Normal pressure hydrocephalus (NPH)

General

AKA Hakim-Adams syndrome,

Do lumbar drain or other CSF testing for other conditions if there is a doubt (vascular dementia)

Epidemiology

Incidence: high (5.5/100,000/year)

3% in elderly in Japan

Usually >60 yrs.
Mean age for iNPH is older than that for secondary NPH.

Slight male preponderance.

Aetiology

Primary (idiopathic-NPH)

Secondary to a predisposing condition (? ICP may be elevated at sometime in the past)

“Secondary NPH” patients don’t have true iNPH but may also respond to shunting.
Risk factors (similar for communicating hydrocephalus)

Post-SAH
Posttraumatic (including concussion)
Post-meningitis
Following posterior fossa surgery
Following radiation therapy to the brain
Tumours, including carcinomatous meningitis
Alzheimer’s disease (AD) (seen in ≈ 15% of patients)
Enlarged head circumference
Deficiency of the arachnoid granulations
Aqueduct stenosis may be an overlooked cause

Pathophysiology

The cause of ventricular enlargement in idiopathic NPH (iNPH) is not as clear.

Could be due to a hydrodyanmic deficit secondary to the following

Cisternal block
Aqueduct stenosis
Problem of cerebrospinal fluid (CSF) absorption due to

Arachnoid cell hyperplasia
Leptomeningeal fibrosis
Other degenerative changes

Clinical deterioration is probably due to

Interstitial oedema → Impaired periventricular blood flow
Enlarging ventricles →

Mechanical stretching of periventricular tissue →

Impairment of BBB
Reduced CSF turnover and disturbed elimination of neurotoxic substances such as β-amyloid, tau-protein, and pro-inflammatory cytokines

Explains the high co-occurrence of Alzheimer-like changes in the cortex of INPH patients and of rats with experimental chronic hydrocephalus

Ependyma disruption
Neuronal injury
Microvascular infarctions
Gliosis
Neuronal degeneration

It has been suggested that these abnormal CSF pressure spikes, called B waves, slowly increase ventricular size by exerting intermittent high pressure on the brain parenchyma that results in ischemic damage.

Abnormalities of the aging brain parenchyma may make it more susceptible to these forces

Clinical features

Clinical triad (Not pathognomonic: also be seen in vascular dementia, Alzheimer’s dementia, and Parkinson’s disease)

Gait disturbance

1st symptoms to present

Almost all have gait disturbance.

Main issue that neurosurgeon can improve

Gait

Wide-based with short,
Shuffling steps
Unsteadiness on turning.

Difficulty initiating steps or turns.
Multistep turning

Patients often feel like they are “glued to the floor” (so-called “magnetic gait”)

Other features: retropulsion, and frequent falls.

Absent: Appendicular ataxia

Test

Supine bicycle test

Lie in bed leg supine in air and bicycle.
NPH can do it but cannot walk properly
Proves walking apraxia not die to ataxia or focal deficit

Dementia

Memory impairment with bradyphrenia (slowness of thought) and bradykinesia.

Cannot be treated with shunt

Other features that are shared with various frontal subcortical disorders:

Apathy or lack of motivation
Daytime sleepiness.

Findings that are not characteristic

Expressive or receptive dyphasias
Dysnomia (impaired naming)
Difficulty recognizing familiar people
Hallucinations

Urinary incontinence

Due to damage of the paracentral lobule which causes loss of voiding inhibition for both bowel and urine

Typically urinary urgency with impaired ability to inhibit bladder emptying.

Incontinence without awareness is not characteristic and may suggest other dementing processes.

Faecal incontinence a late sign

If you have this it is too late

Other clinical features

Speech

True aphasia is unusual, but speech output may be disturbed by impaired motivation or executive dysfunction.
As NPH progresses, cognitive impairment may become more generalized and less responsive to treatment.

Symptoms identical to those of idiopathic parkinsonism may occur in 11%.

Anecdotal

Depression
Bipolar disorder
Aggressiveness
Paranoia

Symptoms not expected with NPH

SIADH,

Syncope

Clinical features not expected solely as a result of NPH include

Papilledema,
Seizures (prior to shunting)
Headaches,
Spasticity,
Hyperreflexia and
Lateralizing findings.

