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78
Specicity
(%) AUC
nICP method accuracy and
correlation measures with ICP Sensitivity (%)
a
prior to shunting was
signicantly increased.
Pre-shunting ICP and PI were
not correlated (R=0.37)
with midline shift as indication
)
of elevated ICP (R=0.66
69
(threshold
of
10mmHg)
99
(threshold
88 (threshold of
10mmHg)
83 (threshold of
20mmHg)
a
(ICP=10.93×PI1.28)
In the ICP range of
5–40mmHg, the correlation
was R=0.94
formula is:
of
20mmHg)
a
)
a
=0.73
2
In this interval, SD for nICP_PI
was ±2.5mmHg in the ICP
ICP=11.5×PI–2.23
(R
ICP and PI was R=0.64
range of 5–40mmHg
95% CI of ±4.2mmHg
D. Cardim and C. Robba
a
=0.22
2
For ICP 20mmHg,
correlation was R=0.82aPI allows early identication of
patients with low CPP and risk
(ICP=23×PI+14)
of cerebral ischaemia
was R
95% CI for a mean ICP of
20mmHg was 3.8 to
43.8mmHg
PI is not a reliable predictor of
ICP
Invasive ICP
monitoring
Epidural PI in patients with elevated ICP
Sample size and
disease
29,
Rainov etal. [59] Investigate a
Method Author Study purpose
Table 8.1 (continued)
Hydrocephalus
possible
relationship
between PI, RI, FV
and ICP changes in
adult patients with
NM Increases in PI were correlated
18, Stroke and
MCA infarction
hydrocephalus.
with clinical
Asil etal. [60] TCD was compared
Intraventricular Correlation between PI and ICP
81 (SAH, TBI
and other
intracranial
relationship
ndings.
between ICP and PI
examination and
neuroradiologic
Bellner etal. [61] Investigate the
disorders)
in neurosurgical
patients.
37, TBI Intraparenchymal Overall correlation between
a tool for detection
of cerebral
haemodynamic
Voulgaris etal. [62] Investigate TCD as
10, INPH Intraparenchymal Correlation between PI and ICP
changes
Behrens etal. [63] Validate TCD as a
method for ICP
determination of
INPH
8 Transcranial Doppler andOptic Nerve Ultrasonography forNon-invasive ICP Assessment
79
88
(threshold
of
20mmHg)
25 (threshold of
20mmHg)
a
No signicant relationships
between PI and ICP when
differences within individuals
or binary examination of PI (PI
<1 and 1) were considered
PI and ICP of R=0.36
PI is not a reliable non-invasive
95 (for
detecting
initial ICH)
94 (for
detecting initial
ICH)
nICP similar to measured ICP,
with nICP of 10.6±4.8 and
indicator of ICP in children
with severe TBI
ICP of 10.3±2.8mmHg
PI 1.31 was observed in 94%
of cases with initially elevated
ICP, and 59% of those with
0.62 (ICP
15mmHg)
a
normal initial ICP values
TCD is an excellent rst-line
examination to screen children
who need urgent treatment and
continuous invasive ICP
monitoring
was R=0.31
0.74 (ICP
35mmHg)
a
95% Prediction interval
>±15mmHg
The value of PI to assess nICP
is very limited
in such situations was R=0.70
(continued)
95% CI of ±21mmHg
NM Marginal correlation between
34 Children,
TBI
relationship
between PI, ICP
and CPP in children
with severe TBI
Figaji etal. [64] Examine the
Intraparenchymal
45, TBI Intraventricular Bellner’s equation resulted in
Brandi etal. [65] Assess an optimal
117 Children,
TBI
nICP and nCPP
following TBI using
TCD.
Evaluate the
accuracy of TCD in
Tude Melo etal.
[66]
emergency settings
to predict
intracranial
hypertension and
abnormal CPP in
290, TBI Intraparenchymal Correlation between PI and ICP
diagnostic tool for
nICP and nCPP
children with TBI.
estimation.
