High risk low grade glioma

High risk low grade glioma

On the basis of two randomized studies from the European Organization for Research and Treatment of Cancer (EORTC1) 2). and a synthesis by Pignatti et al, 3) high-risk low grade glioma LGG were defined by any three of five characteristics, including astrocytic histology, large tumor size (> 6 cm in diameter), midline tumor involvement, neurologic deficits ascribed to the tumor and not to surgery, and age older than 40 years.

This definition differ significantly from the definition used in the RTOG 9802 trial4).

Radiation Therapy Oncology Group (RTOG) 9802 has established postoperative radiation therapy (RT) and chemotherapy sequentially as the new standard of care for patients with high-risk low-grade glioma (LGG) meeting trial criteria. Although this trial investigated sequential chemoradiation therapy (sCRT) with RT followed by chemotherapy, it is unknown whether concurrent chemoradiation therapy (cCRT) may offer advantages over sCRT.

The National Cancer Database (NCDB) was queried for newly diagnosed World Health Organization (WHO) grade II glioma. Patients with unknown surgery, RT, or chemotherapy status were excluded, along with patients below 40 years old who underwent gross total resection to coincide with RTOG 9802 exclusion criteria. The χ, the Fisher exact, or Wilcoxon rank-sum tests evaluated differences in characteristics between groups. Kaplan-Meier analysis was used to evaluate overall survival (OS) between groups (sCRT vs. cCRT). Cox proportional hazards modeling determined variables associated with OS.

In total, 496 patients were analyzed (n=416 [83.9%] cCRT, n=80 [16.1%] sCRT). Sequencing or concurrency of therapy did not independently influence survival on univariable/multivariable analysis. Factors associated with worse OS on multivariable analysis included advanced age (P<0.001), whereas mixed glioma (P=0.017) and oligodendroglioma (P=0.005) were associated with better OS than astrocytoma histologies.

This is the only analysis of which we are aware of cCRT versus sCRT for LGG. There is no evidence that cCRT improves outcomes over sCRT 5).


The level of evidence for adjuvant treatment of diffuse WHO grade II glioma (low-grade gliomaLGG) is low. In so-called “high risk low grade glioma” patients most centers currently apply an early aggressive adjuvant therapy after surgery. The aim of a assessment was to compare progression free survival (PFS) and overall survival (OS) in patients receiving radiation therapy (RT) alone, chemotherapy (CT) alone, or a combined/consecutive RT+CT, with patients receiving no primary adjuvant treatment after surgery.

Based on a retrospective multicenter cohort of 288 patients (≥ 18 years old) with diffuse WHO grade II gliomas, a subgroup analysis of patients with confirmed isocitrate dehydrogenase mutation was performed. The influence of primary adjuvant treatment after surgery on PFS and OS was assessed using Kaplan-Meier estimates and multivariate Cox regression models, including age (≥ 40 years), complete tumor resection (CTR), recurrent surgery, and astrocytoma versus oligodendroglioma.

One hundred forty-four patients matched the inclusion criteria. Forty patients (27.8%) received adjuvant treatment. The median follow-up duration was 6 years (95% confidence interval 4.8-6.3 years). The median overall PFS was 3.9 years and OS 16.1 years. PFS and OS were significantly longer without adjuvant treatment (p = 0.003). A significant difference in favor of no adjuvant therapy was observed even in high-risk patients (age ≥ 40 years or residual tumor, 3.9 vs 3.1 years, p = 0.025). In the multivariate model (controlled for age, CTR, oligodendroglial diagnosis, and recurrent surgery), patients who received no adjuvant therapy showed a significantly positive influence on PFS (p = 0.030) and OS (p = 0.009) compared to any other adjuvant treatment regimen. This effect was most pronounced if RT+CT was applied (p = 0.004, hazard ratio [HR] 2.7 for PFS, and p = 0.001, HR 20.2 for OS). CTR was independently associated with longer PFS (p = 0.019). Age ≥ 40 years, histopathological diagnosis, and recurrence did not achieve statistical significance.

In this series of IDH-mutated LGGs, adjuvant treatment with RT, CT with temozolomide (TMZ), or the combination of both showed no significant advantage in terms of PFS and OS. Even in high-risk patients, the authors observed a similar significantly negative impact of adjuvant treatment on PFS and OS. These results underscore the importance of a CTR in LGG. Whether patients ≥ 40 years old should receive adjuvant treatment despite a CTR should be a matter of debate. A potential tumor dedifferentiation by administration of early TMZ, RT, or RT+CT in IDH-mutated LGG should be considered. However, these data are limited by the retrospective study design and the potentially heterogeneous indication for adjuvant treatment 6).


There was no significant difference in progression-free survival in patients with low-grade glioma when treated with either radiotherapy alone or temozolomide chemotherapy alone. Further data maturation is needed for overall survival analyses and evaluation of the full predictive effects of different molecular subtypes for future individualised treatment choices.

The effect of temozolomide chemotherapy or radiotherapy on HRQOL or global cognitive functioning did not differ in patients with low grade glioma. These results do not support the choice of temozolomide alone over radiotherapy alone in patients with high-risk low-grade glioma 7).