See also unanticipated findings listed under iNPH triad

Treat other conditions before embarking on NPH testing

Diagnostic criteria (international guidelines)

Probable NPH

History: must include

Insidious onset (vs. acute)

Onset age ≥ 40 years

Duration ≥ 3–6 months

No antecedent head trauma, ICH, meningitis, or other known cause of secondary hydrocephalus

Progression over time

No other neurological, psychiatric, or general medical conditions that are sufficient to explain the presenting symptoms

Brain imaging: CT or MRI after onset of symptoms must show

Ventricular enlargement not attributable to cerebral atrophy or congenital enlargement (Evan’s index > 0.3 or comparable measure)

No macroscopic obstruction to CSF flow

≥ 1 of the following supportive features

a) Enlarged temporal horns not entirely attributable to hippocampal atrophy

b) Callosal angle ≥ 40°

c) Evidence of altered brain water content, including periventricular changes not attributable to microvascular ischemic changes or demyelination

d) Aqueductal or 4th ventricle flow void on MRI

Other imaging findings that may support Probable designation but are not required

Pre-morbid study showing smaller or nonhydrocephalic ventricles

Radionuclide cisternogram showing delayed clearance of radiotracer over the convexities after 48–72 hours

Cine-MRI or other technique showing increased ventricular flow rate

SPECT showing decreased periventricular perfusion that is not altered by acetazolamide challenge

Physiological

CSF opening pressure (OP) on lateral decubitus LP: 5–18 mm Hg (70–245 mm H₂O)

Clinical: must show gait/balance disturbance, plus impairment in cognition and/or urinary function

Gait/imbalance: ≥ 2 of the following (not entirely attributable to other conditions)

a) Decreased step height

b) Decreased step length

c) Decreased cadence (speed of walking)

d) Increased trunk sway while walking

e) Widened standing base

f) Toes turn outward while walking

g) Retropulsion (spontaneous or provoked)

h) En bloc turning (≥ 3 steps to turn 180°)

i) Impaired walking balance: ≥ 2 corrections out of 8 tandem steps

Cognition: documented impairment (adjusted for age & education) and/or decrease in performance on cognitive screening instrument (e.g. Mini-Mental State Examination), or evidence of ≥ 2 of the following not fully attributable to other conditions

a) Psychomotor slowing (increased response latency)

b) Decreased fine motor speed

c) Decreased fine motor accuracy

d) Difficulty dividing or maintaining attention

e) Impaired recall, especially for recent events

f) Executive dysfunction: e.g. impairment in multistep procedures, working memory, formulation of abstractions/similarities, insight

g) Behavioral or personality changes

Urinary dysfunction

a) Any one of the following

Episodic or persistent incontinence not attributable to primary urological disorder

Persistent urinary incontinence

Urinary and fecal incontinence

b) Or any 2 of the following

Urinary urgency: frequent perception of a pressing need to void

Urinary frequency (pollakiuria): voiding > 6 times in 12 hours with normal fluid intake

Nocturia: needing to void > 2 times in an average night

Possible NPH

History: reported symptoms may

Have subacute or indeterminate mode of onset

Onset at any age after childhood

Duration: <3 months or indeterminate

May follow events such as mild head trauma, remote history of ICH, or childhood or adult meningitis or other conditions judged not likely to be causally related

Coexist with other neurological, psychiatric, or general medical disorders but judged not to be entirely attributable to these conditions

Be nonprogressive or not clearly progressive

Clinical: symptoms of either

Incontinence and/or cognitive impairment in the absence of observable gait/balance disturbance

Gait disturbance or dementia alone

Brain imaging: ventricular enlargement consistent with hydrocephalus but associated with any of the following

Cerebral atrophy of sufficient severity to potentially explain ventricular enlargement

Structural lesions that may influence ventricular size

Physiological

OP not available or outside of the range delineated for Probable NPH

Unlikely NPH

No ventriculomegaly

Signs of increased ICP (e.g. papilledema)

No component of the clinical triad of NPH

Symptoms explained by other causes (e.g. spinal stenosis)

Levodopa challenge

Non responsive in NPH

Management: diagnosis

Lumbar drain is the best

Imaging

MRI>CT

Prerequisite

Ventricular enlargement without block (i.e., communicating hydrocephalus).

MRI CISS: r/o obs(x) HCP due to aqueduct stenosis

Features that suggest the HCP is not due to atrophy → favourable response to shunt

Periventricular low density on CT or T2 hyerpintensity

May represent transependymal absorption of CSF.
May resolve with shunting

Compression of convexity sulci (as distinct from dilatation in atrophy).

