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EARLY
AND LATE STAGE EEG FINDINGS IN WERNICKE-KORSAKOFF SYNDROME DUE TO LONG-STANDING
STARVATION: CORRELATION WITH THE CLINICAL AND MRI FINDINGS
Demet
Kýnay, Betül Baykan, Ayþen Gökyiðit, Emel Gökmen, Hüseyin Þahin, Candan Gürses,
Rezzan Tuncay, Gencay Gürsoy, Hakan Gürvit
University of Ýstanbul, Ýstanbul Faculty of Medicine Department
of Neurology
Keywords:
Wernicke Encephalopathy, Wernicke-Korsakoff syndrome, EEG, starving, hunger strike,
starvation, death fast
*
This work was presented in part as a poster in the European Neurological Society Meeting
held in 5-9 June 1999 in Milan-Italy
ABSTRACT:
Early
and late stage EEG findings in Wernicke-Korsakoff Syndrome (WKS) due to long standing
starvation were investigated. After a hunger strike performed by political prisoners, 18
patients (15M, 3 F) with a mean age of 30 years were managed in our clinic. Early stage
EEG’s were performed between 20 and 40 days after the termination of the strike and
following the treatment. EEG examinations were repeated in 17 patients one year later.
In
the early stage, abnormal EEG findings were recorded in 5 patients (27.8%). Main
abnormality was theta activity in frontal and frontotemporal regions bilaterally.
Paroxysmal abnormalities were not observed. The abnormal EEGs had no relationship with the
clinical findings at the acute stage and the follow-up findings after one year. There was
no significant correlation between the distribution of abnormal EEG findings and the
subtypes of clinical condition as WE or WKS. At the end of the first year, abnormal EEGs
returned to normal in 3 cases, and showed some improvement in the other 2 patients.
Increased intensity in thalamus and grey matter around the aquaducts were determined in
MRI at the acute stage in 3 of 13 patients whose EEG findings were normal and 4 of 5
patients whose EEGs were pathological. There was a positive correlation between the EEG
and acute stage MRI findings.
INTRODUCTION:
Wernicke’s
encephalopathy (WE) is characterised by nystagmus, gaze palsies, ataxia of the gait, and
confusion. These manifestations may occur singly or in various combinations and may follow
a slowly evolving pattern or conversely they
are characterised by an abrupt onset. Korsakoff’s syndrome refers to an abnormality of
mental activities in which recent memory is affected out of the proportion to other
cognitive functions; the patient is otherwise alert and responsive. Most patients who
present with the manifestations of WE survive the acute illness and are left with an
amnestic state in which case the term Wernicke-Korsakoff syndrome (WKS) is more
appropriate. WKS is due to a deficiency of thiamine (vitamin B1). If thiamine therapy is
not initiated the patient may become comatose and die. On the other hand, when proper
therapy is instituted symptoms resolve rapidly (1-3). Although this syndrome occurs most
frequently in association with chronic alcoholism, recent case reports have emphasised that it can occur in
non-alcoholics as well (2,3). In WKS the lesions usually occur symmetrically in corpora
mamillare, medial thalami, the areas adjacent to the third ventricle, aquaduct, and fourth
ventricle.
There are only a few
reports about EEG findings in patients with WE and WKS. In this paper, we aimed to
investigate early and late EEG findings, and their relations with the MRI findings,
clinical stages and clinical progress of WE/WKS which was due to long term starvation.
MATERIAL AND METHODS
After
the termination of the hunger strike performed by political prisoners, 18 patients were
managed in our clinic. There were 15 male and 3 female patients whose mean age was 29.94 ±
6.38. Their ages ranged from 23 to 36 years with the exception of one patient who was
fifty years old. Duration of hunger was 67 to 69 days for 16 patients (three started 2
days later than the rest), a total of 54 days for one (temporarily ends the strike on the
day 44 and resumes on the day 59) and 39 days for the last patient (becomes comatose and
is started to be fed parenterally by his comrades). All patients were exposed to similar
environmental conditions. Fifteen of them were from the major prison in Istanbul, which
hosted the largest number of strikers. The remaining three were from other prisons in and
close to Istanbul. Dietary intake was restricted to some amount of salt, sugar and liquids
as water, lemonade and linden tea during the strike. Severe lassitude and vomiting
starting around day 60 further restricted, often times prevented this daily allowance.
