Neuro Flashcards
meningeal vessels
Vessels coming off the external carotid artery
- Are in the extradural space - between bones of the skull and the dura
bridging veins?
cross the subdural space - between the dura and arachnoid
circle of willis?
- lies in the subarachnoid space (between the arachnoid and
pia)
white matter v grey matter
White matter contains myelinated axons
• Grey matter contains cell bodies and no myelin sheaths
frontal lobe?
Voluntary movement on opposite side of body
- Frontal lobe of dominant hemisphere controls speech (Broca’s area) & writing
(if right handed, then left hemisphere is dominant etc.) - Intellectual functioning, thought processes, reasoning & memory
pariental lobe?
- Receives and interprets sensations, including pain, touch, pressure, size and
shape and body-part awareness (proprioception)
temporal lobe?
- Understanding the spoken word (Wernicke’s - understanding), sounds as well
as memory and emotion
occipital lobe?
Understanding visual images and meaning of written words
passage of CSF
CSF is produced by ependymal cells in
the choroid plexuses of the lateral
ventricles (mainly)
- From the lateral ventricles it travels to the
3rd ventricle via the interventricular
foramen and then from the 3rd ventricle it
travels to the 4th ventricle via the cerebral aqueduct (Aqueduct of Sylvius)
- From the 4th ventricle it communicates with the subarachnoid space via the
median foramen of Magendie and the two lateral foramen’s of Luschka
- CSF is then absorbed via arachnoid granulations (VILLI) e.g. in the superior
sagittal sinus
hydrocephalus
Abnormal accumulation of CSF in ventricular system
• Often due to a blocked cerebral aqueduct
sympathetic - CNS -
• Leaves the CNS from the thoracic & lumbar regions (T1 - L2) of the
spinal cord
• Most of the ganglia lie close to the spinal cord and form two chains
of ganglia - one on each side of the cord - known as the SYMPATHETIC
TRUNKS
• Uses acetyl-choline (ACh) at preganglionic synapse where there are
nicotinic receptors
• At effector cell synapse the
neurotransmitter noradrenaline is
used where there are adrenergic
receptors (of which there are 5
subtypes)
• Supplies visceral organs and
structures of superficial body regions
• Contains more ganglia than the the parasympathetic division
• Its effects are amplified by the adrenal glands (FORMED BY THE
SYMPATHETIC DIVISION) which in turn release adrenaline directly
into the blood resulting in a high blood pressure & heart rate
parasympathetic CNS
• Leaves the CNS from the brainstem & sacral portion of the spinal cord
• Cranial outflow:
• Comes from brain
• Preganglionic fibres run via; oculomotor nerve CN3 - to pupil, facial
nerve CN7 - to salivary glands, glossopharyngeal nerve CN9 - for
swallowing reflex & via the vagus nerve CN10 - to thorax & abdomen
- remember by 1973
• Cell bodies are located in cranial nerve nuclei in the brainstem
• Innervates the organs of the head, neck, thorax & abdomen
• Sacral outflow: Supplies the remaining abdominal and pelvic organs
• Ganglia lie within/very close to the organs that the postganglionic
neurones innervate
• Uses acetyl-choline (ACh) at the preganglionic neurone synapse
where there are nicotinic receptors
• Uses acetyl-choline (ACh)
at the effector cell synapse
where there are muscarinic
receptors
somatic nerves>?
sensory & motor:
- Bodily segments
- Conscious
branchial
motor only:
- 5 branchial arches
autonomic
sensory & motor:
- Parasympathetic & sympathetic
- No conscious awareness
upper motor neurones v lower motor neurones
• Upper motor neurone:
- The descending pathways and neurones that originate in the motor cortex
- Control the activity of the lower motor neurones
• Lower motor neurone -
known as ALPAH MOTOR NEURONES:
- Alpha motor neurones that directly innervate skeletal muscle that have cell
bodies lying in the grey matter of the spinal cord and brainstem
spasticity?
• Upper motor neurone:
- The descending pathways and neurones that originate in the motor cortex
- Control the activity of the lower motor neurones
• Lower motor neurone - known as ALPAH MOTOR NEURONES:
- Alpha motor neurones that directly innervate skeletal muscle that have cell
bodies lying in the grey matter of the spinal cord and brainstem
rigidity?
- Increased muscle contraction is continuous and the resistance to passive
stretch is constant
how many spinal nerves?
Has 31 pairs of spinal nerves (segments):
- Cervical - 8 nerves
- Thoracic - 12 nerves
- Lumbar - 5 nerves
- Sacral - 5 nerves
- Coccyx - 1 nerve
conus?
