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Neurology > Delta: Trauma and CSF > Flashcards

Delta: Trauma and CSF Flashcards

1
Q

what causes decorticate posturing?

A 
severe brain damage to areas including 
- cerebrum
- internal capsule
- thalamus
(generally have sparing of midbrain)
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2
Q

what is decorticate posturing?

A

flexed arms
hands clenched into fists
legs extended and feet turned inwards
happens due to disruption of lateral corticospinal tracts so the rubrospinal tracts take over causing abnormal flexion of upper limbs and reticulospinal tract takes over causing abnormal extension of the lower limbs

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3
Q

what causes decerebrate posturing?

A

even more severe brain damage and brainstem damage
specifically at a level below the red nucleus in the midbrain
this causes damage to both the lateral corticospinal and rubrospinal tracts so on the reticulospinal tract takes over causing extension of the whole body

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4
Q

what is seen in decerebrate posturing?

A

head arched back

both arms and legs extended

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5
Q

eye opening categories of GCS?

A

spontaneous = 4
verbal command = 3
opens to painful stimuli = 2
none = 1

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6
Q

verbal response categories of GCS?

A 
orientated = 5
confused = 4
inappropriate words = 3
incomprehensible words = 2
none = 1
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7
Q

motor response categories of GCS?

A 
obeys = 6
localizes to pain = 5
withdraws to pain = 4
abnormal flexion (decorticate) = 3
abnormal extension (decerebrate) = 2
none = 1
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8
Q

total volume of CSF? how much is produced daily?

A 
total = 150ml
daily = 450-500ml
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9
Q

what is normal ICP?

A

5-15 mmHg when in the sulpine position

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10
Q

what are the 3 main intracranial components?

A

brain tissue (largest)
CSF
Blood
- compensatory mechanisms to maintain equilibrium between these 3 (if one decreases, other increases in volume to compensate and vice versa)

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11
Q

how does raised ICP affect autoregulation of cerebral blood flow?

A

impaired autoregulation
leads to decrease in CBF and CPP
this causes ischaemia, brain swelling and cerebral herniation

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12
Q

5 clinical features of raised ICP?

A

headache (usually worse on waking up, coughing etc)
nausea/vomiting
drowsiness
cushings triad

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13
Q

what is cushings triad?

A

hypertension
bradycardia
irregular, decreased respiration
(features of raised ICP)

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14
Q

what is uncal herniation and how does it present?

A

medial temporal lobe herniates through tentorium

  • blown pupil (CN III compression)
  • contralateral hemiparesis (compression of pyramidal tracts in crus cerebri)
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15
Q

what is a subfalcine herniation and how does it present?

A

herniation of the cingulate gyrus below falx cerebri

- may cause weakness in lower limbs due to compression of anterior cerebral artery

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16
Q

what is a tonsillar herniation and how does it present?

A

displacement of cerebellar tonsils into the foramen magnum

- can cause medullary compression and ischaemia characterised by neck stiffness, resp abnormalities and coma

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17
Q

what can cause a cerebellar tonsillar herniation?

A

Arnold chiari malformation

posterior fossa space occupying lesion

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18
Q

how may a central herniation of the brainstem present?

A

diplopia due to CN 6 palsy and brainstem dysfunction

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19
Q

which meningeal layer (s) are vascularised?

A 
dura = dural venous sinuses between periosteal and meningeal layers
pia = highly vascularised  to nourish underlying neural structures
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20
Q

what is the arachnoid mater made of?

A

connective tissue

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21
Q

what causes an extradural/epidural haematoma?

A

usually due to rupture of the middle meningeal artery in temporoparietal skull fracture (runs below pterion)
- therefore usually occurs in temporoparietal region but can be anywhere
blood accumulates between dura and bone, the haematoma expands with separation of dura from bone following trauma due to disrupted vessels

22
Q

typical clinical features of extradural haematoma?

A

usually young adult sustaining closed head trauma
brief loss of consciousness followed by period where patient regains consciousness and is normal for a while (Lucid interval) before rapidly deteriorating again
- headache
- vomiting
- contralateral hemiparesis (compression of cerebral peduncle)
- ipsilateral pupil dilation

23
Q

why does the rapid speed of decline in extradural haematoma support the diagnosis?

A

rapid decline = haematoma is from high pressure system (artery)
slower decline = haematoma from lower pressure system (vein)

24
Q

what imaging is used and what is seen on imaging in extradural haematoma?

A

CT

hyperdense lens shaped appearance

25
Q

how is an extradural haematoma managed?

A

immediate neurosurgical evacuation of haematoma if there is significant or ongoing neurological deficit
if small or neurologically intact, conservative measures can be used

26
Q

who is a subdural haematoma most common in?

A

most presentations are adults but more common in children due to absence of adhesions in subdural space which develop with ageing

27
Q

what causes an acute subdural haematoma?

A

acceleration/deceleration in the brain after high impact trauma causing rupture of bridging veins (veins that drain cortex and empty into dural venous sinuses)

28
Q

what happens in the brain in acute SDH?