Their mean weight loss was 21.8 kg (range from 11 to 31) and mean Body Mass Index (BMI)
loss was 16.5 (range from 11.8 to 18.4) during this hunger strike.
Eight
patients were admitted on the termination day and 10 others were referred within 20 days.
All patients showed neurological signs compatible with Wernicke’s encephalopathy, 10 of
whom developed Korsakoff’s syndrome.
Sixteen
of 18 admitted patients returned to prison, after 13 to 40 day-hospital stay. One patient
had already been released. One patient was transferred to the psychiatry department for
further management (Patient no;1). We
followed up all patients for a period of one year.
Clinical
features on admission and at the end of the first year were summarised in Table 1. In
order to follow the course and determine the prognosis in one year period, the patients
were evaluated with a severity scale developed by one of us (HG) (scale 1). The patients
were divided to mild (stage1a and 1b), moderate (stage 2) and severe ( stage 3 and 4)
stages.
EEG
Examinations:
In
17 patients, early stage EEG’s were performed between 20-40 days after termination of
the hunger strike and following the thiamine treatment. In one patient, early stage EEG
was performed 2 months after termination of the hunger strike and after one month of
thiamine therapy. At the time of the first EEG; all blood biochemistry parameters were
normal except low albumin levels.
At
the time of the first EEG examinations, neurological examination revealed a global
confusional state in 6 patients. State of alertness was somewhat comprised in two, and the
other four were alert, yet confused, with evident problems in attentional and mnestic
tasks in neuropsychological testing.
EEG
examinations were repeated in 17 patients one year later.
All
EEG’s had been read and interpreted by two experienced electroencephalographers (AG, BB)
who were blind to the clinical data.
Recordings
were performed with scalp electrodes placed according to the International 10-20 system
with both bipolar and referential montages . Samples, each lasting 30 min, were obtained
while the subject was awake and relaxed, with eyes closed. Standard activating procedures
was performed in all patients. Interictal background activity was studied and selected by
visual inspection in artefact-free EEG samples. Slowing of the background activity was
classified as delta (0.5-3.5 Hz) and theta (4-7 Hz).
MRI Examinations:
MRI
scans were obtained within the first week in 6 patients and within the second week in 3
patients. Nine patients were studied after
the second week .
MRI
scans were performed with an 1.0 T unit (Siemens, Magnetom impact). Spin-echo (SE)
sequences, 2620/17 (TR/TE) and 2900/85 (TR/TE) were obtained with 5-mm thickness (axial)
for the whole brain and a 3-mm thickness (coronal) though the periaquaductal region and
third and fourth ventricles. Sagittal and axial SE 600/15 (TR/TE) scans with a 5-mm
thickness were also obtained. In all patients, sequences included sagittal spin-echo
(TR/TE:600/15) with 5-mm thickness and coronal spin-echo (TR/TE: 600/15) with 3-mm
thickness performed after intravenous administration of Gd-DTPA. Lesions of
paraventricular regions of the thalamus and hypothalamus and periaquaductal regions of the
midbrain were evaluated in all cases by 2 independent observers (RT, GG), as well as
mamillary body, cerebral, and cerebellar shrinkage.
RESULTS:
Early
phase:
In
the early phase of the illness, abnormal EEG findings were recorded in 5 patients (%27.8). Abnormal EEG findings consisted of mild regular
slow activity in theta range which involved frontal regions in 2 patients (no;2,3) and
frontotemporal regions in 2 patients (no;7,13). In the last patient, EEG revealed a
moderate, regular generalised slow activity with the greatest amplitude over the frontal
regions; this was accentuated during hyperventilation (no;1). Paroxysmal abnormalities
were not observed.
