L5 Psych Med Long term consequences of brain injury

Overview

Traumatic brain injury is common, and its consequences unfold in phases: an acute confusional stage dominated by post-traumatic amnesia, a short-term period of biological brain recovery over 3 to 6 months, and a long-term phase in which cognitive, psychological and social effects determine outcome. The lecture covers how TBI severity is classified and why classification predicts outcome imperfectly, the pathology that underlies the clinical picture (focal versus diffuse injury, coup-contrecoup, diffuse axonal injury, secondary injury cascades), what happens neuropsychologically and psychologically at each stage of recovery, and concussion/mild TBI as a separate problem in which persisting symptoms are best understood biopsychosocially. Two cases run through it: Alex, a very severe TBI, and Caroline, a concussion with persisting symptoms.

Why TBI matters, and New Zealand epidemiology

• Prevalence means you are guaranteed to encounter patients with TBI throughout your career. Understanding the impact on patient and family helps with communication, behaviour and treatment adherence, and targeted care may reduce overall costs to the health system.
• Approximately 40,000 TBIs occur in New Zealand each year, roughly 100 new TBIs every day.
• About 93% are mild; moderate to severe injuries account for about 7%. Moderate-severe injury is most common in males aged 15 to 34, and is also high in women over 65.
• Crude incidence is 852 TBIs per 100,000 person-years in New Zealand.
• Many TBIs never present to hospital and are managed in the community, so hospital statistics substantially underestimate true incidence.
• Incidence by mechanism and age (Feigin et al., 2013): falls peak highest in the 0 to 4 age group (around 1000 per 100,000 person-years) and rise again in those 65 and over (around 500); transport accidents and assault both peak at ages 15 to 34 (around 250 and 280 respectively) and decline with age; exposure to mechanical force is roughly flat around 200; other or unknown causes stay low throughout.
• BIONIC (2010-2011) versus BIONIC2 (2021-2022) comparison (Jones et al., 2026), age-standardised incidence per 100,000 person-years: by severity, total 811 then 826, with mild 771 then 767 and moderate-to-severe 40 then 59; by case site detection, hospital 430 then 614, family doctor 51 then 13, other 185 then 227; by area, urban 794 then 933, rural 884 then 593. The ethnicity panel shows a higher overall total in 2021-2022 (Other 1120, European 777, Māori 604) than in 2010-2011 (Other 248 within a total around 1200).

Warning

The exact numeric labels on the stacked and area segments of the BIONIC/BIONIC2 figure are small and some values were inferred from adjacent printed labels; treat them as approximate.

Definitions: acquired brain injury

Acquired brain injury divides into three categories:

• Concussion, also called mild traumatic brain injury.
• Traumatic brain injury, which splits into:
  • Closed brain injury (internal pressure and shearing): assault/abuse, falls, motor vehicle accidents, struck by or against an object, blast exposure.
  • Open brain injury (penetrating): assault/abuse, falls, motor vehicle accidents, struck by or against an object, surgery, gunshot.
• Non-traumatic brain injury: anoxia/hypoxia (near drowning, strangulation), infections, strokes, tumours, metabolic disorders, chemical exposure.

Classification of TBI severity

The classification system uses duration of unconsciousness, Glasgow Coma Scale and post-traumatic amnesia (PTA):

Classification	Duration of unconsciousness	GCS	Post-traumatic amnesia
Mild	<30 minutes	13-15	<24 hours
Moderate	30 minutes to 24 hours	9-12	1-7 days
Severe	>24 hours	3-8	>7 days

• Concussion is a knock to the head, often used interchangeably with mild TBI.
• Very severe is defined by PTA greater than 4 weeks.
• The system works well at predicting severity for moderate to very severe TBI, but depends on when you see the patient: in ED you are unlikely to have PTA information and usually rely on GCS.
• It is less helpful for concussion/mild TBI, where other factors are often at play.
• CBI-M framework (Manley et al., 2025): in 2022 the US National Institute of Neurological Disorders and Stroke launched an international effort towards a better classification, with four components, Clinical, Biomarker, Imaging, Modifiers. It remains a research framework requiring large-scale validation and is not currently widely used.

