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Originally Published 16 July 2009
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Delay in the Diagnosis of Cerebral Vein and Dural Sinus Thrombosis: Influence on Outcome

Abstract

Background and Purpose— Diagnostic delay of cerebral vein and dural sinus thrombosis may have an impact on outcome.
Methods— In the International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVT) cohort (624 patients with cerebral vein and dural sinus thrombosis), we analyzed the predictors and the impact on outcome of diagnostic delay. Primary outcome was a modified Rankin Scale score >2 at the end of follow-up. Secondary outcomes were modified Rankin Scale score 0 to 1 at the end of follow-up, death, and visual deficits (visual acuity or visual field).
Results— Median delay was 7 days (interquartile range, 3 to 16). Patients with disturbance of consciousness (P<0.001) and of mental status (P=0.042), seizure (<0.001), and with parenchymal lesions on admission CT/MR (P<0.001) were diagnosed earlier, whereas men (P=0.01) and those with isolated intracranial hypertension syndrome (P=0.04) were diagnosed later. Between patients diagnosed earlier and later than the median delay, no statistically significant differences were found in the primary (P=0.33) and in secondary outcomes: modified Rankin Scale score 0 to 1 (P=0.86) or deaths (P=0.53). Persistent visual deficits were more frequent in patients diagnosed later (P=0.05). In patients with isolated intracranial hypertension syndrome, modified Rankin Scale score >2 at the end of follow-up was more frequent in patients diagnosed later (P=0.02).
Conclusions— Diagnostic delay was considerable in this cohort and was associated with an increased risk of visual deficit. In patients with isolated intracranial hypertension syndrome, diagnostic delay was also associated with death or dependency.
The identification of variables that delay the diagnosis of cerebral vein and dural sinus thrombosis (CVT) is of clinical and medicolegal relevance. Two previous studies1,2 identified clinical variables associated with admission delay, but could not demonstrate an influence of admission delay on outcome. The purposes of this study were to describe the delay in the diagnosis of CVT and to analyze its predictors and its influence on the outcome of a large cohort of patients with CVT.

