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CSF, Hydrocephalus and LP Flashcards

1
Q

Definition of hydrocephalus

A

A general condition whereby there is an excess CSF within the intracranial space and specifically, the intraventricular spaces within the brain - causing dilatation of the ventricles and a wide range of symptoms

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2
Q

Where is the majority of CSF produced by?

A

Choroid plexus

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3
Q

How is CSF produced?

A

Metabolically active process within the brain (requires ATP) whereby sodium is pumped into the subarachnoid space, and water follows from the blood vessels

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4
Q

Where is choroid plexus located?

A 
Lateral ventricles
- temporal horn roofs
- floor of bodies
Posterior 3rd ventricle roof
Caudal 4th ventricle roof
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5
Q

Where is the biggest choroid plexus found?

A

Lateral ventricle

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6
Q

What is the mechanism of CSF flow?

A

Flows from the two lateral ventricles into the 3rd ventricle (through the foramen of munro) then down the aqueduct into the 4th ventricle.
Then out through the megendie foramen (single and midline) and two Luschcka foramen (lateral)
After exiting the 4th ventricle, flows through subarachnoid space over and around the brain and spinal cord and is eventually reabsorbed into the venous system through numerous arachnoid granulations along the dural venous sinuses (esp the superior sagital sinus

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7
Q

How many cc’s does an average adult brain produce?

A

450 - 600 ccs

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8
Q

Normally, production of CSF = what?

A

Resorption of CSF

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9
Q

What do arachnoid granulations contain?

A

Arachnoid villi

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10
Q

Two types of hydrocephalus

A 
Communicating hydrocephalus (CoH)
Non communicating hydrocephalus (NCH)
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11
Q

What is communicating hydrocephalus also known as?

A

Non obstructive hydrocephalus

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12
Q

What is non communicating hydrocephalus also known as?

A

Obstructive hydrocephalus

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13
Q

What is communicating hydrocephalus?

A

CSF pathway open from “start to finish”, meaning CSF can travel freely from the choroid plexus to the arachnoid granulations, then you have “no obstruction” and a communicating hydrocephalus

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14
Q

What is non communicating hydrocephalus?

A

If CSF cannot travel freely from start to finish, then youve got an “obstruction” and non communicating hydrocephalus

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15
Q

What does communicating hydrocephalus usually represent a problem with?

A

CSF reabsorption - which cannot keep up with the rate of CSF production

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16
Q

Result of communicating hydrocephalus

A

As the ventricular system dilates uniformly, the ICP rises

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17
Q

Pathology of communicating hydrocephalus

A

Underabsorption of CSF

Overproduction of CSF (RARE)

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18
Q

Presentation of communicating hydrocephalus

A

Young children whose sutures havent fused yet
- disproportional increased in head circumference
- failure to thrive
Children with fused sutures / adults
- symptoms of increased ICP; Headache, nausea and vomiting, gait distrubance, 6th cranial nerve palsy, papilloedema, upgaze difficulty

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19
Q

Causes of Communicating hydrocephalus

A

Infection (e.g. bacterial meningitis)
Subarachnoid haemorrhage (blood and blood breakdown products cause scarring of arachnoid granulations)
Post op
Head trauma

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20
Q

Causes of non communicating hydrocephalus

A 
Aqueductal stenosis
Tumours / cancers / metastases
Cysts
Infection 
Haemorrhage/haematoma 
Congenital malformations/conditions
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21
Q

How quickly do the symptoms of non communicating hydrocephalus come on?

A 
Processes that have developed over long periods of time - more gradual symptoms (i.e. masses etc)
Acute processes (i.e. intraventricular bleed) can cause acute obstruction with rapid mental status decline
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22
Q

What is the earliest radiographic finding of non communicating hydrocephalus?

A

Dilatation of temporal horns of the lateral ventricles

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23
Q

Radiographic findings of non communicating hydrocephalus

A

First dilatation of temporal horns
Third ventricle becomes ballooned
Lateral ventricle will increase in size
Peripheral sulci effaced

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24
Q

An evans ratio greater than or equal to 0.3 defines what?

A

Ventriculomegaly

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25
Q

Treatment of acute hydrocephalus

A

Urgent or emergency placement of extra ventricular drain (EVD)

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26
Q

How does an EVD work?