Clinical and pathological correlates

Key concepts: diffuse versus focal injuries, coup versus contrecoup, acceleration/deceleration, diffuse axonal injury, “talk and die” syndrome, and brain bleeds.

• Coup-contrecoup: the initial (coup) injury occurs where the brain collides against the skull at the point of impact, with rotary force; the contrecoup injury occurs as the brain collides against the opposite side of the skull. Both produce microscopic damage to brain cells.
• Diffuse axonal injury: impact force to the head damages axons through three force types acting on the axon: tensional forces (stretching), rotational forces (twisting), and shearing forces (axon segments sliding sideways).
• Secondary injury cascade (Bigler, 2016): a primary injury leads over hours to days to molecular secondary injury factors, including glutamate release causing Na+/K+ efflux and influx and Ca2+ entry, generating reactive oxygen and nitrogen species and axonal injury, together with mitochondrial dysfunction, coagulopathy and apoptosis, with associated markers of reduced regional cerebral blood flow, raised ICP, reduced cerebral perfusion pressure and altered glucose. These lead to clinical secondary injury factors: hypoxaemia, hypotension, seizures and fever. Over months these contribute to final injury: progressive brain damage, epilepsy and hypopituitarism, though the pathway from clinical secondary factors to final injury is marked with a question mark, indicating uncertainty.
• Different pathological features map onto different imaging modalities: MRS for dendrites; T1/T2/FLAIR for white matter (astrocyte, axon, oligodendrocyte); T1-based volumetrics for cell death, atrophy and encephalomalacia; GRE/SWI for haemorrhage; fMRI/BOLD/ASL for functional activity at axon terminals.

Why severity markers predict outcome imperfectly

• LOC and GCS are important features of TBI but provide limited information about underlying neuropathology or how the injury relates to outcome.
• PTA is often a good marker of severity.
• Identical LOC, GCS and even PTA scores may correspond to similar or widely different neuropathological findings on imaging. For example, one mild TBI scan showed old contusion with frontal encephalomalacia at GCS 14, another mild case had GCS 15 with no LOC, while two severe cases both had GCS 3 with LOC yet different underlying neuropathology.
• Essentially, two people with the same injury, in the same place, can have vastly different long-term outcomes.

Acute phase

• Post-traumatic amnesia: an acute confusional state in which the brain is unable to form new memories. The INCOG guidelines (INCOG 2.0, Ponsford et al.) offer up to date information on PTA management.
• Whole brain effects.
• Neurogenic fatigue.
• Shock, denial and insight issues.
• Focus at this stage is regaining function of basic activities of daily living.

Short-term phase

• Brain recovery (3 to 6 months): brain cells previously connected to cells that died need to make new functional connections; neurons strengthen or form new synaptic connections. Management balances rest against targeted rehabilitation.
• Early recovery focuses on regaining physical functioning and performing activities of daily living.
• Cognitive effects take time to understand. Hospitals are highly structured environments, so the extent of cognitive effects is difficult to observe. Patients are consequently often labelled as “lacking insight” when they simply may not yet have had an experience of failure. Denial can occur, though it is often psychologically protective.
• Neurogenic fatigue: daily tasks are highly effortful.
• Psychological impact: how did this happen, what will my life be like.

Long-term phase

• The trajectory of recovery is highly variable from mild to very severe TBI; two people with the same injury can have different outcomes. Improvement and decline can both be observed even after many years.
• US TBI Model Systems Study (Corrigan et al., 2014), longitudinal data on nearly 15,000 participants over 25 years:
  • Older age at injury predicts poorer outcomes and a faster rate of decline on functional outcomes.
  • Among those who received acute inpatient rehabilitation, by 5 years after injury approximately 1 in 5 had died, 12% of survivors were living in institutional settings, and more than a third had deteriorated from a previously achieved level, across all ages.
• TBI is often an “invisible” injury once physical injuries resolve, so physical and cognitive effects must be accommodated.
• Neuropsychological effects: slowed thinking; attention/concentration; memory; executive dysfunction (planning, problem solving, multitasking); social skills.
• These impact day to day functioning: planning the day ahead, remembering medications, generating plans and completing tasks, interpreting tone, sarcasm and social cues.
• Psychological effects: depression, anxiety and PTSD are common; changes to life roles such as employment and independence; changes to family and friend relationships.

