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Brain Dysfunction & Stroke Part 2 - Coggle Diagram
Brain Dysfunction & Stroke
Part 2
Head injury
Classification of Head injury
Closed Head injury
Result of Blunt Trauma
may Cause diffuse axonal injury/ Focal Brain injury
Skull intact, Brain damaged due to external indirect cause/ internal pathological process
Open Head Injury
Result of Penetrating trauma
may cause Focal brain injury
skull penetrated, brain damaged by direct force (e.g. bone fragments, foreign body)
Mechanisms of Head injury:
3 mechanism types
Secondary injury includes:
-Cerebral oedema
-Haematoma
-infection
-
Increased Cranial Pressure
Intracranial Pressure:
Cranium is solid, therefore increase content= increase pressure (Skull=box)
(Brain is compliant)
--> Can be accommodated before Intracranial Pressure (ICP) rises
Damage to Blood vessels:
.Haematoma=Space filling lesion
. Compresses neural tissue & blood vessels supplying other regions
Inflammation of neural tissue:
-Oedema- generalised compression
Signs
depending on injury type
Arterial Bleeding:
Rapid onset (hrs)
.High risk of re-bleed
Venous Bleeding:
*Days/weeks to develop
.Common in newborn/elderly
Effects of Increasing Intracranial Pressure
Headache:
Pathophysiology:
Stretching/ Distortion of meninges/walls of larger blood vessels
Vomiting:
Pathophysiology:
Pressure on emetic centre in Medulla
Decreasing Level of Consiousness
:
Pathophysiology:
*Pressure on RAS (Brainstem)/Cerebral Cortex
Vital Signs:
Increasing BP + Pulse Pressure
Slow Heart rate
Pathophysiology:
Cushings Reflex-response to cerebral Ischemia- Systemic Vasoconstriction
Response to increasing BP (Baroreceptors)
Intracranial Pressure increase:
Blood pressure increases ( Increasing pulse pressure= Systolic increases whilst diastolic remains somewhat stable)
Pulse and Respiration decreases
Signs affecting vision:
Papilledema
Pupils fixed & Dilated
Pathophysiology:
*Increasing Pressure of CSF- swelling around optic disc
*Pressure on Cranial nerve 3 (occulomotor)
Tertiary injury:
-Apnoea
-Hypotension
-respiratory and cardiovascular effects of primary and secondary injuries
Primary injury:
Cause: Impact
-Acceleration/Deceleration
-Direct impact
-direct injury
Affect: Neurons, Glia & Blood vessels
e.g. impact forward,
contrecoup
(back of brain rebounds off back of skull)
Anatomical Considerations
Meninges (Membranous covering of brain)
Cranium--> Dura Mater-->Dura Sinus-->Subdural Space--> Arachnoid--> Subarachnoid--> PIa Mater--> Cerebral Cortex
Anatomy of the Brain
Reticular formation:
Neurological pathway controls Arousal & ability to respond to stimuli
Ascending Reticular Activating System (RAS)
.* Input from all sensory systems
Maintains alertness/arousal/sleep
Descending Reticular Activating system (RAS
)
input from Cerebrum to
Cerebral Blood Supply
Cerebral blood supply (cerebro-arterial circle, Circle of Willis)
Cerebral Venous drainage
Progression of Head Injury:
*Consciousness level vary due to:
-Extent of injury
-Intervention
-Fever
-Environment
Deterioration of brain function progresses from:
Higher cerebral functions
to
fundamental reflexes of brainstem
Respiratory pattern Changes and Brain injury:
Apneustic-Pons
Cluster-base of Pons
Central Neurogenic Hyperventilation
Ataxic-Medulla
Cheyne-Stokes-Parietal Lobe
Glasgow Coma Scale-Assessment
-Tool assess severity of injury
-relates presentation to outcome
-set standard set of stimuli
-gives score of 3 (worst) to 15 (best)
Clinical Management:
Sedation ( Clinical Coma)
Damage to brain tissue (Contusion etc) --> cause-->inflammatory oedema, increasing intracranial pressure + effects
Therapies:
Oxygen (& Ventilation)
Steroids
Diuretics (Mannitol)
Post Traumatic Amnesia:
Post traumatic confusional State
Loss of memory around time of trauma
Agitation, disorientation, decrease in cognitive ability and attention
Duration varies= indicates injury level
Westmead PTA Scale= indicates injury severity as a function of PTA duration
-PTA less than 5 minutes: very mild injury
-PTA between 5-60 minutes: mild injury
-PTA between 1-24 hours : moderate injury
-PTA 1-7 days: severe injury
-PTA greater than 7 days: very severe injury
Evidence of vascular disruption + Mitochondrial mitochondrial damage
-Cell damage/death possible