Focal sulcal dilation may sometimes be seen and may represent atypical reservoirs of CSF, which may diminish after shunting and should not be considered as atrophy

Rounding of the frontal horns

DESH (disproportionately enlarged subarachnoid space hydrocephalus): Japanese guidelines for iNPH also identify the following features

Enlarged subarachnoid spaces primarily in the Sylvian fissure and basal cisterns
Effacement of the subarachnoid space over the convexity (“tight high convexity”)

If dilated subarachnoid space in the high convexity it is suggestive of atrophy

Has high positive predictive value in identifying shunt responsive iNPH pts

Yellow: inferior choroidal point of the choroidal fissure

Red: choroidal plexus of lateral ventricle

Green: Ambient cistern

Purple: temporal horns

H: Head of hippocampus

sNPH: secondary NPH

iNPH: idiopathic

See 2nd image of iNPH the inferior choroidal point of choroidal fissure is open.

Inferior choroidal point is where the anterior choroidal arteries and inferior choroidal veins enter the lateral ventricle

SILVER index: The ratio between the area of the Sylvian fissure and the area at the vertex

Enlarged at 11.52 in DESH
Normal control is 1.68

Screenshot of a CT scan MPR created with the MPR button (red arrow).

(A) Coronal viewport. The coronal plane obtained through the previous adjustment is used to calculate the SILVER index.

(B) Sagittal viewport. The axial orientation line (blue) is rotated to be parallel to the frontal fossa.

(A) After deactivating the orientation lines from the viewport via the specific button (red arrow), the subarachnoid area at the vertex and the Sylvian fissure are calculated with the free-hand measurement tool. Areas are showed in squared millimeters (red boxes).

(B) Close-up of the area at the vertex. Measurement starts from the most cranial point of the superior frontal gyrus medial part (arrow), follows the medial surface of the brain until no space between the brain and the falx is recognizable or (as in this case) until the gyrus cinguli (arrowhead). The measurement is completed following the falx to the inner skull point immediately overhead the starting point (asterisk).

(C) Close-up of the Sylvian fissure. Measurement starts from the most lateral aspect of the inferior frontal gyrus (arrow), contours the Sylvian fissure and the insular cortex (asterisks) to the most lateral aspect of the superior temporal gyrus (arrowhead). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Callosal angle

Due to deformation of the corpus callosum

Impingement on the falx

Measure coronal MRI perpendicular to the AC-PC line, passing through the posterior commissure

Normal >90°

NPH: < 90°

Phase-contrast MRI may demonstrate hyperdynamic flow of CSF through the aqueduct

Although some patients improve with no change in ventricles, clinical improvement most often accompanies reduction of ventricular size.

A: Evans index

B: Temporal horn size

C: Callosal angle

Radionuclide cisternography

❌ High false-positive rate.

One study found that the cisternogram does not increase the diagnostic accuracy of clinical and CT criteria.

Use has been abandoned by most researchers

It is not recommended

iNPH Radscale

Interpretation

iNPH Radscale scores of >8 have been shown to have high sensitivity (>90%) for NPH in patients with clinical symptoms
Although iNPH Radscale scores alone may not predict response to shunt surgery.

Feature	Finding	Points
Evan’s index: ratio of the maximum width of the frontal horns of the lateral ventricles to the maximum BPD on the same CT or MRI slice	≤ 0.25 0.25–0.3 > 0.3	0 1 2
Narrow CSF spaces in high convexity & high parafalcine sulci on coronal and high axial MRI slices	None Parafalcine Vertex	0 1 2
Sylvian fissure enlargement in the coronal plane compared to surrounding sulci	Normal Enlarged	0 1
Focally enlarged sulci in coronal or transverse planes compared to surrounding sulci	Absent Present	0 1
Temporal horns (TH): mean width of the left & right TH measured on axial images	< 4 mm ≥ 4 and < 6 mm ≥ 6 mm	0 1 2
Callosal angle: angle between the lateral ventricles under the falx (on a coronal MRI slice at a right angle to the AC-PC line passing through the PC)	> 90° > 60° and ≤ 90° ≤ 60°	0 1 2
Periventricular hypodensities in the vicinity of the lateral ventricles: anterior to the frontal horns (“caps”) or diffusely surrounding the ventricle	Absent Frontal horn caps Diffusely surrounding	0 1 2
“iNPH Radscale” score = Total Points	ㅤ	0-12

Not testing for NPH but looking for shunt responsiveness

Tap test PPV>075 NPV<0.2

Drainage test PPV>0.95 but meningitis risk 1/300

Infusion study wikkelso et al JNNP 50% "failure" responded to shunt

Two LP needles

Infusion of saline
Measure ICP

Measures compliance
Results

Normal plateau
Abnormal increases

Ancillary tests for NPH

CSF labs

R/O infection, elevated protein (e.g. with tumor), SAH

Lumbar puncture (LP)

Opening pressure at left lateral decubitus position

Normal

12.2 ± 3.4cm H2O (8.8 ± 0.9mm Hg) and should be< 18 cm H2O
OP> 24cm H2O suggests noncommunicating hydrocephalus rather than NPH.

