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FRCS Part 2 > Hydrocephalus > Flashcards

Hydrocephalus Flashcards

1
Q

What is the definition of hydrocephalus?

A

An abnormal accumulation of CSF within the ventricles

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2
Q

What is the prevalence of hydrocephalus?

A

1-1.5% overall and 1/1000 for congenital hydrocephalus

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3
Q

What are the congenital causes of hydrocephalus?

A

Chiari 1 and 2 Aqueductal stenosis Dandy Walker malformation X-linked inherited disorder

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4
Q

What are the acquired causes of hydrocephalus?

A

Infection SAH / IVH Neoplastic obstruction Post-op (iatrogenic)

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5
Q

What are the symptoms or raised ICP?

A

Headache Papilloedema N&V Gait ataxia 6th nerve palsy Up-gaze palsy

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6
Q

How does hydrocephalus present in children?

A

Enlarged OFC Irritiability / poor feeding / poor head control Bulging fontanelle Frontal bossing Engorged scalp veins Sun setting 6th nerve palsy Crack pot skull Splaying of the sutures

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7
Q

What is the normal OFC?

A

Same as crown to rump length

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8
Q

When should changes in OFC signify further investigation?

A

If crossing centiles (curves) on growth chart OFC >2 S.D. above normal Head circumference out of proportion to body length

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9
Q

Through which mechanisms can hydrocephalus cause blindness?

A

Papilloedema causing optic nerve damage PCA infarction from herniation 3rd ventricle dilatation compressing the optic chiasm

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10
Q

What are Lundberg waves?

A

Describe mean ICP patterns in patients

A = mean wave ICP >50 mmHg lasting between 5-20 minutes. Suggests ICP exceeding cerebral compliance

B = mean wave ICP 20-50 lasting < 5 minutes. Seen in sleep.

C = mean wave ICP < 20 occuring every 10 seconds. Due to oscillations in baroR and chemoR control.

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11
Q

What are the characteristics of pregeniculate blindness?

A

Marked optic nerve atrophy Loss of pupillary reflex

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12
Q

What does postgeniculate injury cause?

A

Cortical blindness. May be associated with Anton’s syndrome (denial of the deficit) and Ridoch’s phenomenon (appreciation of moving but no stationary objects)

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13
Q

What is the blood supply to the occipital pole?

A

MCA and PCA - hence why there is macular sparing with PCA infarcts

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14
Q

What imaging features are suggestive of hydrocephalus?

A
  1. Temporal horn diameter >2mm with barely visible sylvian fissure 2. Temporal horn diameter >2mm and FH/ID ratio >0.5 3. Ballooning of the 3rd ventricle 4. Periventricular oedema 5. Evan’s ratio 6. Thinning or bowing of the corpus callosum
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15
Q

What is Evan’s ratio?

A

FH diameter divided by biparietal diameter. If >0.3 then suggests hydrocephalus

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16
Q

What are the causes of pseudohydrocephalus?

A

Ex vacuo hydrocephalus - due to cerebral atrophy Agenesis of the CC Septo-optic dysplasia Hydranencephaly

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17
Q

What is external hydrocephalus?

A

Enlarged subarachnoid spaces and increased OFCs. Usually ventricles are also mildly dilated.

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18
Q

What are the features of chronic hydrocephalus?

A

Beaten copper cranium Empty sella Erosion of the dorsum sella Macrocrania Atrophy of corpus callosum Suture diastasis or delayed closure in infants

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19
Q

How can external hydrocephalus be distinguished from chronic subdural collections?

A

Cortical vein sign - these are seen with external hydrocephalus but not with chronic subdural collections

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20
Q

What is the pathophysiology of X-linked hydrocephalus?

A

X-linked so only affects males. Females are asymptomatic carriers. L1CAM mutation - integrin cell adhesion molecule important for axonal migration. Causes L1 syndromes.

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21
Q

What are L1 syndromes?