Methods

Diagnostic delay was defined as the interval (days) between the onset of symptoms (day of first symptom judged to be related to CVT by the investigator) and the confirmation of CVT by MR and/or angiography. We also measured the interval (days) between onset of symptoms and hospital admission (first hospital). Early admission was defined as an admission delay below the median of the sample.
We used the International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVT) cohort consisting of 624 consecutive symptomatic patients with CVT with a mean follow-up of 478 days.3 Follow-up visits were performed at 6 and12 months and yearly thereafter.
The primary outcome was death or dependency defined as a modified Rankin Scale score (mRS) >2 at end of follow-up. Secondary outcomes were all deaths, complete recovery (mRS 0 to 1) at the end of follow-up, and any persistent visual deficit related to CVT (decreased visual acuity or visual field defect) at final follow-up. Confrontation testing of visual fields and measurement of visual acuity were recommended at each follow-up, but perimetry was optional.
We compared diagnostic delay for potential explanatory and confounding variables listed in Table 1.
Table 1. Association Between Diagnostic Delay and Potential Predictors
VariableDays Between Onset and DiagnosisP
<44–78–16>16
nPercentnPercentnPercentnPercent
Age         
    <37 years9129.28025.67323.46821.80.069
    ≥37 years7423.87925.47724.88126.0 
Gender         
    Female13028.012126.111524.89821.10.014
    Male3522.03823.93522.05132.1 
Center         
    European14229.312225.211423.510722.10.006
    North-American1522.11927.91927.91522.1 
    South-American712.11525.91424.12237.9 
    High GNI*14829.112825.211823.211422.40.013
    Medium-low GNI*1714.83127.03227.83530.4 
    <10 patients8031.75622.26124.25521.80.104
    ≥10 patients8522.910327.88924.09425.3 
Referred         
    Yes7928.17627.05624.07025.30.826
    No8325.28324.69127.07823.1 
Intra-arterial angiography for diagnosis         
    Yes3624.83222.13926.93826.20.225
    No12927.012726.611123.211123.2 
Headache         
    Yes14231.914526.213223.913424.20.553
    No2231.91420.31826.11521.7 
Isolated headache         
    Yes1629.61324.11324.11222.20.539
    No14826.114625.713724.213624.0 
Papilledema         
    Yes2112.13218.45431.06738.50.001
    No14031.912528.59521.67918.0 
IIHS         
    Yes3323.12920.34028.04128.70.035
    no13227.513027.111022.910822.5
GCS 14–15
    Yes11423.611924.612626.112425.70.001
    No4337.73429.82118.41614.0 
GCS <9         
    Yes1445.2619.4516.1619.40.045
    No14325.314726.014225.113413.7 
Mental disturbance         
    Yes3827.74935.82417.52619.00.042
    No12726.111022.612625.912325.3 
Seizure         
    Yes8133.17028.65422.04016.30.001
    No8422.28923.59625.410928.8 
Motor deficit         
    Yes6728.96628.45222.44720.30.061
    No9825.19323.89825.110226.1 
(Continued)
Table 1. Continued
VariableDays Between Onset and DiagnosisP
<44–78–16>16
nPercentnPercentnPercentnPercent
Note. Percent is within condition (yes or no) of variable in each quartile of delay.
*World Bank categories.
†Patients referred from other hospitals versus patients coming directly to the participating hospital.
IIHS indicates isolated intracranial hypertension syndrome; GCS, Glasgow Coma Score; GNI, gross national income.
Aphasia         
    Yes3126.13327.72319.33226.90.930
    No13426.212625.012725.211723.2 
Sensory loss         
    Yes823.5720.6823.51132.40.197
    No15726.715225.814224.113823.4 
Brain lesion         
    Yes11830.211328.98221.07819.90.001
    No4720.34619.96729.97130.7 
Venous infarct         
    Yes9231.78930.75719.75217.90.001
    No7322.07021.19227.79729.2 
Hemorrhagic lesion         
    Yes6727.56727.55221.35823.80.232
    No9825.99224.39725.79124.1 
Occlusion of multiple sinuses         
    Yes8426.98025.67022.47825.00.860
    No8025.87925.58025.87122.9 
We used nonparametric statistics (median and quartile distribution, Mann-Whitney U and Kruskal-Wallis tests). We performed the following subgroup analysis: (1) low CVT risk score (<3) and high risk (CVT risk score ≥3) patients4; (2) patients presenting as isolated intracranial hypertension syndrome; (3) patients in coma (Glasgow Coma Score <9); (4) patients with brain lesions on admission CT/MR; and (5) patients who were anticoagulated in therapeutical dosages after the diagnosis of CVT. Additionally, we performed logistic regression for the primary outcome, forcing diagnostic delay in the ISCVT prognostic model, considering the interactions with unbalanced predictors.

Results

There were 623 valid cases for analysis with information on onset to diagnosis delay. The median delay was 7 days and the interquartile range 3 to 16 days. The distribution showed a strong left-sided skew (skewness=11.36). There were 619 patients with valid information on admission delay. The median admission delay was 4 days and the interquartile range 1 to 11 days.
Early admission was associated with higher gross national income (P=0.02), disturbance of consciousness (P=0.001), mental disturbance (P=0.03), seizure (P=0.001), motor deficit (P=0.02), and parenchymal lesion on admission CT/MR (P=0.001).