NPH: 15 ± 4.5cm H2O (11 ± 3.3mm Hg), slightly higher than, but overlapping with, normal.

An upper limit of 24cm H2O (17.6mm Hg) is suggested for the definition of NPH.
Patients with an initial OP> 10cm H2O have a higher response rate to shunting.

“Tap Test” (AKA Miller Fisher test)

Consists of lumbar puncture with removal of a specific quantity of CSF and assessment of response.

The tap test has not undergone rigorous prospective evaluation.

A positive response to withdrawal of 40–50ml of CSF has a PPV in the range of 73–100%, but sensitivity is low (26–61%).

A significant “response” has not been standardized;

Most experts prefer demonstrating objective improvement in gait, taking into account the fact that NPH patients can have day-to-day fluctuations in symptoms.

Resistance testing

Principles

Davson equation

Use to calculate Rout

Higher the measured resistance greater response to shunting
CSF Ro (CSF outflow resistance) is considered to be the impedance of CSF absorptive mechanisms.
1/Ro is the conductance.

ICP = Rout * If + PSS

Rout: resistance of CSF outflow
If : CSF formation
PSS: sagittal sinus pressure
This equation is valid if ICP is greater than PSS. Below PSS, ICP may have any value

A key deficit in NPH is a disturbance in the Rout variable and treatment for NPH, shunt surgery, is aimed at manipulating Rout

Techniques and thresholds are center-specific.

No clinical study has adequately addressed the fact that Ro normally increases with age.

Determination of CSF Ro may have a higher sensitivity (57–100%) but a similar PPV (75–92%) to the tap test.

Methodology

Numerous methods have been devised to measure Ro

Bolus method

A known volume (usually ≈ 4ml) is injected via LP at a rate of 1 ml/sec

Katzman test: infuse saline through LP at a known rate

Up to 19% of patients experience H/A after infusion studies

Ro = [(final steady state pressure)-(initial pressure)]/infusion rate

This formula came from Davson equation

The prope way to calculate Rcsf results from the well known Davson’s formula

ICPbₐₛₑₗᵢₙₑ=Rcsf*Formation of CSF+Pss; where Pss is sagittal sinus pressure

ICP reached during infusion is equal to

ICPₑₙd₋ₑqᵤᵢₗᵢbᵣᵢᵤₘ=Rcsf*(Formation of CSF+Infusion rate)+Pss

Subtracting the first equation from the second it can be derived

ICPₑₙd₋ₑqᵤᵢₗᵢbᵣᵢᵤₘ-ICPbₐₛₑₗᵢₙₑ=Rcsf*Infusion rate

Analysis of lumbar infusion tests: (a) a plot showing our conventional method of performing a lumbar infusion test, using constant-rate infusion at 1.5 ml/min of Ringer solution.

The plot of mean CSFP against time incorporates the period before infusion (opening pressure; P₀), and during the infusion period (infusion rate of 1.5 ml/min). The plateau pressure (Pₚ) is indicated. The resistance to CSF outflow (Rout) is calculated as (Pₚ - P₀)/infusion rate. Two 6 s time windows of the continuous CSFP signal from (b) the start and (c) the termination of the infusion test are indicated, illustrating the single CSFP pulse waves. (d) Plot of mean CSFP pulse amplitude against time, indicating the period after lumbar puncture and before infusion (opening phase), and the 10 min period during the infusion. For comparison between patients we compared the CSFP pulse amplitude during the first 10 min of infusion.

Use two spinal needles one to infuse and one to measure

Trakeuchi et al measured Ro in 25 patients: (these values vary a lot between publications)

Average Ro for shunt responsive patient: 35.3mmHg/ml/min
Average Ro for shunt unresponsive patient: 9.1mmHg/ml/min

In the Dutch NPH study, outflow resistance greater than 18 mmHg/mL/min had a specificity of 87% and a sensitivity of 46%.

Positive predictive values

92% for an Rcsf of 18 mm Hg/ml/minute,
100% for an Rcsf of 24 mm Hg/ml/minute.
Negative predictive values were low (for both)

More important was the highest likelihood ratio of 3.5 for an Rcsf of 18 mm Hg/ml/minute.