A

Catheter passed through the patient’s scalp and skull into the lateral ventricle, that drains CSF to a collecting system kept at the patients bedside

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27
Q

Treatment of communicating hydrocephalus

A

Shunt placement

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28
Q

Types of shunt used to treat communicating hydrocephalus

A

Ventriculo-peritoneal
Lumbar peritoneal
Ventricular atrio

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29
Q

What is the most common type of shunt used in communicating hydrocephalus?

A

Ventriculo-peritoneal shunt

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30
Q

Treatment of non communicating hydrocephalus

A

Removing obstructive lesion
+/- Shunt
Possibly a third ventriculostomy

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31
Q

How does a third ventriculostomy work?

A

Often performed in conjunction with BP shunt placement
Hole is opened surgically in the floor of the third ventricle so CSF flows out into the interpeduncular cistern and pre-pontine space (bypasses cerebral aqueduct)

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32
Q

Causes of VP shunt failure

A 
Mechanical failure from occlusion/disconnection 
Migration 
Overdrainage/underdrainage 
Infection 
Skin erosion
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33
Q

What % of shunts fail 5 years after placement?

A

50%

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34
Q

What % of shunts can fail in the first year?

A

40%

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35
Q

What does NPH stand for?

A

Normal pressure hydrocephalus

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36
Q

What is NPH a rare preventable cause of?

A

Dementia

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37
Q

Classic triad of NPH

A

Wet, wobbly and wacky

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38
Q

Presentation of NPH

A 
Urinary incontinence
Gait disturbance 
- wide stance
- short, shuffling steps 
Quickly progressive dementia
39
Q

What is usually the first symptom to present of NPH?

A

Gait disturbance

40
Q

Investigations of NPH

A

CT/MRI
LP
- normal opening pressure

41
Q

What do symptoms of NPH improve with?

A

CSF removal

42
Q

Treatment of NPH

A

VP shunt placement

43
Q

Prognosis of NPH

A

Outcome improved if symptoms been present for shorter period of time

44
Q

What is the least likely symptom of NPH to improve with shunting?

45
Q

What position should the patient be in for LP?

A

Lateral decubitus position

46
Q

What level does the spinal cord end?

47
Q

What level are LPs done at?

A

L3-L4 or L4-L5

48
Q

What position are infants held in for LP?

A

Seated position with maximal spinal flexion

49
Q

Indications for LP; to obtain CSF for the diagnosis of…..

A 
Meningitis (WCC)
Meningoencephalitis (WCC)
SAH (bilirubin)
Malignancy 
Idiopathic intracranial HTN
Other neurological syndromes
Infusion (e.g. NPH studies) of drugs or contrast
50
Q

Contraindications for LP

A

Unstable patient with CVS or Resp system instability
Localized skin/soft tissue infection over puncture site
Evidence of unstable bleeding disorder
Platelets < 50,000 or clotting factor deficiency
For bleeding diathesis
Increased intracranial pressure
Caution in patients with chiari malformations

51
Q

Complications of LP

A 
Headache 
Apnea 
Back pain 
Bleeding or fluid leak around the spinal cord
Infection 
Pain 
Haematoma 
Ocular muscle palsy (transient)
Nerve trauma 
Brainstem herniation 
Subarachnoid epidermal cyst
52
Q

Who is headache after LP uncommon in?

53
Q

What is the most common complication of LP?

A

Spinal headache

54
Q

Risk factors for spinal headache post LP

A 
Female
Age 18-30 
Lower BMI
History of Headache 
Prior spinal headache
55
Q

Features of spinal headache post LP

A

Bilateral

Improves when supine

56
Q

Treatment of spinal headache post LP

A

Supine position for at least 2 hours
Hydration
Caffeine either PO or IV
Epidural blood patch

57
Q

Prevention of spinal headache

A

Passing needle bevel parallel to longitudinal fibres of the dura
Replacing stylet before removing needle
Using smaller diameter needes
Using atraumatic needles

58
Q

Presentation of nerve root trauma/irritation

A

Electric shocks
Dysesthesias
Back pain persistent for months

59
Q

If cause nerve root irritation during LP, what should be done?

