Ventricles and Sinuses B&B Flashcards

1
Q

what is the flow of CSF in the brain?

A
  1. lateral ventricles
  2. interventricular foramen (of Monroe)
  3. third ventricles
  4. cerebral aqueduct
  5. fourth ventricles
  6. central canal (center of spinal cord)
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2
Q

CSF is produced by ______, absorbed by ______, and drained by ______

A

production: ependymal cells of choroid plexus (one in each ventricle)

absorption: arachnoid villi

drainage: superior sagittal sinus (onward to venous system)

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3
Q

choroid plexus cysts are associated with…

A

chromosome abnormalities, esp. trisomy 18

however, often a normal variant

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4
Q

what is the problem in communicating hydrocephalus?

A

decrease in CSF absorption by arachnoid, increasing intracranial pressure (ICP)

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5
Q

what are the key clinical features of communicating hydrocephalus? (3)

A
  1. headache (chief complaint)
  2. papilledema (fundoscopic exam)
  3. dilation of ALL ventricles (CT scan)

note PMH of meningitis is common (causes scarring)

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6
Q

Pt with PMH of meningitis presents to your neurology practice complaining of severe headache. Fundoscopic exam reveals papilledema. A CT scan is ordered, which shows dilation of all the ventricles. What is the diagnosis?

A

communicating hydrocephalus

  1. headache (chief complaint)
  2. papilledema (fundoscopic exam)
  3. dilation of ALL ventricles (CT scan)

PMH of meningitis is common (causes scarring)

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7
Q

what are 3 congenital causes of non-communicating hydrocephalus?

A
  1. aqueductal stenosis: congenital or intrauterine infection
  2. Chiari malformations: malformations of cerebellum and brain stem
  3. Dandy Walker malformation: developmental anomaly of 4th ventricle
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8
Q

give 1 genetic cause and 4 infectious causes of aqueductal stenosis

A

congenital: X-linked (boys)

inflammatory due to intrauterine infection: Rubella, CMV, toxo, syphilis

[blocked drainage from 3rd to 4th ventricles —> non-communicating hydrocephalus]

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9
Q

how does aqueductal stenosis present in a baby?

A

enlarging head circumference (due to non-communicating hydrocephalus)

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10
Q

what is the consequence of a Chiari II malformation?

A

downward displacement and herniation of the cerebellar tonsils and medulla

causes obstruction of CSF flow from 4th ventricle —> non-communicating hydrocephalus

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11
Q

Chiari II malformations are almost always associated with…

A

[downward displacement and herniation of the cerebellar tonsils and medulla —> non-communicating hydrocephalus]

associated with myelomeningocele (spina bifida) - failure of spine/meninges to close around cord

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12
Q

what congenital malformation causes downward displacement and herniation of the cerebellar tonsils and medulla

A

Chiara II malformation —> non-communicating hydrocephalus

associated with spina bifida (myelomeningocele)!!!

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13
Q

what are the consequences of Dandy Walker malformation? explain the 2 root causes of these

A

developmental anomaly of 4th ventricle

  1. cysts —> hydrocephalus —> macrocephaly
  2. very large ventricle —> hypoplasia/agenesis of cerebellar vermis, small cerebellum —> motor dysfunction (crawling/walking) —> delayed development
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14
Q

Parent comes in to the office worried that their child is not crawling yet. On PE, you note the child has a very large head (macrocephaly). Delayed development and motor dysfunction is apparent. You might want to think about…

A

Dandy Walker malformation: developmental anomaly of 4th ventricle

  1. cysts —> hydrocephalus —> macrocephaly
  2. very large ventricle —> hypoplasia/agenesis of cerebellar vermis, small cerebellum —> motor dysfunction (crawling/walking) —> delayed development
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15
Q

pseudotumor cerebri

A

idiopathic intracranial HTN —> increased ICP in absence of tumor/ other cause

causes intractable/ disabling headaches, papilledema, visual loss, pulsatile tinnitus (rushing water/ wind sound)

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16
Q

what are the symptoms of pseudotumor cerebri? which one is most key?

A

idiopathic intracranial HTN —> increased ICP in absence of tumor/ other cause

causes intractable/ disabling headaches, papilledema, visual loss, pulsatile tinnitus (rushing water/ wind sound)

17
Q

who is the classic patient affected by pseudotumor cerebri?

A

idiopathic intracranial HTN

causes intractable/ disabling headaches, papilledema, visual loss, pulsatile tinnitus

classically overweight women of childbearing age

18
Q

how is pseudotumor cerebri diagnosed? how is it treated?

A

idiopathic intracranial HTN

causes intractable/ disabling headaches, papilledema, visual loss, pulsatile tinnitus

diagnose via spinal tap to measure the ICF pressure
tx: acetazolamide (mild diuretic)

19
Q

what is the key neuroimaging finding of normal pressure hydrocephalus (NPH)?

