TBI PDF - Traumatic Brain Injury and Rehab - PSY3010S

Traumatic brain injury (TBI) and rehab Course 🧠 PSY3010S Last Edited @September 16, 2024 8:07 PM Head injury (HI): ➥ This is not the same as a TBI any trauma to face, s...

Traumatic brain injury (TBI) and rehab Course 🧠 PSY3010S Last Edited @September 16, 2024 8:07 PM Head injury (HI): ➥ This is not the same as a TBI any trauma to face, scalp, skull or brain broad range of injuries but might not necessarily include damage to the brain TBI: alteration in brain function or other evidence of brain pathology caused by an external force i.e. disruption in the normal function of the brain that can be caused by a bump, blow or jolt to the head or penetrating head injury specifically refers to an injury to the brain and the force results in an alteration of brain functioning TBI Types: 1. Closed/non-penetrating brain injury : no penetration of skull, the head suffers concussive or forceful blow most common cause = motor vehicle accident (MVA) these are high velocity deceleration forces brain is shaken around within skull cavity Traumatic brain injury (TBI) and rehab 1  acceleration , deceleration and rotational forces coup injury: point of impact Damage to axons: contrecoup injury: opposite pole e.g. initial blow at back of head, brain accelerated into frontal and sphenoid plates where obtained large contusion results in: frontal lobes and temporal poles will rub against tentorial skull plates acceleration-deceleration forces = diffuse axonal injury by shearing subcortical white matter most vulnerable causes attention and processing speed deficits, memory deficits, emotional regulation deficits retrograde degeneration: axon torn and degenerates back to cell body anterograde degeneration: tear/rupture of cell body leads to axon degenerating = neuron dies so axon cannot be activated and causes ‘domino effect”: metabolic changes in postsynaptic neurons and possible cell death Traumatic brain injury (TBI) and rehab 2  2. Open/penetrating brain injury : a foreign object enters or penetrates skull (dura and brain tissue) focal injury: cerebral pathology is usually localised around the path of movement through brain the track: pathway projectile: moving object e.g. bullet higher risk of complications: infection haemorrhages (bleeding) oedema (swelling) seizures Measuring injury severity: mild = +- 80% moderate= +- 10% severe = +-10% dose-response relationship: the more severe the injury = the more severe the functional outcomes Severity determined by: Traumatic brain injury (TBI) and rehab 3  1. loss of consciousness (LOC) : period of time unconscious 2. posttraumatic amnesia (PTA): period of confusion and disorientation and alertness once gain consciousness, emerge from coma or following TBI i.e. no memory anterograde and retrograde 3. Glasgow coma scale: measures degree of impairment of consciousness limitations: incorrect assessment due to confounding variables: eye swelling, poor brainstem functioning, seizure at time of measurement, patient is sedated, endotracheal tube small lesion in brainstem can cause coma although most of brain not injured = not good indicator of overall brain damage 4. CT scan initially 5. MRI if further complications suspected Primary injuries: ➥ occur as result of the initial trauma and the biomechanical forces acting on the brain Skull fractures: Traumatic brain injury (TBI) and rehab 4  can result in: infection, CSF leaks, bleeding epidural and subdural hematomas ( rupture veins/sinuses) 75-90% Relation between skull fractures and neuropsychological functioning has been debated Types: 1. linear fracture: distinct, straight line = relatively benign 2. depressed skull fracture: impact has often driven fragments of skull into underlying dura and brain Secondary injuries: result of primary injuries ➥ occur because of the presence of the primary injury and as a result of changes at cellular or biomolecular level as well as physiological changes in brain often result of secondary complications Cerebral edema: Traumatic brain injury (TBI) and rehab 5  Trauma causes excessive fluid build up in tissue which can lead to swelling and increased ICP causes diffuse damage to brain in mod and severe TBI severe and uncontrollable ICP = main cause of death will see widened gyri and narrowed sulci Brain herniation: represents shift of brain through or across regions to another site generally complications of mass effect: from tumor, trauma, haemorrhage or infection associated with inc ICP which is usually related to presence of a hematoma (large pocket of blood) transtentorial herniation: downward displacement of the brain through tentorial hiatus tentorium cerebelli: invagination of dura that separates occipital and temporal lobes of cerebrum from cerebellum and brain stem c = transtentorial herniation puts pressure on lower brainstem structures Traumatic brain injury (TBI) and rehab 6  restricts blood flow (compress blood vessels) Haemorrhage: haemorrhage: active, ongoing process of bleeding hematoma: localised collection or pooling of blood outside of a blood vessel occurs when blood has leaked out of a vessel but has intracranial hematomas/haemorrhages