doi:10.1111/ncn3.

117

REVIEW ARTICLE

Clinical manifestations of hydrocephalus: A review

Richard Schwamb, Amanda Dalpiaz, Yimei Miao, Jacquelyn Gonka, and Sardar Ali Khan
Department of Urology and Physiology, State University of New York Health Science Center, Stony Brook, New York, USA

Key words Abstract

adams triad, cerebrospinal fluid, normal
pressure hydrocephalus, shunt, urinary
incontinence.
Accepted for publication 18 August 2014.
Correspondence
Sardar Ali Khan, HSC Level 9 Room 040
SUNY at Stony Brook, Stony Brook, NY
11794-8093, USA. Email: skysalik@gmail.com
Background: Normal Pressure Hydrocephalus is a disease, which results from
excess cerebral spinal fluid, it is often misdiagnosed for other degenerative diseases.
Symptoms of Normal Pressure Hydrocephalus may be reversed with new treat-
ment techniques such as shunting.
Aims: The aim of this article is to review the pathophysiology of Normal Pressure
Hydrocephalus, discuss how to distinguish it from other diseases and discuss treat-
ment options, which show potential for treating Normal Pressure Hydrocephalus.
Methods: PubMed was used to conduct searches regarding the subject matter of
this article.
Results: Gait, dementia and urinary incontinence, which are also referred to as
Adam’s Triad, are typical associated with Normal Pressure Hydrocephalus. The
pathophysiology of these conditions has been outlined in this article. Review arti-
cles have been outlined which discuss the potential certain shunt operations have
to treat Normal Pressure Hydrocephalus.
Discussion: There are several known treatment options that have been successful
when treating Normal Pressure Hydrocephalus. With the use of shunts to drain
excess cerebral spinal fluid, it is possible to improve the patient’s symptoms and
thus improve their quality of life.
Conclusion: Normal Pressure Hydrocephalus should be considered when treating
elderly patients that show signs of Adam’s Triad. There are numerous types of
treatment options available that show promise as to relieving some of the symp-
toms that are associated with Normal Pressure Hydrocephalus.

CSF decreases as the age of an individual increases, result-

Introduction
Hydrocephalus is a disorder characterized by a buildup of
cerebrospinal fluid (CSF) in brain ventricles and cavities.
Typically found in infants, hydrocephalus is also reported in
elderly adults. Hydrocephalus is categorized into two classi-
fications: communicating and non-communicating. Commu-
nicating hydrocephalus occurs when there is an
overproduction of CSF, non-communicating hydrocephalus
occurs when an obstruction blocks CSF flow. Normal pres-
sure hydrocephalus (NPH) is a type of communicating
hydrocephalus in which the cerebral ventricles become
enlarged and CSF pressure fluctuates. Common clinical
manifestations of NPH include gait disturbances, dementia
and urinary incontinence (UI), referred to as the Adams
triad.1 The cause of NPH remains undetermined; however,
the decrease in reabsorption of CSF through arachnoid
granulations is the speculated trigger.
The normal CSF production rate produced in the choroid
plexus is 500 mL/day. Of this, 100–150 mL is reabsorbed.
The normal intracranial pressure of the brain is between
7 mmHg and 15 mmHg; therefore, treatment should be con-
sidered for anything above 20 mmHg.2 The turnover rate of
ing in the onset of neurogenic diseases. CSF also plays a sig-
nificant role in the interstitial fluid homeostasis, which has
an effect on neuronal functions.3
Normal pressure hydrocephalus affects patients aged
between 60 and 70 years,1 and is misdiagnosed as Alzhei-
mer’s disease (AD) because of the similar manifestations
between the two.4 Unlike AD, symptoms of NPH can be
reversible through shunt implantations and other medical
procedures.3 Different techniques used to diagnose NPH
include radiological testing, clinical diagnostic testing and
invasive diagnostic testing. One technique that can be
implemented to differentially diagnose AD from NPH is to
examine the distribution of cortical retentions of Pittsburgh
compound B (PIB). A study by Kondo took 10 patients
with idiopathic NPH (iNPH) and observed the cerebral
retention of PIB and compared them with seven patients
with AD. The results showed that three of the patients had
an increase in cortical PIB retention. The characteristic of
an increased PIB retention can be used to help differentiate
iNPH from AD.5
Parkinson’s disease and AD have similar characteristic
traits to NPH. It is important to differentiate these diseases

