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Neurology > Hydrocephalus > Flashcards

Hydrocephalus Flashcards

1
Q

What are the normal values for CSF pressure?

A

Mean CSF pressure = 10mmHg >15mmHg represent abnormally high values

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2
Q

At what rate is CSD produced?

A

0.35ml/min = 20ml/hour = 500ml/day Largely independent of CPP (cerebral perfusion) and ICP Choroid plexus secretion is hypertonic to CSF (accounts for 3/4 of all CSF production)

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3
Q

CSF is produced in a circadian rhythm, at what time of day is it at it’s maximum and minimum respectively?

A

Maximum at 2am, minimum at 6pm

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4
Q

What can decrease CSF formation?

A

Production rate decreases in elderly. Acetazolamide reduced production by >50%

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5
Q

Where is CSF absorbed?

A

Via arachnoid granulations. Absorption is passive and depends upon the ICP being greater than the pressure in the sagittal sinus and on the resistance to outflow across the arachnoid granulations

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6
Q

What are the physical functions of CSF?

A

Buoyancy - reduces effective brain weight by 96% Accommodates physiological changes in vascular volumes in the head being displaced into the spinal canal ie. the mediator of compliance

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7
Q

What are the chemical functions of CSF?

A

Provides certain micro-nutrients to cerebral tissue e.g. vitamin C, thyroxine Clears some waste products of nerve cell metabolism e.g. 5HIAA Ionic homeostasis

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8
Q

What are some examples of CSF pathologies?

A

Hydrocephalus, spontaneous intracranial hypotension, syringomyelia, intracranial arachnoid cysts, Dandy Walker cysts, spinal arachnoid webs

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9
Q

What are the causes of spinal arachnoid webs?

A

May be idiopathic or secondary to previous inflammatory processes caused by infection or intracranial haemorrhage

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10
Q

What are some examples of pathologies where there is abnormal accumulation of water within the parenchyma of the CNS?

A

Cerebral oedema, benign intracranial hypertension, spinal dural arteriovenous fistulae, syringomyelia

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11
Q

How is hydrocephalus classified?

A

Obstructive vs communicating Infantile vs childhood/adult (acute or chronic)

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12
Q

What are the features of hydrocephalus from birth?

A

An unusually large head, a thin and shiny scalp with easily visible veins, a bulging or tense fontanelle, downward looking eyes

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13
Q

What can congenital hydrocephalus cause?

A

Poor feeding, irritability, vomiting, sleepiness, muscle stiffness and spasms in a baby’s lower limbs

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14
Q

When can congenital hydrocephalus be picked up?

A

Sometimes picked up before a baby is born during an ultrasound scan

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15
Q

What are some common causes of paediatric hydrocephalus?

A

Congenital - chiari malformation or spina bifida, aqueductal stenosis, Dandy-Walker complex, congenital arachnoid cysts, atresia of foramen of Munro Acquired causes - haemorrhage, infection, traumatic head injury, tumour

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16
Q

How long do ventriculoperitoneal shunt valves typically last?

A

Function satisfactory after insertion in 80% of cases but 80% are no longer functioning after 12 years 40% revision rate in first year!

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17
Q

What are complications of shunt valves?

A

Over-drainage - acute subdural haematomas (SDH), slit ventricles Under-drainage - blockage, displaced/disconnected catheter Infection - reduced by use of antibiotic or silver impregnated shunts., use iodine!! Intracerebral haemorrhage, seizures, craniosynostosis, umbilical fistula, ascites, hydrocele

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18
Q

What are the clinical features of a blocked shunt?

A

Headache and vomiting Sunsetting in children, lack of upward gaze in adults Blurred vision - papilloedema precedes blindness!

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19
Q

How is a blocked shunt managed?

A

Tap the shunt in extremes but can send CSF to microbiology CT head to show hydrocephalus Urgent surgery to replace shunt!

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20
Q

What can be used as an alternative to insertion of a shunt in some cases?

A

Endoscopic 3rd ventriculostomy (ETV)

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21
Q

What is the success rate for inserting an ETV?

A

Around 70% succeed with aqueduct stenosis and tumours. With hindbrain hernia group the success rate is only 50%. There is a high failure rate in vascular, congenital and post-meningitic groups

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22
Q

What is normal pressure hydrocephalus?

A

Enlarged cerebral ventricles with normal/intermittently raised ICP

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23
Q

What are the triad of symptoms associated with normal pressure hydrocephalus (NPH)?

A

Ataxia, memory decline and incontinence

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24
Q

How is NPH managed and why is it especially important to treat?

A

Potential to respond to CSF diversion - 70% success but not permanent It is one of very few potentially treatable causes of dementia

25
Q

What are some of the causes of NPH?

A

Idiopathic Post-inflammatory - SAH, meningitis, trauma, craniotomy

26
Q

What are some of the features of NPH dementia?

A

Delay in answering questions, loss of spontaneity, may progress to akinetic mutism, often fluctuates in severity, urinary incontinence

27
Q

What are some of the features of NPH ataxia and why is it so important?

A

Difficulty rising from a chair, tendency to fall backwards, difficulties initiating gait, broad based, shuffling gait Essential to the diagnosis, precedes all other symptoms

28
Q

What are some of the differential diagnoses for NPH?

A

Causes of ataxia - cerebellar, myelopathy Causes of dementia - Huntington’s, Wilson’s, syphilis, encephalitis, hypothyroidism, alcohol, cerebral tumours, cerebrovascular disease, Alzheimer’s, frontotemporal, Parkinson’s, major head injury, demyelination

29
Q

How is NPH investigated?

A

Diagosis is made with hydrocephalus in the context of one or more of the classic triad i.e. clinical + CT MRI, tracer diffusion studies, ICP measurement, LP tap-test, lumbar drainage tests, infusion studies

30
Q

How is treatment method decided and what are the treatment options for NPH?