A

CRASH = corpus callosum hypoplasia, retardation, adducted thumbs, spastic paralysis and hydrocephalus due to aqueductal stenosis. Other features are aphasia, shuffling gait, vermis hypoplasia etc

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22
Q

What feature is pathognomonic of L1 syndrome?

A

Rippled ventricular wall after VP shunt insertion

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23
Q

What is arrested hydrocephalus?

A

Where there is no progression or deleterious sequelae of the hydrocephalus (may decompensate in the future). There should be near normal ventricle size, normal head growth curve and continued development.

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24
Q

What groups of patients are most likely to develop a trapped 4th ventricle?

A

Chronic lateral ventricle shunting, Fungal intracranial infection and Dandy walker malformation

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25
Q

How can a trapped 4th ventricle be shunted?

A
  1. Insertion under direct vision from below the tonsils (through Fr. Magandie) - this is preferred 2. Through the cerebellar hemisphere (risk of damage to the floor of the 4th ventricle by the catheter) 3. Torkildsen shunt (ventriculocisternal shunt)
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26
Q

What is the triad of NPH>

A

Gait ataxia Incontinence Dementia

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27
Q

When was NPH first described?

A

1965 aka Hakim-Adams syndrome

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28
Q

What are the causes of a secondary NPH?

A

Post-SAH Post-meningitis After posterior fossa surgery After radiotherapy

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29
Q

What are the characteristics of gait disturbance in NPH?

A

Wide based gait, short shuffling steps and unsteady with turning aka magnetic gait. Retropulsion and frequent falls. Truncal ataxia is absent.

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30
Q

What is the classical feature of incontinence associated with NPH?

A

Urgency with impaired ability to inhibit bladder emptying. Incontinence without awareness would suggest another cause.

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31
Q

What are the NPH mimics that need to be investigated?

A

AD / PD incl PSP and MSA Huntington’s disease Lewy body dementia FTD ALS CJD Vascular dementia Lyme / HIV / Syphilis Urological disorders / UTI

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32
Q

How would you investigate a patient with NPH?

A

Dementia screening bloods (FBC, U&E, B12, Folate, TSH, Vit D) Neuropsychology MRI of head and spine (rule out myelopathy) Urodynamic testing (Syphilis and Lyme testing only if clinical suspicion)

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33
Q

What features on MRI are consistent with a favourable response to shunting in NPH?

A

Based on the iNPH Radscale: No cerebral atrophy (suggests AD) Periventricular oedema Convexity crowding / DESH Rounding of the frontal horns Acute callosal angle <90 deg Cine MRI may demonstrate hyperdynamic CSF flow through the aqueduct

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34
Q

What is the normal OP on LP in the left lateral position?

A

10-15 cmH20

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35
Q

What is the average OP in NPH?

A

15cmH20 (upper limit for NPH is 24cmH20). Those with OP >10 have a higher shunt response rate.

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36
Q

What are Lundberg B waves?

A

Slow increases in ICP lasting 20 sec to 2 minutes. If Lundberg B waves are present for >80% of the ICP monitoring time is suggestive that shunting will be helpful in NPH.

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37
Q

How can CSF absorption resistance be measured?

A

Infusion studies

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38
Q

What is the management algorithm for NPH?

A

Clinical history/examination Neuropsychology Imaging Lumbar drainage (5 days) better than Tap test Continuous CSF pressure monitoring

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39
Q

What are the diagnostic guidelines for probable NPH?

A

Chronic / progressive >40 years Duration of symptoms >6 months No cause for secondary hydrocephalus No other explanation for symptoms Evan’s >0.3 Supportive MRI features LP<24cmH20 Clinical features of gait imbalance + cognitive impairment or urinary dysfunction

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40
Q

What shunt valve would you use in NPH?

A

Programmable so pressures can be reduced gradually reducing the chance of subdural haemorrhages. If not available then a medium fixed pressure shunt.

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41
Q

What are the complications of shunting in NPH?

