Week 4 - TBI Flashcards
What is TBI?
an acquired brain injury due to damage to hte brain resulting from sudden application of mechanical energy from external physical forces
Difference between penetrating and contact TBI
penetrating (bullet) - damage tends to be concentrated around the path of penetration
contact - the brain moves behind the skulls and hits itself repeatedly against the skull surface (more widespread damage)
Estimation of prevalence?
600 cases of TBI per 100 000 patients
Most often will be mild (most common form)
not everyone who survives a TBI will seek medical attention
Prevalence of hospitalized TBI
higher proportion of male (2 x 3 times higher)
Majority of these are from ages 15-24 - at this time, memory is particularly susceptible to disruption - and the ability to learn new information and store it is most likely to be affected by TBI
What are the main causes of TBI
In young children and adults over 45 = a fall
in adolescence and young adults = violence or motor vehicle accidents
TBI more often occurs in lower socioeconomic classes, unemployed, substance abuse, poor academic performance - you have to differentiate between pre-existing state and the condition.
A traumatic brain injury can occur due to both:
Contact forces to the head
Acceleration / deceleration of movements (linear forces or angular rotation)
Brain effects are usually described in terms of primary/immediate, secondary and tertiary processes
What are primary effects (immediate)
Immediate (Primary) = occurs at the time of injury and represents the direct result of rapid acceleration and deceleration of the head
Injury to scalp
Fractures to skull
Surface brain contusions (bruising) and cerebral laceration s(tearing from the bony underside of the skull)
Intracranial hematoma (bleeding)
Diffuse axonal injury (different parts of the brain move relative to one another - grey matter, white matter, ventricles)
Frontal and temporal lobes are particularly susceptible (to lesions) because of the irregular surface
Tell me about contusions
Contusion - bruises
coup contusion - site of impact
contrecoup contusion - opposite of the site of impact
What are the 3 layers you have under the skul
-dura mater
- arachnoid
- pia mater
These 3 layers represent areas where you could get tearing of blood vessels
Outline intracranial bleeds
- due to haemorrhage and haematoma through tearing of blood vessels - can occur immediately or over hours
- if neurological state starts to deteriorate, its a sign there’s bleeding going on
Types: - extradural (bleed between skull and dura mater)
- intradural (subdural, subarachnoid, etc)
These collections of blood can exert pressure on underlying brain tissue
Acceleration-deceleration phenomena
Diffuse white matter shearing:
- when the head suddenly rotates, different parts of the brain, meninges and CSF move relative to one another
- shearing strains cause widespread tearing of nerve fibres, synapses and blood vessels
- results in extensive white matter lesions and generalized disconnection between cortical and subcortical structures
- shearing strains are exaggerated at brain surfaces between substrates of different densities and at positions of least brain movement
Outline diffuse axonal and diffuse vascular injury
The axonal injury is the principle pathology which causes the neurological dysfunction.
The most significant pathology will be a result of traumatic axonal injury.
Least severe - axons are stretched (mild TBI)
Most severe - axons are torn, macroscopic haemorrhages (mod - severe)
Results in very small haemorrhages due to bleeding
Secondary effects
Instigated by TBI
Example:
ischemia (reduced blood supply to brain tissues)
hypoxia (lack of oxygen)
swelling (odema)
raised intra-cranial pressure (ICP)
Delayed effects
Ongoing atrophy (degeneration) of white matter
Hydrocephalus (occurs due to problems of reabsorption of CSF)
Meningitis and brain abscess (most common following depressed or base of skull fractures, surgery)
PT epilepsy (incidence of 5%)
How to measure the severity of TBI
2 parameters measured:
- level of coma / impaired consciousness using the Glasgow Coma Scale
- post-traumatic amnesia measured by the Westmead Post-Traumatic Amnesia scale
Describe the Glasgow Coma Scale
Measures the presence, duration and depth of impaired consciousness and coma.