Important

Despite long-term disability, changes in outcome are more strongly associated with psychological factors such as depression, anxiety, stress and self-esteem than with initial injury severity or cognitive impairment (Thornhill et al., 2000; Whitnall et al., 2006; McMillan et al., 2012).

Recommendations for doctors

• Consider the human element of the individual’s experience: balance optimism and hope against realism when delivering news, and validate distress at each part of the journey, managing expectations while tolerating uncertainty.
• Cognitive difficulties make it hard for patients to follow instructions or remember information: write down even one key point, provide handouts where possible, and consider how this might affect treatment adherence.

Concussion / mild TBI

• Approximately 93% of TBIs are mild. Mild TBI and concussion are used interchangeably in the literature, which makes it confusing.
• Concussion is commonly associated with sport, but is most frequently caused by falls and motor vehicle accidents. Repeated concussion also occurs in people experiencing domestic violence and assault, in youth, and in incarcerated individuals.
• Symptoms usually resolve within a few weeks and approximately 80% are resolved within 3 months. Presentation can be delayed, and some develop persisting symptoms.

Symptoms and signs (bpacnz, 2022)

Common symptoms:

• Physical: headache; neck pain or tenderness (mild to moderate); nausea or vomiting; tinnitus; taste or smell impairment; dizziness or vertigo; photosensitivity or sensitivity to noise; transient diplopia; balance or motor incoordination.
• Cognitive: confusion or disorientation; brief loss of consciousness (<2 minutes); difficulty concentrating; difficulty remembering things; feeling “slowed down” or “in a fog”; witness reports that the person was slow to get up after the injury.
• Behavioural/emotional: irritability and other transient personality changes such as disinhibition; emotional lability; psychological adjustment problems or depressive/anxious symptoms; difficulty attending work or school; fatigue, drowsiness and sleep disturbance (insomnia or sleeping more than usual).

Red flags for emergency referral:

• Physical: worsening of initial symptoms; severe or increasing headache; severe neck pain; repeated vomiting (as a general guide, more than one vomit in an adult or any vomiting in a child); seizures or convulsion; ongoing diplopia or other significant visual disturbance; weakness, tingling or burning in the arms or legs; ongoing or severe dizziness or vertigo.
• Cognitive: prolonged loss of consciousness (2 minutes or more) or deteriorating conscious state; inability to recognise people or places; dysarthria; prolonged post-traumatic amnesia (>12 hours).
• Behavioural/emotional: increasing restlessness, agitation, confusion or combative behaviour; significantly unusual or inappropriate behaviour or personality change.

ACRM diagnostic criteria for mild TBI (Silverberg, Iverson et al.)

Five criteria combine to a diagnosis: criterion 1, plausible mechanism of injury; criterion 2, clinical signs (1 or more); criterion 3, acute symptoms (2 or more); criterion 4, clinical examination and laboratory findings (1 or more); criterion 5, neuroimaging abnormality (if completed). A case that does not meet other criteria sufficient for diagnosing TBI, but has 2 or more acute clinical signs or 2 or more clinical or laboratory findings, is routed to “unclear” or, if not better accounted for by confounding factors, to “suspected” and then mild TBI.
The “mild” qualifier is not used if any of these severity indicators are present:

• Loss of consciousness longer than 30 minutes.
• A GCS score below 13 after 30 minutes.
• Post-traumatic amnesia greater than 24 hours.

