- To demonstrate basic knowledge of recovery of movement in the lower limb after
brain injury (rehabilitation)
- To demonstrate basic knowledge of the effect of cerebral oedema and seizure on
the cerebral cortex
- To demonstrate basic knowledge of the treatment of fractures in this case
Recovery depends on the mechanism of damage:
Concussion
o A reversible impairment of neurological function for minutes to hours
following head injury.
o Loss of consciousness, ‘seeing stars’, headache, dizziness, nausea and
vomiting are common symptoms
o Treatment is typically rest
Contusion/Laceration
o Petechial haemorrhage, oedema and tissue destruction typically from
mechanical forces. This displaces and compresses the hemispheres of the brain
against the skull.
o Symptoms depends on the location of the contusion/laceration
o Recovery results in glial scarring and immune cell filtration. These can cause
haemosiderin-stained depressions in the cortex that can result in epilepsy
Cerebral Oedema
o Vasogenic oedema – influx of fluid and solutes into the brain via an
incompetent BBB
o Cytotoxic Oedema – cellular swelling due to trauma or infarction
Elevated ICP
o Presents with drowsiness and reduced consciousness with later signs of coma
and pupillary changes
o Treated by elevating the head to 30 degrees. Emergent treatment includes
intubation, hyperventilation high dose barbiturates, decompressive
hemicraniectomy and possibly hypothermia.
Seizure
o Temporary loss of function of brain activity due to excessive neural activity
o Cortical scars from contusions may result in seizures
o Can be focal or generalised
Brain damage can occur due to trauma through a variety of mechanisms:
Axonal shear injury – damage to the white matter
Petechial haemorrhage – spots of blood in the white matter
Intracranial heamorrhage – large spots of blood in the white matter
Cerebral contusion
Penetrating trauma
Cerebral oedema
1
Guillaume Antem – MBChB Y2
, A craniotomy is a procedure that involves drilling a home in the skull, exposing the dura and
then elevating said dura to reduce ICP.
The GCS is a tool used to record the conscious state of the patient:
Severe – GCS <8
Moderate – GCS 9-12
Minor – GCS >13
As a primary survey assessment for consciousness, the abbreviated coma scale can be used:
A Alert
V Vocal stimuli
P Pain
U Unresponsive
- To demonstrate basic knowledge of sleep and consciousness
The ascending arousal system increases arousal and facilitates consciousness by maintaining
a desynchronised EEG. This system consists of monoaminergic and cholinergic neurons in
the brainstem and hypothalamus which project into the thalamus and cortex:
Cholinergic neurons in the pedunculopontine nucleus and basal nucleus of Meynert
are important in arousal
These neurons project to the diencephalon and cortex
Sleep and wakefulness
Sleep-wake cycles are determined by the circadian rhythm. This system works as follows:
The sleep-wake cycle is regulated by the suprachiasmatic nucleus (SCN)
SNC cells produce CLOCK and BMAL1, which promotes PER and CRY gene
transcription
PER and CRY proteins bind together, inhibiting their own gene transcription
PER and CRY degrade, allowing CLOCK and BMAL1 to promote PER and CRY
transcription
The whole process takes about 24hrs
The SCN uses light information to adjust the circadian rhythm via the retinohypothalamic
tract.
Stage of sleep
Sleep can be divided in non-REM (desynchronised) and REM (synchronised) stages:
There are typically 4-6 cycles in 8hrs of sleep.
80% of sleep is spent in non-REM sleep.
2
Guillaume Antem – MBChB Y2
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