3 aspects measured: verbal responses, motor responses, eye opening
GCS: eye opening
Spontaneous - 4
Speech - 3
Pain - 2
Pain, no eyes - 1
GCS Motor response
Commands -6
Pain (pulls examiners hand away) - 5
Pain (pulls own body part away) - 4
Pain (flexes innapropriately) - 3
Pain (body becomes rigid) -2
Pain (no motor response) -1
CGS Verbal response
Oriented (name, place, why, month, year) - 5
Seems confused and disoriented - 4
Talks but nonsensicle - 3
Makes sounds that cannot be understood -2
Makes no noise - 1
Total GCS score
ranges from 3 - 15
A GCS of 8 is a the critical score - 8 or less means there’s been a loss of consciousness
Can still have a TBI even if you score 15/15
Also used as a measure of the severity of TBI
13-15 = mild
9-12 = moderate
3- 8 = severe
Define post-traumatic amnesia
- acute but temporary period following TBI during which the patient is confused, disoriented
- the patient is unable to record events in memory in a continuous or connected way
- patient must be amnesiac for a period
- PTA represents the BEST measure of TBI severity and most accurate index of the likelihood of permanent cog and behavioural change - if divergence between GCS and PTA, use PTA
- best predictor of recovery
PTA duration classification
Up to 24 hours = mild
between 1 and 7 days = moderate
7 or more days = severe
When is the Westmead PTA scale used?
For cases of moderate - severe TBI
Test the patient each day to see if they can answer.
Testin begins when patient communicates intelligibly and is able to follow commands (i.e. GCS motor score = 6)
A person is judged to be out of PTA when they can achieve a perfect score over 3 consecutive days.
When PTA is very prolonged, we just require one single score, because they are likely to have ongoing problems.
How is the WPTAS administered
7 orientation questions
age, dob, month, time, day, year, place
5 memory question s
examiner’s name and face, 3 picture cards
When is the abbreviated Westmead PTA scale used?
If the person is suspected of having a mild TBI, the abbreviated Westmead PTA scale will be administered.
Aminitered hourly up for up to 4 hours - can be administered at any time within 24 hours of injury.
Patient is out of PTA on the first score of 18/18/
Involves motor, eye opening, verbal, and then 3 picture cards.
What is retrograde amnesia?
Failure to recall events prior to the TBI - and more remote memories are spared.
Usually RA is much shorter duration than PTA, and may shrink over time as the individual recovers.
Length of RA associated with TBI severity.
Neuropsychological screening in the acute phase
We may have to verify PTA status
Assess if they are able to be discharged if they are living alone/
Manage rehabilitation
Address issue of returning to productivity (education or work)
What is the selective reminding task?
Its a word list learning task - where you read the words to the patient and the patient tells you what they can remember.
After trial 1, you only remind them of the words they didn’t say, and they repeat the ones from trial 1 they remember plus the new ones.
Might uncover that stored memory is impaired - i.e. he repeats the words that she just said but not the ones from before.
Neuropsychological assessment in the chronic phase (>3 months to years after an injury)
Typically seeing the patient as an outpatient post injury.
Neuropsych measures (takes 3-4 hours in a f2f assessment) evaluate: intelligence, memory, executive function, motivation/effort)
- looking to see if there’s a disparity of IQ and memory that is atypical
Psych measures: PTSD checklist, depression/anxiety/stress scale, post concussion checklist
Following Mild TBI - GCS of 13-15, PTA <24 hrs
Neuropsych impairment: attention (inattentive, difficulty sustaining / focusing attention), learning and memory, speed of information processing
Neuropsych recovery
- occurs most quickly during the first few weeks
- return of baseline at 1-3 months
Moderate to severe TBI - GCS<12 or PTA>1
Memory for past is left intact because well established. Usually the ability to learn new information, retrieve info and retain it over time is impacted.
Have an inability to adapt, regulate and control responses in accord with novel and unusual task demands.