Concussion pathology

• Neurometabolic cascade of concussion: 1. neurons stretch and shear at the initial trauma; 2. electrolytes (K+, Na+, Ca2+) move across gradients, with potassium leaking out and calcium rushing in; 3. neurons fire indiscriminately via calcium entry and indiscriminate glutamate release; 4. an energy deficit results from the work of restoring the electrolyte gradient.
• Axon shear occurs particularly at the grey matter / white matter boundary.
• Neuroinflammation is part of the pathological picture.
• Usually there are no findings on CT or MRI because there are no macroscopic changes. Even among those sent for CT, only 5 to 9% will have an abnormality and only 0.5% have an actionable lesion.
• Diffusion weighted imaging can detect changes in white matter pathways in mild TBI, correlating with ongoing symptoms.
• Blood biomarkers (emerging evidence, Kobeissy et al., 2024): neuronal ubiquitin C-terminal hydrolase-L1 (UCH-L1), a neuron injury marker, and glial fibrillary acidic protein (GFAP), an astrocyte injury marker. Both are usually present in small amounts in healthy individuals and are elevated after brain injury; they show promise as a blood test to indicate the need for CT brain.

Persisting symptoms after concussion

• Nearly half of adults report persistent symptoms 12 months after a concussion (Theadom et al., 2016).
• Risk factors: female sex (possibly neck strength); cervical spine pathology; vestibular symptoms; oculomotor symptoms; psychological symptoms, both pre- and post-injury.
• Best conceptualised within a biopsychosocial model of predisposing, precipitating and perpetuating factors (Rickards et al., 2022; Faulkner & Snell, 2023).

Predisposing factors (pre-injury vulnerabilities): individual/demographic (older age, female sex); mental health history (depression, anxiety, PTSD, somatization); medical history (prior concussion/mTBI, migraine, ADHD, chronic pain); psychosocial (low resilience, poor coping, low social support).
Precipitating factors (injury-related): injury severity (high acute symptom burden, LOC, amnesia, severe headache, dizziness, nausea); acute symptoms (early symptom severity, vestibular or cognitive issues); psychological response (acute stress reaction, fear or catastrophic beliefs).
Perpetuating factors (maintenance of symptoms): psychological (anxiety, depression, PTSD, catastrophizing, hypervigilance, fear of activity); behavioural (avoidance, reduced activity, poor sleep, fatigue, maladaptive coping); social/environmental (work stress, litigation, lack of support, compensation issues); physiological (cervical injury, vestibular dysfunction, oculomotor problems, autonomic dysregulation).
All three groups feed into persistent post-concussion symptoms: headache, dizziness, cognitive issues, mood changes, fatigue and sleep problems. Key points: the model is multifactorial, with biological, psychological and social factors interacting; early identification allows early intervention (education, rehabilitation, CBT, exercise); address both risk and maintenance factors.

Case 1: Alex (very severe TBI)

Presentation: 20-year-old man. After a party, five friends piled into a car travelling 100 km/h; the driver lost control and crashed. The driver died at the scene and two passengers were critically injured. Alex was unconscious with no pulse detected by ambulance on arrival, and GCS was 3/15 at the scene. Brain scans showed multifocal haemorrhagic contusions, bilateral frontal and left temporal. PTA duration was 58 days.

• Classification: Alex’s presentation meets criteria for a very severe TBI (GCS 3 in the severe 3-8 band, PTA far beyond 4 weeks).
• Pathology: multifocal haemorrhagic contusions suggest both focal and diffuse injury, likely to impact a whole host of cognitive, behavioural and psychological factors.
• Acute phase: Alex was in a period of PTA and unable to make new memories, describing the experience as “islands of memories”. His family worried about discussing the death of his friend. Focus was on regaining basic activities of daily living.
• Short-term phase: no longer in PTA and mobilising on the ward; had noticed some memory difficulties but was not entirely aware of them; keen to leave hospital and “get back to things”; his parents asked when he might return to work.
• Neuropsychological assessment before discharge from rehabilitation: no longer in PTA, but had difficulty remembering what people had said to him; he was not aware of this and it did not worry him in hospital as his long-term memory was okay; his thinking was slowed; he had executive functioning difficulties with generating ideas, impulse control, recognising emotions in others, and multitasking.
• Psychological: in good spirits because he was going home; understood his friend had died and was processing this okay; eager to return home and get on with things.
• Management: discharge home with parents; ACC therapy to access the Training for Independence Programme, identifying long-term goals such as living independently and returning to work, use of cognitive strategies, and speech and language therapy to support social cognition. Under NZTA guidelines there is no driving for a minimum of 6 months, with visual assessment required before returning to driving, and occupational therapy on-road driving assessment advised given his cognitive complaints.

