The following lecture has been approved for University

The following lecture has been approved for University Undergraduate Students This lecture may contain information, ideas, concepts and discursive anecdotes that may be thought provoking and challenging It is not intended for the content or delivery to cause offence Any issues raised in the lecture may require the viewer to engage in further thought, insight, reflection or critical evaluation

Introduction to Brain Injury Dr. Craig Jackson Senior Lecturer in Health Psychology School of Health and Policy Studies Faculty of Health BCU

What was Michael Angelo’s Hidden Message? Michelangelo. The Creation of Adam (detail, Sistine Chapel). 1510. Fresco, Sistine Chapel, Vatican, Rome.

Objectives List major structures and function of nervous system Name types of head and spine injuries; describe clinical features Describe mechanisms of neurological injury Describe assessment of head injuries Describe functional affects and symptoms Describe imaging techniques

Neurological Injuries Responsible for 50+% of trauma deaths Approx. 1, 000 patients in UK attend A&E with head injury per year Can be prevented (some extent) by helmets and PPE Major cause of chronic disability Mostly from Falls, RTAs and Assaults Flannery & Buxton, 2001

Anatomy Principles Neuron specialized nerve cell Dendrites and Axons short and long processes of neurons Peripheral neurons sheathed with myelin Impulses transmitted from synapses to dendrites

Anatomy Principles 2 Central Nervous System = brain, spinal cord Peripheral Nervous System = nerves, branches Meninges = protective triple layer cover Dura matter Arachnoid Pia matter = = = outer layer middle layer inner layer Cerebral Spinal Fuid (CSF) circulates in middle layer

Anatomy Principles 3 Cerebrum (hemispheres) Cerebellum, brainstem Cranial nerves originate at base of brain Sensory / motor supply to head and face Motor nerves = brain to muscle units Sensory nerves = skin back to brain Somatic Nervous System = voluntary action Automatic Nervous System = involuntary action

Anatomy Principles 4

RTA figures In 1990, road traffic crashes caused 5, 563, 000 Intra-cranial injuries worldwide Murray CJL, et al. 1996 HI major cause of death and injury in RTAs (80% of serious RTA injury is to head) 1 concussion every 15 seconds in USA 15, 000 Brain Injuries per year in USA Car injuries Playgrounds Sports

RTA figures

RTA figures

RTA figures 1, 200, 000 killed per year in RTAs 10, 000 injured per year in RTAs Most Head Injuries are mild, but any lefy with long-lasting problems RTA most common cause of HI Young males at biggest risk Alcohol implied Data suggests female drinking catching up with male Implications for Female RTAs?

RTA figures

RTA figures

Mechanics of RTAs Occupant RTAs Driver Hazards Steering wheel / column Instrument panel Seatbelt Windscreens Passenger Hazards

Mechanics of RTAs Pedestrian RTAs

RTA Brain injuries Skull Fractures Open Head Injury Closed Head Injury

RTA Brain injuries Contusion / Concussion Contre-Coup Epidural haematoma Diffuse axonal injury

RTA Brain injuries Subdural haematoma Intracerebral haemorrhage Epidural haematoma

Swelling Brain matter pushed and swollen Painful Exacerbates affects Accelerates symptoms

How are brain injuries assessed? PTA Post Accident Amnesia – memory problems when regaining consciousness • Minor Brain Injury Unconscious for < 15 mins • Moderate Brain Injury Unconscious > 15 mins but < 6 hrs + PTA < 24 hrs • Severe Brain Injury Unconscious > 6 hrs OR PTA > 24 hrs • Very Severe Brain Injury

How are brain injuries treated? Trepanning (Gk – trupanon – borer) Popular Japanese treatment George Morland. Trepanning a Recruit. c. 1790 Oil on canvas

How are brain injuries treated?