Conus (end of spinal cord) finishes BEFORE L2
spinal nerve exits from cords?
- Cervical segments: around 1 vertebra HIGHER than their corresponding
vertebra [EXCEPY C8 which exits below one vertebra] - Thoracic segments: around 1-2 vertebra BELOW their corresponding vertebra
- Lumbar segments: 3-4 vertebra BELOW their corresponding vertebra
- Sacral segments: around 5 vertebra BELOW
sensory innervation of hand - nerves?
- Little finer (ulnar nerve) - C8
- Index finger (median nerve) - C7
- Thumb - C6 - The thumb is C6, always remember this!
cervicle nipple medial arm umbilicus knee perianal areal anus DERMANTOME
- Clavicle - C4
- Nipples - T4
- Medial side of arm - T1
- Umbilicus - T10
- Knee - L4
- Perianal area - S4
- Anus - S5
ascending tracts?
- dorsal/medial leminicus columns
- spinothalamic
- spino-cerebellar
dorsal leminscal columns?
Consist of the Fasciculus cuneatus & Fasciculus gracilis • Carry proprioception, vibration & fine touch • Fasciculus cuneatus - LATERAL and carries information from the UPPER body to the cuneate tubercle in the medulla
• Fasciculus gracilis - MEDIAL and
carries information from the LOWER
body to the gracile tubercle in the
medulla
Ascends to the medulla and then DECUSSATES to become the medial
lemniscus then ascends to the thalamus then to the SOMATOSENSORY
CORTEX
• Thus decussates AFTER LEAVING SPINAL CORD
spinothalamic
• LATERAL: pain & temperature • MEDIAL/ANTERIOR: crude touch • Ascends on the same side for 1 to 2 segments then DECUSSATE (substansia gelatinosa) before ascending to the thalamus (unlike other sensory modalities that travel to the cortex, PAIN reaches consciousness in the THALAMUS) • Thus decussates SOON UPON ENTRY INTO SPINAL CORD • The tract terminates at the thalamus • PAIN REACHES CONSCIOUSNESS AT THE THALAMUS - unique
spino-cerebellar tract?
Posterior spinocerebellar tract: carries information on proprioception to
the IPSILATERAL INFERIOR CEREBELLAR PEDUNCLE
• Anterior spinocerebellar tract: carries information on proprioception to
the CONTRALATERAL SUPERIOR CEREBELLAR PEDUNCLE
• Both carry the same information so difficult to clinically differentiate
descending tracts?
Originate from the cerebral cortex and brainstem (UPPER MOTOR
NEURONES)
Divided into pyramidal and extrapyramidal:
pyramidal tracts
- 2 neurone pathway originating in the cerebral cortex of cranial
nerve nucleus (for facial innervation) - DECUSSATE in the medulla and descend CONTRALATERALLY
- Neurones innervating our axial muscles (muscles of the trunk and
head) mostly DO NOT DECUSSATE - Synapses with the cell bodies of the ventral horn of the spinal grey
matter - E.g. Corticospinal tract
extra-pyramidal tracts?
- Originate in the brainstem and carry motor fibres to the spinal cord
- Responsible for involuntary autonomic control of all musculature
- E.g. Rubrospinal tract, Tectospinal tract & Vestibulospinal tract
corticospinal tract?
• Transmits control of voluntary
muscles (motor)
• Lateral corticospinal tract
(75%): pyramidal (MEDULLARY)
DECUSSATION - limb muscles
- Originates from the
contralateral motor cortex
• Medial (25%): DECUSSATES as it leaves via the anterior white commissure (a bundle of nerve fibres that cross the mid-line of
the spinal cord) - axial muscles (head & trunk - muscles needed
to keep upright et.)
- Originates from the
contralateral motor cortex
• Upper motor neurones (UMN) originate in the motor cortex - a UMN
lesion can occur anywhere from the cortex all the way down to the ventral
horn
• Neurones (cell bodies) located in the ventral horns project to limb and
axial muscles - these are the lower motor neurones (LMN)
Vestibulospinal tract:
- Muscle tone, balance & posture (by innervating antigravity muscles)
- Originates from vestibular uncles (CN8)
- NON-DECUSSATING thus IPSILATERAL
Tectospinal tract:
- Head turning in response to visual stimuli
- Originates from the tectum; superior (visual) colliculus
- DECUSSATES at the midbrain thus is CONTRALATERAL
rubrospinal
- Facilitates flexors and inhibits extensors - fine hand movements
- Originates from the red nucleus
- DECUSSATES at the midbrain thus is CONTRALATERAL
brown squard syndrome?