Case 2: Caroline (concussion with persisting symptoms)

Presentation: 34-year-old woman who sustained a fall with headstrike and no LOC. She did not think much of the injury at the time and carried on with her day, then developed headaches, irritability, eye strain and fatigue the following day. Her GP gave a medical certificate for a week and advised rest; she returned the next week with ongoing symptoms. A graded return to work over the next 2 months had limited success. She has a history of migraines and anxiety, and was referred to ACC concussion services.
Course: occupational therapy gave advice on pacing and management strategies. She avoided certain tasks such as reading because they were effortful, and described feeling overwhelmed and overstimulated. Her partner had lost work, creating additional financial pressure. At 6 months post injury she had ongoing symptoms and was becoming frustrated by the recovery process.
Formulation using the biopsychosocial model:

• Predisposing: anxiety history, migraine history, female sex.
• Precipitating: headstrike from a fall, headache, dizziness.
• Perpetuating: catastrophic cognitions, symptom avoidance and poor pacing, maladaptive coping, possible oculomotor symptoms.

Warning

The transcript flags that the Predisposing/Precipitating/Perpetuating dot-scale bars beneath Caroline’s formulation diagram are not legible or numerically labelled, so their scale interpretation is unclear.

Management options:

• Consider referral for neuro-optometry.
• Psychological support to address fear avoidance behaviours and frustration; these behaviours might be keeping her stuck in boom/bust cycles, and frustration at the recovery process calls for psychological coping strategies or acceptance. Graded return, slow and steady.
• Address social factors such as financial strain; a social work referral may support the family.

Self-test

1. State the duration of unconsciousness, GCS range and PTA duration that define mild, moderate and severe TBI, and the criterion for very severe.
2. What is the annual number of TBIs in New Zealand, what proportion are mild, and why do hospital statistics underestimate the true incidence?
3. List the three categories of acquired brain injury given in the lecture, with the distinguishing feature or example causes of each.
4. Describe the three force types that produce diffuse axonal injury.
5. Explain what coup and contrecoup injuries are.
6. Describe the sequence of secondary injury after TBI, from primary injury through to final injury, with the timescales given.
7. Two patients both present with GCS 3 and documented LOC. Predict what this tells you about their underlying neuropathology and their long-term outcomes, and explain why.
8. Define post-traumatic amnesia and state what the clinical focus is during the acute phase.
9. Explain why cognitive effects are often missed in hospital, and why the label “lacking insight” may be misleading.
10. State the 5-year outcomes reported by the TBI Model Systems Study for patients who received acute inpatient rehabilitation, and what older age at injury predicts.
11. List the neuropsychological effects seen in the long-term phase and give one everyday functional consequence of each domain.
12. Which factor group is more strongly associated with change in outcome after TBI: initial injury severity and cognitive impairment, or psychological factors? Give the psychological factors named.
13. List three practical steps a doctor should take when giving information to a patient with cognitive difficulties after TBI, and explain why.
14. Describe the four steps of the neurometabolic cascade of concussion.
15. What proportion of patients with concussion who are sent for CT have an abnormality, and what proportion have an actionable lesion? What imaging modality can detect white matter change in mild TBI?
16. Name the two blood biomarkers under investigation for mild TBI and the cell type each indicates injury to.
17. List the three severity indicators that mean the “mild” qualifier cannot be used under the ACRM criteria.
18. Distinguish predisposing, precipitating and perpetuating factors for persistent post-concussion symptoms, giving two examples of each.
19. List four red flags in a concussed patient that should prompt emergency referral.
20. What proportion of adults report persistent symptoms 12 months after concussion, and what are the risk factors for persisting symptoms?
21. A 34-year-old woman with a history of migraine and anxiety has ongoing headache, fatigue and overstimulation 6 months after a headstrike with no LOC, avoids reading because it is effortful, and faces financial pressure at home. Explain how you would formulate and manage this, using the model from the lecture.
22. Integrative: Alex sustained a very severe TBI with GCS 3 and 58 days of PTA, while Caroline sustained a concussion with no LOC. Explain why injury severity alone does not predict which of them will have the better long-term outcome, drawing on the classification limitations, the pathology and the psychological evidence.