Diagnostic Delay

Median delay (interquartile range) was 9 days (5 to 18) for countries with low-middle gross national income per capita and 7 days (3 to 15) for countries with high gross national income per capita (P=0.013). Diagnostic delay was decreased females and in patients with decreased vigilance, mental disturbance, seizure, and venous infarct on admission CT/MR. There were no significant differences in diagnostic delay in relation to age, centers with <10 patients, patients referred from other centers and patients requiring intra-arterial angiography for diagnosis, focal deficits (motor, sensory or language), the number or site of thrombosed sinus and veins, and any of the associated conditions or risk factors. Diagnostic delay was longer in patients with papilledema and isolated intracranial hypertension syndrome. More patients with diagnostic delay above the median were not prescribed anticoagulants in therapeutic dosages: 11% (22.4% versus 11.4%, χ2=13.5, P<0.001).
No statistically significant differences were found in the primary outcome and in secondary outcomes: mRS 0 to 1 or death. Persistent visual loss (visual field defects in 6 patients and decreased visual acuity in 21 patients; median visual acuity in right and left eyes 8 of 10; range, 9.5 to 5.5 of 10) was more frequent in patients diagnosed later (Table 2). We performed logistic regression with mRS >2 at final follow-up as the outcome and the variables of the ISCVT prognostic model and diagnostic delay as predictors. Diagnostic delay was not retained in the model either when dichotomized in below/above the median (P=0.056; adjusted OR, 0.60; 95% CI, 0.35 to 1.01) or when quartiles were considered (P=0.24; adjusted OR, 0.87; 95% CI, 0.69 to 1.10).
Table 2. Delay in Diagnosis of CVT and Outcome
Outcome*Days Between Onset and DiagnosisP
<44–78–16>16
nPercentnPercentnPercentnPercent
Note. Percent is within condition (yes or no) of variable in each quartile of delay.
*At the end of follow-up.
†Kruskal-Wallis test.
mRS >2
    Yes2630.61517.62124.72327.10.329
    No13925.814426.812924.012623.4 
mRS 0–1         
    Yes12826.012926.211924.211623.60.858
    No3728.23022.93123.73325.2 
Death         
    Yes1528.81019.21630.81121.20.526
    No15026.314926.113423.513824.2 
Visual deficit         
    Yes311.1725.9518.51244.40.049
    No16227.215225.514524.313723.0 

Subgroup Analysis

Diagnostic delay was significantly associated with visual loss in patients with isolated intracranial hypertension syndrome and in the low CVT risk score subgroups (Table 3). In patients with isolated intracranial hypertension syndrome, poor outcome was significantly more frequent in patients with longer diagnostic delay.
Table 3. Delay in Diagnosis of CVT and Outcome: Subgroup Analysis
Subgroup Outcome*Days Between Onset and DiagnosisP
<44–78–16>16
nPercentnPercentnPercentnPercent
Isolated intracranial hypertension syndrome         
    mRS >2         
        Yes00110.0220.0770.00.022
        No3324.82821.13828.63425.6 
    mRS 0–1         
        Yes3124.02821.73728.73325.60.093
        No214.317.1321.4857.1 
    Death         
        Yes0000233.3466.70.117
        No3324.12921.23827.73727.0 
    Visual deficit         
        Yes216.718.318.3866.70.023
        No3123.72821.43929.83325.2 
Coma on admission         
    mRS >2         
        Yes758.3325.0216.7000.194
        No736.8315.8315.8631.6 
    mRS 0–1         
        Yes538.5215.4215.4430.80.602
        No950.0422.2316.7211.1 
    Death         
        Yes654.5327.3218.2000.252
        No840.0315.0315.0630.0 
    Visual deficit         
        Yes000000001.00
        No1445.2619.4516.1619.4no
Low-risk patients (CVT risk score <3)         
    mRS >2         
        Yes1728.8915.31627.11728.80.352
        No12325.312525.712425.511423.5 
    mRS 0–1         
        Yes11325.311325.311425.510723.90.876
        No2727.62121.42626.52424.5 
    Death         
        Yes822.9514.3134.31028.60.373
        No13225.912925.312825.112123.7 
Visual deficit         
        Yes311.5623.1525.11242.50.043
        No13726.412824.713326.01122.9 
High-risk patients (CVT risk score ≥3)         
    mRS >2         
        Yes934.6623.1519.2623.10.426
        No1530.61836.748.21224.5 
    mRS 0–1         
        Yes1433.31535.749.5921.40.753
        No1030.3927.3515.2927.3 
    Death         
        Yes741.2529.4423.515.90.112
        No1729.31932.858.61729.3 
    Visual deficit         
        Yes001100.000000.547
        No2432.42331.1912.21824.3 
(Continued)
Table 3. Continued
Subgroup Outcome*Days Between Onset and DiagnosisP
<44–78–16>16
nPercentnPercentnPercentnPercent
Note. Percent is within condition (yes or no) of variable in each quartile of delay.
*At the end of follow-up.
†Kruskal-Wallis test.
Brain lesion on admission CT/MR         
    mRS >2         
        Yes2536.81420.61522.11420.60.361
        No9328.89930.76720.76419.8 
    mRS 0–1         
        Yes8629.98830.65820.15619.40.666
        No3231.12524.32423.32221.4 
    Death         
        Yes1435.01025.01127.5512.50.438
        No10429.610329.37120.27320.8 
    Visual deficit         
        Yes320.0533.3426.7320.00.830
        No11530.610828.77820.77519.9 
On therapeutic anticoagulation         
    mRS >2         
        Yes2436.41116.71522.71624.20.182
        No12427.412828.310723.69420.8 
    mRS 0–1         
        Yes11527.911327.49924.0256.10.778
        No3330.82624.32321.52523.4 
    Death         
        Yes1536.6717.11024.4922.00.457
        No13327.813227.611223.410121.1 
    Visual deficit         
        Yes312.0728.0520.0440.00.071
        No14529.413226.711723.79720.2 
No significant differences for any of the outcomes were detected in the other subgroup analysis (Table 3).