- Hemi-section of the spinal cord
- Ipsilateral & contralateral are in relation TO THE LESION
• Ipsilateral weakness (i.e. less motor etc.) below the lesion - due to damage to the ipsilateral descending motor corticospinal tract (decussated at the medulla already) • Ipsilateral loss of dorsal column proprioception below lesion - sine the ascending tracts are damaged before they could decussate in the medulla • Contralateral loss of spinothalamic pain & temperature below the lesion since spinothalamic fibres decussate just after entering cord within the spinal cord
- ***** Overall:
- Ipsilateral loss of; proprioception, motor & fine touch
- Contralateral loss of; pain, temperature & crude touch
olfactory nerve?
sense of smell
- sensory
optic nerve?
vision
- sensory
- test -> snellen test
oculomotor
- motor
- parasympathetic
- test pupillary constriction and accommodation
PALSY -> down and out eye
trochlear?
innervetes superior oblique
- motor
trigeminal
- sensory and motor
- function -> Chewing Face and mouth touch and pain
abducens
lateral rectus
- motor
facia nerve
- sensory and motor
- parasympathetic
- Controls most facial expressions Secretion of ears and saliva
- anterior 2/3 of tongue
vestibulochlear
- sensory
- hearing
glossopharyngeal?
- sensory and motor
- parasympathetic
- taste (posterior 1/3)
- Senses carotid blood pressure
- Muscle sense –proprioception, sensory awareness of the bod
vagus nerve?
- motor and sensory
- parasympathetic
- senses aortic blood pressure
- Slows heart rate - Stimulates digestive organ
accessory nerve?
- motor
- controls trapezius and sternocleidomastoid
hypoglossal nerve
- motor
- Controls tongue movements
parasympathetic cranial nervers
1973
10, 9, 7, 3
cranial nerve brainstem nuclei location
- 3,4 - Midbrain
- 5,6,7,8 - Pons
- 9,10,11,12 - Medulla
Brocas area?
Broca’s area is the language area of the DOMINANT (normally left if right handed)
FRONTAL LOBE
- damage causes expressive aphasia -> they will understand what you are saying but unable to express words into meaningful language
Wernickes area?
Wernicke’s area is the comprehension area in the DOMINANT (normally left if right
handed) TEMPORAL LOBE and is responsible for understanding speech:
- comprehension aphasia -> difficult understanding but fluent speech that is scrambled
external and internal carotid
- External carotid supplies everything in
head & neck EXCEPT the brain
• Internal carotid supplies the brain ONLY!
internal carotid braches
- Anterior cerebral artery (ACA): • Supplies motor cortex and top of brain • If there is ischaemic stroke in ACA the lower limbs will be effected e.g. legs
- Middle cerebral artery (MCA):
• Supplies the majority of the outer surface of
brain
• If there is ischaemic stroke in MCA then the
region affected will be from the chin to the
hip - Posterior cerebral artery (PCA):
• Supplies peripheral vision - ischaemic stroke will result in peripheral
vision loss but not macular vision - The PICA supplies the medulla (CN 9,10,11,12) and an emboli can result in
lateral medullary syndrome: dsypgaia, slurred speech, facial pain
- The PICA supplies the medulla (CN 9,10,11,12) and an emboli can result in
where does common carotid arteries bifurcate
- The common carotid arteries BIFURCATE into the internal (larger than the
external) & external carotid arteries at C4:
visual fields from nasal and temporal
Fibres from the nasal portion (closest to the nose) of the retina (carrying the
TEMPORAL VISUAL FIELDS) cross at the optic chiasm which is located JUST
ANTERIOR to the PITUITARY INFUNDIBULUM
Fibres from the temporal portion (furthest from the nose) of the retina (carrying the
NASAL VISUAL FIELDS) do the same as mentioned above ↑
where do optic tracts go after optic chasm
The optic tracts carry the fibres posterolaterally around the cerebral peduncles to
terminate at the geniculate bodies of the thalamus
After the lateral geniculate body, the optic radiations split into two
• The fibres carrying information from the inferior portions of the retina (and thus the
SUPERIOR VISUAL FIELDS) travel by looping laterally through the TEMPORAL
LOBE to the visual cortex - this is known as MEYER’S LOOP. VLS
• The fires carrying information from the superior portions of the retina (and thus the
INFERIOR VISUAL FIELDS) travel by looping superiorly through the PARIETAL
LOBE to the visual cortex - this is knows as BAUM’S LOOP AIM
damage to optic chasm causes?