How are brain injuries treated? Stop bleeding Prevent ICP Control pressure Maintain blood flow Remove any blood clots Positioning (head up) Fluid restriction (of patient) Medication barbiturate (coma) anticonvulsants diuretics

How are brain injuries treated? Ventricular drain (Ventriculostomy) Ventilator Surgery Craniotomy Burr holes Bone flap removal

Injury Development Recovery from Brain Injury is possible Less likely as severity of injury increases Permanent brain problems from minor head injury are rare Post-concussional symptoms / Post-concussion syndrome Headache Dizziness Sensitive to loud noise or bright light Insomnia Slow thinking Tinnitus Blurred vision Tiredness Irritation PCS usually pass within 3 months

Injury Development “Focal Brain Injury”

Development of mood problems Memory Headache Overload Sleep disorders Fatigue Anger Depression Cognitive loss and muddle • 33% of head injury patients develop depression within < 1 year • Only 20% for non-head injury patients • Neuro-Rehab services need to plan ahead

Development of mood problems PTSD in kids after accident 34% of children in RTAs suffer PTSD Within 6 weeks of RTA Stallard, P et al. 1998 20% suffer acute stress reaction afterwards 25% suffer psychiatric problems within 1 year Mayou et al. Mood disorder Phobic travel anxiety PTSD all common Psychological de-briefing after RTAs may help Hobbs et al. 1996

Traumatic Brain Injury Physical force causes nerve cells to stretch, tear and pull apart Unable to relay messages through brain Force causes brain to slam against skull interior: “Traumatic Brain Injury” Injury to brain cells affects processing: thinking remembering seeing control & coordination mood

Traumatic Brain Injury TBI ranges from mild to severe: degree of force multiple trauma neurological complications speed of assistance

Head Injuries Severity depends on amount of Primary and Secondary brain injury Main cause of Secondary injury = hypoxia Categories: Open or Closed Forces: Shearing and Compression

Non Loss of Function 41 yr old Mike Hill Attacked from behind Full recovery after removal No infection Left hospital 1 week after removal Epileptic medication and some memory problems

Functional Status SPECT image with Technetium (T 99)

Pathophysiological Disturbance Involve scalp, cranium, or underlying brain Depends on mechanism of injury Scalp: lacerations, contusions, abrasions Skull fractures: vault / base, simple or compound, depressed or planar Primary Brain Injury: contusion) Focal (intra-cranial haematoma, Diffuse (diffuse axonal injury) Categories: Open or Closed

“Closed” or “Open” Head Injury Closed Head Injury (CHI): No penetration of the skull Usually a TBI Not always though Open head Injury (OHI): Bullet, Knife, or Fracture Skull breeched Brain injury depends on power of physical force injury If great enough, forces radiates through skull, causes sudden brain movement Results in damaged nerve cells May result in “soft tissue” injury cervical strain myofascial trauma

“Mild” Traumatic Brain Injury Head injury graded on: unconsciousness (i) length of (ii) length of amnesia Both caused by sudden trauma and nerve cell tearing Brain cannot maintain functioning and shuts down either: fully (unconsciousness) or partially (dazed) MBI refers to loss of consciousness for 30 mins or less Unconscious Amnesia Altered consciousness Injury neurological deficits Any of these Diffuse Axonal indicates MBI

Diffuse Axonal Injury Thinking slows down Memory poor Mild Brain Injury Processing slower Concentration haphazard “Roadblocks of damaged unconnected neurons” Individual feels: Incomplete Unconfident Frustrated Irritable Struggling emotional problems Described as “ mental fog” cognitive problems

Brain Injury without Direct Trauma Whiplash & Shaking Sudden movement inside cranium damages neurons Acceleration – Deceleration RTAs – even with airbag deployment –can cause brain injury Brain is torn, squashed, bruised Rollercoasters

Types of Head Injuries Concussion: Temporary alteration in neurological function or LOR Cerebral Contusion: Bruised brain Cerebral Haemotoma or bleed epidural sub-arachnoid intra-cerebral

Signs and Symptoms Headache Dizziness Nausea / Vomiting Amnesia Decreased responsiveness Confusion Combativeness Loss of responsiveness