A

Infection Subdural haemorrhages ICH Seizures Shunt malfunction / failure

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42
Q

What is the therapeutic benefit of ETV in NPH?

A

Reported to be 70%

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43
Q

Which symptoms improve most with shunting in NPH?

A

Urinary > gait > dementia

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44
Q

What factors give the best response in NPH shunting?

A

Clinical triad LP OP>10 Lundberg B waves on continuous pressure monitoring MRI - DESH

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45
Q

What does shunt failure in pregnancy mimic?

A

Pre-eclampsia (headache, N&V, seizures etc)

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46
Q

How would you investigate shunt failure in pregnancy>

A

MRI Shunt tap

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47
Q

How would you shunt a gravid patient with hydrocephalus?

A

1st trimester - peritoneal shunt 2/3rd trimester - pleural shunt

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48
Q

Should prophylactic abx be given during delivery for patients with a shunt?

A

Yes - reduces the risk of shunt infection. Normal vaginal delivery is performed if patient is well. C-section if become symptomatic of hydrocephalus

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49
Q

What is Binswanger’s disease?

A

Subacute vascular dementia - produces a frontal dysexecutive symptom

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50
Q

What proportion of dementia is due to NPH?

A

5% so rule out Alzheimer’s disease first!

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51
Q

What is an abnormal bicaudate ratio?

A

>0.25

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52
Q

In NPH what does continuous ICP monitoring demonstrate?

A

Waves of increased ICP during REM sleep called B waves. These result in enlargement of the ventricles.

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53
Q

How do you measure CSF outflow resistance?

A

Lumbar infusion test. An outflow resistance >18 mmHg/ml/min was 87% specific for NPH

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54
Q

What are the risks of endoscopic aqueductoplasty?

A

Damage to the periaqueductal gray, dysconjugate gaze, parinaud syndrome and cranial nerve palsies. Retrograde aqueductoplasty can be performed if the ventricles are small.

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55
Q

Does unilateral optic nerve sheath fenestration improve vision in both eyes?

A

YES

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56
Q

What is the failure rate of LP shunts in IIH?

A

50%

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57
Q

What is the most efficacious treatment for acute visual deterioration in IIH/

A

Optic nerve sheath fenestration > VP shunt insertion

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58
Q

Which valve types show a sigmoid pressure flow curve?

A

Flow regulated devices e.g. Integra Orbis-Sigma II

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59
Q

What is the lower limit of normal ICP when standing?

A

-8mmHg

60
Q

What organism is most likely to cause shunt infection?

A

Staph. epidermidis

61
Q

What organism is most likely to cause a delayed shunt infection?

A

Proprionobacterium / Corynebacterium

62
Q

How do you manage VP shunt infection?

A

IV abx, removal of all hardware and EVD insertion followed by reimplantation when CSF is sterile

63
Q

Why can patients become bradycardic during ETV?

A

During perforation of the 3rd ventricular floor irrigation can cause a Cushing’s response. Stimulation of the pre-optic area and hypothalamus can cause tachycardia. Memory loss can result from damage to the fornix.

64
Q

What are the theories for syrinx formation in Chiari?

A

Waterhammer theory Craniospinal dissociation theory Piston theory Virchow-Robin space theory

65
Q

What are the causes of macrocephaly?

A

Familial (most common)

Hydrocephalus (aqueduct stenosis or post-meningitis)

Benign Enlargement of the Subarachnoid Spaces

Neurophakomatosis (due to increase in brain volume)

Haemorrhage

AVM (due to venous hypertension)

Cyst/Tumour

Endocrine causes (hypoparathyroidism and adrenal insufficiency)

66
Q

What is the risk of a shunt tap causing an infection?

A

2 in 1000

67
Q

What is thought to be the underlying etiology of BESS?

A

Immaturity of the arachnoid villi

68
Q

What is the triad of shaken baby syndrome?

A

Subdural haemorrhages

Retinal haemorrhages

Encephalopathy

69
Q

What are the MRI findings associated with aqueductal stenosis?

