TBI & SCI Flashcards
Traumatic brain injury facts
Acute trauma to head and brain with or without skull fracture
10000-20000 severe traumatic brain injuries per year
Men 2x more likely
15-24 yrs old and over 80s most at risk
Common causes of TBI
Motor vehicle accidents
Cycling (helmet reduces 88% chance)
Sports injuries
Violence
Falls and accidents
Potential effects of head injury
Behaviour and personality changes - anxiety, depression, loss of motivation, difficulty controlling anger, impulsivity
Cognitive impairment- problems with memory, attention, concentration. Low tolerance for noise or stressful environments, loss of insight and initiative
Motor and sensory deficit changes- loss of coordination, muscle rigidity, epilepsy, speech issues, sight/smell/taste loss, fatigue, sexual problems, paralysis
Glasgow coma scale (GCS) - TBI diagnosis
Monitors changes in consciousness
Monitors motor response, verbal response and eye opening
Score ranges from 1 to 4-6
<8 is a severe head injury (coma)
9-12 moderate head injury
>12 mild head injury
Traumatic brain injury: closed injury
Trauma cause brain to be violently shaken inside of skull eg blast injury. No visible wound
Traumatic brain injury: open/penetrating injury
Object goes through the skull and enters brain
Traumatic brain injury: crush
Head is sandwiched between two hard objects
Traumatic brain injury: coup
Primary injury cause when the head stops suddenly and the brain rushes forward. Brain incurs a primary impact injury at the site of skull stroke as well as surrounding tissue
Traumatic brain injury: counter coup
Secondary injury caused when brain bounces off the primary surface of impact and goes on to impact the opposite side of the skull. Brain incurs focal area of damage as well as damage to nearby surrounding tissue
Traumatic brain injury: coup and contrecoup forces
Rotational forces - shearing and twisting
Coup - blow
Countrecoup - contusion, swelling, blood clots
Whiplash injury, TBI and cervical vertebrae
Hyperextension of the neck followed by hyperflexion
Major area of damage done to anterior longitudinal ligament
Vertebrae can become dislocated and/or fractured
Whiplash: hyper extension
Sudden backwards acceleration of skull. Once skull stops moving, the frontal lobe strikes the front of skull
Whiplash: Hyperflexion
Head recoils forward and stops
Occipital lobe strikes back of skull
Key events in TBI: primary
Skull fracture (open)
Contusions (bruising, damage to blood vessels)
Haemorrhage (bleeding from raptured blood vessels)
Haematoma (localised pooling of blood)
Diffuse axonal injury (DAI) (damage to axons through the brain)
Concussion (temporary - neuronal dysfunction)
Key events in TBI: secondary
Intracranial - evolves over hrs, days, week after impact
Brain swelling, cerebral oedema, hydrocephalus
Increased intracranial pressure
Intercranial haemorrhages, traumatic haematomas, infections
Blood flow changed and metabolic changes
Epilepsy
Hypoxia-ischaemia (reduced o2 to brain)
What can haemotoma lead to?
Increased intracranial pressure and shifting of brain tissue so increased pressure in brain tissue
What do all the key events in TBI lead to?
Atrophy of brain tissue and wide ranging symptoms
Neuropathology of TBI
Atrophy and increased ventricles
(Seen through T1 weighted MRI)
TBI - intracranial pressure (ICP)
Cerebral perfusion pressure = mean arterial pressure - intracranial pressure
CPP should not fall below 70mmHg - risk of hypoxia and ischaemia
Normal ICP
7-15mmHg
Drowsy and confused patients ICP
20mmHg
Severe brain swelling ICP
30mmHg
Monroe Kellie doctrine
V intracranial = V brain + V blood + V CSF
Brain = 80%
Blood = 10%
CSF = 10%
Increase in one results compression of others
ICP: homeostasis and treatments
Diuretic
Medically induced coma
Placement of shunt
Craniectomy (partial skull removal)
Key events in TBI: secondary injury - Neurochemical injury
Excessive production of free radicals
Excessive release of excitatory neurotransmitters
Alterations in glucose metabolism
Decreased cerebral blood flow
Neuro inflammation
Key events in TBI: late/delayed injury
White matter degeneration and cerebral atrophy
Postraumatic hydrocephalus
Post traumatic seizures
Secondary injury - Neuroinflammation
Activation of microglia, astrocytes, neurons
Activation and recruitment of macrophages
Microglia secrete pro inflammatory modulators- degrade BBB and release cytokines in response to DAMPs
Astrocytes - up regulate extracellular matrix to wall off areas of lesion
Oligodendrocytes - violin that sits around lesion but don’t do much after
AD and TBI comparison - MRI
Both have accentuated gyri
Both have neuronal atrophy
Diffuse axonal injury (DAI)
Injury to axon - twist and tear
BAPP is produced by neurones in response to injury
Accumulates at points of damage (construction/transection)
Some axons have multiple swellings (beaded appearance) may persists for years