Ambulatory lumbar drainage (ALD)

The drip chamber is placed at the level of the patient’s ear when they are recumbent, or at the level of the shoulder when sitting or ambulating.

A properly functioning drain should put out ≈ 300ml of CSF per day.

If symptoms of nerve root irritation develop during the drainage, the catheter should be withdrawn several millimeters.

Daily surveillance CSF cell counts and cultures should be performed (NB: a pleocytosis of ≈ 100 cells/mm3 can be seen normally just as a result of the presence of a drain).

A 5-day trial is recommended (mean time to improvement: 3 days).

Baseline Test

Walking assessment

Qtug video
Quantitative time up and go test.

Neuropsychology test - Addenbrookes' cognitive assessment

Continuous CSF pressure monitoring

Some patients with a normal OP on LP demonstrate pressure peaks > 270mm H₂O or recurrent B waves.

These patients may also have a higher response to shunting than those without these findings.

Miscellaneous

Cerebral blood flow (CBF) measurements

Although some studies indicate otherwise, CBF measurements show no specific findings in NPH, and are not helpful in predicting who will respond to shunting.
However, increased CBF after shunting correlates with clinical improvement.

EEG: There are no specific EEG findings in NPH.

Treatment

Management algorithm

Based on diagnostic criteria

Probable NPH
Possible NPH
Unlikely NPH

For probable and possible NPH, without further testing, the degree of certainty of the diagnosis of NPH is ≈ 50–61%.
In an otherwise healthy patient in whom the diagnosis of NPH seems highly probable, it is not unreasonable to proceed to shunting

To increase the certainty of response to shunting, one or more of the following is recommended

“Tap test” (AKA Miller Fisher test): withdrawal of40–50ml of CSF via LP

Positive response increases likelihood of responding to a shunt (PPV) to the range of 73–100%
Due to low sensitivity (26–61%), a negative response does not rule out the possibility of responding, and a subsequent supplemental test should be performed
OP> 17.6mm Hg (24cm H2O), consider further search for cause of secondary hydrocephalus (does not rule out shunting as a treatment)

Resistance testing

Sensitivity (57–100%) > tap test
Similar PPV (75–92%) to tap test

External lumbar drainage

CSF diversionary procedures

Types

VP shunt

Procedure of choice.

Lumbar-peritoneal shunts

Disadvantages include: tendency to overshunt, difficult to tap, tendency to migrate.

VPleural shunt	VA shunt
- Can cause pleural effusion and most of the time is not due to an increase in cerebral CSF production. - The younger, the higher failure rate	- Can take high volume - Can cause immune mediated glomerulonephritis

Settings

Medium pressure valve

(Closing pressure 65–90mm H₂O)
Most commonly used
To minimize the risk of subdural hematomas

Low-pressure valve

May be higher response rate
Higher risk of subdurals

If have low pressure symptoms

Gradually sit patient up over a period of several days;
Proceed more slowly

Programmable shunts

Pros

Dec. risk of developing SDH

Initially at a high pressure (to reduce risk of subdural hematoma) and gradually decreasing the pressure setting over a number of weeks.

Follow patients clinically and with CT for ≈ 6–12 months.

Responder

Patient improves with smaller ventricles

Non-responder

Definition: no clinical improvement despite a reduction in ventricular size
The failure to improve might be attributed to

An incorrect diagnosis, OR
A shunt nonresponder (e.g. if valve at lowest setting and shunt patency confirmed).

Uncertain

No clinical improvement + ventricles do not change
Evaluated for

Shunt malfunction.
If not obstructed, and if no subdural fluid collections have developed, a lower pressure valve may be tried (or a lower pressure selected on a programmable shunt).

Potential complications of shunting for NPH Complication rates may be as high as ≈ 35% (due in part to the frailty of the elderly brain)

Subdural hematomas or hygroma

Higher risk with low pressure valve and older patients who tend to have cerebral atrophy.
Usually accompanied by headache, most resolve spontaneously or remain stable.
1/3 require evacuation and tying off of shunt (temporarily or permanently).
Risk may be reduced by gradual mobilization post-op

Shunt infection

Intracerebral hemorrhage

Seizures

Delayed complications include:

Shunt obstruction or disconnection

Endoscopic third ventriculostomy (ETV)

Can’t explain why ETV would work for NPH, but it has been advocated by some in highly selected patients, using nonvalidated outcome measures, quoting post-op improvement in 69% of patients.