Zweifel etal. [67] Assess PI as a
345, TBI Intraparenchymal Correlation between PI and ICP
relationship
between PI and
CVR in situations
where CVR
increases (mild
hypocapnia) and
decreases (plateau
waves of ICP) in
TBI patients.
De Riva etal. [8] Assess the
80
Specicity
(%) AUC
81.1 96.3 0.84
a
nICP method accuracy and
correlation measures with ICP Sensitivity (%)
0)
2
(threshold
20cmH
Binomial logistic regression
indicated a strong signicant
relationship between raised ICP
and PI (OR: 2.44; 95% CI:
1.57–3.78)
(CSF pressure) was R=0.65
with rapid elevations of PI.On
Initial 24h
post-injury
82
Initial 24h
post-injury
100 (threshold
a
recording day 4, PI was
reported to be 1.93 (considering
a normal range of 0.6–1.2). ICP
was deemed elevated according
to clinical status (level of
consciousness, headache) and
papilledema
Initial 24h post-injury
Correlation between PI and ICP
was R=0.6
(threshold
20
mmHg for
PI of 1.3)
diastolic ow velocity, ICH intracra-
d
20mmHg for
PI of 1.3)
Beyond 24h
post-injury
47 (threshold
20mmHg for
PI of 1.3)
a
Beyond 24h post-injury
Correlation between PI and ICP
was R=0.38
D. Cardim and C. Robba
Invasive ICP
monitoring
LP Correlation between PI and ICP
Sample size and
disease
78,
Miscellaneous
intracranial
disorders
correlation between
PI with CSF
pressure.
Wakerley etal. [68] Assess the
NM Increasing ICP was associated
Case report,
sagittal sinus
thrombosis
where TCD serves
as an effective tool
for nICP
monitoring.
Wakerley etal. [69] Present a case
Intraventricular/
intraparenchymal
36 Children,
TBI
d
and ICP in children
with severe TBI.
relationship
between PI, FV
O’Brien etal. [70] Determine the
coefcient of determination, RI resistance index, SAH subarachnoid haemorrhage, SD
2
jugular bulb venous blood oxygen saturation, TBI traumatic brain injury
2
Method Author Study purpose
Table 8.1 (continued)
ABP arterial blood pressure, AUC area under the curve, CI condence interval; CT computerised tomography, CSF cerebrospinal uid, FV
Correlation coefcient is signicant at the 0.05 level
nial hypertension, INPH idiopathic normal pressure hydrocephalus, LP lumbar puncture, MCA middle cerebral artery, NA not available, NM not measured, NPV negative predic-
tive value, OR odds ratio, PPV positive predictive value, R correlation coefcient, R
a
standard deviation, SJO
()
Pm
=-
8 Transcranial Doppler andOptic Nerve Ultrasonography forNon-invasive ICP Assessment
81
8.3 Methods Based ontheCalculation ofNon­invasive CPP (nCPP)
Many authors have also investigated methods based on the primarily intended calculation of non­invasive cerebral perfusion pressure (nCPP), and secondarily calculating non-invasive ICP based on the assumption that “nICP=ABPnCPP”. nICP methods based on TCD-derived cerebral perfusion pressure are listed in Table8.2.
8.3.1 Aaslid etal. [12] (nICP
Aaslid etal. (1986) [12] were the pioneers in the development of a mathematical model for non- invasive estimation of CPP based on TCD waveform analysis. Supported by the knowl­edge that increased ICP was related to decreases of the ow waveform in the internal carotid artery [13], the authors deemed feasible that less evident changes in the ow pattern could be detected by more rened methods of wave­form analysis. TCD, in such a perspective, could be used to obtain an estimate of ICP. Considering CPP as the driving force to ow through the cerebral vascular bed and the main factor determining pulsatile dynamics, the ow would be approximately proportional to CPP [12].