Two
patients with clouded consciousness (no;1,2) and one of the 4 alert but confusional
patients (no;3) had pathological changes of the EEG.
Two patients who had abnormal EEG findings were not confusional and showed only motoric
signs of WE (no;7,13). There was no significant correlation between abnormal EEG findings
and mental state of the patients (Fisher’s
Exact Test; P=0.2682).
Two
of the 8 patients who were classified as WE (no;7,13) and 3 of the 10 patients who were
classified as WKS (no;1,2,3) had pathological EEG changes. There was no significant
relation between the distribution of abnormal EEG findings and the subtypes of clinical
condition as WE or WKS (Fisher’s Exact Test; P=1.0000).
Nine
of the 13 patients whose EEGs were normal had been rated being in severer clinical stages (stages 4 and 3) and 4 of
them were in moderate clinical stage (stage 2) according to our scaling system. On the
other hand, four of the 5 patients who had abnormal EEG findings, were in those severer
clinical stages (stages 4 and 3) and the last one was in moderate stage (stage 2). No
significant correlation was found between the EEG findings and the severity of clinical
findings at this early stage (Fisher’s Exact Test; P=1.0000).
Late
Phase:
EEG
examinations repeated in 17 patients showed abnormalities in 3 patients one year later. In
2 patients, abnormal EEG findings included slight theta activity over one frontotemporal
(no;15) and temporal region (no;13) and these were observed only during hyperventilation.
The 3rd patient had a slight slow
activity over the frontotemporal regions bilaterally in the routine EEG. This abnormality
was accentuated during hyperventilation (no;1).
The
abnormal EEG findings performed in the early period and at the end of the first year were
summarised in Table 2. Two of the 3 patients who had abnormal EEG findings at the end of
the first year had also abnormal EEG findings in the early period (no1,13), but the 3rd
patient had a normal EEG in the early period. (no;15).
All
of the abnormal EEGs in the early phase of the illness found to improve to a certain
degree (more or less) at the end of the first year. In the patient whose EEG had been
grossly abnormal, generalised slow activity diminished and localised to frontotemporal
regions (no;1). The slow-wave activity were observed only during hyperventilation in one
patient (no;13).
Prognosis
of the patients after one year according to the clinical stages was seen in table 3. There
was no significant correlation between abnormal EEG and the prognosis after one year
follow-up (Fisher’ Exact Test; P=0.3260).
Clinical
course was also not different in the patients who still have abnormal EEG findings
compared with the patients whose EEGs returned to normal.
The exceptional patient who had abnormal EEG at the end of the first year,
although his first EEG was normal, did not show any deterioration in the clinical course
(no,15).
MRI
findings of the patients are listed in Table 4. In the early phase of the illness,
symmetrical signal abnormalities on T2-weighted images in the periaquaductal areas and in
the medial thalami were found in 4 of 5 patients (Figure 1) whose EEGs were abnormal (no;1,2,3,7) and 3 of 13 patients whose EEGs were
normal (no;4,5,9). We found a significant correlation between the results of the EEG and the symmetrical signal abnormalities
on T2-weighted MRI images in the periaquaductal areas and in the medial thalami (Spearman
correlation coefficient r= 0.53, p=0.023). There was also a weak correlation between EEG
findings and cortical atrophy on MRI (Spearman correlation coefficient r= 0.47, p=0.045).
No significant correlation could be shown between EEG findings in the early period and MRI
findings such as mamillary atrophy, third ventricular and aquaductal dilatation and
cerebellar and vermian atrophy ( Spearman correlation coefficient r=0.01, p=0.95; r=0.19,
p=0.44; r=0.026, p=0.918; r=-0.02, p=0.919; respectively) .
