Review Normal Pressure Hydrocephalus

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Review Normal Pressure Hydrocephalus

• Supattra Tribuddharat
• 13/10/48

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Ventricular system
CSF production 0.2-0.35 ml/min total volume 120
ml
lateral ventricle ? foramen of Monro? third
ventricle,? cerebral aqueduct ?fourth ventricle
?foramina of Luschka and Magendie? subarachnoid
space ? arachnoid granulations? dural sinus ?
venous drainage.
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Hydrocephalus

• A disturbance of formation, flow, or absorption
  of CSF ? an increase in volume in CNS
• Communicating / non Communicating
• (full communication between ventricles and
  subarachnoid space)
• Cerebral atrophy and focal destructive lesions?
  vacant space filled with CSF
• (hydrocephalus ex vacuo)

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Normal pressure hydrocephalus (NPH)

• First described in 1965 by Hakim and Adams
• Clinical triad of symtoms
• - gait disturbance
• - dementia
• - incontinence
• Image communicating hydrocephalus
• Potenially reversible by shunting symptoms lt2y

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Etiology of NPH

• Idiopathic 50,elderly gt 60 y, worse response
  to shunting (3050)
• Secondary 50, younger age, better response to
  shunting (5070)
• - head injury
• - subarachnoid haemorrhage
• - meningitis
• - neurosurgery

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Etiology of idiopathic NPH

• Combination of mechanisms gt a single cause
• Decreased CSF resorption at arachnoidal villi or
  granulations ? increases transmantle pressure
  (CSF pressure within ventricles gt in subarachnoid
  space) ? ventricular enlargement
• Short-lasting CSF pulsations (B waves)
  periodically apply pressure to the ventricular
  walls and have a water-hammer effect that
  enlarges the ventricles

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Anatomy

• Enlarged third ventricle
• Dilation of the occipital, frontal, and temporal
  horns of the lateral ventricles.
• Presumably, the periventricular white matter is
  stretched and dysfunctional as a result of
  inadequate perfusion, without actually being
  infarcted

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Clinical features

• Considerable variation in nature, severity, and
  course of progression
• Gradually progressive disorder
• Gait disturbance the most readily recognized
  feature
• Cognitive disturbances not occur in all
  patients
• Signs and symptoms of INPH are typically
  bilateral

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Gait disorder

• An initial manifestation of NPH
• Mechanisms enlargement of the ventricles
• 1. compression motor neuron fibers passing
  through corona radiata (an early hypothesis
  pyramidal tract not supported by recent study)
• 2. a disorder of subcortical motor control
• with progression of extensive subcortical white
  matter changes, pyramidal tract involvement may
  become more likely

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• described as apractic, bradykinetic,
  glue-footed, magnetic, parkinsonian,
• short-stepped, and shuffling.
• Bradykinetic, broad-based, and shuffling
• Mimics PD start hesitation, difficulty turning,
  freezing
• Increased tone and with brisk tendon reflexes in
  the lower limb
• Plantar responses may be flexor or extensor,
  unilaterally or bilateral

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• Differentiate NPH from PD
• May occur but less commonly rigidity, tremor,
  and slowing of rapid, alternating movements
• Does not respond significantly to
  carbidopa/levodopa
• No true ataxia or weakness, described as gait
  apraxia.
• Parkinsonian symptoms in INPH abnormal
  pulsatile CSF flow affecting the substantia
  substantia nigra and/or striatum,

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Dementia

• Mental deterioration is frequently mild and
  subcortical
• Memory problems, poor attention, bradyphreni and
  slowing of information processing
• It progresses less rapidly than the dementia of
  Alzheimer disease

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Incontinence

• Usually urinary but may be fecal.
• Increased frequency and urgency may be seen in
  early stages progression to frank urinary
  incontinence with disease progression.
• Results from disruption of periventricular
  pathways to the sacral bladder center ? decreased
  inhibition of bladder contractions and ?
  instability of bladder detrusors
• more advanced stages indifference to the
  episodes of incontinence, is associated with
  frontal executive dysfunction.

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Unexpected manifestration

• Papilledema
• Seizure
• headache

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Brain Imaging

• MRI or CT must be performed to assess ventricular
  size and to rule out ventricular obstruction.
• Either CT or MRI can document noncommunicating
  ventriculomegaly sufficient to satisfy the brain
  imaging requirements for routine diagnosis of
  INPH.