During increases in ICP, the proportion of the systolic to the diastolic CPP increases as ICP approaches the diastolic ABP.Consequently, the pulsatile component of CPP increases propor­tionally to its mean value and this would also be reected in the FV waveform. Thus, the ratio between mean FV (FVm) and pulsatile amplitude of FV (f1) would be expected to be related to CPP.The simplest approach, in this case, would be using this ratio as an index for CPP.However, it does not consider changes in the ratio caused by variations in the amplitude of ABP waveform. Such limitation was solved by multiplying the ratio described above by the amplitude of the rst harmonic of ABP (a1) [12]:
nCPP FV mmHg
=
Aaslid m
´/ fa11
Aaslid
)
This method was tested in patients with supra­tentorial hydrocephalus undergoing ventricular infusion tests. The linear regression determined for nCPP estimation considering all cases was
CPPnCP
11 5.
Aaslid
mHg
In the individual case, there was a strong corre­lation between nCPP and CPP, R=0.93–0.99. The standard deviation between nCPP and CPP was
8.2mmHg at 40mmHg, while the mean deviation was only 1mmHg. Overestimation occurred in two cases, 10 mmHg and 18 mmHg, respectively. Underestimation was present in other two cases, 9 and 8mmHg, respectively. For the six remaining cases, the estimates were within ±5mmHg of mea­sured CPP. The method could differentiate cor­rectly between low (<40 mmHg) and normal (>80mmHg) CPP in all patients. At higher levels of CPP, the estimates presented with low accuracy, showing correct differentiation between CPPs of 70 and 100mmHg in 80% of the cases.
8.3.2 Czosnyka etal. [14] (nICP
FVd
)
Some studies have demonstrated that certain pat­terns of the TCD waveform, like a decrease in FVd, reect impaired cerebral perfusion caused by a CPP decrease [14, 15]. Czosnyka et al. [14] described this relationship as the following formula:
FV
nCPP ABP
=´+ 14mmHg
FV
d
FV
d
m
The correlation between nCPP and invasively measured CPP in traumatic brain injury (TBI) patients was R= 0.73, p<0.001. In 71% of the examinations, the estimation error was below 10mmHg, and in 84% of the examinations, the error was less than 15mmHg. The method had a high positive predictive value (94%) for detecting low CPP (<60 mmHg). Estimated CPP was highly specic for detecting changes in measured CPP over time, caused by either increases in ICP (plateau waves) or systemic hypotension. In six patients presenting plateau waves, nCPP com­pared with measured CPP had an average goodness- of-t coefcient R2 of 0.82.
82
94 (CPP
60mmHg)
D. Cardim and C. Robba
(20mmHg)
nICP/nCPP method accuracy and
correlation measures with ICP/CPP AUC PPV (%) NPV (%)
40mmHg
Able to differentiate between low
(40mmHg) and normal (80mmHg) CPP
in all cases
Low accuracy (80%) at higher levels of CPP
Invasive ICP
monitoring
Intraventricular SD for nCPP estimation of 8.2mmHg at
Sample size and
disease
10, Supratentorial
hydrocephalus
Sensitive to detect changes of CPP over time
(70–100mmHg)
. 96, TBI Intraparenchymal 95% PE for nCPP estimation was >27mmHg
Aaslid
Describe and assess a
method for nCPP
calculation based on
FV and ABP.
Aaslid etal.
[12]
Assess nICP
Czosnyka
etal. [14]
a
Estimation error was less than 10 and
R=0.73
=0.82
2
15mmHg in 71% and 84% of the cases,
respectively
Highly specic for detecting changes over
time: R
Averaged correlation considering day-by-day
variability between CPP and nCPP was
R=0.71
96, TBI Intraparenchymal Correlation between nCPP and CPP was
Describe and assess a
method for nCPP
calculation based on
FV (using the
concept of FVd) and
ABP.