Axonal transport stopped
Severe white matter degeneration and atrophy of corpus callosum
Chronic traumatic encephalopathy (CTE)
Progressive and degenerative brain condition that has been linked to repeated head injuries and repeated concussion
Aka dementia puglistica and punch drunk syndrome
Chronic traumatic encephalopathy (CTE): symptoms
Begins gradually - years after initial trauma(s)
Memory loss
Confusion
Impaired judgement
Impulsive control problems
Aggression
Depression
Parkinsonism
Progressive dementia
Molecular/cellular changes found in CTE
Abnormal tau accumulation and neurofibrillary tangles
Microgliosis, astroiosis
Brain atrophy
Englarged ventricles
Abnormalities in TBL-43 (frontotemporal dementia and ALS)
Woodpeckers
Less CSF
Tongue has a bone to act as a spring - dampens force on brain
Recent evidence shows that smaller brain size allows larger concussion threshold
Spinal cord injury (SCI) facts
1000-2000 new cases in uk a year
42 avarage age at injury (20s and old)
Males more likely
Pneumonia and septicaemia - common cause of death of SCI patient
Spinal cord anatomy
Cervical 1-8
Thoracic 1-12
Lumbar 1-5
Sacral 1-5
Coccygeal 1
What information is carried in which tract
Lateral corticospinal tract - motor control (motor descending tracts)
Posterior columns - vibration, light touch, proprioception (sensory ascending tracts)
Anterior spinothalamic tract - pain and temperature (sensory ascending tracts)
Paraplegia versus quadriplegia
Quadriplegic - no longer control any of limbs (C4 and C6 injury)
Paraplegia - don’t have use of legs but have arms (T6 and L1)
Priorities for recovered function amongst SCI patients
Arm/ hand function highest priority for quadriplegics
Sexual function highest priority for paraplegics
SCI - partial lesions
brown sequard syndrome of spinal cord -
Same side as lesion UMN weakness, loss of position and vibration
Side of opposite lesion loss of pain and temp
Central cord syndrome -
Lesion interrupts fibres crossing to enter spinothalamic tracts (stretch reflex, autonomic function)
ASIA (American spinal injuries association)
A (complete injury) -E (normal) levels
Determines sensory lvls for right and left
Motor levels for right and left
Single neurological lvl - lowest spinal level that is normal on both sides
Injury complete or incomplete
Spinal shock
State of temporary loss of function in spinal cord (often lasts a day can be up to month) (replaced by spastic paralysis after spinal shock)
Flaccid paralysis below the lesion
Loss of tendon reflexes
Impaired sympathetic outflow to vesicular smooth muscle can cause decreased blood pressure (high cervical injury)
Absent sphincter reflexes and tone
SCI and TBI - comparisons of initial injury
Lesions - contusion, necrosis, apoptosis, hemorehage, oedema, breakdown of BBB, swelling, excitotoxicity, DAI, hyperthermia, inflammation
Loss of function - local vs global
Acute versus chronic (primary vs secondary)
SCI - impact of injury
Acute injury, lesion spread, chronic injury
Contusion injury - lesion in centre and tissue responding for days becoming bigger. After week has a hole with debris, 2 weeks to month - strong capsule as fluid filled
CNS injury - spinal cord, astrocytes and glial scar
Astrocytes become reactive - become hypertrophic, secrete chondroitin sulfate proteoglycans (CSPGs), increase expression of normal molecules eg glial fibrillation acidic protein (GFAP)
Result = glial scar
Glial scar + myelin debris = area which growing axon cannot get through
GFAP as a stain
Injury dark
Area around bright
Mechanism of Inflammatory cells in SCI
Flood lesion and release pro inflammatory cytokines so affect neuronal viability
Diffusable inflammatory mediators (nitrous oxide) affect neuronal excitably
Axons/neurons die or degenerate
Wallerian degeneration in PNS
Axon becomes fragmented at injury site
Myelin debris released and Schwann cells become reactive
Macrophages recruited and both clear debris
Schwann a cells for regeneration tubes (bands of bungner), axons sprout and regrowth through tube
Wallerian degeneration in adult CNS
Injury
Microglia and astrocytes activated
Macrophages begin to remove debris
Myelin debris not fully removed
Oligodendrocytes survive
Glial scar firmed.
Cell body undergoes chromatolysis and synaptic terminal retract
Axons attempt to sprout but regeneration fails due to persistent myelin debris and glial scar
Damaged neurons - chromatolysis
Nissl substance stains RE and poly ribosomes - no axon present
Neurones undergoing chromatolysis have a displacement of nucleus, Nissl substance only at cell body periphery
Neurones usually undergo apoptosis
Spinal cord injury and traumatic brain injury - issues for repair and recovery
Major biomedical problem and increasing in frequency
Prevention better than cure
Prevent secondary damage, anti inflammatory response, increase neuro protection, increase axon protection
Repair damage?