= Loss of
vision of the temporal visual fields - this is
called hemianopia
damage to left optic tract
Damage to the left optic tract = Loss of
vision of the temporal field of the left eye & the
loss of the nasal field of the right eye - another
type of hemianopia
damage to left Meyers loop
Damage to the left Meyer’s loop carrying
information from the inferior retina and thus the
SUPERIOR VISUAL FIELD resulting in loss of
vision in the superior nasal field of the left eye
and the superior temporal field of the right eye
damage to left Baums loop?
carrying
information from the superior retina and thus the
INFERIOR VISUAL FIELD resulting in loss of
vision in the inferior temporal field of the right
eye and the inferior nasal field of the left eye
where does spinal cord finish?
SPINAL CORD FINISHED AT L1
epidural below L1
best place for lumber puncture?
L3/4 or L4/L5
complication with where C3 runs?
• CN3 runs over the petrous apex of the
temporal bone:
- If there is a fracture or inflammation then
CN3 can get pushed against the bone
resulting in a CN3 nerve palsy resulting in
a FIXED DILATED PUPIL
cerebellar symtoms?
- Ataxia - loss of full control of body movements - limb unsteadiness
- Nystagmus - rapid eye movements
- Deficit is ON SAME SIDE AS CEREBELLAR LESION (IPSILATERAL)
what passes through cavernous sinus?
Oculomotor nerve (3) • Trochlear nerve (4) • Opthalmic trigeminal (5.1) • Maxillary trigeminal (5.2) • Carotid (INTERNAL) • Abducens (6) - only one going medially • Trochlear nerve (4)
3 main investigations for head injury?
- GCS - Glasgow coma scale - measure of level of consciousness:
• Score adds to 14 and consists of 3 categories: - Motor response - most important
- Verbal response
- Eye opening response
- Look at lateralising signs;
• To identify which hemisphere issue is with
• For example can check painful stimuli response: - Pinch behind ear and will see what side has issue e.g. the R hand
may come up but the L will not
Look at pupils for signs of raised ICP:
• Fixed dilated pupils - CN3 palsy
• Papilloedema
- Monitor vital signs
clinical management of head injury?
- IV MANNITOL a diuretic to reduce oedema and thus ICP
- Management of seizures e.g Diazepam for status epilepticus
TIA?
Definition:
- A brief episode of neurological dysfunction due to temporary focal cerebral
ischaemia without infarction
<24 HRS
TIA, epidemiology?
M>F
blacks more at risk
aetiology of TIA?
- Small vessel occlusion
- Atherothromboembolism from the carotid is the CHIEF CAUSE
- Cardioembolism resulting in MICROEMBOLI
- Hyperviscosity
risk factor for TIA?
- Age - risk increases with age
- Hypertension
- Smoking
- Diabetes
- Heart disease - valvular, ischaemic or atrial fibrillation
pathophysiology of TIA?
- The commonest cause of a TIA is cerebral ischaemia resulting in a lack of O2
and nutrients to the brain resulting in cerebral dysfunction - however in a TIA
this period of ischaemia is short-lived, with symptoms usually only lasting a
maximum of 5-15 minutes after onset, and then resolves with before
irreversible cell death occurs - Symptoms that gradually progress suggest a different pathology such as
demyelination, tumour or migraine
clinical presentation of TIA?
- SUDDEN loss of function, usually lasting for minutes only, with complete
recovery and no evidence of infarction on imaging - Site of TIA is often suggested by symptoms
- 90% of TIA’s affect the anterior circulation (carotid artery):
• Supplies the frontal and medial part of the cerebrum
• Occlusion may cause a weak, numb CONTRALATERAL leg +/- similar, if
milder, arm symptoms
• Amaurosis fugax:
- 90% of TIA’s affect the anterior circulation (carotid artery):
- Sudden transient loss of vision in one eye
- 10% affect the posterior circulation (vertebrobasilar artery):
• Diplopia - double vision
• Vertigo - the feeling that your surroundings are moving
investigations of TIA?
- Bloods: • FBC - look for polycythaemia • ESR - will be raised in vasculitis • Glucose - to see if hypoglycaemic • Creatinine, electrolytes • Cholesterol
- Carotid artery doppler ultrasound to look for stenosis/atheroma
- MR/CT angiography if stenosis to determine extent
treatment of TIA?