become confined within the tissues often clotted and encapsulated during injury, cerebral blood vessels may tear = producing blood within and between meninges Hematoma types: Traumatic brain injury (TBI) and rehab 7  1. Subdural: beneath dura symptoms occur weeks after injury classic symptom: initial period of unconsciousness and then function normally : due to tightness of dura bleeding occurs so slowly bleed enlarges, pushes brain downwards = herniation consciousness deteriorates quickly 2. Extradural/epidural: between skull and dura less frequent Most common is damage of middle meningeal artery Frequently associated with skull fractures initial period of unconsciousness then period of alertness (a few hours) then loss of consciousness and brain function decline Leads to raised ICP 3. Intracerebral: within brain tissue itself Traumatic brain injury (TBI) and rehab 8  15% of fatal TBIs space-occupying clots = ICP will inc , herniation will occur most frequent: microscopic haemorrhages ( torn blood vessels) in subcortical white matter, corpus callosum, orbital surfaces of FLS and TLs technically: subdural and epidural hematomas are NOT intracerebral hematomas PTE: Post-traumatic epilepsy major complication after TBI Related to the presence of scar tissue – can occur even 2 yrs after trauma. Risk factors Penetrating type head injury Traumatic brain injury (TBI) and rehab 9  Severity of brain damage Prolonged periods of trauma Inflammation associated with the wound Residual neurologic symptoms Assessing brain injury: Challenges: Estimating preinjury/premorbid functioning levels Evaluating comorbid factors (history of alcohol or substance use; prior concussions; preexisting learning conditions; emotional risk factors like hysteria, somatization, secondary gain, pain syndrome, frequently co- occurring injuries, sleep) Exploring interactions among post-injury problems Impairment index – if falls 2 SDs below the mean (but leads to false negatives) Neuropsychological outcomes: Cognitive problems: attention, memory Mood alterations & psychiatric manifestations Personality changes (e.g., FL damage) Patient’s wellbeing and QoL: quality of life Symptoms may only appear later when go back to work/ home Most recovery within first 6 months, continues to 2 years (spontaneous recovery) Rehab most effective if started as early as possible Cognitive outcomes: Traumatic brain injury (TBI) and rehab 10  Dependent on the area damaged in the injury Some common functional impairments seen: Attention and concentration Memory Executive functions (e.g., working memory, disinhibition, planning; abstraction, problem solving) Processing speed Visuospatial difficulties Motor speed General intellectual functioning Behavioural and emotional consequences Factors affecting outcomes: Recovery from brain damage: Chronological process of recovery Plasticity is dependent on the extent of redundancy Redundancy – the extent to which remaining undamaged brain areas are able to take on functional adaptation Traumatic brain injury (TBI) and rehab 11  1. Acute phase: Acute neurophysiological response to brain insult ‘Damage control’ 2. Advantage stages: Adaptation phase – “healing stage” Diaschises Reorganisation plasticity and redundancy Functional adaptation plasticity and redundancy Recovery: Restitution: spontaneous recovery = brain’s innate ability to heal after an injury and occurs without external interventions brain attempts to restore normal function through several mechanisms: 1. Diachisis: distant but connected areas recovery function Traumatic brain injury (TBI) and rehab 12  brain areas that are connected to injured region temporarily and reversibly lose function areas are not damaged , just connected to damaged areas as recovery progresses areas will regain function and contribute to overall recovery = if injury caused by shock or other temporary mechanism = diachisis can “ unmask” functioning neuronal systems 2. Regeneration: new connections form between neurons growth of new neurons/connections via axonal and collateral sprouting: new axons from neurons that were damaged sprouting of new branches (collaterals) from undamaged axons to re- establish connections significant in PNS where greater capacity for regeneration - but limited in brain 3. Denervation supersensitivity: compensatory mechanism where neurons become more responsive to compensate for lost input neurons are more sensitive to other signals after losing their normal input increased sensitivity can help restore some function by making the remaining connections more effective = neurons damaged through shearing and tearing may reorganise through axonal resprouting, collateral sprouting or denervation supersensitivities to NTs Substitution: = brain’s ability to adapt through plasticity. After injury, brain can compensate for lost functions by using different pathways or regions = When neuronal damage is complete, depending on plasticity, the brain may sometimes be able to substitute other functioning neurons or neuronal systems or rely on some redundancy to take over 1. anatomical reorganisation: reassignment of functions within same hemisphere (intra) or between