Discussion

In this multicenter cohort, the median interval between onset of symptoms and confirmation of CVT diagnosis was 7 days. Patients with more severe clinical presentations, women, and patients in high-income countries tend to be diagnosed earlier. In the overall sample, diagnostic delay had no influence on death or dependency or complete recovery. However, diagnostic delay was associated with an increased risk of poor outcome and of visual deficit in patients presenting with a syndrome of isolated increased intracranial hypertension.
Although visual acuity and confrontation testing of the visual fields were performed in the majority of the patients with visual complaints, information on visual acuity was not always recorded by the investigators and its frequency is probably underestimated. A standardized evaluation of visual consequences of CVT would require formal neuro-ophthalmological examination. We used a pragmatic approach considering any objective visual deficit not explained by an ocular cause as CVT-related. Another limitation of the research on diagnostic delay in CVT is the difficulty in establishing the onset of symptoms in patients with subacute or chronic presentations. This is certainly subject to considerable interexaminer variation, which was not studied in our investigation. Results of this study cannot be generalized to world regions that did not participate or were underrepresented in ISCVT such as Africa or Asia. Median admission delay and predictors of admission delay were consistent with the findings of the 2 previous studies with smaller sample sizes.1,2
Early diagnosis is more likely to have a favorable influence in outcome if an intervention has increased efficacy if applied earlier. There are no studies analyzing the influence on outcome of the delay on starting anticoagulation. Starting treatment earlier in patients with good initial condition may prevent pulmonary embolism and thrombus progression. Local thrombolysis, hematoma evacuation, or hemicraniectomy were used in a minority of patients in serious condition who, as we have shown, tend to present and be diagnosed earlier.

Acknowledgments

We thank the investigators who participated in the ISCVT. Their names and centers are listed in reference 3.
Sources of Funding
This study was supported by grants from the “Fundação para a Ciência e Tecnologia” PRAXIS C/SAU/10248/1998 and the “Associação para o Desenvolvimento da Investigação da Doença Vascular Cerebral.”
Disclosures
None.

References

1.
Ferro JM, Lopes MG, Rosas MJ, Fontes J; for the VENOPORT Investigators. Delay in hospital admission of patients with cerebral vein and dural sinus thrombosis. Cerebrovasc Dis. 2005; 19: 152–156.
2.
de Bruijn SFTM, de Haan RJ, Stam J; for the Cerebral Venous Thrombosis Study Group. Clinical features and prognostic factors of cerebral venous sinus thrombosis in a prospective series of 59 patients. J Neurol Neurosurg Psychiatry. 2001; 70: 105–108.
3.
Ferro JM, Canhão P, Stam J, Bousser M-G, Barinagarrementeria F; for the ISCVT Investigators. Prognosis of cerebral vein and dural sinus thrombosis: results of the International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVT). Stroke. 2004; 35: 664–670.
4.
Ferro JM, Rodrigues T, Bacelar-Nicolau L, Bacelar-Nicolau H, Canhão P, Crassard I, Dutra A, Massaro A, Mackowiak-Cordiolani MA, Leys D, Fontes J. Development of a risk score to predict the prognosis of cerebral vein and dural sinus thrombosis (CVT). Cerebrovasc Dis. 2007; 23 (suppl 2): 141.

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On the cover: The illustration (the author’s own reconstruction of Marlowe’s carotid artery wound) is taken from an article in this issue, “Reflections on the Carotid Artery: 438 BC to 2009 AD: The Karolinska 2008 Award Lecture in Stroke Research” by Barnett (Stroke. 2009;40:3143–3148).

