApoE e4 allele

female

history of head injury

negative relationship with educational level

cognitive reserve = more highly educate you are, the more cognitive reserve (resilient) your brain deals with pathology

AD risk factors

Anterograde episodic memory is impaired in

AD

Time of onset of symptoms to diagnosis = 2-3 years

Diagnosis to nursing home placement = 3-6 years

Nursing home to death 3 years

10 year progression from onset to death

AD onset and prognosis

Increases AD risk 20 fold

Age of onset 10 years younger

Associated with more severe cholinergic deficit (don't have as many acetylcholine receptors), increases amyloid beta burden, more neurofibrillary tangles (neuropathology worse)

ApoE e4 allele

Acetylcholinesterase (enzyme that breaks down acetylcholine) inhibitors - Ach hanging in synapse for longeer

Donepezil

Rivastigmine

Galantamine

Inhibit enzyme action - prolongs Ach activity in synaptic cleft

Reduce progression, but do not restore function (no cure)

AD treatment: acetylcholinesterase inhibitors

N-methyl-D-aspartate (NMDA) receptor antagonist - involved in apoptosis (cytotoxicity and cell death due to over activity of neurons)

AD treatment: memantine

Antidepressants (SSRIs) to treat mood symptoms

Antipsychotics (risperidone) to treat behaviour symptoms

AD treatment

Umbrella term for neurodegenerative disorders that affect anterior parts of the brain (frontal lobe and anterior parts of the temporal lobe)

Frontotemporal dementia FTD_

Earlier onset than AD

More rapid progression than AD (5-7yrs rather than 10yrs)

FTD: onset and prognosis

Behavioural variant

Primary Progressive Aphasia (temporal variant) i.e. Progressive Non-fluent Aphasia, Semantic Dementia, Logopenic Progressive Aphasia

FTD subtypes

Cortical atrophy of frontal and anterior temporal lobes

Can be asymmetrical - particularly for language variants (attacking left side of brain first)

Pick bodies (tau accumulation)

Beta amyloid plaques and neurofibrillary tangles

Blood flow and metabolism significantly reduced in frontal and temporal lobes

FTD neuropathology

Aphasia Dysnomia (problem naming objects)

Impaired repetition (different to PNFA) and comprehension of sentences (singlee word is okay)

Smantic knowledge INTACT

Logopenic PPA

· loss of semantic knowledge (poor semantic memory)

· Conversation is fluent and non-dysarthric (clear)

· Intact episodic memory

· Little evidence of dysarthria or reduced speech output

· Social withdrawal and depression common due to intact insight

· Not associated with personality/behavioural changes

Semantic Dementia

· Language deficits

· Significant frontal executive dysfunction

· Greater executive impairment in frontal lobes as opposed to memory impairment

· Visuospatial skills, orientation and arithmetic intact

· Memory impairment variable - encoding and retrieval difficulties rather than rapid forgetting

· Behavioural/personality changes - core diagnostic

LACK OF INSIGHT

bv-FTA

Progressive decline in speech and writing

Increasing phonological and grammatical errors

Agrammatism (grammar inaccessible)

Effortful speech/non-fluent (similar to Broca's Aphasia)

Eventually becomes telegrammatic (e.g. single words)

Comprehension of words intact

Repetition intact

Dysarthria and worsening speech output

Social withdrawal and depression common due to intact insight

PNFA

Can vary

Relatively abrupt onset; stepwise deterioration; fluctating course of congitive functioning; more insidious course with small vesseel dementia; mood and behavioural changes

Vascular cognitive impairment: presentation

1. Dementia

2. Cerebrovascular Disease

3. Relationship between onset of problems and evidence of CVD manifested/inferred by the presence of:

a) onset of dementia within 3 months following strok

b) abrupt deterioration in cognitive functions, or fluctuating stepwise progression of cognitive deficits

NINDS-AIREN criteria (vascular CI)

Mixed etiology dementia is common

Vascular dementia and AD