DISCUSSION
The
true prevalence of Wernicke’s encephalopathy is clearly higher than what is diagnosed
clinically. The adult autopsy incidence of up to 2.2% (4,5) emphasises the underdiagnosis
of this syndrome, which is recorded clinically in only 0.04% to 0.13 % of all hospital
admissions (4,6) It may be difficult to formulate a clinical diagnosis in patients who
have an atypical history and the incomplete
or attenuated forms of the syndrome, so that better tools for the early and definite
identification of this disease (and the prediction of the prognosis) are needed in
clinical practice (2). Most studies have reported that imaging modalities such as MRI may
contribute greatly by providing an early diagnosis for this life-threatening disease
(7-9). There are only a few reports about EEG findings in patients with WE and they are
usually anectodal case reports.
In
this study, EEG findings were examined in a homogenous group of WE/WKS cases who have
suffered from long term and severe lack of food for similar periods. The
electroencephalograms were performed after the institution of thiamine therapy and slight
improvement was observed in clinical findings of all our patients. We followed up our
patients in the prison for a period of one year and their EEGs were reevaluated at the end
of this period. In the early phase of the illness, the EEG abnormalities were recorded in
27.8% of patients in our study. Victor et al. reported that about half of the patients
with Wernicke-Korsakoff disease show EEG abnormalities from a mild to moderate diffuse
slow activity (4). In their monograph, almost all patients were alcohol addicts. Kelley
and Reilly have reported varying degrees of background slowing with increased amounts of
theta and delta activity in WE (10). EEG
abnormalities in reported cases with WE/WKS showed diffuse slow wave activity or frontal/
frontotemporal dominance of the frequent slow waves (9, 11-15). Martinez-Barros et al.
emphasised that EEG showed non-specific changes which can appear with many kinds of
diffuse encephalopathy regardless of etiology (15).
It
is noteworthy that pathologic EEG findings in our group were consisted of mild slowing
observed predominantly in frontal, frontotemporal regions. Fratzen has also reported three
cases with WE whose EEGs showed a moderate to severe degree of slowing with the greatest
amplitude over the fronto-temporal regions (11). The cause of WE in one of his cases was
hunger strike as in our cases. Fournet and Lanternier reported diffuse sharp and slow wave
complexes in severely ill patients (16). Paroxysmal abnormalities were not observed in any
of our patients.
No
statistically significant difference could be demonstrated in means of pathological EEG
findings between the WE and WKS subgroups in our patients. This is an original finding not
reported before.
There
was no relationship between the pathologic EEGs and severity of the neurological clinical
findings. EEG examinations were normal in most of the cases with severe clinical findings
of WE/WKS. Victor et al. have also reported that in some patients with the full-blown
acute syndrome, who later proved to have extensive lesions in the diencephalon in
postmortem examinations, the EEG was entirely normal (4).
Total
cerebral blood flow and cerebral oxygen and glucose consumption may be greatly reduced in
the acute stages of the disease, and these defects may still be present after several
weeks of the treatment (3). These observations indicate that profound reductions in brain
metabolism need not be reflected in EEG abnormalities or in depression of the state of
consciousness (3).
We
would like to emphasise some improvement in the EEG findings after treatment. In our
cases, all of the EEG abnormalities detected in the early phases of the illness improved
to a lesser or more extend at the end of the
first year. The improvement of the EEG abnormalities paralleled clinical improvement. In
only one of our cases who had the most severe abnormalities in the early phases, EEG
abnormalities continued one year later, although slight improvement was observed. Similar
to ours, in three cases reported by Fratzen, EEG abnormalities detected in the early
phases became less within several months after the thiamine therapy and returned to normal
one year later (11). In a case report with WK caused by psychogenic food refusal,
Doraiswamy et al. have reported that the diffuse slowing detected in the first EEG was
replaced by mild background (7 Hz) and bitemporal (4 to 5 Hz) slowing seven months later
high dose thiamine treatment (14). In another
case report with WE, Yokote et al have reported that the EEG showed basic rhythms of 6-7
Hz theta waves without laterality at the beginning. Two weeks after the administration of
thiamine and the patient regained consciousness, the EEG demonstrated improvement with
basic rhythms of 8-9 Hz slow alpha waves with frontal-dominant frequent theta waves (9).
Dreyfus and Victor found that EEG changes could range from mild to severe and in general,
paralleled the severity of neurological deficits (17).