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History

Received: 2 April 2009
Accepted: 8 May 2009
Published online: 16 July 2009
Published in print: 1 September 2009

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Keywords

  1. cerebral vein thrombosis
  2. diagnostic delay
  3. dural sinus thrombosis
  4. medicolegal
  5. outcome

Authors

Affiliations

José M. Ferro, MD, PhD
From the Department of Neurology (J.M.F., P.C.), Hospital Santa Maria, University of Lisboa, Lisboa, Portugal; the Academic Medical Centre (J.S.), Amsterdam, The Netherlands; Hôpital Lariboisière (M.G.B.), Paris, France; Instituto Nacional de Neurologia y Neurocirurgia (F.B.), México City, México; Hospital das Clínicas (A.M.), Universidade de São Paulo, São Paulo, Brazil; Hôpital Central (X.D.), Nancy, France; and the University of Pennsylvania Medical Center (S.E.K.), Philadelphia, Pa.
Patrícia Canhão, MD
From the Department of Neurology (J.M.F., P.C.), Hospital Santa Maria, University of Lisboa, Lisboa, Portugal; the Academic Medical Centre (J.S.), Amsterdam, The Netherlands; Hôpital Lariboisière (M.G.B.), Paris, France; Instituto Nacional de Neurologia y Neurocirurgia (F.B.), México City, México; Hospital das Clínicas (A.M.), Universidade de São Paulo, São Paulo, Brazil; Hôpital Central (X.D.), Nancy, France; and the University of Pennsylvania Medical Center (S.E.K.), Philadelphia, Pa.
Jan Stam, MD
From the Department of Neurology (J.M.F., P.C.), Hospital Santa Maria, University of Lisboa, Lisboa, Portugal; the Academic Medical Centre (J.S.), Amsterdam, The Netherlands; Hôpital Lariboisière (M.G.B.), Paris, France; Instituto Nacional de Neurologia y Neurocirurgia (F.B.), México City, México; Hospital das Clínicas (A.M.), Universidade de São Paulo, São Paulo, Brazil; Hôpital Central (X.D.), Nancy, France; and the University of Pennsylvania Medical Center (S.E.K.), Philadelphia, Pa.
Marie-Germaine Bousser, MD
From the Department of Neurology (J.M.F., P.C.), Hospital Santa Maria, University of Lisboa, Lisboa, Portugal; the Academic Medical Centre (J.S.), Amsterdam, The Netherlands; Hôpital Lariboisière (M.G.B.), Paris, France; Instituto Nacional de Neurologia y Neurocirurgia (F.B.), México City, México; Hospital das Clínicas (A.M.), Universidade de São Paulo, São Paulo, Brazil; Hôpital Central (X.D.), Nancy, France; and the University of Pennsylvania Medical Center (S.E.K.), Philadelphia, Pa.
Fernando Barinagarrementeria, MD
From the Department of Neurology (J.M.F., P.C.), Hospital Santa Maria, University of Lisboa, Lisboa, Portugal; the Academic Medical Centre (J.S.), Amsterdam, The Netherlands; Hôpital Lariboisière (M.G.B.), Paris, France; Instituto Nacional de Neurologia y Neurocirurgia (F.B.), México City, México; Hospital das Clínicas (A.M.), Universidade de São Paulo, São Paulo, Brazil; Hôpital Central (X.D.), Nancy, France; and the University of Pennsylvania Medical Center (S.E.K.), Philadelphia, Pa.
Ayrton Massaro, MD
From the Department of Neurology (J.M.F., P.C.), Hospital Santa Maria, University of Lisboa, Lisboa, Portugal; the Academic Medical Centre (J.S.), Amsterdam, The Netherlands; Hôpital Lariboisière (M.G.B.), Paris, France; Instituto Nacional de Neurologia y Neurocirurgia (F.B.), México City, México; Hospital das Clínicas (A.M.), Universidade de São Paulo, São Paulo, Brazil; Hôpital Central (X.D.), Nancy, France; and the University of Pennsylvania Medical Center (S.E.K.), Philadelphia, Pa.
Xavier Ducrocq, MD
From the Department of Neurology (J.M.F., P.C.), Hospital Santa Maria, University of Lisboa, Lisboa, Portugal; the Academic Medical Centre (J.S.), Amsterdam, The Netherlands; Hôpital Lariboisière (M.G.B.), Paris, France; Instituto Nacional de Neurologia y Neurocirurgia (F.B.), México City, México; Hospital das Clínicas (A.M.), Universidade de São Paulo, São Paulo, Brazil; Hôpital Central (X.D.), Nancy, France; and the University of Pennsylvania Medical Center (S.E.K.), Philadelphia, Pa.
Scott E. Kasner, MD
From the Department of Neurology (J.M.F., P.C.), Hospital Santa Maria, University of Lisboa, Lisboa, Portugal; the Academic Medical Centre (J.S.), Amsterdam, The Netherlands; Hôpital Lariboisière (M.G.B.), Paris, France; Instituto Nacional de Neurologia y Neurocirurgia (F.B.), México City, México; Hospital das Clínicas (A.M.), Universidade de São Paulo, São Paulo, Brazil; Hôpital Central (X.D.), Nancy, France; and the University of Pennsylvania Medical Center (S.E.K.), Philadelphia, Pa.
for the ISCVT Investigators
From the Department of Neurology (J.M.F., P.C.), Hospital Santa Maria, University of Lisboa, Lisboa, Portugal; the Academic Medical Centre (J.S.), Amsterdam, The Netherlands; Hôpital Lariboisière (M.G.B.), Paris, France; Instituto Nacional de Neurologia y Neurocirurgia (F.B.), México City, México; Hospital das Clínicas (A.M.), Universidade de São Paulo, São Paulo, Brazil; Hôpital Central (X.D.), Nancy, France; and the University of Pennsylvania Medical Center (S.E.K.), Philadelphia, Pa.