Attention and speed of information processing deficits - slowed thinking, particularly with complex tasks
Dose-response relationship
Neuropsychological recovery
rapid recovery in first 3-6 months, continued slower recovery over 1-2 years
overall neuropsych function at 6 months and >24 months is significantly below that of matched controls
decrease in learning and processing speed at 1 year predict long term disability
behavioural changes may be present
Neuropsychiatric Disorders
There is a high frequency of psychological disorder across severity of TBI
Preinjury history of mood or anxiety disorder is more frequent in patients who develop PostTBI depression, PTSD, etc
PTSD is a big one!
What is a brain tumour
- mass or growth of abnormal cells in the brain - benign = noncancerous
- malignant = cancerous
- primary = begin in the brain
- secondary = cancer begins in other parts of the body and spreads to the brain
Tumours can destroy brain cells directly or damage cells by producing inflammation and increasing pressure in the skull.
Prevalence of brain tumours
less than 1% chance of developing a brain tumour in life time
1900 malignant brain tumours are diagnosed in Australia
5 year survival rate is 22%
Causes of primary brain tumours
- family history
- genetic conditions (NF1)
- exposure to certain chemicals (vinyl chloride)
- high doses of radiation to the head (radiation therapy - used to treat cancers - contributes to the risk of having cancers in the future)
Diagnosis of brain tumours
- neurological exam = checking reflexes, muscle strength, balance, coordination, etc
- viewing the optic nerve (may bulge)
- neuroimaging (CT, MRI, PET)
- lumbar puncture (more invasive test - tapping the CSF)
- biopsy
How do we classify brain tumours?
- site of occurrence
- type of tissue involved
- whether it is benign or malignant
Graded on a scale from 1-4, measuring how fast the tumour is growing and how likely it is to spread.
More than 120 different types of brain tumour - the most common is gliomas and meningiomas.
Outline a glioma
- most prevalent adult BT, accounting for 30% of all brain tumours and 78% of malignant brain tumours
- more common in men
- they grow and often mix with normal brain tissue (actual cells in the brain)
- arise from supporting cells of the brain (glia)
3 types of glia:
Astrocytomas: most common
Ependymomas: neoplastic transformation of ependymal cells lining ventricular system
Glioblastoma multiforme - most invasive - grows rapidly, poor prognosis
Meningiomas
most prevalent types of non-cancerous brain tumour - 10-15% of all brain tumours
- more common in women
- most benign
- arises from the membranes surrounding the brain and spinal cord (meninges)
Medullobastomas
- grows quickly and develops at base of skull
- most common form of primary malignant brain tumour in children
Pituitary adenoma
- starts in PG, slow growing, usually benign
- 1 in 5 people will develop them at some point
Schwannoma
starts in schwann cells (which surround nerves in the brain and spinal cord)
- usually benign
- includes vesitbular schwannomas
Symptoms of brain tumours
- headaches
-seixures - weakness or paralysis
- loss of balance
- irritability / drowsiness
- nausea / vomitting
- disturbed senses
- increased confusion
Treatment of brain tumours
Surgery - most common form
- simple if tumour is isolated and separated from brain matter (i.e. meningiomas)
- can be complex if mixed in with normal brain matter (glioma)
- may remove just some parts of the tumour
Radiation therapy
- directing high energy beams at the BT
- can be internally or externally, specific or whole brain
Chemotherapy
- drugs delivered in pill form or IV
Targeted drug treatment
Rehab
Sequalae of BT
- cognitive impairment is usually present at the time of diagnosis –> they can be easily ignored if other symptoms are quite intense
- localized cognitive deficits associated with focal lesions
- cognitive impairment is more generalized than expected for focal lesions
- treatment can damage healthy brain tissue (radiation has more long term impacts, chemo is more short term)
- exhaustion, medication and depression exacerbate cognitive impairment
- impairments to attention, information processing speed, executive functions, memory
What is epilepsy?
- a disease of the brain characterised by the tendency to have spontaneous, recurrent seizures
- disorder characterised by an enduring predisposition to generate seizures - 2 or more recurrent unprovoked seizures occurring more than 24 hours apart.
- 4th most common brain disorder
- more likely to be diagnosed in childhood or senior years
What is the difference between seizures and epilepsy?