Czosnyka
etal. [14]
a
Mean values of nCPP and CPP were
66.10±10.55mmHg and
and 13mmHg in 89% and 92% of the cases,
respectively
95% CI of ±12mmHg
R=0.92
65.40±10.03mmHg, respectively
Bias of 5.6mmHg and 95% CI of
±17.4mmHg
nCPP:
45, TBI Intraparenchymal nICP:
. 25, TBI Intraparenchymal Error for nCPP estimation was less than 10
FVd
Assess nICP
Schmidt
. 47, TBI Intraparenchymal Correlation between nCPP and CPP was
FVd
Assess an optimal
nICP and nCPP
following TBI using
Assess nICP
etal. [71]
Gura etal.
[72]
TCD.
Brandi etal.
[65]
Bias of 6.2mmHg and 95% CI of 11.8mmHg 0.96
Bias of 5.5mmHg and 95% CI of
±20.6mmHg
28
Intraparenchymal,
10 intraventricular
injury
. 38, Acute brain
FVd
Assess nICP
Rasulo etal.
[73]
Aaslid
Method Author Study purpose
Table 8.2 nICP methods based on non-invasive cerebral perfusion pressure estimation
nICP
FVd
nICP
8 Transcranial Doppler andOptic Nerve Ultrasonography forNon-invasive ICP Assessment
83
0.91
(20mmHg)
0.34
(20mmHg)
a
(R=0.17)
R=0.30
nCPP and CPP were correlated (slope, 0.76;
intercept, 10.9; 95% CI, 3.5 to 25.4mmHg)
During hypercapnia:
nCPP and CPP were correlated, but with
increased discrepancy, as reected in
Intraparenchymal Correlation between ICP and nICP was
ischaemic brain
injury after
cardiac arrest
20, TBI Intraparenchymal During normocapnia:
. 100, TBI Intraparenchymal No correlation between ICP and nICP
. 11, Hypoxic-
FVd
FVd
reactivity
2
>0.8
a
Bias of 6.8mmHg and 95% CI ±19.7mmHg
nCPP:
condence interval (slope, 0.55; intercept,
32.6; 95% CI, 16.3–48.9mmHg)
Bias of 6.8mmHg and 95% CI ±45.2mmHg
Bias ± SD of 4.02±6.01mmHg
R=0.85
280, TBI Intraparenchymal Correlation between nCPP and CPP was
. 45, TBI Intraparenchymal nICP:
Edouard
nCPP estimation error was below 10mmHg in
83.3% of the cases
Temporal analysis:
Mean correlation in time domain was R=0.73
(0.23–0.99)
a
Correlation between nCPP and CPP was
Bias of 3.45mmHg (range: 4.69–9.03mmHg)
Mean SD of 5.52mmHg (range: 1.52–
R=0.67
10.76mmHg) and 95% CI of the SD of
1.89–5.01mmHg
Bias of 19.61mmHg
95% CI: ± 40.1mmHg
Temporal analysis:
Mean correlation in time domain was R=0.55
(±0.42)
2
coefcient of determination, SD standard deviation, SAH subarachnoid haemorrhage, TBI traumatic brain injury
Assess nICP
Assess nICP
Cardim etal.
[74]
Cardim etal.
[42]
Describe and assess a
method for nCPP
calculation based on
Edouard
etal. [16]
Edouard
test.
FV and ABP under
stable conditions and
during CO
nICP
Assess nICP
Brandi etal.
[65]
Describe and assess a
method for nCPP
calculation based on
FV (using the
concept of CrCP) and
ABP.
Varsos etal.
[18]
CrCP
nICP
Describe and assess a
method for nCPP
calculation based on
FV and ABP.
Abecasis &
Cardim etal.
[24]
Spectral
nCPP
AUC area under the curve, ABP arterial blood pressure, CI condence interval, FV cerebral blood ow velocity, NPV negative predictive value, PPV positive predictive value,
PE prediction error, R correlation coefcient, R
Correlation coefcient is signicant at the 0.05 level
a
84
()
ë
û
D. Cardim and C. Robba
Furthermore, nCPP was very sensitive to detect­ing decreases in ABP below 70 mmHg (in ten patients) with an average R2 of 0.92. A good cor­relation was found between the average measured CPP and nCPP when day-by-day variability was assessed in a group of 41 patients (R=0.71).