At this time, ETV should not be considered a first line treatment for most cases of NPH.

Outcome

Most to least likely symptom to improve with shunting is incontinence > gait disturbance > dementia.

Black et al give the following markers for good candidates for improvement with shunting

Clinical

Presence of the classic triad
Also 77% of patients with gait disturbance as the primary symptom improved with shunting.

Patients with dementia and no gait disturbance rarely respond to shunting

OP > 10cm H2O

Continuous CSF pressure recording

Pressure > 18cm H2O
Frequent Lundberg B waves for more than 80% of ICP monitoring period

CT or MRI

Large ventricles with flattened sulci (little atrophy)

Response is better when symptoms have been present for a shorter time.

NPH patients with co-existing Alzheimer’s disease (AD) may still improve with VP shunts

Thus AD should not exclude these patients from shunting.
However, patients with AD alone (without NPH) did not respond to shunting in an RPDB placebo-controlled trial.
In general, most responders eventually relapse, often after ≈ 5–7 years of good response.

Shunt malfunction and subdural collections must be ruled out before ascribing this to the natural course of the underlying condition.

Degree of improvement?

See Klinge et al 2012
If you shunt everyone with features of NPH percentage of patients

Evidence for not denying anyone with a shunt

Changes in modified Rankin Scale (mRS) scores 1 year after shunt insertion

Economic benefit to society

See Kameda et al 2017

Natural course

See Andrén et al 2013

Quicker the surgery better the outcome

Differential diagnosis

Neurodegenerative disorders

Alzheimer’s disease

Parkinson’s disease

Lewy body disease

Huntington’s disease

Frontotemporal dementia

Corticobasal degeneration

Progressive supranuclear palsy

Amyotrophic lateral sclerosis

Multisystem atrophy

Spongiform encephalopathy

Vascular dementia

Cerebrovascular disease

Multi-infarct dementia

Binswanger’s disease

CADASIL

Vertebrobasilar insufficiency (VBI)

Other hydrocephalic disorders

Aqueductal stenosis

Arrested hydrocephalus

Long-standing overt ventriculomegaly syndrome

Noncommunicating hydrocephalus

Infectious disease

Lyme disease

Syphilis

Urological disorders

Urinary tract infection

Bladder or prostate cancer

Benign prostatic hypertrophy (BPH)

Miscellaneous

Vitamin B12 deficiency

Collagen vascular diseases

Epilepsy

Depression

Traumatic brain injury

Spinal stenosis

Chiari malformation

Wernicke’s encephalopathy

Carcinomatous meningitis

Spinal cord tumor

To differentiate Table 24.4 compares some features of NPH, Alzheimer’s disease, and Parkinson’s disease. Tests used to rule out common NPH mimics

Bloods

FBC
U/E
B12
Folate
TSH
Additional blood tests when indicated

Rapid plasma reagin (RPR): screening for syphilis antibodies (in neurosyphilis) 2. ELISA screening test for Lyme disease; then if positive, Western blot to confirm 3. vitamin D level

Neuropsychological testing

Imaging

Cervical and/or thoracic as appropriate if concern about myelopathy
Lumbar if there is pain with ambulating

Electrodiagnostic studies (EMG/NVC) if peripheral neuropathy is possible

Urology consultation

Comparison of NPH, Alzheimer’s & Parkinson’s diseaseᵃ

Feature	NPH	AD	IPA
Gait disturbanceᵇ	+	±	±
Postural instability	±	ㅤ	+
Urinary disturbance	±	±	±
Memory or cognitive impairment	±	+	±
Difficulty performing familiar tasks	±	+	±
Behavioral changes	±	+	±
Limb rigidity	ㅤ	ㅤ	+
Limb tremor	ㅤ	ㅤ	+
Bradykinesia	ㅤ	ㅤ	+

ᵃAD = Alzheimer’s disease; IPA = idiopathic paralysis agitans (Parkinson’s disease); + = feature present; ± = feature partial or late
ᵇin NPH, the gait is often wide based, in IPA often narrow stance
Alzheimer: fully active but cant remember anything
NPH: is poor concentration rather poor memory

To be sorted

Shunt setting formula

IAP: intraabdominal pressure
OPV:
H: height
G: gravitty
Rou:
IVP: intra-ventricular pressure

Acetazolamide is a carbonic anhydrase inhibitor, hence causing the accumulation of carbonic acid. Systemically it primarily acts at the kidneys.

The correct answer is: Metabolic acidosis with respiratory compensation