ABCD2 score risk of stroke after TIA
- Age > 60yrs = 1
- Blood pressure > 140/90mmHg = 1
- Clinical features:
- Unilateral weakness = 2
- Speech disturbance without weakness = 1
- Duration of symptoms:
- Symptoms lasting more than 1hr = 2
- Symptoms lasting 10-59mins = 1
- Diabetes = 1
meds
- - Antiplatelet drug:
• ASPIRIN IMMEDIATELY + DIPYRIDAMOLE (↑cAMP and ↓ thromboxane
A2) for two weeks then lower dose
• P2Y12 inhibitor longterm e.g. CLOPIDOGREL
- Statin longterm e.g. SIMVASTATIN
- Control cardiovascular risk factors:
• Antihypertensives such as ACE-inhibitor e.g. RAMIPRIL or angiotensin
receptor blocker e.g. CANDESARTAN
stroke?
Syndrome of RAPID onset of neurological deficit caused by focal, cerebral,
spinal or retinal INFARCTION
- Characterised by RAPIDLY DEVELOPING signs of focal or global disturbance
of cerebral functions, lasting for MORE THAN 24HRS or leading to death
stroke epidemiology?
M>F
increasing age
higher in Asian and black African
aetiology of stroke?
- Ischaemic/infarction account for 80% of strokes
- Haemorrhagic account for 17% of strokes
pathophysiology go stroke?
- Ischaemic (70%):
• Arterial disease and atherosclerosis is the main pathological process - Haemorrhagic (17%):
• Hypertension resulting in micro aneurysm rupture (Charcot-Bouchard
aneurysms)
clinica presentation of stroke?
- Anterior cerebral artery (ACA) territory:
• Leg weakness (more likely than arm weakness
since more of leg in ACA - Middle cerebral artery (MCA) territory:
• CONTRALATERAL ARM & LEG WEAKNESS - hemianopia
- Posterior cerebral artery (PCA) territory - visual issues:
• CONTRALATERAL HOMONYMOUS HEMIANOPIA
(loss of half the vision of the same side in both
eyes
investigations of stroke?
- Urgent CT head/MRI head BEFORE TREATMENT:
• Urgent if suspected cerebellar stroke, unusual presentation (i.e.
alternative diagnosis likely), high risk of haemorrhage (low GCS and
signs of raised ICP)
• To rule out haemorrhagic stroke before starting thrombolysis - Pulse, BP & ECG:
• Look for AF - Bloods:
• FBC: look for thrombocytopenia & polycthaemia
treatment for stroke?
• Treatment:
- Maximise reversible ischaemic tissue:
• Ensure hydration
• Keep O2 sats > 95%
ischemic
• Give tissue plasminogen activator e.g. IV ALTEPLASE
• Then start antiplatelet therapy e.g. CLOPIDOGREL 24hrs after
thrombolysis
haemorragic
• Antiplatelets contraindicated
• Any anticoagulants should be reversed for Warfarin reversal use
BERIPLEX and VITAMIN K
• Control hypertension
• Manual decompression of raised ICP, can also reduce ICP by giving
diuretic e.g. MANNITOL
subarachnoid haemorrhage
- Spontaneous bleeding into the subarachnoid space - between the arachnoid
layer of the meninges and the pia mater - Can often be catastrophic
subarachnoid haemorrhage
- Spontaneous bleeding into the subarachnoid space - between the arachnoid
layer of the meninges and the pia mater - Can often be catastrophic
epidemiology of subarachnoid haemorrhage?
- Typical age 35-65
- most common = berry aneurysm
aetiology of subarachnoid haemorrhage?
- Rupture of saccular aneurysms (80%) e.g. berry aneurysms
- Atriovenous malformation (AVM) (10%)
- no cause found eg, tumours or bleeding disorder
risk factors for subarachnoid haemorrhage?
- hyper tension
- family history
- PCKD, eheler danlos
- smoking
pathophysiology of subarachnoid haemorrhage?
- Most common cause is ruptured aneurysm which leads to tissue ischaemia
(since less blood can reach tissue) as well as rapid raised ICP as the blood
(fast flowing since arterial), acts like a space-occupying lesion, puts
pressure on the brain, resulting in deficits if not resolved quickly
clinical presentation of subarachnoid haemorrhage?
