This document discusses radiological imaging techniques for evaluating hydrocephalus. It describes various imaging findings in different types of hydrocephalus like congenital hydrocephalus and hydrocephalus secondary to tumors. It focuses on techniques for evaluating normal pressure hydrocephalus (NPH), including phase contrast MRI to quantify cerebrospinal fluid flow. It hypothesizes that NPH may be caused by a combination of naturally enlarged ventricles and later deep white matter ischemia restricting CSF flow, leading to symptomatic hydrocephalus. Quantitative CSF flow studies can help diagnose shunt-responsive NPH.

1. Radiological imaging of hydrocephalus.
Dr/ ABD ALLAH NAZEER. MD.

21. The contrast among a normal brain in a normal adult (left), the brain of a normal
man with impressive hydrocephalus and an equally impressive hydrocephalus in a
54-year-old man with deep cognitive and motor impairment since childhood (right;

22. A 25-week premature male with an intraventricular hemorrhage and
subsequent development of hydrocephalus: ( a ) CUS shows the right-sided
intraventricular hemorrhage; ( b ) CT also shows parenchymal hemorrhage

23. Congenital hydrocephalus.

24. Congenital hydrocephalus.

25. Congenital hydrocephalus.

26. A 4-month-old male with vein of Galen malformation: ( a ) MRI
shows the dilated vein of Galen; ( b ) cerebral angiogram shows the
dilated vein of Galen and the surrounding vasculature

27. ( a – b ) A 8-year-old female with a posterior fossa brain tumor and hydrocephalus.

28. A 13-year-old male with hydrocephalus secondary to aqueductal stenosis, status
post endoscopic third ventriculostomy (ETV). CSF cine flow study demonstrates
CSF flow across the fenestration in the anterior third ventricle: ( a ) phase-contrast
magnitude cine MRI; ( b ) phase contrast directional cine MRI.

29. CT/MRI axial scans demonstrating ventriculomegaly with relatively well- identified
sulci. Periventricular edema is observed in case 4 which suggest acute onset.

30. Pineal body tumour with hydrocephalus.

31. Communicating hydrocephalus.

32. Communicating hydrocephalus.

34. Communicating Hydrocephalus.

35. Aqueductal Stenosis

38. Tectal Glioma.

40. Giant cell astrocytoma with hydrocephalus.

41. Choroid plexus papilloma.

42. Choroid plexus tumors with hydrocephalus.

43. Choroid plexus carcinoma with hydrocephalus.

44. Fourth ventricular medulloblastoma with hydrocephalus.

45. Fourth ventricle tumour with hydrocephalus.

46. Posterior fossa immature teratoma with hydrocephalus.

47. Posterior fossa cystic mass with hydrocephalus.

48. Tuberculous meningitis with hydrocephalus.

49. Normal Pressure Hydrocephalus
• Described by Hakim, Adams, et al (1965).
• 50% known cause (SAH, meningitis).
• 50% idiopathic (older).
• Diagnosis primarily clinical: Gait apraxia,
dementia, incontinence.
• Radiology: communicating hydrocephalus.

51. Physiologic Tests for NPH
• Nuclear cisternography
– Communicating hydrocephalus
• Pressure monitoring
– Water hammer pulse
– Plateau waves
• Saline Infusion (outpatient)
– If resistance > 4mmHg/ml/min, 82% respond
to ELD
• 50 cc Tap test: PPV 73-100%; sensitivity 26-62%
• External lumbar drainage (inpatient)

53. External Lumbar Drainage
• 16 gauge lumbar puncture; catheter
drainage
• 10 cc/hour for 3 days; gait assessed.
• Of 151 patients* with iNPH,100 improved
with ELD.
– Gait only (88%), gait/dementia (84%), triad
(59%).
• Of responders, 90% improve with VP shunt.
• Of nonresponders, 22% improve with shunt.