8.3.3 Edouard etal. [16] (nICP
Edouard
)
This method is based on a non-invasive assessment of CPP using a combination of phasic values of both FV in the MCA and
æ
FV
nCPP
Edouard
=
ç
FV FV
-
md
è
m
ABPm and ABPd represent the mean and dia-
stolic ABP, respectively.
Twenty adults with bilateral and diffuse brain injuries were included in the study and subdi­vided into two groups. In group A (N=10), the comparison was repeatedly performed under sta­ble conditions. In group B (N=10), the compari­son was conducted during a CO2 reactivity test. nICP was not estimated in this study. In group A, nCPP and measured CPP were correlated (slope,
0.76; intercept, +10.90; 95% CI, 3.50 to +25.40). The relationship persisted during ICP increase caused by the reactivity test in group B (slope, 0.55; intercept, +32.60; 95% CI, +16.30 to +48.90). However, the discrepancy between nCPP and measured CPP increased as reected by the increase in bias and variability.
8.3.4 Varsos etal. [18] (nICP
CrCP
)
The concept of critical closing pressure (CrCP) was first introduced by Burton’s model,
ABP.It was primarily validated in preeclamp­tic and healthy pregnant women by comparing nCPP with CPP measured at the epidural space [17].
In Edouard etal.’s prospective study [16], the objective was to assess the adequacy of such method for TBI patients with invasive ICP moni­toring, in both a stable state and during a rapid change in cerebrovascular tone following an induced alteration in arterial blood carbon diox­ide pressure (PaCO2).
The non-invasive CPP (nICP
Edouard
) was calcu-
lated using the following formula:
ö
ABPABP mmHg
´-
÷ ø
md
described as the sum of ICP and vascular wall tension (WT) [19]. WT represents the active cerebral vasomotor tone that combined with ICP determines the CrCP. Clinically, CrCP represents the lower threshold of ABP below which blood pressure in the brain microvascu­lature is inadequate to prevent the collapse and cessation of blood flow [19]. CrCP can be assessed non-invasively using TCD, by com­paring the pulsatile waveforms of FV and ABP.Given the relationship with the vasomo­tor tone of small blood vessels, CrCP can pro­vide information regarding the state of cerebral haemodynamics and reflect changes in CPP [1923].
The conception and assessment of the model for the non-invasive estimator of CPP (nCPP
) were performed using a cohort of
CrCP
280 TBI patients, divided into two subgroups: the formation group with 232 patients (including 455 recordings) and the validation group with 48 patients (including 325 recordings):
nCPP ABP
=´ -
CrCP
é ê
.
ê ê
()
0 266
.
CVRC HR
×× ×
a
21
ù ú
-0 734
2
ú
p
+
ú
.
7 026
m
mmHg
ABP
FV
C
CBV
a
1
1
8 Transcranial Doppler andOptic Nerve Ultrasonography forNon-invasive ICP Assessment
85
CVR
=
a
=
a
CVR (mmHg/(cm/s)) represents cerebral vas-
cular resistance, C
(cm/mmHg) denotes compli-
a
ance of the cerebral arterial bed (arteries and arterioles) and HR represents heart rate given in beat/s. a1 represents the pulse amplitude of the rst harmonic of the ABP waveform; f1 the pulse amplitude of the rst harmonic of the FV wave­form; and CaBV1 the pulse amplitude of the rst harmonic of the cerebral arterial blood volume waveform (CaBV). The pulse amplitude of rst harmonics is determined with fast Fourier trans­formation (FFT).