A

Tap test LP or lumbar drain + measure NPH triad pre and post CSF drainage. If there is an improvement -> shunt. Lumboperitoneal shunts, VP shunt, endoscopic ventriculostomy

31
Q

What is used to safeguard against over-drainage and subdural haematoma formation in the use of VP shunts for NPH?

A

Valves - anti-syphon, adjustable pressure

32
Q

How effective a treatment is shunting in NPH?

A

If gait problems predominate or the underlying cause is known - good prognosis If there is pronounced dementia the prognosis is poor so NPH patients are best treated before cognitive decline is too great

33
Q

What are some conditions associated with idiopathic intracranial hypertension (IIH)?

A

Female sex, obesity, sleep apnoea, hypothyroidism, Addison’s disease, uraemia, SLE, vitamin A, antibiotics, steroid withdrawal, lithium

34
Q

What symptoms are associated with IIH?

A

Headaches, visual losses - intervene wen visual field loss before patient develops visual acuity loss

35
Q

What are some of the signs associated with IIH?

A

Papilloedema, constriction of visual fields, loss of visual acuity

36
Q

How is IIH investigated?

A

LP pressure >25cm Normal CSF chemistry and cytology Normal CT and MRI findings No evidence of venous sinus thrombosis

37
Q

How is IIH treated?

A

Treat underlying cause (heparin), diuretics, LP, LP or VP shunt, optic nerve sheath fenestration, sub-temporal decompression, venous stents, WEIGHT LOSS! Tends to resolve spontaneously but there is a lifetime predisposition to raised pressure

38
Q

What are some of the potential complications of LP shunts?

A

Blockage, infection, nerve root irritation, low pressure headaches, subdural haemorrahges, arachnoiditis, tonsillar herniation (TH)

39
Q

What are the symptoms associated with spontaneous intracranial hypotension (SIH)

A

Orthostatic headaches, neck/interscapular/arm pain, diplopia/visual field defects, dizziness, muffled hearing, galactorrhoea, impaired sphincter control, symptomatic subdural haematomas

40
Q

What can cause SIH?

A

Idiopathic, collagen disorders, dural diverticula, trauma

41
Q

How is SIH investigated?

A

MRI head - meningeal enhancement, chronic SDH, hindbrain herniation Lumbar puncture - low pressure, pleocytosis, raised protein, xanthochromia CT myelography, spinal MRI, isotope myelography

42
Q

How is SIH treated?

A

Conservative - bed rest, fluids, analgesics Epidural blood patches Surgical repair

43
Q

What causes galactorrohea in SIH?

A

Hyperaemia through the pituitary gland (increased blood flow)

44
Q

When does syringomyelia typically present?

A

Mean age - 31-35

45
Q

When is syringomyelia common?

A

In cases of traumatic paraplegia victims

46
Q

What is the morphology of syringomyelia?

A

Dilated central canals, spindles, holocord (whole spinal cord), tethered conus medullaris

47
Q

How is syringomyelia classified?

A

Craniovertebral junction e.g. chiari type 1 malformation, hindbrain hernia., spinal canal e.g. arachnoiditis, trauma and idiopathic Conus medullaris syrinxes in association with tethered cords form a sub-group of their own

48
Q

How common are persisting central canal of spinal cords?

A

Persisting central canal of cord is seen in 1.5% of spinal MR scans. Patency rate is 100% under 12 months of age. Marked reduction in 2nd decade, occlusion takes place with advancing age

49
Q

How does syringomyelia classically present?

A

Dissociated sensory loss, cuts + burns on hands, small muscle wasting, clawed hands, loss of upper limb reflexes, increased lower limb reflexes

50
Q

What is a feature of early stage syringomyelia?

A

Hyperhidrosis - indicates hyperactivity in pre-ganglionic neurons

51
Q

How else might syringomyelia present?

A

A wide variety of involuntary movements are seen as presenting features of syringomyelia Segmental myoclonus, paroxysmal arm posturing, isolated Horner’s, orofacial pain, limb hypertrophy, orthostatic hypotension, reduced intestinal motility

52
Q

How do hindbrain hernias commonly present?

A

Headaches following coughing, sneezing, straining, bending forward. Visual disturbances, dizziness, deafness/tinnitus, dysarthria/dysphagia, somatic sensory disturbances, sleep apnoea (72% of people with craniovertebral junction abnormalities have sleep apnoea)

53
Q

What proportion of patients with hindbrain hernia have an associated syrinx?

A

65%

54
Q

What is the outlook for syringomyelia like?

A

Poorly defined, progression to quadraplegia is rare, 50% remain stable for long periods, occasional sudden deterioration, ageing exacerbates burden

55
Q

How is syringomyelia treated?

A

Open up obstructed CSF channels e.g. craniovertebral decompression, laminectomy + duroplasty., drain syrinx cavity, lower overall CSF pressure, conservative management

56
Q

What can happen as a result of craniovertebral decompression surgery?

A

Blood and other products released into the CSF pathways during surgery lead to recurrent adhesion formation and persistence of the syrinx cavity

57
Q

When would a syrinx be drained instead of creating a conduit?

A

When the syrinx is particularly large

58
Q

Where can fluid from a syrinx be diverted to?

A

Spinal subarachoid channels, pleural cavity, peritoneal cavity

59
Q

What are the outcomes of craniovertebral decompression (CVD) in the mangement of hindbrain hernia related syringomyelia?

A

Pressure dissociation headaches usually relieved. 80% rate of syrinx collapse following CVD. Motor deterioration commonly stopped but dysaesthetic pains commonly persist.

Neurology (18 decks)

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