Notes

Correspondence to José M. Ferro, MD, PhD, Department of Neurology, Hospital Santa Maria, 1649-035 Lisboa, Portugal. E-mail [email protected]

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  1. Re-optimizing the Time Frame for Classifying Cerebral Venous Sinus Thrombosis: An Unmet Need, Cureus, (2024).https://doi.org/10.7759/cureus.75951
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  2. A Case Report of Simultaneous Intracranial Hemorrhage and Cerebral Venous Sinus Thrombosis in a Young Indian Male: Diagnostic and Therapeutic Challenges, Cureus, (2024).https://doi.org/10.7759/cureus.55642
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  3. Lower cranial neuropathy as a presentation of cerebral venous sinus thrombosis secondary to antiphospholipid syndrome: A case report, International Journal of Case Reports and Images, 15, 1, (30-35), (2024).https://doi.org/10.5348/101440Z01AR2024CR
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  4. Health Care Encounters Prior to Hospitalization for Cerebral Venous Thrombosis Patients, Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques, 52, 2, (225-231), (2024).https://doi.org/10.1017/cjn.2024.48
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  5. Machine learning-based Cerebral Venous Thrombosis diagnosis with clinical data, Journal of Stroke and Cerebrovascular Diseases, 33, 9, (107848), (2024).https://doi.org/10.1016/j.jstrokecerebrovasdis.2024.107848
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  6. Clinical Course and Visual Outcomes of Papilledema in Pediatric Cerebral Venous Sinus Thrombosis, American Journal of Ophthalmology, 263, (126-132), (2024).https://doi.org/10.1016/j.ajo.2024.02.001
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  7. Clinical value of neuroimaging indicators of intracranial hypertension in patients with cerebral venous thrombosis, Neuroradiology, 66, 7, (1161-1176), (2024).https://doi.org/10.1007/s00234-024-03363-6
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  8. Diagnostic and Therapeutic Challenges of Concurrent Intracranial Hemorrhage and Cerebral Venous Thrombosis in a Patient With Acute Lymphoblastic Leukemia: A Case Report and Literature Review, Cureus, (2023).https://doi.org/10.7759/cureus.37482
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  9. Analysis of 6 pediatric nephrotic syndrome cases with complications of cerebral sinovenous thrombosis and literature review, Frontiers in Pediatrics, 11, (2023).https://doi.org/10.3389/fped.2023.1226557
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  10. Diagnosis and Treatment of Cerebral Venous Thrombosis, CONTINUUM: Lifelong Learning in Neurology, 29, 2, (519-539), (2023).https://doi.org/10.1212/CON.0000000000001211
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