We
demonstrated that there was no relation between the initial EEG findings and clinical
status at the end of the first year. We can, therefore, assume that EEG abnormalities in
WE/WKS are not useful in the prediction of
the prognosis.
We
found an interesting significant correlation between the results of EEG and the
symmetrical signal abnormalities on T2-weighted MRI images in the periaquaductal areas and
bilateral medial thalami. Follow-up MRI scans in some reports have revealed atrophy of
mamillary bodies, cortical atrophy and third ventricular and aquaductal dilatation (7-9,
14). Early thiamine replacement may result in complete resolution of thalamic and midbrain
MR signal abnormalites (7,8,14). Galluci et al have reported that the high signals on
T2-weighted images represent pathologically non-specific findings such as edema,
demyelination and gliosis (8). Comparison of the MRI with the pathological findings showed
that the high signals seen on the T2-weighted images corresponded to edematous change
induced by spongy disintegration of the neurophil (18). In some reports, the mamillary
bodies have been enhanced on MRI in acute WE (19,20). Mamillary body atrophy has been
reported as the sign of chronic WE (21). The exact mechanisms underlying the pathogenesis
of the lesions observed in WE are not understood completely. The role of thiamine in the
pathophysiology of WE may be related to its involvement in the function of excitable
membranes and neurotransmitter production (8). Antunez et al have that MRI is useful in
confirming the diagnosis of acute WE, but the absence of abnormalities on MRI does not
exclude the diagnosis and the sensitivity of MR imaging in revealing evidence of this
disease was 53% and the specificity, 93% (22).
In
conclusion; abnormal EEGs were found in 27.8% of the cases with WE/WKS, consisting of slow
wave activity in frontal and frontotemporal regions which improved markedly after one
year. The abnormal EEGs had no relationship with the neurological findings and the
subtypes of clinical condition as WE versus WKS. There was a significant correlation
between the pathologic results of the EEG and
the T2 hyperintensity on MRI in the periaquaductal areas and in the medial thalami.
REFERENCES
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M, Adams RD, Collis GH. The Wernicke-Korsakoff syndrome and related neurologic disorders
due to alcoholism and malnutrition, 2nd ed. Philadelphia; Davis, 1989:1-117.
2. Victor
M. MR in the diagnosis of Wernicke-Korsakoff syndrome. AJNR 1990;11:895-896.
3. Adams
RD, Victor M, Ropper AH. Principles of neurology. New York:McGraw-Hill,1997.
4. Victor
M, Adams RD, Collins GH. The Wernicke-Korsakoff Syndrome: A Clinical and Pathological
Study of 245 Patients, 82 with Post-Mortem examinations. Philadelphia, Davis Co,
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5. Harper
C. Wernicke’s encephalopathy: a more common disease than realised. A neuropathological
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CG. The incidence of Wernicke’s encephalopathy in Australi: a neuropathological study of
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JF, Heinz ER, Burger PC. MR
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M, Bazzao A, Splendiani A, Masciocchi C, Passariello R. Wernicke encephalopathy: MR
findings in five patiens. AJNR 1990;11:887-892.
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K, Miyagi K, Kuzuhara S, Yamanouchi H, Yamada H. Wernicke encephalopathy: Follow-up study
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Frantzen E. Wernicke’s encephalopathy. Acta Neurol Scand 1966; 42:426-441.
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Fournet A, Lanternier M. Consultation electroenceplographique dans 17 cas
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Suzuki S, Ichijo M, Fujii H, Matsuoka Y,
Odawa. Acute
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D’Aprile P, Gentile MA, Carella A. Enhanced MR in the acut phase of Wernicke
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Shogry MEC and Curnes JT. Mammillary body enhancement on MR as the only sign of acute
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Antunez E, Estruch R, Cardenal C, Nicolas JM, Fernandez-Sola J, Urbano-Marquez A.