A

Ventriculomegaly affecting the lateral and third ventricles but not the 4th ventricle and signs of increased ICP e.g. periventricular oedema.

70
Q

What are the possible surgical treatments for a patient with aqueductal stenosis?

A

CSF diversion through a: 1) VP shunt or 2) ETV.

ETV requires a functioning CSF absorption pathway distal to the obstruction and avoids the complications of overdrainage.

71
Q

What are the risks of ETV?

A

Early or late failure, fornix injury, ICH, hypothalamic injury, basilar artery injury and uncontrollable bleeding.

72
Q

What is the ETV success score?

A

Age: <1 month = 0, 1-6 months = 10, 6-12 moths = 30, 1-10 years = 40 and >10 years = 50

Etiology: Infection = 0, MMC/IVH/tumour = 20, Aqueductal stenosis = 30

Shunt previously: No = 10

Provides the 6 month ETV success rate.

73
Q

What are the features of CSF infection in a young child?

A

Fever, bulging fontanel, somnolent, irritable or obtunded.

74
Q

How would you investigate a child with a shunt, fever and bulging fontanel?

A

CT scan if signs of raised ICP, tap the shunt for CSF MC&S and full septic screen incl. CXR, urinalysis, BCs etc.

75
Q

What is the most common cause of shunt infection within 6 months of insertion?

A

Skin colonisation (gram positive cocci) from the time of surgery.

76
Q

How would you treat a child with an early shunt infection?

A

Systemic antibiotics and externalisation of the shunt. Externalisation is through removal of the catheter from the abdomen initially and then treatment with antibiotics until the CSF is clear / normal WCC and then replacement of the cranial catheter at a different site.

77
Q

What is the initial antibiotic regime of choice?

A

Ceftriaxone and Vancomycin +/- gentamicin.

78
Q

What is the rate of initial shunt infection in children?

A

10%

79
Q

What is the rate of shunt infection in children who have had a shunt infection previously?

A

25%

80
Q

What factors reduce the rate of shunt infections?

A

Double gloving, short duration of surgery, reduced manipulation of the hardware, antibiotic impregnated shunts etc.

81
Q

A young patient with a long standing VP shunt presents with headaches and slit ventricles. What is the cause of the headache?

A

Slit ventricle syndrome maybe from over-drainage of CSF or shunt failure (BIH type picture where the ventricles remain small even with small ventricles). ICP monitoring, CT head and shunt series and or nuclear medicine shuntogram can be performed. Opthalmology assessment for papilloedema.

82
Q

What is the management of slit ventricle syndrome in the absence of shunt malfunction?

A

With stable ventricle size and normal shunt function then referral to neurology for migraine treatment.

83
Q

What are the features of neonatal hydrocephalus?

A

Enlarged head circumference greater than the 97th percentile, bulging fontanel, splayed sutures and distended scalp veins. Always check for associated spinal dysraphism and skin changes for neurocutaneous syndromes!

84
Q

What are the surgical options for paediatric mega-hydrocephalus?

A

VP shunt, VA shunt or ETV +/- choroid plexus coagulation within 24-48 hours.

85
Q

What are the different shunt types that can be used in children?

A

Fixed or programmable shunts with or without anti-siphon devices.

86
Q

Which pressure should the shunt be initially set at (for a programmable shunt)?

A

This depends on the opening pressure from the ventricle.

87
Q

What are the complications of VP shunt insertion?

A

CSF leakage, overdrainage, skin / wound breakdown, cranial deformity (children only), SDH, shunt failure / infection, bowel injury if VP shunt and complications of anaesthesia.

88
Q

Post-shunting the child presents with a fluctuant subgaleal collection. What is the cause?

A

CSF leakage through the burr hole due to the lower resistance pathway than the shunt.

89
Q

How would you manage a child with CSF leak causing a subgaleal collection?

A

Revise the shunt with a lower pressure valve / adjust the setting to a lower pressure +/- repair the site to close the space between the shunt and the burr hole (with fascia and tissue sealant).