Neurology and Clinical Neuroscience 2 (2014) 173–177 173

ª 2014 Japanese Society of Neurology and Wiley Publishing Asia Pty Ltd
Manifestations of hydrocephalus
from one another before pursuing a treatment plan for the
patient. Ivkovic et al.6 showed that the shape of a mean dif-
fusivity histogram could differentiate NPH, AD and Parkin-
son’s disease from one another. Moore et al. carried out a
study with five NPH patients, five normal control (NC) par-
ticipants and 10 AD participants. Imaging measures that
were used to compare the separate groups were total intra-
cranial volume (TICV), Evans index, cortical thickness and
ventricular volume. The five NPH participants each had an
Evans index that was above the cut-off for ventricular
enlargement. Five AD participants and one NC participant
also scored above the cut-off. The NPH group had a larger
total intracranial volume than the other participants. Mea-
surements such as this one can be taken with magnetic reso-
nance imaging (MRI) to help differentiate NPH patients
from those with AD and Parkinson’s disease.7
Pathophysiology of urinary
incontinence
Sakakibara et al. inspected UI as a result of NPH. The
study used single-photon emission computed tomography
(SPECT) and statistical brain mapping to determine the
pathophysiology of UI. That study involved 97 NPH
patients with a mean age of 74 years. The results showed
that patients with severe UI had decreased tracer activity in
the right-side-dominant bilateral frontal cortex and left infe-
rior temporal gyrus. A relationship between UI and right
frontal hypoperfusion was noted. Positron emission tomog-
raphy scans carried out on normal patients showed that the
anterior cingulate, prefrontal cortex and insula play a role
in bladder filling. The cause of UI in NPH is associated with
right frontal hypoperfusion. Furthermore, urodynamic test-
ing in NPH patients showed detrusor muscle overactivity,
which is a loss of micturition reflex, indicating primary auto-
nomic dysfunction. This further exacerbates the symptoms
of UI in NPH patients.8 Another study showed a decreased
concentration of dopaminergic D2 receptor density in NPH
patients, which could also contribute to UI.9 The findings in
these studies can contribute to the pathophysiology of UI in
patients with NPH.
As the autonomic nervous system is crucial in controlling
UI, there should be a link between this system and NPH.
Kuriyama et al. carried out a study in which 18 patients
with NPH and 31 control patients were used to identify
autonomic function parameters that could affect bladder
control. A lumbar test was carried out while monitoring
heart rate. High frequency (HF) showed parasympathetic
activity, whereas low to high (L/H) frequency showed sym-
pathetic activity. The results from the study showed that HF
values were on average 190.3 for control patients and 237.2
for NPH patients. However, lumbar puncture resulted in the
average HF value dropping to 160.3 in the NPH patients.
This suggested that NPH is associated with increased para-
sympathetic activity, which returns to normal after lumbar
puncture.10
To see if there were other links to brain abnormalities
and NPH, Ishii et al. aimed to investigate cerebral blood
flow patterns in patients with NPH. A total of 84 patients
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R Schwamb et al.
with NPH who underwent shunt operation were studied.
Results showed that after surgery, frontal-dominant perfu-
sion and whole-brain perfusion declined in NPH patients,
with 88% of patients having a significant reduction in fron-
tal perfusion. Brain anatomy showed dilated ventricles and
a Sylvian fissure. Furthermore, the study showed increased
perfusion in the parietal lobe and medial portion of the
frontal lobe.11
Along with MRI, cystometry is another important tool
used to evaluate bladder dysfunction. Jonas et al.12 used
cystometry to diagnosis patients with neurogenic bladder,
which is caused by neurological dysfunction. Magnetic reso-
nance diffusion tensor imaging (DTI) can be used to diag-
nose NPH, and obtain a fractional anisotropy (FA) brain
map. Koyama et al. carried out a study that analyzed 24