A

cerebral blood flow can be reduced and the blood volume in the brain decreases as a result of compression with midline shift and cerebral oedema due to raised ICP

29
Q

what causes chronic SDH?

A

brain atrophy is main driver (ageing, alcoholism etc)

in atrophy, the bridging veins are stretched meaning that even minor trauma can cause them to rupture

30
Q

what happens in the brain in SBH?

A

ruptured veins cause accumulation of blood in subdural space
osmotic gradient forms which draws more fluid into that space
ICP rises causing decreased blood perfusion in the brain (causing symptoms to appear)
(inflammation and angiogenesis can also contribute)

31
Q

clinical features of SDH?

A 
acute = severely decreased state of consciousness
chronic = insidious course, headache and confusion, urinary incontinence, weakness, seizures, cognitive dysfunction and gait abnormalities
32
Q

what imaging is used and what is seen in SDH?

A

CT
acute = hyperdense crescent appearance (acute blood products)
chronic = hypodense crescent appearance

33
Q

what causes normal pressure hydrocephalus?

A 
impaired resorption or overproduction of CSF
mainly idiopathic but can be due to
- trauma
- meningitis
- subarachnoid haemorrhage
34
Q

clinical features of normal pressure hydrocephalus?

A 
normal opening pressure on lumbar puncture
patient has triad of:
- apraxia of gait (shuffling)
- dementia (can be reversible)
- urinary incontinence
35
Q

how is normal pressure hydrocephalus managed?

A

ventriculoperitoneal shunt
- usually reserved for patients with marked ventriculomegaly with severe symptoms or marked improvement after removal of CSF

36
Q

what is communicating hydrocephalus and what causes it?

A

enlargement of ventricles but with no obstruction of flow between ventricles and subarachnoid space
problem with CSF absorption due to impairment of arachnoid granulations

37
Q

what is non-communicating hydrocephalus and what causes it?

A

obstruction in the flow of CSF in ventricular system causing a back up of CSF leading to enlarged ventricles
commonly caused by tumours compressing ventricles, colloid cyst obstructing 3rd ventricle or stenosis of aqueduct

38
Q

what can be seen in non-communicating hydrocephalus?

A

4th ventricle is small in comparison to the 3rd and laterals

39
Q

clinical features of congenital hydrocephalus?

A 
failure to thrive
dilated scalp veins
increased head circumference 
impaired upgaze (due to compression of tectal plate)
sun setting appearance of eyes
raised ICP and diplopia
vomiting
Macewen sign (cracked pot/hyperresonant sound on head percussion)
40
Q

what can cause a congenital hydrocephalus?

A

mainly due to aqueductal stenosis
Arnold chiari malformation
spina bifida

41
Q

clinical features of acquired hydrocephalus?

A 
headaches (more prominent in mornings)
vomiting
diplopia
impaired upgaze
raised ICP
papilloedema
drowsiness
incontinence 
gait abnormalities
42
Q

how is hydrocephalus investigated?

A 
measure head circumference and fullness of anterior fontanelle
check for dilated scalp veins
ophthalmoscope
MRI = best diagnosis
CT can be used in an acute situation
43
Q

how is hydrocephalus managed?

A

CSF shunt if ventriculomegaly and evidence of raised ICP

44
Q

what is a chiari malformation?

A

congenital or acquired malformations of the hindbrain affecting the structural relationships between cerebellum, medulla and upper cervical spinal cord which causes impaired CSF circulation through foramen magnum

45
Q

what is chiari 1 malformation?

A

most common and least severe
caudal displacement of cerebellar tonsils below foramen magnum
- may have associated syringomyelia

46
Q

signs and symptoms of chiari 1 malformation?

A

headache (on coughing and neck extension)
downbeat nystagmus
central cord symptoms
may have ataxic gait

47
Q

what is chiari 2 malformation?

A

“Arnold chiari malformation”
less common but more severe
more common in children
caudal displacement of the cerebellum and medulla below the foramen magnum with herniation of 4th ventricle
association with myelomeningocoele (spina bifida)

48
Q

clinical features of chiari 2 malformations?

A

hydrocephalus and syringomyelia are common
tend to be symptomatic during infancy
severe brainstem dysfunction (dysphagia, apnoea, stridor and nystagmus)
weakness which may progress to quadriplegia

49
Q

how is chiari malformation managed?

A

surgical - suboccipital craniectomy and upper cervical laminectomy (decompress)
non-surgical if mild

50
Q

clinical features of idiopathic intracranial hypertension?

A

throbbing, worse in morning
papilloedema
nausea and vomiting
can have CN 6 palsy in few cases

51
Q

investigations in idiopathic intracranial hypertension?

A

CT or MRI - normal or reduced ventricle size (“slit like ventricles”)
visual fields and fundoscopy
lumbar puncture

52
Q

management in idiopathic intracranial hypertension?

A

weight loss
diuretics (e.g acetazolamide etc)
surgical - CSF shunt

Neurology (53 decks)

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