90
Q

Following shunting in a neonate the child develops positional plagiocephaly. What is the management?

A

Mulitpositional stimulation +/- correction bands and helmets initially. If still deformed by age of one year then a cranial reduction procedure with multiple cranial osteotomies and reconstruction can be performed.

91
Q

What is the LCAM1 mutation associated with?

A

X-linked hydrocephalus

92
Q

What is a birds nest appearance of distal shunt tubing associated with?

A

Migration of distal catheter out of the peritoneum into the subcutaneous tissue

93
Q

What rate do neonated produce CSF?

A

25 ml/day. This increases to adult capacity as a toddler.

94
Q

What rate do neonated produce CSF?

A

25 ml/day. This increases to adult capacity as a toddler.

95
Q

What is the pH of CSF?

A

7.33-7.35

96
Q

What proportion of CSF is produced by the choroid plexus?

A

80% Most of the rest of intracranial production occurs in the interstitial space. CSF is also produced by the ependymal lining of the ventricles, and in the spine, in the dura of the nerve root sleeves.

97
Q

What is the total volume of CSF in the newborn?

A

5ml (150ml in Adults)

98
Q

What is the production rate of CSF in newborns?

A

25ml/day (450-750ml/day in adults - 0.3ml/min)

99
Q

Most accurate way to confirm CSF leak?

A

Beta transferrin

100
Q

Where is Rosenmullers fossa?

A

Potential site of CSF leak found behind the openingo of the Eustachian tube. It is inferior to cavernous sinus and can be exposed by drilling off anterior clinoids to access ophthalmic artery aneurysms.

101
Q

What proportion of head injury patients have a CSF leak?

A

2-3%

102
Q

What proportion of CSF leaks resolve spontaneously?

A

70% within 1 week, the rest usually by 6 months. in non-traumatic leaks only 33% resolve spontaneously

103
Q

How would you investigate a CSF leak?

A

Hx, test with Beta transferrin, if CSF +ve the water soluble CT cisternogram (Iohexol) or intraoperatively with fluorescein

104
Q

Would you treat CSF leaks with prophylactic antibiotics?

A

Not for traumatic causes, as likely to resolve spontaneously

Prophylactic abx for CSF leak controversial - There was no difference in the incidence or morbidity of meningitis between treated and untreated patients. (Klastersky 1976 Surg Neurol)

Furthermore, the risk of selecting resistant strains appears real and is therefore usually avoided. (Spetzler 1986)

105
Q

How would you treat a spontaneous CSF leak?

A

Conservative

  • bed rest, avoid straining, blowing nose etc

Medical

  • can give acetazolamide 250 mg QDS if due to raised ICP (not otherwise)

Surgical

  • Lumbar drain
  • repair
106
Q

What are the indications for surgical intervention in CSF leaks?

A
  1. traumatic CSF leak that persists > 2 weeks in spite of non-surgical measures
  2. spontaneous leaks and those of delayed onset following trauma or surgery: usually require surgery because of a high incidence of recurrence
  3. leaks complicated by recurrent meningitis
107
Q

How does CSF protein vary with age?

A

Lowest at 1-2 years of age (15mg/dl) then increases preemie - 150 term - 80 young child 20 Young adult 30 senile 40

108
Q

What are the imaging findings seen in intracranial hypotension?

A

Remember ‘SEEPS’:

Sagging brain, pachymeningeal Enhancement, Engorged veins, Pituitary hyperaemia and Subdural collections

109
Q

How would you manage intracranial hypotension?

A

Identify site of leak: MRI head and whole spine, consider cisternogram if cranial or myleogram if spinal.

Conservative treatment options - bed rest, caffiene, hydration / IV fluids

Medical - Theophylline

Epidural blood patch

Surgical repair of CSF leak

110
Q

How can CSF leaks through the cribiform plate be repaired?

A

Extradural (endonasal)

Intradural (bifrontal bone flap)

111
Q

What visual field loss pattern is classical of raised intracranial pressure?