patients with NPH. All participants underwent DTI, with
imaging focused on the corpus callosum, posterior limb of
the internal capsule and cerebral peduncle. The results
showed that NPH patients had significantly lower FA values
compared with the control group; specifically, the corpus
callosum region had significantly lower FA values, whereas
the posterior limb of the internal capsule had higher values
than average. Additionally, the lower FA values were associ-
ated with higher severity of gait.13
Urinary incontinence naturally increases as people age.
There are different classifications of UI including urge, over-
flow, stress, mixed and functional. Initially, a patient ques-
tionnaire is carried out to evaluate UI. This questionnaire
consists of questions that evaluate the severity of UI. Stress
incontinence can be tested through a cough stress test, which
is currently the preferred method for diagnosis. Urge is the
most prevalent type of UI, and is caused by detrusor over-
activity. UI patients generally complain of a loss of urine
during physical activity or activities involving intra-abdomi-
nal pressure. Other causes of UI include anatomical defects
of cognitive disabilities. In order to help diagnose UI,
doctors might ask patients to keep a voiding diary, which
will allow for a better-tailored treatment plan prescribed by
the doctor.14
Pathophysiology of gait
Gait disturbances are common in NPH patients.15 Gait
symptoms are seen in elderly patients and are associated
with NPH. Gait increases in severity as NPH progresses.
When diagnosing gait disturbances, it is important to assess
one’s feet and posture, both might cause gait abnormalities.4
Gait disorder characteristics typically include falls, impaired
motion and an overall depressed quality of life.16 Gait is
one of the easily treated symptoms of NPH, as it typically
resolves after a patient is shunted.
The pathophysiology of gait occurrence related to NPH
has been linked to midbrain diameter. A study carried out
by Lee et al. correlated the mesencephalic locomotor region
to the onset of hypokinetic gait. That study used 20 patients
with NPH showing gait disturbance, and measured the max-
imum diameter of the midbrain and pons along with the
width of the lateral and third ventricles. That study showed
that the maximal midbrain diameter was smaller in NPH
Neurology and Clinical Neuroscience 2 (2014) 173–177
ª 2014 Japanese Society of Neurology and Wiley Publishing Asia Pty Ltd
R Schwamb et al.
patients than the control group. The width of the midbrain
was also adversely correlated to the severity of the patient’s
gait. That study suggested that midbrain diameter has a neg-
ative correlation to gait severity in patients with NPH.17
Hiraoka et al. also hypothesized that the midbrain region
is responsible for gait disturbances in NPH patients. A total
of 21 patients undergoing shunt surgery had their MRI
scans studied before and after surgery. The MRI scans did
not show any changes in diameter and cross-sectional area
of the midbrain after shunting.18 Because shunting has been
proven to improve gait function in NPH patients,19 the lack
of change in midbrain diameter reported by Hiraoka et al.18
serves as evidence that refutes the original hypothesis that
midbrain abnormalities are associated with gait dysfunction
in NPH. The gait associated with NPH can appear similar
to the shuffling gait commonly seen in Parkinson’s disease.
Therefore, when making a diagnosis of NPH it is important
to rule out Parkinson’s disease.
Pathophysiology of dementia
Another clinical manifestation of NPH is dementia, which is
a cognitive impairment that results in multiple deficits, such
as slowed speech, short-term memory impairment, loss of
concentration and fine motor skill decline. Dementia is an
early clinical sign of NPH, and should be used to differenti-
ate NPH from other disorders during this stage.1 Diagnostic
tests for dementia include Stroop, digit span, Rey auditory-
verbal learning and grooved pegboard tests, as well as radio-
logical findings.4 Shunting has been successful in decreasing
dementia caused by NPH in approximately 80% of patients.