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• CT scan or MRI
• - Ventricular enlargement out of
  proportion to sulcal atrophy
• - Prominent periventricular hyperintensity
  (transependymal flow of CSF)
• - Prominent flow void in the aqueduct and third
  ventricle, the so-called jet sign, (presents as
  a dark aqueduct and third ventricle on a
  T2-weighted image where remainder of CSF is
  bright)
• Thinning and elevation of corpus callosum on
  sagittal images
• Rounding of frontal horns
• May have hyponatremia (SIADH)

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• a rounded frontal horn

The arrow points to transependymal flow.
T2-weighted MRI showing dilatation of ventricles
out of proportion to sulcal atrophy
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Measurement of CSF-OP

• Normal CSF-OP averages 122 34mmH2O
• INPH, CSF-OP averages 150 45 mmH2O
• (60-240 mm H2O)
• Transient high pressures (B waves) are
  detectable during prolonged intraventricular
  monitoring in adults with symptomatic INPH
• OP is elevated gt 18 mm Hg indicate secondary or
  noncommunicating hydrocephalus than INPH

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DIAGNOSING IDIOPATHIC NPH

• Require clinical history, physical examination,
  and brain imaging
• Diagnosis of INPH is complicated
• Resemble, or occur in combination with, various
  disorders that are prevalent in the elderly, such
  as CVD, neurodegenerative disorders (e.g., AD,
  PD, LBD), primary urological disorders, spinal
  stenosis, and other conditions.
• May be useful to classify INPH into probable,
  possible, and unlikely categories,

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PROGNOSTIC TESTS FORPREOPERATIVE ASSESSMENT OF
INPH

• 1. CSF Removal via High-volume Tap Test
• Remove large volumes of CSF (4050 ml)
• An objective improvement in gait
• Complications headaches
• 62 sensitivity , 33 specificity
• Good PPV for shunt response INPH
• Specificity is low, ?many patients who might
  benefit from shunting will be missed
• Therefore, INPH candidates not be excluded on the
  basis of a negative tap test.

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• 2. CSF Ro (outflow resistance)
• A pump introduces CSF or saline 4ml at a rate
  1ml/sec through a needle placed in the lumbar
  subarachnoid space
• Complications headaches and meningismus
• Sensitivity 46, specificity87
• CSF Ro may be helpful in increasing prognostic
  accuracy for identifying SRINPH when tap test
  results are negative

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• 3. ELD Test (external lumbar drainage)
• Draining 10 ml CSF/ hour for 72 hrs (total, 720
  ml)
• Complications bacterial meningitis and root
  irrigation
• more patients who do not improve with CSF tap
  test will show improvement with prolonged
  drainage and benefit from shunting
• The PPV is high, 80 to 100,
• However, hospital admission is required.
• Reported complication rates with ELD are
  generally low but may be significant in terms of
  added

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Treatment

• Medication
• No definitive evidence exists that
  medication can successfully treat NPH.
• Surgical Care
• Surgical CSF shunting remains the main
  treatment modality.

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• No randomized prospective clinical trials were
  conducted comparing different measures or
  protocols of shunt outcome assessment.
• no validated, universally accepted scale for
  assessment of treated or untreated INPH outcome.
• Shunt outcome can be based on the documentation
  of either the clinical impairment, improvement
  after treatment, or both. Grading of either the
  functional status or the clinical criteria of
  gait, incontinence, and dementia

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• Patients with a good response to the above
  procedure
• are candidates for ventriculoperitoneal or
• ventriculoatrial shunting.
• Best results - patients who have no adverse risk
  factors -responded favorably to
  a large-volume LP
  -definite evidence of dementia and ataxia,
  - CT scan or MRI evidence of chronic
  hydrocephalus,
• - a normal CSF at lumbar
  puncture.
• Some evidence indicates that patients with gait
  disturbance, mild or no incontinence, and mild
  dementia fare best among shunt surgery patients.

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• Thank you

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• a baseline neuropsychological evaluation and a
  timed walking test.
• undergo a lumbar puncture with removal of
  approximately 50 cc of CSF. The above evaluations
  are repeated 3 hours later.
• A clear-cut improvement in mental status and/or
  gait predicts a favorable response to shunt
  surgery.
• Improvement in gait may be seen in the form of
  reduced time to walk a fixed distance, reduced
  gait apraxia, or reduced freezing of gait.
• Reduction in bladder hyperactivity also may be a
  sign of good outcome from shunting. Occasionally,
  improvement may be delayed and appear 1-2 days
  after the large-volume lumbar punctures.
• When clinical suspicion is high and the patient
  is a good candidate for surgery, repeated lumbar
  punctures are indicated over the next 1-2 days.
• Some clinicians use an indwelling CSF catheter in
  lieu of repeated lumbar punctures. This method
  carries a higher risk of meningeal infection but
  may allow for a more accurate prognosis.