11: Hydrocephalus Flashcards

1
Q

Ursachen

A

• Meningitis
• Congenital
• Traumatic
• Following brain trauma
• Brain tumors
• Degenerative
• Acquired

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2
Q

CSF

A

• production by choroid plexus in ventricles
• 350-500ml CSF production / day
• Active production, independent from blood pressure/ICP
• Resorption in brain tissue, nerves, lymphatic vessels (2/3) and spinal (about 1/3)
• Connected with spinal dural sac
• conus medullaris reaches only to Th12 or L1 -> at L4/5 puncture is possible with minimal risk
• ICP depends on place in brain, body position and activity (15 lying, 0 sitting)
• Wird meist am Foramen Monroe gemessen

Brain:
- 80% brain tissue
- 12% blood
- 8% CSF
-> build together ICV

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3
Q

Brain perfusion

A

• CPP = MAP - ICP
• For survival of brain tissue, stable perfusion is mandatory -> autoregulation of the vessels‘ diameters allows that

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4
Q

Pressure-volume curve:

A

• CPP depends on medium arterial pressure and intracranial pressure
• If ICP raises above 20 mmHg over longer period -> autoregulation fails and brain perfusion goes down

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5
Q

Signs of acute ICP elevation:

A

• Mild: Headache, Nausea, Emesis
• Acute: Optic sheath hydrops (hügeli), neurological symptoms
• Severely: Coma
-> pupil dilation (brain gets pressed on occulomotor nerve)

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6
Q

Diagnostic

A

• Lumbar puncture -> Only in lying position and clear origin!!! (otherwise incarceration/brain sagging)

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7
Q

Forms of Hydrocephalus:

A

• occlusive (acute/chronic) -> occlusion of CSF pathways
• Maleresorptive (acute/chronic) -> Impaired balance btw CSF production and absorption
• NPH (normal pressure hydrocephalus) -> reduced tissue compliance

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8
Q

Occlusive

A

• acute: most dangerous - die in few hours
• Chronic: not so dangerous, large ventricles
• Enlarged ventricles
• Enlarged ff. monroe
• Thinned c. callosum
• Small 4th ventricle
• Enlarged 3rd ventricle
• Outwardly shifted l.terminalis and floor of 3rd ventricle

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9
Q

Malresorptive

A

• not extremeley high danger
• Often hemorrhage or tumor

Acute:
- enlargement of ventricles
- decreased compliance (stiff tissue)
- compresses arteries, breakdown of windkessel effect
- increased ventricular pulsations
- ventricular dilation

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10
Q

NPH

A
  1. Enlarged ventricles reduce neto-CSF flow into subarachnoidal space
  2. production exceeds drainage
  3. Enlargement of ventricles -> higher mechanical stress on periventricular white matter
  4. Reduced compliance lowers «bulk flow» through aqueduct and the Ff. Luschkae/Magendie -> Further enlargement of ventricles
  5. Enlargement of ventricles distributes pressure to larger surface. When pressure exceeds elastic resistance of ventricular walls-> enlarge further + pressure normalizes
  6. Despite normal pressure, pressure of ventricular walls is raised proportionally to ventricular enlargement

->Reduction of blood flow, hypoxy, ischemia -> demyelinization and apoptosis
->Venous congestion, reduction of transependymal CSF passage
->Accumulation of toxic metabolites in the tissue

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11
Q

Symptoms

A

• dementia
• Incontinence
• Walking disorder

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12
Q

NPH in neuroimagin: (DESH signs)

A
  • Enlarged ventricles
  • Large Sylvian fissures
  • Narrow parasaggital sulci
  • Pointed callosal angle
  • Sulcal enlargements
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13
Q

Treatment

A

Ventriculo-peritoneal shunt
-> treatment for all kinds of Hydrocephalus
-> to drain CSF (controls how much CFS will be drained)

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