A

Withdraw needle immediately

If pain or motor weakness persists, start corticosteriods

60
Q

What should be scheduled if nerve root pain continues after trauma?

A

Electromyogram/nerve conduction velocity studies

61
Q

What does brain herniation manifest as?

A

Altered mental status
Followed by cranial nerve abnormalities
Cushings triad
May be rapidly fatal

62
Q

Treatment of brain herniation due to LP

A

Immediately remove the needle and raise the head of the bed to 30 - 45 degrees to improve venous return from the brain
Mannitol or 3% saline
Intubate patient and ventilate
Emergency neurosurgical consult

63
Q

When does an epidual inclusion cyst occur?

A

Occurs when a core of skin is driven into spinal or paraspinal space with a hollow needle
Rare due to use of stylet

64
Q

What does CSF look like?

A

Clear

Colourless

65
Q

Opening pressure of CSF

A

6 - 16 MM/H20

66
Q

Protein level of CSF

67
Q

Glucose level of CSF

68
Q

WCC of CSF

69
Q

Who is idiopathic intracranial HTN often seen in?

A

Young, overweight females

70
Q

Risk factors for idiopathic intracranial HTN

A

Obesity
Female
Pregnancy
Drugs - OCP, sterioids, tetracycline, vit A, lithium

71
Q

Presentation of idiopathic intracranial HTN

A 
Headache
Blurred vision 
Papilloedema
Enlarged blind spot
Sixth nerve palsy may be present
72
Q

Treatment of idiopathic intracranial HTN

A 
Weight loss
Diuretics
Topiramate 
Repeated LP
Surgery - to prevent optic nerve damage (decompression of optic nerve and fenestration) and can also insert a shunt
73
Q

What is normal pressure hydrocephalus a reversible cause of in the elderly?

74
Q

What is normal pressure hydrocephalus secondary to? What else could it be secondary to?

A

Reduced CSF absorption at the arachnoidal villi - most common
Head injury
SAH
Meningitis

75
Q

Classic triad of normal pressure hydrocephalus

A
  1. Urinary incontinence
  2. Dementia and bradyphrenia
  3. Gait abnormality (may be similar to PD)
76
Q

Definition of bradyphrenia

A

Slowness of thought

77
Q

How long a time period do the symptoms of hydrocephalus develop over?

78
Q

Investigations for normal pressure hydrocephalus

A

Imaging

  • enlarged 4th ventricle
  • ventriculomegaly
  • absence of substantial sulcal atrophy
79
Q

Management of normal pressure hydrocephalus

A

Ventriculoperitoneal shunting

80
Q

What % of patients with shunts experience significant complications and what are these complications?

A

10%
Seizures
Infection
ICH

81
Q

What is syringomyelia?

A

A collection of CSF within the spinal cord

82
Q

Causes of syringomyelia

A

Chiari malformation (STRONG association)
Trauma
Tumours
Idiopathic

83
Q

Presentation of syringomyelia

A

Neck and arms loss of sensation to temp but preservation of light touch, proprioception and vibration
Spastic weakness (predominantly of upper limbs)
Paraesthesia
Neuropathic pain
Upgoing plantars
Bowel and bladder dysfunction

84
Q

What may occur over years if syringomyelia is not treated?

A 
Scoliosis 
Horners syndrome (rare)
85
Q

Investigations of syringomyelia

A 
Full spine MRI (to exclude tumours or tethered cord)
Brain MRI (chiari malformation)
86
Q

Treatment of syringomyelia

A

Treat cause

If symptomatic or persistent - a shunt can be placed into it

87
Q

Treatment of idiopathic intracranial hypertension

A

Acetazolamide

88
Q

What does an isolated result of high protein in the CSF indicate?

A

Guillian barre syndrome

89
Q

Types of cerebral oedema

A

Vasogenic
Cytotoxic
Interstitial

90
Q

Pathology of vasogenic cerebral oedema

A

Increased capillary permeability

91
Q

Causes of vasogenic cerebral oedema

A

Trauma
Tumour
Ischaemia
Infarction

92
Q

Causes of cytotoxic cerebral oedema

93
Q

Causes of interstitial cerebral oedema

A

Obstructive hydrocephalus

Hyponatraemia

Neuro Pathology (21 decks)

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