- seizures: definition - bust of electrical activity in the brain that temporarily affect how it works –> up to 5% of australians will experience a one-off provoked seizure
- epilepsy: a tendency for recurrent seizures unprovoked by systemic or neurologic insults
–> 250 000 aussies living with epilepsy
What are the causes of epilepsy?
- Genetics: 1/3 people with epilepsy have a family member with it
- head trauma, stroke, infectious disease of the brain, abnormalities
- half the people with epilepsy never know the cause of their epilepsy
Diagnosis of epilepsy
- EEG: most successful means of epilepsy diagnosis as it measures energy in the brain (can be helpful to diagnose epliepsy even when they aren’t having a seizure)
- brain imaging that looks at structure of the brain (MRI, CT, PET)- will help determing what may be causing the epilepsy
- neurological exam
- blood test (rules out infections)
- description/observation/recording of seizures
Classification of Seizures
3 primary groups based on: where they begin, consciousness, other features
3 seizure types =
- focal (partial/local) onset (originating from a particular part of the brain) –> aware/implied, motor/nonmotor
- generalized onset (start throughout the brain) –> motor/nonmotor
- unknown onset –> motor/nonmotor
Generalized tonic-clonic seizures
most universally recognised seizures
characterised by:
sudden loss of consciousness
tonic phase: stiffening
clonic phase: jerking
breathing becomes shallow
might bite tongue/ lose bladder control
postictal phase: confusion, agatation, fatigue, headache, muscle soreness
What are some other motor seizures>
tonic seizures = increased tone / stiffening
atonic seizures = patient loses all muscle tone
clonic seizures = convulsions
myoclonic seizures = twitching or jerking of a particular muscle group
Generalized absence seizures
usually start in childhood and can be mistaken for daydreaming and inattentiveness - misdiagnosed as ADHD
only lasts 2-20 seconds
characterised by: sudden start and end, may stare, lose facial expression, become unresponsive
can occur multiple times per day
immediate recovery
Focal onset seizures
These start from a particular part of the brain: can be ‘aware’ or ‘impaired awareness’
Focal aware seizures
Person retains consciousness
Usually brief
Symptoms: sensory changes (numbness, tingling, burning) movement (jerking, twitching) autonomic changes (blushing, palpitations) emotions (fear) cognition (deja vu, hallucinations)
Focal impaired awareness seizures
May or may not respond, or may respond appropriately
Can last 30 seconds - 3 minutes
- task arrest
- oral or hand automatisms
short period of confusion after
Temporal Lobe epilepsy
Most common form of focal epilepsy! 6/10 of people with focal epilepsy have this!
2 types =
- mesial temporal lobe epilepsy: medial or internal structures of the temporal lobe, accounts for almost 80% of temporal lobe seizures, associated with abnormality on MRI like hippocampal scloerosis
- neocrotical or lateral temporal lobe epilepsy involving the outer part of temporal lobe
What are the typical sequence of events for temporal lobe epilepsy?
Before seizure starts - experience an ‘aura’
- stomach discomfort, deja vu
Early signs = blank stare, behavioural arrest, automatisms, motor restlessness
Motor symptoms = tonic upper limb extension, hand and eye deviation
Late signs = autonomic changes, dystonic posturing, arrest o fall behaviours
Postictal = confusion, headache, aphasia
Status epilepticus
Continuous seizure activity lasting longer than 5 mins - or multiple seizures wihtout regaining full consciousness between them
increased risk of brain damage or even death
Management and treatment of epilepsy
medication –> up to 70% respond positively to first drug they try, after being seizure free for 3 years, 75% discontinue medication
surgery - only considered when seizures are medication resistant, or they originate from one small area of the brain –> up to 60-70% of people become seizure free after surgery
vagus nerve stimulation
-> device implanted under chest skin connecting to vagus nerve in neck, sending electrical bursts reducing seizures by 20-40%
Seizure don’ts
don’t: restrain the person, try to put anything in the person’s mouth to stop them from swallowing their tongue, don’t offer the person food or water until fully alert