Answers

Reveal answers

1. Mild: LOC <30 minutes, GCS 13-15, PTA <24 hours. Moderate: LOC 30 minutes to 24 hours, GCS 9-12, PTA 1-7 days. Severe: LOC >24 hours, GCS 3-8, PTA >7 days. Very severe: PTA greater than 4 weeks.
2. Approximately 40,000 per year, roughly 100 per day; about 93% are mild. Many TBIs do not present to hospital and are managed in the community, so hospital statistics substantially underestimate true incidence (crude incidence 852 per 100,000 person-years).
3. Concussion (also called mild TBI); traumatic brain injury, subdivided into closed injury (internal pressure and shearing; assault/abuse, falls, MVAs, struck by or against an object, blast exposure) and open/penetrating injury (the same causes plus surgery and gunshot); and non-traumatic brain injury (anoxia/hypoxia such as near drowning or strangulation, infections, strokes, tumours, metabolic disorders, chemical exposure).
4. Tensional forces (stretching of the axon), rotational forces (twisting) and shearing forces (axon segments sliding sideways), each producing damage at the affected site of the axon.
5. The coup injury is the initial injury where the brain collides against the skull at the point of impact, with rotary force; the contrecoup injury occurs when the brain collides against the opposite side of the skull. Both produce microscopic brain cell damage.
6. Primary injury leads over hours to days to molecular secondary injury factors: glutamate release with Na+/K+ efflux and influx and Ca2+ entry, generating reactive oxygen and nitrogen species and axonal injury, plus mitochondrial dysfunction, coagulopathy and apoptosis, with reduced rCBF, raised ICP, reduced CPP and altered glucose. These produce clinical secondary injury factors: hypoxaemia, hypotension, seizures and fever. Over months these contribute to final injury: progressive brain damage, epilepsy and hypopituitarism. The slide marks the link from clinical secondary factors to final injury with a question mark, indicating uncertainty.
7. Very little about the neuropathology, and it does not predict their outcomes. LOC and GCS give limited information about underlying neuropathology or how injury relates to outcome; patients with identical GCS and LOC can have quite different findings on imaging, and two people with the same injury in the same place can have vastly different long-term outcomes.
8. PTA is an acute confusional state in which the brain is unable to form new memories. The acute focus is on regaining function in basic activities of daily living; INCOG guidelines cover PTA management.
9. Hospitals are highly structured environments, so the extent of cognitive effects is difficult to observe. Patients are then labelled as lacking insight when they simply may not yet have had an experience of failure; where genuine denial exists it is often psychologically protective.
10. Following nearly 15,000 participants over 25 years, by 5 years after injury approximately 1 in 5 had died, 12% of survivors were living in institutional settings, and more than a third had deteriorated from a previously achieved level, across all ages. Older age at injury predicts poorer outcomes and a faster rate of decline on functional outcomes.
11. Slowed thinking; attention/concentration; memory (for example forgetting medications); executive dysfunction such as planning, problem solving and multitasking (planning the day ahead, generating plans and completing tasks); social skills (interpreting tone, sarcasm and social cues).
12. Psychological factors. Despite long-term disability, changes in outcome are more strongly associated with depression, anxiety, stress and self-esteem than with initial injury severity or cognitive impairment.
13. Write down even one key point; provide handouts where possible; consider the impact on treatment adherence. Cognitive difficulties make it hard for patients to follow instructions or remember information.