A

Restriction of the peripheral field and enlargement of the blind spot.

112
Q

Why do you request a CTV/MRV in patients with IIH?

A

To detect venous sinus thrombosis / stenosis

113
Q

Define pseudotumour cerebri / IIH?

A

ICP >20 cmH20 in the absence of an intracranial mass or infection. Often due to venous outflow obstruction.

114
Q

What is the cause of blindness with IIH?

A

Optic atrophy

115
Q

What are the management options for IIH?

A

Acetazolamide & diuretics (salt restriction) + methylprednisolone / weight loss incl bariatric surgery / optic nerve sheath fenestration / VP shunt / Sinus stenting and Subtemporal decompression

116
Q

What is the main demographic for IIH?

A

Women of childbearing age (3rd decade) Overweight

117
Q

Why does IIH occur?

A
  1. Reduced venous outflow 2. Hormonal theory - adipocytes > high estrogen > high CSF production rates
118
Q

What are the diagnostic criteria for IIH?

A

Modified Dandy criteria: No signs of symptoms of high ICP No localising signs except CN6 Normal CSF composition Normal/small ventricle size

119
Q

What symptoms and signs are related to IIH?

A

Headache, nausea, visual loss, diplopia, tinnitus, dizziness and neck stiffness. Worse with bending / valsalva. Transient visual obscurations. Papilloedema, loss of acuity, CN6 palsy and constricted visual fields.

120
Q

What are the main differentials that should be excluded before diagnosing IIH?

A

Venous sinus thrombosis (MRI/V) Chiari 1 (MRI) Intracranial infection (LP) Inflammatory CNS condition e.g. neurosarcoid / SLE (LP) Vascuilits (serum & LP)

121
Q

How do you investigate IIH?

A

MRI/V LP for OP and cell counts / biochemistry Routine bloods incl vasculitis screen Opthalmology BP to rule out hypertension

122
Q

What MRI findings suggest raised ICP in IIH?

A

Flattening of the optic discs Tortuosity of the optic nerve Enhancement of the optic nerve Distention of the subarachnoid spaces Empty sella Small sinuses Encephalocoeles

123
Q

How does acetazolamide work?

A

Carbonic anhydrase inhibitor Water reabsorption is by H20+CO2 forming H+ and HCO3-. The HCO3- and Na+ are cotransported. The Acetazolamide therefore prevents H20 and Na uptake.

124
Q

What shunts are placed in IIH patients?

A

VP or LP

125
Q

What is done for patients with IIH and visual loss despite VP shunting?

A

Optic nerve sheath fenestration or subtemporal decompression

126
Q

How do you perform a subtemporal decompression?

A

Bilateral ?mark incisions Splitting of the temporalis Craniectomy 3 cm diameter Expansion duraplasty Close muscle and skin

127
Q

What distinguishes empty sella syndrome from a sella arachnoid cyst?

A

In empty sella syndrome the infundibulum can be seen traversing the sella

128
Q

What is secondary empty sella syndrome?

A

Where resection of a pituitary mass causes the chiasm to kink into the sella causing visual dysfunction.

129
Q

What is the management algorithm for IIH?

A

Weight loss

Acetazolamide / low Na diet

VP shunt (LP shunts have a tendency to block or become displaced)

Subtemporal decompressions

Optic nerve sheath fenestration

Venous sinus stenting if pressure gradient across stenosis

130
Q

What questions should you ask a patient with a shunt?

A

Patient - cause of hydrocephalus

Shunt - where is the distal end (peritoneal, pleural, atrial), type of shunt and pressure setting, when it was inserted, last revision etc.

Symptoms associated with previous blockages, infection symptoms, abdominal pain.

131
Q

How do you clinically assess a patient with ?shunt malfunction?