However, shunting will not improve dementia in AD
patients or patients suffering from other neurological disor-
ders.4,17 Frontal temporal lobar degeneration (FTLD) is a
common cause of dementia with patients that are aged
60 years and younger. Biomarkers for dementia, using MRI
scans, focus on frontal and/or anterior temporal atrophy.20
The pathophysiology of dementia from the progression of
NPH could be related to a chemical imbalance caused by a
reduction in CSF. Kaiya et al. reviewed a beta-endorphin-
like immunoreactivity that is present in CSF. This beta-
endorphin was observed in lower amounts in patients with
dementia symptoms. This relates to NPH, because patients
with NPH show a decrease in CSF, which results in a
decrease in beta-endorphin. This could be one of the main
pathophysiologies behind dementia in NPH.21
The clinical manifestation of dementia relating to NPH is
not very well understood, although there are case studies
that point to some plausible causes of dementia. In a cast
report carried out by Smith et al., a 70-year-old patient was
observed and treated for NPH. The patient complained of
worsening memory problems and was then examined. After
computed tomography (CT) scans, there was worsening dila-
tion of frontal horns of the lateral ventricles, and the
patient’s posterior portion of the ventricular system col-
lapsed entirely. The worsening dilation leads to poorer
blood flow. It has been speculated that impaired cerebral
blood flow is linked to the onset of symptoms associated
with NPH.22
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ª 2014 Japanese Society of Neurology and Wiley Publishing Asia Pty Ltd
Manifestations of hydrocephalus
Diagnosis
Diagnosis of NPH can be made based on radiological find-
ings, or through invasive testing. MRI or CT scans can be
used look for disproportionate widening of the ventricles
compared with the cerebral sulci as a marker for NPH.
When running tests, the coronal section from the level of
posterior commissure shows a narrow subarachnoid space
surrounding the outer brain with an enlarged third ventri-
cle.2 Evans index with the corpus callosum angle on a MRI
screening is also very useful to show differential diagnosis
with cerebral atrophy.
Spinal taps along with continuous spinal drainage can
be used not only for diagnosis, but also for improving
symptoms of NPH.2 The spinal tap test involves removal of
30–50 mL of CSF, and assessment of the patient’s gait
before and after the test. Improvement in gait confirms the
diagnosis of NPH.23
Treatment
The use of shunts, either ventriculoperitoneal (VP) or lum-
boperitoneal shunts, has been shown to improve symptoms
of NPH.21 Poca et al.24 studied 244 patients who were
shunted. The results showed that 82.4% of patients exhib-
ited clinical improvement in sphincter control. Valves
located within the pump are either programmable or drain
based. Tests have been carried out to determine whether
gravitational valves better reduce the risk of overdrainage in
comparison with programmable valves. Lemcke et al. com-
pared the data of NPH patients that had shunts with a grav-
itational valve compared with those with a programmable
valve after VP surgery. VP shunts are prone to overdrai-
nage, which occurs with postural changes. The study used
clinical and radiological signs, such as nausea, headache,
vomiting, slit ventricle or subdural effusion, as primary end-
points. The results of the study concluded that the use of a
gravitational valve over another type reduced the risk of
overdrainage in 33% of patients.25 The standard treatment
for NPH is a VP shunt.21
Ventriculoperitoneal shunt implantation has a complica-
tion rate of 38%, with a hemorrhage rate that approaches
10%.21 Giesemann et al. described an 82-year-old patient
who had a VP implanted years before the study, who com-
plained of visual problems and headaches. CT scans showed
that the catheter tip was placed too deeply, with the tip tra-
versing the third ventricle and penetrating the midbrain tec-
tum precisely in the midline.26 Placement of VP shunts
might result in the formation of a subdural hematoma.
Patients with NPH are at an increased risk for a subdural