- SUDDEN ONSET severe OCCIPITAL headache - ‘thunder clap’, like being
kicked in the head, SEVERE PAIN 12/10!! - Vomiting, collapse, seizures and coma often follow
- papiloedema
signs
- Kernig’s sign (unable to extend patients leg at
the knee when the thigh is flexed)
- Brudzinski’s sign (when patients neck is flexed
by doctor, patient will flex their hips & knees)
investigations of subarachnoid haemorrhage?
- ABG
- Head CT - GOLD STANDARD DIAGNOSTIC:
• Detects >90% of SAH within 1st 48hrs
• Seen as a ‘star shaped lesion’ due to blood filling in gyro patterns
around the brain and ventricles
- Head CT - GOLD STANDARD DIAGNOSTIC:
- lumber puncture - • Xanthochromia ( due to breakdown products of Hb -> bilirubin)
treatment of subarachnoid haemorrhage?
- Maintain cerebral perfusion by keeping well hydrated (IV FLUIDS) and aim
for BP < 160mmHg - Administer Ca2+ blocker to reduce vasospasm and consequent morbidity
from cerebral ischaemia e.g. IV/ORAL NIMODIPINE - Endovascular coiling:
• Preferred to surgical clipping since has lower complication rate where
possible
• Promotes thrombosis and ablation of aneurysm
• FIRST LINE TREATMENT
subdural haemorrhage?
• Caused by the accumulation of blood in the subdural space - between the
arachnoid and dura mater following rupture of a BRIDGING VEIN between cortex
and venous sinus (vulnerable to deceleration injury)
epidemiology of subdural haemorrhage
- MOST COMMON where patient has a small brain e.g. alcoholics or dementia
etc. or babies that have suffered a trauma or elderly that have brain atrophy
that makes the bridging veins more vulnerable
pathophysiology of subdural haemorrhage?
- Trauma either due to deceleration due to violent injury or due to dural
metastases results in bleeding from bridging veins between the cortex and
venous sinuses - Bridging veins bleed and form a haematoma (solid swelling of clotted blood)
between the dura and arachnoid - this reduces pressure and bleeding stops - Days/weeks later the haematoma starts to autolyse due to the massive
increase in oncotic and osmotic pressure thus water is sucked into the
haematoma resulting in the haematoma enlarging - This results in a gradual rise in intra-cranial pressure (ICP) over many weeks
- Shifting midline structures away from the side of the clot and if untreated
leads to eventual tectorial herniation and coning (brain herniates through
foramen magnum - causes significant damage)
clinical presentation of subdural haemorrhage?
- Interval between injury and symptoms can be days to weeks or months
- Fluctuating level of consciousness (35%) +/- insidious physical or
intellectual slowing - Sleepiness
- Headache
- Personality change
- Signs of raised ICP e.g. headache, vomiting, nausea, seizure and raised BP
investigations of subdural haemorrhage?
- CT head:
• Diffuse spreading, hyperdense CRESCENT SHAPED
collection of blood over 1 hemisphere: - SICKLE/CRESCENT SHAPE DIFFERENTIATES subdural blood
from extradural haemorrhage!!
treatment of subdural haemorrhage?
- Assess and manage ABCs, prioritise head CT
- Stabilise patient
- IV MANNITOL to reduce ICP
extradural haemorrhage?
• Collection of blood between the dura mater and the bone usually cause by head
injury
aetiology of extradural haemorrhage?
- MOST COMMONLY due to a traumatic head injury resulting in fracture of the
temporal or parietal bone causing laceration of the MIDDLE MENINGEAL
ARTERY, typically after trauma to the temple
epidemiology of extradural haemorrhage?
- Usually occurs in young adults (rare < 2 and > 60)
pathophysiology of extradural haemorrhage?
- Blood accumulates RAPIDLY over minutes-hours between the bone and
dura
clinical presentation of extradural haemorrhage?
• Head injury
• Brief post-traumatic loss of consciousness or initial drowsiness
- Severe headache, nausea and vomiting, confusion and seizures - due to
rising ICP +/- hemiparesis (weakness of half the side of the body) with brisk
reflexes (faster than usual)
investigations of extradural haemorrhage
CT • Shows hyperdense haematoma that is biconvex/lense
shaped/lemon shaped and adjacent to the skull:
- Blood forms a more rounded shape compared with the sickle-
shaped subdural haematomas as the tough dural attachments to
the skull keep it more localised
treatment of extradural haemorrhage?
- ABCDE emergency management - asses and stabilise patient
- Give IV MANNITOL if increased ICP
epilepsy?
- The recurrent tendency to spontaneous, intermittent, abnormal electrical
activity in part of the brain, manifesting in seizures
chronic disorder >2 seizures
