Brain Injury Treatment Flashcards
What is acquired brain injury?
Any non-congenital, non-degenerative injury to the brain, including TBI
Incidence of ABI is _____________ in the developed world due to _____________ but ______________ in the developing world.
▪️Decreasing
▪️Better road safety
▪️Increasing
What are the main risk factors for ABI?
▪️Male gender
▪️Age 15-24 and over 75
▪️Alcohol abuse
▪️Risk-taking behaviour
▪️Lower socioeconomic status
▪️Psychiatric history
What are the main types of closed TBI?
▪️Direct impact
▪️Coup/contrecoup
▪️Acceleration/deceleration
▪️Blast injury (e.g. shockwave)
What are the two parts of a coup/contrecoup injury?
- Primary impact - brain hits skull on side of impact, usually front of brain
- Secondary impact - brain hits posterior area of the skill as it goes back (occipital pole)
What pathogy is commonly seen in acceleration/deceleration injuries?
Diffuse axonal injury - the shearing forces cause axonal tear and retraction
Where is cerebral oedema most commonly seen following brain injury?
In regions of contusions, infarcts, and haematomas
What are the three sectilms of the Glasgow Coma Scale?
- Eye opening response
- Best verbal response
- Best motor response
When should the GCS be used?
In acute scenarios, best straight after injury
What does GCS score of 13-15 suggest?
Mild TBI
What does a GCS score of 9-12 indicate?
Moderate TBI
What does a GCS score of 3-8 indicate?
Severe TBI - patient is unresponsive or comatose
What are the three main classifications of TBI according to the Mayo system?
▪️Definite moderate-severe TBI
▪️Probable mild TBI
▪️Possible TBI
What is a concussion?
Immediate, transient alteration/loss of consciousness after force to the head
What symptoms may be present in the acute stage of a mild TBI?
▪️Confusion/Disorientation
▪️Altered mental state (e.g. panic)
▪️Headache
▪️Transient loss of function (e.g. freezing)
What intervention may be required during the acute stage of mild TBI?
▪️Possibly analgesia or anxiolytics
▪️May not need hospital admission
What may be present in the acute stage of severe TBI?
▪️Loss of consciousness
▪️Severe autonomic disturbance
▪️Compromised vital functions
▪️Coma and death
What intervention may be required in the acute stage of a severe TBI?
▪️Ventilation
▪️Life support
▪️Neurosurgery (e.g. evacuation of haematoma)
What might delayed post-traumatic amnesia indicate?
The development of a secondary complications such as an extradural haemorrhage
Who is at risk of longer confusion and disorientation following TBI?
▪️The elderly
▪️People with cerebrovascular disease
▪️Alcohol abuse
▪️Medication withdrawal
What is retrograde amnesia?
The time between moment of injury and the last clear memory before the injury
What memories are more vulnerable to retrograde amnesia?
Emotionally salient events such as the RTA
How does retrograde amnesia usually compare to PTA?
It’s usually much shorter - typically a few seconds to minutes
What might longer retrograde amnesia indicate?
▪️More severe injuries
▪️Psychogenic origin?
What is anterograde amnesia?
A deficit in forming new memories after injury.
What is usually the last function to return after consciousness is regained?
Anterograde amnesia
What are considered good indicators of head injury severity?
▪️Depth of unconsciousness (GCS)
▪️Duration of LoC
▪️Duration of PTA
▪️Delirium immediately after injury
▪️Neurological symptoms and signs
▪️Skull fracture
▪️Imaging abnormalities
▪️Blood in CSF
What are considered poor indicators of head injury severity?
▪️Duration of retrograde amnesia
▪️EEG abnormalities
▪️Facial injuries
What chronic cognitive sequelae may be present in severe head injury?
Minimally conscious state (used to be persistent vegetative state)
What chronic cognitive sequelae may be present in less severe head injury?
▪️Cognitive slowing
▪️Apathy
▪️Dysarthria
▪️Emotional lability
▪️Motor disability
▪️Incontinence
What are symptoms of post-concussional syndrome?
▪️Headache
▪️Dizziness
▪️Fatigue
▪️Noise intolerance
▪️Irritability
▪️Emotional lability
▪️Insomnia
▪️Impaired concentration/memory
What might chronic postconcussional syndrome indicate?
A psychological basis
How long does postconcussional syndrome last?
50% recover by 2 month, and 99% by 12 months
What factors may contribute to postconcussional syndrome?
▪️Premorbid personality
▪️Emotional factors
▪️Compensation/litigation
▪️Cognitive impairment
▪️Epilepsy
What are symptoms of orbitofrontal damage?
▪️Disinhibition
▪️Euphoria
▪️Emotional lability
▪️Poor judgement
▪️Environmental dependency
What are the symptoms of anterior cingulaye cortex damage?
▪️Impaired motivation
▪️Akinetic mutism
▪️Apathy
What are the symptoms of dorsolateral prefrontal cortex damage?