hematoma as a result of reduced intracranial pressure
caused by overdrainage of CSF. Hayes et al. described a
63-year-old patient who experienced head trauma with a VP
shunt placement. CT scans showed a subdural hematoma.
Treatment involved a change in the valve setting, which
reduced the drainage of CSF. After a couple days, the
patient began to complain of gait ataxia and UI. CT scans
showed an acute subdural hematoma and dilated ventricles,
175
Manifestations of hydrocephalus
Table 1 Different types of shunt procedures and their use
Type of shunt Uses
Ventriculoperitoneal Drains excess CSF into the abdomen30
Ventriculoatrial Drains excess CSF into right atrium
of the heart31
Ventriculopleural Drains excess CSF into the lungs or chest32
Ventriculogallbladder Drains excess CSF into the gall bladder33
Lumboperitoneal shunt Drains excess CSF into the peritoneal
cavity34
CSF, cerebrospinal fluid.
indicating the re-emergence of NPH. The settings on the
valve were once again changed, resulting in more CSF
drained, causing a complete resolution in the patient’s symp-
toms.27 Even though shunts have been shown to resolve
symptoms of NPH, they are typically inserted by a free-
handed technique that is guided by landmarks, which can
result in complications. One case reported a patient who suf-
fered bilateral palsy after the catheter damaged the trochlear
nerve.26
Chung et al. aimed to help relieve overactive bladder
problems that were associated with VP shunt implantations
in 53 iNPH patients. The study tested a drug called solifena-
cin in the hope of increasing bladder capacity to treat
patients with overactive bladders. After the trial was com-
pleted, the overactive bladder symptom score and Interna-
tional Prostate Symptom Score had both improved in the
remaining 38 patients who completed the trial. The overall
consensus for that experiment was that solifenacin is effec-
tive in the treatment of patients with overactive bladder.28
An alternative to a VP shunt is a lumboperitoneal shunt
(LP) with horizontal vertical valves (HVV). Bloch et al.
reported of the 33 patients treated with LP-HVV, 100% had
gait improvement, 46% had an improvement in incontinence
and 55% had an improvement in memory. LP-HVV shunt
usage is safe and effective, and should be considered as an
alternative to ventriculoperitoneal shunt placement. Bloch
et al. reported that out of 33 patients that had an LP shunt,
27% had failure of the shunt requiring surgery, whereas 6%
had an infection. Overdrainage of CSF and neurological
complications, such as hemorrhage, are low risk, making
LP-HVV a safe procedure.29 Table 1 shows the different
types of shunt procedures and their use.30–34
The delayed treatment of NPH has serious consequences.
Andren et al. studied 102 NPH patients in whom shunt
placement was delayed. The study took 33 patients who
waited 6 months for shunt placement, and 69 who waited
3 months. After receiving implantation, both groups had
improvements of their symptoms, but the final outcome for
the group that waited 6 months was significantly worse.35
Conclusion
Controversies as to whether shunts are effective in all
patients were discussed in a study carried out by Hamilton
et al. That study was composed of 37 patients with iNPH
who were studied to see whether their symptoms of gait, UI
and dementia improved, worsened or stayed the same. It
176
R Schwamb et al.
was found that patients with moderate pathology had an
improvement in their symptoms, whereas patients with
severe pathology did not show significant signs of improve-
ment after shunting.36 This could be as a result of the condi-
tion worsening and becoming untreatable after a certain
period of time.
Normal pressure hydrocephalus should be taken into con-
sideration when dealing with a patient that shows all of the
symptoms of the Adams triad. Through diagnostic testing, it
is possible to identify NPH and administer treatment for the
patient. The risks and benefits of a shunt surgery should be
considered before surgery is carried out in order to deter-
mine the best option for the patient.
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