14. 1. Neurons stretch and shear at the initial trauma. 2. Electrolytes (K+, Na+, Ca2+) move across their gradients, with potassium leaking out and calcium rushing in. 3. Neurons fire indiscriminately, with indiscriminate glutamate release. 4. An energy deficit results from restoring the electrolyte gradient.
15. Between 5 and 9% of those sent for CT will have an abnormality, and only 0.5% have an actionable lesion. Diffusion weighted imaging can detect white matter pathway changes in mild TBI, correlating with ongoing symptoms.
16. Neuronal ubiquitin C-terminal hydrolase-L1 (UCH-L1), a neuron injury marker, and glial fibrillary acidic protein (GFAP), an astrocyte injury marker. Both are present in small amounts in healthy people and elevated after brain injury, and show promise for indicating the need for a CT brain.
17. Loss of consciousness longer than 30 minutes; a GCS score below 13 after 30 minutes; post-traumatic amnesia greater than 24 hours.
18. Predisposing are pre-injury vulnerabilities (for example older age or female sex; depression or anxiety history; prior concussion or migraine; low resilience or low social support). Precipitating are injury-related (for example high acute symptom burden, LOC or amnesia; early vestibular or cognitive symptoms; acute stress reaction or catastrophic beliefs). Perpetuating maintain symptoms (for example catastrophizing or fear of activity; avoidance, reduced activity or poor sleep; litigation or compensation issues; cervical, vestibular, oculomotor or autonomic dysfunction).
19. Any four of: worsening or severe/increasing headache; severe neck pain; repeated vomiting (more than one vomit in an adult, any vomiting in a child); seizures or convulsion; ongoing diplopia or significant visual disturbance; limb weakness, tingling or burning; ongoing or severe dizziness/vertigo; prolonged LOC of 2 minutes or more or deteriorating conscious state; inability to recognise people or places; dysarthria; PTA >12 hours; increasing restlessness, agitation, confusion or combative behaviour; significantly unusual or inappropriate behaviour or personality change.
20. Nearly half of adults report persistent symptoms at 12 months. Risk factors are female sex (possibly related to neck strength), cervical spine pathology, vestibular symptoms, oculomotor symptoms, and psychological symptoms both pre- and post-injury.
21. Formulate biopsychosocially. Predisposing: anxiety and migraine history, female sex. Precipitating: headstrike from a fall, headache and dizziness. Perpetuating: catastrophic cognitions, symptom avoidance and poor pacing, maladaptive coping, possible oculomotor symptoms. Management: consider neuro-optometry referral; psychological support for fear avoidance and frustration, since these behaviours may keep her stuck in boom/bust cycles, developing coping strategies or acceptance; a slow and steady graded return; and address social factors such as financial strain, with social work referral to support the family.
22. The severity classification predicts outcome only broadly and works best for moderate to very severe injury; identical LOC, GCS and even PTA can accompany widely different neuropathology, and two people with the same injury in the same place can have vastly different long-term outcomes. Alex’s multifocal haemorrhagic contusions indicate both focal and diffuse injury, but recovery trajectory is highly variable and both improvement and decline occur over years. Caroline’s mild injury carries a substantial risk of persisting symptoms, since nearly half of adults report persistent symptoms at 12 months and her predisposing, precipitating and perpetuating factors are all loaded. Crucially, change in outcome is more strongly associated with psychological factors (depression, anxiety, stress, self-esteem) than with initial injury severity or cognitive impairment, so Alex’s good psychological adjustment and rehabilitation access and Caroline’s anxiety, catastrophizing, avoidance and financial strain matter more than the initial severity labels.