55. What Causes Idiopathic NPH?
• Consider normal bulk flow of water in brain
• Consider association of deep white matter ischemia
(DWMI) and NPH.
Normal Bulk Flow of Extracellular Brain Water
• Water leaves upstream arterioles under pressure-osmotic
gradients (e.g, mannitol).
• Normal and excess water resorbed by downstream
capillaries and venules.
• Vasogenic edema flows centripetally to be absorbed
by ventricles
• Interstitial edema flows centrifugally to subarachnoid
space via extracellular space.

56. Possible Etiology of NPH
• Hypothesis: NPH patients have always had large
ventricles (“slightly enlarged”)
– Decreased CSF resorption (saline infusion test)
– Unrecognized benign external hydrocephalus?
• No evidence for previous SAH or meningitis
• Significant CSF resorption pathway is via extracellular
space of brain (like tectal gliomas)
• Everything fine until “second hit”: DWMI
DWMI is “Second Hit” in NPH
• No symptoms until DWMI occurs later in life
• Resistance to peripheral CSF flow through extracellular space
increases slightly due to DWMI.
– loss of myelin lipid: more hydrophilic environment
– Greater attraction of out flowing CSF to myelin protein
• CSF production continues unabated
– Accumulates in ventricles -hydrocephalus worsens
– Increased tangential shearing forces.
– NPH symptoms begin.

57. NPH.

59. NPH.

63. CSF Flow Void.

64. Proposed Causes of CSF Motion
• Production by choroid plexus
(500 ml/day).
• Cardiac pulsations.
– Choroid plexus (Bering, 1959).
– Large arteries.
– Cerebral hemispheres (phase-contrast
MRI).

65. Normal flow.

66. Hyperdynamic flow.

69. Enlarged
Sylvian
cisterns
in NPH

70. Association of DWMI and NPH: Clinical
• Some cases of L’etat Lacunaire (Marie, 1901)
may have been NPH (Fischer, 1981)
• Coexistence of NPH and Hypertensive
Cerebrovascular Disease Noted Previously
(Earnest 1974, Goto 1977, Graff-Radford 1987)
• CSF flow void is useful indicator of favorable
response to CSF diversion
• Presence of DWMI is not contraindication to
shunting
• NPH and DWMI may be related

71. CSF Flow Measurement
• CSF flow void on conventional MR images represents
average motion during 256 spin echo acquisitions.
• Since CSF motion is due to cardiac pulsations, it is better
evaluated using cardiac gated techniques.
Phase Contrast CSF Velocity Imaging
• “Velocity” is speed plus direction
• Flow sensitization along craniocaudal axis
– Flow up: shades of black
– Flow down: shades of white
– No flow: gray
– Set aliasing velocity
– Quantification of velocity or flow

72. Qualitative
CSF Velocity
Imaging.

73. Quantitative CSF Flow Study
• 512x512; 16 cm FOV
• .32 mm pixels
• 4mm slice angled perpendicular to aqueduct
• Velocity-encode in slice direction
• Retrospective cardiac-gating (not EKG triggering)
Through-plane flow-encoding
• Venc= 10, 20, 30 cm/sec (NPH)
• Venc= 5 cm/sec (shunt malfunction)

77. Quantitative CSF Velocity Imaging
• Calculates “Aqueductal CSF stroke volume”
• Stroke volume: microliters of CSF flowing back or
forth over cardiac cycle
• Verified by pulsatile flow phantom using ultrasound
flow meter (Mullin, 1993)
Quantitative CSF Velocity Imaging

80. CSF Flow Study: No Flow.

84. Conclusions
• NPH diagnosed by symptoms, not MRI
• MRI used to confirm diagnosis of
shunt-responsive NPH
• Asymptomatic patients may have dilated
ventricles and elevated CSF flow: Pre NPH?
• Not everyone with benign external
hydrocephalus gets NPH
• Keep your extracellular space open

85. Thank You.