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Scale
1:
Activities of Daily Living Scale for Hunger Strikers
0
|
No
symptoms or signs accountable to hunger strike |
0.5 |
Mild
symptoms and signs, unrelated to WKS |
1a |
Very
mild or residual WE (e.g. Isolated nystagmus) |
1b |
Mild
ataxia, no assistance needed; dysarthria |
2 |
Moderate
ataxia, walks with assistance;
or
mild but definite amnesia |
3 |
Severe
ataxia, unable to sit unless supported; or prominent amnesia, apathy, depression or
psychosis |
4 |
Clouding
of consciousness, bedridden |
5 |
Death |
*developed
by one of us (HG)
Table
1: Neurological findings at the admission and after one year
Symptoms
and signs |
Admission
|
One
year later |
Change
of consciousness
(mild
confusion, somnolence, stupor) |
1,
2, 3, 4, 5, 6, 9, 15 |
- |
Korsakoff-like
amnesia |
1,
2, 3, 4, 5, 9, 15, 16, 17, 18 |
1,
2, 3, 4, 5, 9, 15, 16, 17, 18 |
Apathy |
2,
9, 15, 18 |
1,
15, 16, 18 |
Euphoria
or disinhibition |
3,
4, 5 |
5 |
Depression
or psychosis |
1,
16 |
2,
3 |
Horizontal
nystagmus |
1,
2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, |
1,
2, 4, 5, 6, 7, 8, 9, 10, 12, 13, 15, 16 |
Vertical
nystagmus |
1,
2, 3, 4, 5, 6, 7, 10, 14, 15 |
2 |
Ophtalmoparezis |
1,
2, 3, 4, 5, 6, 7, 8, 10, 11, 14, 15 |
1,
2, 6, 9, 10, 13 |
Horizontal
and vertical conjugated gaze palsy |
1,
2, 4, 15 |
- |
Horizontal
conjugated gaze palsy |
3,
4, 5, 6, 7, 8 |
- |
VI.
nerve palsy |
10,
11, 14 |
1,
2, 6, 9, 10, 13 |
Truncal
ataxia |
1,
2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18 |
1,
2, 4, 5, 6, 8, 9, 11, 12, 15, 16
|
Dysmetria
in the extremities |
1,
2, 4, 13, 15, 16 |
1,
2, 4, 5, 6, 9, 10, 13, 14,
15,
16 |
Dysarthria |
4,
9 |
2,
4, 6, 8, 9, 11, 13, 15, 16 |
· Numbers
represent individual patients
Table
2. The pathological EEG findings in the
early period and one year later
No: |
Diagnosis |
Initial
State |
The
first year |
7 |
WE |
Theta
activity over the bilateral frontotemporal
regions |
Normal
|
13 |
WE |
Theta
activity over the bilateral frontotemporal regions |
Unilateral
slow activity in temporal region during only hyperventilation |
1* |
WKS |
Moderate
generalised slow activity with the greatest amplitude over the frontal regions
(accentuated during hyperventilation) |
Mild
slow activity over bilateral frontotemporal regions; accentuated during hyperventilation |
2 |
WKS |
Theta
activity over bilateral frontal regions |
Normal
|
3 |
WKS |
Theta
activity over bilateral frontal regions |
Normal |
15 |
WKS |
Normal |
Mild
slow activity in unilateral frontotemporal region during
hyperventilation |
*This
patient had the most severe EEG abnormality in the early period and also after one year.
Table
3 . Prognosis of the patients after 1 year
GROUP |
Stages |
Initial
State |
The
first year |
WA
(n=8)
|
4
3
2
1b
1a
|
6
7L;8
10,11,12,13L,14
-
-
|
-
-
6,12
8,10,13L
7L,11,14 |
WKS
(n=10) |
4
3
2
1b
1a
|
1L,2L,3L,4,5,9,15,18
-
16,17
-
-
- |
-
1L,2L,3L,4,15,16,18
-
5,9,17
-
- |
*the
numbers indicates individual patients
L:
disclosed
the patients whose EEG were abnormal in the early stage (no; 1,2,3,7,13)
**
Stage 4 and 3=severe, stage 2= moderate, stage 1b and 1a= mild. |
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