Assessment First impression: Responsive or Unresponsive Urgent Survey: LOR ABC’s Open airway with C-spine Check breathing: Ventilate; Oral airway; O 2 when available Check carotid artery pulse – CPR if indicated Control any major bleeding

Assessment continued Rapid Body Survey Sample, DCAP-BTLS Stabilize head between knees Call for equipment, assistance, transport Maintain body temp. Transport (head uphill) Non-Urgent Survey Ongoing Survey – seizures, vomiting, change in LOR

Assessment continued Brain Swelling Increased Intracranial Pressure (ICP) Hypoxia Further Secondary Brain Injury More Swelling Increased ICP

Localised Neurological Signs (ICP) GENERAL SIGNS + PLUS + Change in pupil size / light reactivity Slowing pulse Rising BP Change in respiration Unilateral weakness Incontinence Seizure

Urgent Interventions - ATLS Presume C-Spine injury Immobilize neck Open airway: administer oxygen Treat bleeding and shock Prevent aspiration of vomit / secretions Transport immediately Elevate head 6” Transport head uphill

Imaging Xray, MRI and CT cannot show traumatic brain injury Techniques rely on tissue density Diffuse damage will not show on these techniques SPECT or PET measure brain cell metabolism Can detect changes in function due brain injury

Behavioural Changes Speech Cognition Memory Mood Mental health psychoses delirium Tremor Gait Symmetry of function simplification Visual Auditory Gross over-

Other Causes of Brain Injury Drug effects Tumor Metastases Physical assault Surgery Traumatic birth Hypoxia

Glasgow Coma Scale Scores 8 or less = needs urgent anaesthetic assessment. Danger of airway compromise 13 -15 = mild 9 -12 = moderate 3 -8 = severe

Queen’s Medical Centre

Cerebral Asymmetry of Function Hemispheric asymmetry of function is relative Asymmetries have been overblown by popular media into fads (e. g. golf with your right brain) Anterior-posterior differences far outweigh left-right differences Asymmetry is not uniquely human

Cerebral Asymmetry of Function LEFT HEMISPHERE Convolutions mature more rapidly Extends further posteriorly Higher in density (more gray matter; more neurons) Planum temporale larger on left (in 60 -90%) of cases Larger insula Longer Sylvian fissure (gentler slope) Double cingulate gyrus Larger lateral posterior nucleus (to parietal cortex) Wider occipital lobe Larger total area of frontal operculum (much buried in sulci) Larger inferior parietal lobule

Cerebral Asymmetry of Function RIGHT HEMISPHERE Convolutions mature less rapidly Extends further anteriorly Larger and heavier Primary auditory (Heshl's gyrus) larger on right Shorter (steeper slope) Single Larger medial geniculate nucleus Narrower Larger area of convexity in frontal lobe; wider frontal lobe

Cortical Lesions Human cognitive and sensory dysfunction different following lesions (due to strokes, surgery, accident, etc. ) Differences noted in lesions to left and right hemispheres Lesions can provide clues about brain organization Do specific areas possess special unique functions? Does a lesion to a specific area demonstrate a dysfunction + Lesions to other brain locations do not cause a similar

Dissociation Lesion site Speaking Reading Writing 100 normal impaired 102 impaired 104 normal impaired normal

Hemispherical Function Left Vision Right linguistic stimuli patterns faces steropsis language sounds Audition rhythm Somatosensation Motor tactile recognition complex movement Memory memory Language spatial movement verbal memory speech non-verbal reading writing Emotion emotions prosody arithmetic social emotions primary

Split Brain and Commissurotomy Corpus Callosum joins hemispheres Sever corpus callosum Two hemispheres cannot communicate

Brain Injury - Summary 1. The main cause of secondary damage to the brain is _ _ __? 2. Head injury alone rarely causes damage. T / F? 3. Temporary loss of consciousness or function from a head trauma is a _____? 4. Brain injury can occur without any impact trauma. T / F 5. Axons being damaged / shredded is the simple reason for