nCPP
using data from the validation group. nCPP
was tested against invasive CPP
CrCP
CrCP
was correlated with measured CPP (R = 0.85, p<0.001), with a bias of 4.02±6.01mmHg, and in 83.3% of the cases with an estimation error below 10mmHg. nCPP
prediction analysis at
CrCP
low CPP limits (50, 60 and 70mmHg) resulted in AUCs greater than 0.8 for all limits. nCPP
CrCP
was found to be strongly correlated with CPP changes in the time domain (mean R = 0.73, range 0.23–0.99). For each patient, nCPP
CrCP
pre­sented a mean difference from CPP of 3.45mmHg (range 4.69–19.03mmHg), and a mean standard deviation of this difference of 5.52mmHg (range
1.52–10.76mmHg). nCPP
could predict CPP
CrCP
between multiple recording sessions with a 95% CI of 1.89–5.01mmHg.
8.3.5 Abecasis andCardim etal.
(Spectral nCPP) [24]
This recently proposed method is based on accounting for changes in pulsatile cerebral arte­rial blood volume (CaBV) applied to the analysis of a simplied hydrodynamic model of CBF and CSF dynamics [2527]. The spectral feature of the method has some advantages: it creates par­tial independence from the inaccuracy associated with zeroing ABP transducers at heart level (a common clinical practice) and partially elimi-
nates the issue of the time delay between periph­eral ABP and FV in the MCA.The dynamical model of CSF and cerebral blood circulation pro­posed by Ursino and Lodi [25, 26] is the theoreti­cal basis for the spectral nCPP method; the former has also been modied by other authors to incorporate changes in cerebral blood volume and adapted to nICP or nCPP estimations. nICP
[28] described in Sect. 8.4 is one exam-
Heldt
ple. Similarly to this method, spectral nCPP pro­duces patient-specic CPP estimates and does not require calibration datasets of reference patients.
Abecasis and Cardim etal. [24] assessed spec­tral nCPP on a retrospective analysis from 19 children (69 TCD recordings). Spectral nCPP presented good correlation with CPP measure invasively (R= 0.67 (p< 0.0001)), and a good mean correlation in time domain (R=0.55±0.42). Spectral nCPP also demonstrated strong ability to predict values of CPP below 70mmHg (AUC of 0.908 (95% CI=0.83–0.98)). The agreement between spectral nCPP and invasive CPP assessed by Bland-Altman analysis revealed that nCPP overestimated invasive CPP by 19.61 mmHg with a wide 95% CI of ±40.4mmHg.
8.4 Methods Based
onMathematical Models Associating Cerebral Blood Flow Velocity andArterial Blood Pressure
Several authors have proposed mathematical models that simulate the cerebrovascular dynam­ics using simultaneous FV and ABP measure­ments. nICP methods based on mathematical models are listed in Table8.3.
8.4.1 Black-Box Model forICP
Estimation (nICP
In this model, the intracranial compartment is considered a black-box (BB) system, with ICP being a system response to the incoming signal ABP [29]. This mathematical model originates
)
BB
86
Specicity
(%) AUC
Sensitivity
(%)
CSF
D. Cardim and C. Robba
For Mx: 92
For PRx: 67
For Mx: 97
CSF
CSF
CSF
a
For PRx: 61
and R
CSF
a
nICP method accuracy and
correlation measures with ICP
1.8mmHg
In this cohort a maximum 95% CI of
±12.8mmHg was found
Correlation between nR
was R=0.73
Invasive ICP
monitoring
Sample size and
disease
11, TBI Epidural Bias of 4.0mmHg and SDE of
Epidural Analysis across all records:
21, Different
types of
hydrocephalus
and R
CSF
a
prediction of 2.2mmHg minute/ml
Analysis specic to different
subtypes of hydrocephalus:
Bias of 4.1mmHg and SDE for R
Correlation between nR
was R=0.89
during ICP increase was R=0.98
prediction of 1.7mmHg min/ml
Bias of 2.7mmHg and SDE for R
Intraparenchymal Correlation between nICP and ICP
17, TBI (plateau
(A) waves
.
