Consciousness and Head Injury Flashcards
3 components of consciousness
Alertness - reticular formation responsible for wakefulness
Attention - limbic system and frontoparietal areas affect mood, attention and motivation
Awareness - cerebral cortex responsible for awarenss and interaction with environment
Caues of decrease in conscious level
Trauma - concussion, contusion, intracranial haemorrhage
Infection - meningitis, abscess, subdural empyema, encephalitis
Tumour
Metabolic - hypoperfusion, hypoxaemia, hyercalcaemia, hypoglycaemia
Intoxication - drugs, alcohol, toxins
Causes of progressive change of consciousness
Metabolic abnormality: electrolytes, sugar, liver and renal damage
Sepsis
Intracranial space occupying lesion
hydrocephalus
DDx for sudden loss of consciousness
Stroke
Head trauma
Hydrocephalus
Hypoglycaemia
Hypoxia
Drug intoxication
Subarachnoid haemorrhage
Cause of a transient loss of consciousness
Syncope
Seizure
Subarachnoid haemorrhage
Brain concussion
Extradural/Subdural haemorrhage
Focal signs of neurological deficit
Motor: weakness, paralysis
Speech: expressive or receptive dysphasia
Los of memory/confusion
Visual defects
Decorticate response
Flexion and adduction of arms, extension of the legs
Indicates severe bilateral damage above the midbrain
Decrebrate response
Extension and internal rotation of all four limbs
Indicates brainstem damage or damage to the midbrain.
Proression from decorticate to decrebrate indicates uncal herniation.
Describe the pathophysiology of raised ICP
The cranium is an enclosed space. Excessive accumulation of fluid/mass in the brain causes a rise in intracranial pressure.
Can be due to infection, tumour, trauma, tumour, haemorrhage.
Small increases in ICP are accommodated by the CSF which becomes redistributed to the lumbar cisterna.
As intracranial pressure increases the veins collapse because the pressure within them is low. This favours further rises in pressure.
Rise in ICP reduces the cerebral perfusion pressure, eventually the arterioles become compressed and there is a decrease in blood flow. The brain is not adequately perfused and becomes ischaemic
Vegetative state
Caused by diffuse damage to the cerebral cortex
Reticular formation (non-cognitive function) is intact but the cerebral cortex is non-functional.
Patient is awake, eyes are open, sleep wake cycles present however there is lack of awareness and no meaningful response to verbal commands or pain
Locked-in syndrome
Results from an extensive lesion of the ventral pons which interrupts the corticobulbar and corticospinal tracts.
Reticular formation and cortical function is intact. Patients are awake and alert but unable to speak or move their face or limbs.
Symptom progression in coning
Headache/nausea/vomiting
Hypertension, bradycardia and wide pulse pressure
Pupillary changes
Hemiparesis
Stupor
Coma
Abnormal respiratory pattern
Death
Pupillary changes seen in comatose patients
Pinpoint pupils - pontine lesions, opiates (sympathetic affected)
Dilated, unreactive pupil - midbrain lesion or herniation compressing CN3, overdose
Fixed mid-size: brainstem compression
Enlarged slowly reactive: metabolic or toxic
Signs of raised intracranial pressure
Headache
Nausea and vomiting
Papilloedema
Assessment of outcome of head injury
Glasgow outcome score
- Dead
- Vegetative state (sleep/wake cycle but not sentient)
- Severely Disabled (conscious but dependent)
- Moderately disabled (independent but disabled)
- Good recovery (may have minor sequelae)