hemisphere (inter) Traumatic brain injury (TBI) and rehab 13  2. functional adaptation: brain develops new strategies or methods to perform tasks that were affected by injury e.g. relying on different senses enhancing the use of remaining abilities creating new ways to achieve similar outcomes e.g. visual cues to compensate for impaired motor function. Plasticity: = brain’s ability to adapt and change in structure/function as a result of experience persists throughout life changes neural connectivity : it occurs by changing the pattern of synaptic connectivity between neurons greatest in childhood : brain is immature and less susceptible to impact of cerebral damage = greater capacity for transference of functions from damaged cerebral tissue to health tissue Early vulnerability: although children have higher plasticity brain insults occurring during childhood = detrimental to development and long-term cog deficits due to vulnerability of immature brain Crowding effect: functions in two hemispheres are crowded into one with general depression of all abilities competition occurs where one will be more pronounced/”better” than the over but overall they are both low Growing into deficit: cog deficits not immediately apparent post-injury and show up later greater deficits may emerge later in childhood when these functions are expected to mature (and havent) Traumatic brain injury (TBI) and rehab 14  Adult vs child: adult models cant be applied to children brains similar in structure but have differences due to different stages of cognitive development of children children are in process of development, especially in terms of brain maturation and cog development if you disrupt this process then there will be disruption/interference neuropsychologically, cognitively, developmentally and socially Adult Child Impact apparent soon after Effects of injury may only be evident later on in injury development (‘growing into deficit’) Brain is anatomically, physiologically, & Brain is still developing functionally mature Previously acquired Injuries disrupt the acquisition of developmental abilities abilities break down Cognitive and behavioural functions can vary dramatically Greater stability and (depending on current developmental stage & on the predictability of behaviour nature & quality of the child’s biopsychosocial environment) Rehabilitation: What it is: multidisciplinary team to try restore pre-morbid functioning as best as possible cognition managing behavioural outcomes emotional = clincial Approaches: Traumatic brain injury (TBI) and rehab 15  1. restorative: restoring a function and retrain impaired, existing pathways to redevelop the pathway that was lost = restitution there has to still be a little bit of functioning remaining if an area is completely gone/ necrotised = will not work Tasks: “drills” repetitive overtime get harder and more complex controversial approach: only really good at the task and cant really see if task extends outside of training ecological validity not confirmed 2. Compensatory: supplementation rather than fixing the problem that is there The aim is to enhance the patient’s ability to function in daily life despite the ongoing cognitive challenges resulting from the brain injury context -driven = must be in their own environments Externally focused strategies: Modifying the environment Undertaken by parents, teachers or caregivers e.g. once intervention is complete and psych can no longer be there decreasing distractions / organising workspace Involves training injured individual External cues e.g. checklists or devices that remind or cue individual Alter expectations for functioning of patient and family Alter demand or need for certain skills or abilities E.g. recognition rather than recall tests Specialised teaching strategies Traumatic brain injury (TBI) and rehab 16  Facilitate learning, memory or behavioural change 3. Eclectic model : combination Case study: 1. Moderate: loss of conc between 30-24 hours and GCS was 9 2. Closed injury: damage to brain tissue but no damage to skull and meninges Traumatic brain injury (TBI) and rehab 17  3. areas Region Mechanism functional fallout PFC/FL coup ( direct impact) executive function posterior parietal- cortical sensory loss - visual contrecoup occipital disturbances grating against tentorial temporal lobe memory plate acceleration-deceleration diffuse axonal injury attention processing speed forces 4. disinhibition ( stroop test - trial 3 * google other trials) , planning (rey), abstraction ( word association, similarities) 5. swelling, oedema , herniation , intracerebral haemorrhage - sub and epidural is usually if skull penetration or person is old and vasculature is compromised, post-traumatic epilepsy 6. time since injury, injury severity, familial support, access to resources 7. “functional adaptation” : compensation for loss of functions 8. spontaneous recovery can occur in any brain injury (6mo-2 years), she's in acute stage 9. checklist, memory aids , someone is there to facilitate and monitor 10. strategy’s applicable beyond intervention itself and to context person exists in Traumatic brain injury (TBI) and rehab 18