A

enlarged ventricles on imaging causing compression of the corona radiata (fibers projecting from corpus colosum)

note the CSF pressure is normal when measured (may be due to impaired absorption of CSF)

classic triad: urinary incontinence, gait disturbance, dementia (wet, wobbly, wacky)

20
Q

what is the classic triad of normal pressure hydrocephalus (NPH)?

A

enlarged ventricles on imaging causing compression of the corona radiata (but normal CSF pressure when measured)

classic triad: urinary incontinence, gait disturbance, dementia (wet, wobbly, wacky)

21
Q

how is normal pressure hydrocephalus (NPH) treated?

A

enlarged ventricles on imaging causing compression of the corona radiata (but normal CSF pressure)

tx: ventriculoperitoneal (VP) shunt - drains CSF to abdomen

22
Q

what is the cause of hydrocephalus ex vacuo?

A

ventricular enlargement that occurs with age (60+) due to shrinkage of the cortex (but may be accelerated with Alzheimer’s, Pick, HIV, etc)

23
Q

how can hydrocephalus ex vacuo be differentiated from hydrocephalus on neuroimaging?

A

hydrocephalus ex vacuo: ventricular enlargement with age

size of ventricles should increase in proportion to increasing size of sulci (as cortex atrophies) - if out of proportion, you’re dealing with hydrocephalus

24
Q

what is the function of the dural sinuses?

A

large venous channels traveling through dura, drain blood from cerebral veins and receive CSF from arachnoid granulations —> empty into internal jugular vein

25
Q

which dural sinus receives CSF first?

A

sagittal sinus

26
Q

which 6 nerves travel through the cavernous sinus? which important artery travels through the cavernous sinus?

A

between temporal/sphenoid bones, collects blood from the eye/cortex and drains into internal jugular vein

nerves: CN III, IV, V1, V2, VI, sympathetics (all going to orbit)
artery: internal carotid

27
Q

what are the symptoms of cavernous sinus syndrome?

A

between temporal/sphenoid bones, drains into internal jugular vein, includes:
nerves: CN III, IV, V1, V2, VI, sympathetics (all going to orbit)
artery: internal carotid

symptoms: headache, swollen eyes, impairment of ocular motor nerves, Horner’s syndrome, loss of sensation supplied by V1/V2

28
Q

Pt presents to their GP with complaint of a “head cold” that has gotten worse. They complain of headache and sensory loss to their upper face. Examination reveals swollen eyes, impairment of the ocular motor nerves, and Horner’s syndrome. What is the likely diagnosis?

A

Cavernous sinus syndrome - due to infection spreading (septic thrombosis)

between temporal/sphenoid bones, drains into internal jugular vein, includes:
nerves: CN III, IV, V1, V2, VI, sympathetics (all going to orbit)
artery: internal carotid

29
Q

which of the dural sinuses often becomes enlarged in patients with AV malformations?

A

artery to vein connection with no capillary bed, enlarge over time —> headaches, seizures

commonly result in Vein of Galen enlargement

30
Q

describe the presentation of hydrocephalus in adults vs children

A

adults: headache, N/V, papilledema + periodic visual obscurations (transient vision loss), cranial nerve palsies (esp. abducens/CN VI), cognitive impairment + urinary difficulties, gait instability (frontal lobe dysfunction)

children: non-specific signs, head enlargement, tense fontanelles, developmental delay, sun-setting phenomenon (vertical gaze palsy - can’t look up)

31
Q

what 2 findings are necessary to confirm diagnosis of hydrocephalus?

A
  1. establish ventriculomegaly - are lateral ventricles more than 1/3 of the diameter of the skull?
    AND
  2. confirm signs of increased ventricular pressure - are the temporal horns dilated? Is there transependymal flow of CSF (bright white around rim of ventricles)?
32
Q

what is a colloid cyst and what type of CNS issue does it cause?

A

colloid cyst: non-malignant, mucin-filled lesions in roof of third ventricle —> obstructs foramen of Monro —> non-communicating hydrocephalus

can cause acute life-threatening hydrocephalus that causes hemorrhage!

33
Q

most common cause of congenital hydrocephalus

A

aqueductal stenosis —> non-communicating hydrocephalus

34
Q

hyperdensity on CT scan =

A

hemorrhage

35
Q

vast majority of absorption of CSF in the brain is by…

[why is this relevant regarding communicating hydrocephalus?]

A

capillaries! not actually the arachnoid granulations! (recall CSF = ECF in brain)

therefore, the real cause of communicating hydrocephalus is loss of elasticity of the blood vessels within the brain (decreased vascular compliance) - they have less capacity to hold a big volume of CSF, and thus more leaks out (global problem, not focal)