A

GCS - level of alertness

Papilloedema

Fontanelle/suture splaying in young children

Dilated scalp veins

Up-gaze palsy

Reservoir depression

Erythema / pseudomeningocele around the valve

Shunt tap

Assess for any signs of infection

If there is any concern about the shunt function then a CT head and shunt series are required and compared to baseline.

132
Q

What are the possible findings with a shunt tap?

A

Opening pressure high - aspirates easily = distal block

Dry or poor aspiration = proximal block

Opening pressure low - aspirates easily = suggests functioning OK

Send for MCS and gram stain

133
Q

What is the cause of slit ventricle syndrome?

A

Poor ventricular compliance as a result of periventricular gliosis from chronic overdrainage. Due to LaPlace’s law (Wall tension = Pressure x Radius) a large pressure is required to dilate smaller ventricles.

134
Q

How do you manage a shunt infection?

A

Remove the shunt system

Place an EVD for CSF sampling and possibly intrathecal antibiotics

IV Vancomycin and meropenem

Identify the source of infection

Re-insert the shunt once the CSF is sterile

135
Q

What are the sources of shunt infection?

A

Inoculation at time of insertion - usually from the skin flora

Wound dehiscence / CSF leak

Contamination of the distal end (peritonitis)

Haematogenous (systemic sepsis)

136
Q

What is the BASICs trial?

A

Multicenter RCT. Antibiotic or silver versus standard VP shunt.

Antiobiotc impregnated catheters with Clindamycin and Rifamipicin.

Shunt infection rates with standard and silver catheters were 6% compared to 2% with antibiotic-impregnated. 25% in all groups had an adverse event associated with valve or catheter dysfunction.

No age restriction. Follow up time 6 months - 2 years.

137
Q

When should intrathecal antibiotics also be administrated?

A

Multi-drug resistant organisms.

138
Q

What is a normal WCC in the CSF?

A

<5. Slightly higher in neonates due to permeability of the BBB. If a bloody tap then the ratio to RBC = 1:500

139
Q

How sensitive is CSF gram stain?

A

60%

140
Q

What are the concerns about inserting a VP shunt in a child with very dilated ventricles?

A

Subdural haemorrhages. In such cases, a medium-high pressure valve (instead of a medium-low) should be considered. If the child develops a subdural then the valve will need to be temporarily tied off and the valve up-regulated (potentially with a programmable valve) after the subdural has resolved.

141
Q

What are the valve opening pressures for different fixed pressure valves?

A

Very low = 1

Low = 4

Medium low = 7

Medium high = 10

Hihg = 13

(they go up by 3 cmH20)

142
Q

What are the causes of a dissociated sensory loss in the extremities?

A

Syrinx, demyelination, inflammation or spinal cord tumour

143
Q

How do you investigate a patient with syrinx?

A

MRI of the brain and spine with contrast for spinal cord tumour, Chiari malformation and spinal cord tethering.

Flexion / ext xrays and CT scan if concerns over spinal cord instability.

144
Q

How do you treat a symptomatic syrinx associated with a chiari 1 malformation?

A

ICP monitoring. If ICP high then VP shunt.

If ICP normal then Foramen magnum decompression with expansion duroplasty +/- C1 laminectomy and tonsillopexy.

If FMD fails then syringo-subarachnoid shunt insertion through a midline dorsal myelotomy and pial retention suture..

145
Q

What are the causes of subdural hygromas after FMD?

A

Brain slump or hydrocephalus. If there are low pressure symptoms then likely due to slump due to large FMD. Treatment is post-fossa reconstruction or ventriculo-thecal shunt.

146
Q

What is the positive preditive value of CSF outflow resistance for VP shunt success in NPH?

A

92% if the CSF outflow resistance is >18mmHg/ml/min

147
Q

How do you perform an infusion study?

A

1 or 2 needles into the subarachnoid space/shunt reservoir connected to an infusion pump and pressure monitor. CSF is infused at 1.5ml/min and the increase in ICP is measured. Change in ICP divided by 1.5 = resistance to CSF outflow (normal is 12).

FRCS Part 2 (17 decks)

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