▪️Apathy
▪️Loss of initiative
▪️Slowing of thought and action
▪️Inattention
▪️Distract ability
▪️Poor planning and judgement
Cortical sensory loss, astereognosis, body schema disturbance, and anosognosia might indicate damage to which area?
Parietal lobe
What is Gerstmann syndrome and lesions in which area is it associated with?
▪️Dyscalculia
▪️Dysgraphia
▪️Finger agnosia
▪️R-L Disorientation
Indicative of dominant parietal lesion
Patients with lesions to which brain area may present with auditory deficits, sensory dysphasia, prosopagnosia, memory impairments and psychosis?
Temporal lobe
What is associated with post-TBI personality change?
▪️Moderate/severe injury
▪️Longer period of PTA
▪️Confabulations
▪️Behavioural disturbance
▪️Frontal and temporal damage
What premorbid factors may increase risk of post injury personality change?
▪️Cognitive status
▪️Psychiatric illness
▪️Personality disorder
▪️Premorbid personality
▪️Substance misuse
What post injury factors may increase risk of post injury personality change?
▪️Poor care/supprt
▪️Poor access to neurorehabiliation
▪️Complicating effects of legal proceedings
How does personality change post injury present over time?
It usually fluctuates, but tends to persist
What does cortical blindness indicate?
Bilateral occipital damage
What does homonymous hemianopsia indicate?
Unilateral occipital damage
What are the anatomical correlates of post injury personality change?
Mostly the frontal lobe, particularly the orbitofrontal cortex.
BUT not always - damage to connections to frontal lobe?
What are the main principles of pharmacological interventions for brain injury?
▪️Wait for spontaneous recovery
▪️One med at a time
▪️Start low and titrate slowly
▪️Avoid anything which may cause symptoms or confusion
▪️Stop it if it doesn’t work
▪️Avoid length prescriptions in the community
What medication shows good evidence for reducing early agitatoom following injury?
Propranolol (a beta blocker)
▪️Requires ECG monitoring!
What classes of medication show negative evidence for their use in early post-injury agitation?
▪️Benzodiazepines
▪️Opiates
▪️Psychostimulants
▪️Phenytoin
What are the best medications for the longer term management of agitation, aggression and impulsivity post injury?
▪️Anticonvulsants, particularly carbamazepine and valproate
▪️Propanolol
▪️Antipsychotics, particularly olanzapine
▪️Potentially antidepressants, such as sertraline and amitriptyline
When is olanzapine most useful and why should you be cautious?
In acute crisis
Some evidence that it impairs neuronal plasticity
What should you consider when choosing a medication for long term management of TBI sequelae, particularly agitation and aggression?
▪️Comorbidities, such as depression, mood disturbance, epilepsy, paranoia, or psychotic symptoms
▪️PTA - danger of increasing confusion
▪️Other medical problems and medications
▪️Tolerability
What are the main roles of psychology in the multidisciplinary treatment of TBI?
▪️Neuropsychological assessment
▪️CBT and other therapies
▪️Cognitive training
▪️Relaxation training and mindfulness
▪️Anger management
▪️Social skills training
What is the role of occupational therapy in brain injury treatment?
Helping the individual to maintain ‘real world’ skills such as:
▪️Self care
▪️Shopping
▪️Cooking
▪️Household tasks
▪️Planning and managing life demands
What symptoms can be helped by a speech and language therapist?
▪️Dysphasia
▪️Dysphagia
▪️Dysarthria
▪️Communication problems (e.g. conversational style)
What is akinetic mutism?
Intact consciousness and sensorimotor capacity but with a significant decrease in goal-directed behaviour and emotions.
Extreme apathy with slowed or nearly absent movement and speech.
Lesions in which area is associated with akinetic mutism?
Anterior cingulate cortex
Damage to which structures is associated with apathy following brain injury?
▪️Medial prefrontal cortex
▪️ACC
▪️Insula
▪️Subcortical structures, such as thalamus and basal ganglia
What roles do the insula and ACC supposedly play in apathy?
Form a system for registering internal and external events and selecting response
Insula = input
ACC = output
What pharmacological interventions show evidence for the management of post injury apathy?
▪️Dopamine agonists (particularly amantadine)
▪️Psychostimulants (particularly methylphenidate)
▪️Antidepressants (particularly if comorbid depression)
What class of medication may be particularly helpful for cognitive apathy?
Psychostimulants - may improve alertness and sustain attention
What are the main symptoms of cerebellar cognitive-affective syndrome?
▪️Emotional dysregulation
▪️Impaired use of language
▪️Executive dysfunction
▪️Visuospatial deficits
(similar clinically to prefrontal cortex lesions)
Damage to which brain region is associated with cerebellar cognitive-affective syndrome?
Posterior lobe of the cerebellum
Why is cerebellar damage thought to mimic frontal damage?
Reciprocal connections between the cerebellum and cortical regions