BB
during plateau
BB
Analysis considering the baseline of
plateau waves:
Bias of 8.3mmHg and SDE of
5.4mmHg
Analysis considering the top of
plateau waves:
Bias of 7.9mmHg and SDE of
4.3mmHg
Increases of nICP and direct ICP
Correlation between nMx and Mx
during plateau waves:
R=0.98 (p<0.001)
Intraparenchymal/
observed in 7
patients)
145 (135 TBI, 10
a
was R=0.90
Correlation between nPRx and PRx
was R=0.62aMedian bias of 6.0mmHg
Only TBI:
Bias of 7.1mmHg
Only stroke:
Bias of 4.3mmHg
intraventricular
stroke)
using nICP
Describe and assess a method
for nICP calculation based on
FV and ABP using a black-box
model.
This study aimed at predicting
Schmidt
etal. [29]
Schmidt
BB
Method Author Study purpose
Table 8.3 nICP methods based on mathematical models
nICP
CSF
the time course of raised ICP
during CSF infusion tests and
its suitability for estimating the
R
etal. [75]
waves of ICP.
Assess nICP
Schmidt
etal. [76]
to adapt to the SCA,
BB
using Mx and PRx as
This study aimed at
Schmidt
parameters
investigating the ability of
nICP
etal. [77]
8 Transcranial Doppler andOptic Nerve Ultrasonography forNon-invasive ICP Assessment
0.83
(20mmHg)
0.88
(20mmHg)
70
80
83
90
(linear)
BB
0.92
87
resistance to cerebrospinal
CSF
Correlation between nICP and ICP
was R=0.90
Bias of 1.6 and SDE of ±7.6mmHg
Inferred 95% CI of ±14.9mmHg
Across bilateral TCD records:
Correlation between nICP and ICP
was R=0.76
Bias 1.5 and SDE 5.9mmHg
Inferred 95% CI of ±11.6mmHg
On a patient record basis:
Intraparenchymal Across all TCD records:
37 (45 TCD
recordings in
total, 30 bilateral),
TBI
Describe and assess a method
for nICP calculation based on
FV and ABP.
Kashif and
Heldt etal.
[28]
Biases for non-linear models were
<6.0mmHg compared to 6.7mmHg
Correlation between nICP and ICP
was R=0.90 (N=45 recordings)
of the nICP
Inferred 95% CIs for non-linear
models were ±10.8mmHg,
Intraparenchymal/
intraventricular
23 (14 TBI, 9
hydrocephalus)
.
BB
Describe and assess a method
for nICP calculation based on
FV and ABP, using an
appropriated model for nICP
Xu etal.
[33]
mining nICP and ICP was R=0.80
compared to 10.6mmHg of the
linear model
9, TBI Intraventricular Median correlation between data
Describe and assess a method
for nICP calculation based on
[38]
Decision curve analysis showed that
method presented a median bias of
57, TBI NM Kernel spectral regression-based
FV and ABP based on the
concepts of data mining.
Describe and assess a method
for nICP calculation based on
Kim etal.
[39]
the semi-supervised method is more
4.37mmHg
Intraparenchymal/
intraventricular
90 (44 TBI, 36
SAH, 10 NPH)
Describe and assess a method
for nICP calculation based on
FV and ABP based on the
concepts of data mining.
Kim etal.
[40]
accurate and clinically useful than
the supervised or PI-based method
coefcient of determination, SDE standard deviation of the error, R
2
; NPH normal pressure hydrocephalus, TBI traumatic brain injury, SAH subarachnoid haemorrhage, SCA state of cerebral
CSF
FV and ABP based on the
concepts of semi-supervised
machine learning.
nICP-derived R
CSF
Heldt
nICP
BB
Modied
nICP
Data mining Hu etal.
Semi-
supervised
learning
Correlation coefcient is signicant at the 0.05 level
Inferred 95% CI was calculated as 1.96*SDE
a
AUC area under the curve, CI condence interval, R correlation coefcient, R
uid (CSF) outow, R
autoregulation