References

1)

van den Bent MJ, Afra D, de Witte O, et al. (2005) Long term efficacy of early versus delayed radiotherapy for low-grade astrocytoma and oligodendroglioma in adults: The EORTC 22845 randomised trial. Lancet 366:985–990.
2)

Karim AB, Afra D, Cornu P, et al. (2002) Randomized trial on the efficacy of radiotherapy for cerebral low-grade glioma in the adult: European Organization for Research and Treatment of Cancer Study 22845 with the Medical Research Council Study BRO4—An interim analysis. Int J Radiat Oncol Biol Phys 52:316–324.
3)

Pignatti F, van den Bent M, Curran D, et al. (2002) Prognostic factors for survival in adult patients with cerebral low-grade glioma. J Clin Oncol 20:2076–2084.
4)

Chamberlain MC. Does RTOG 9802 change practice with respect to newly diagnosed low-grade glioma? J Clin Oncol. 2013 Feb 10;31(5):652-3. doi: 10.1200/JCO.2012.46.7969. Epub 2013 Jan 7. PubMed PMID: 23295807.
5)

Ryckman JM, Appiah AK, Lyden E, Verma V, Zhang C. Concurrent Versus Sequential Chemoradiation for Low-grade Gliomas Meeting RTOG 9802 Criteria. Am J Clin Oncol. 2019 Feb 12. doi: 10.1097/COC.0000000000000519. [Epub ahead of print] PubMed PMID: 30768441.
6)

Paľa A, Coburger J, Scherer M, Ahmeti H, Roder C, Gessler F, Jungk C, Scheuerle A, Senft C, Tatagiba M, Synowitz M, Wirtz CR, Schmitz B, Unterberg AW. To treat or not to treat? A retrospective multicenter assessment of survival in patients with IDH-mutant low-grade glioma based on adjuvant treatment. J Neurosurg. 2019 Jul 19:1-8. doi: 10.3171/2019.4.JNS183395. [Epub ahead of print] PubMed PMID: 31323633.
7)

Reijneveld JC, Taphoorn MJ, Coens C, Bromberg JE, Mason WP, Hoang-Xuan K, Ryan G, Hassel MB, Enting RH, Brandes AA, Wick A, Chinot O, Reni M, Kantor G, Thiessen B, Klein M, Verger E, Borchers C, Hau P, Back M, Smits A, Golfinopoulos V, Gorlia T, Bottomley A, Stupp R, Baumert BG. Health-related quality of life in patients with high-risk low-grade glioma (EORTC 22033-26033): a randomised, open-label, phase 3 intergroup study. Lancet Oncol. 2016 Nov;17(11):1533-1542. doi: 10.1016/S1470-2045(16)30305-9. Epub 2016 Sep 27. PubMed PMID: 27686943.

APOEε4

APOEε4

Apolipoprotein E (ApoE) is a glycoprotein with a major role in brain lipoprotein metabolism. It has three isoforms encoded by distinct alleles: APOEε2, APOEε3 and APOEε4.

The presence of this genotype portends a worse prognosis following traumatic brain injury 1)

Furthermore, the incidence of severe traumatic brain injury in individuals with the apoE-4 allele greatly exceeds the rate of the allele in the general population 2). This allele is also a risk factor for Alzheimer’s disease 3) 4) 5) as well as for chronic traumatic encephalopathy.

Among patients with lobar hemorrhage, those with the apoE ε4 allele typically have their first hemorrhage >5 yrs earlier than noncarriers (73 ± 8 yrs vs./ 79 ± 7 yrs) 6).


Findings suggested that APOEε4 allele is a risk factor to brain function aggravation in the early stage of aneurysmal subarachnoid hemorrhage, and it may contribute to early brain injury after SAH 7).

Finding also suggests that the patients with APOEε4 allele predispose to cerebral vasospasm after spontaneous SAH 8).


The presence of APOE ε4, an elevated international normalized ratio, and a higher glucose level (≥ 10 mmol/L) are predictors of progressive traumatic intracerebral hemorrhage. Additionally, APOE ε4 is not associated with traumatic coagulopathy and patient outcome 9).


APOE ε4 and ε2 alleles appear to affect lobar ICH risk variably by race/ethnicity, associations that are confirmed in white individuals but can be shown in Hispanic individuals only when the excess burden of hypertension is propensity score-matched; further studies are needed to explore the interactions between APOE alleles and environmental exposures that vary by race/ethnicity in representative populations at risk for ICH 10).

APOEε4 may induce cerebral perfusion impairment in the early phase, contributing to early brain injury (EBI) following aneurysmal subarachnoid hemorrhage (aSAH), and assessment of APOE genotypes could serve as a useful tool in the prognostic evaluation and therapeutic management of aSAH 11).

The APOΕε4 polymorphism was analysed in 147 patients with aSAH. Allele and genotype frequencies were compared to those found in a gender- and area-matched control group of healthy individuals (n = 211). Early cerebral vasospasm (CVS) was identified and treated according to neurointensive care unit (NICU) guidelines. Neurological deficit(s) at admittance and at 1-year follow-up visit was recorded. Neurological outcome was assessed by the National Institute of Health Stroke Scale, Barthel Index and the Extended Glasgow Outcome Scale.

APOEε4 and non-APOEε4 allele frequencies were similar in aSAH patients and healthy individuals. The presence of APOEε4 was not associated with the development of early CVS. We could not find an influence of the APOE polymorphism on 1-year neurological outcome between groups. Subgroup analyses of patients treated with surgical clipping vs endovascular coiling did not reveal any associations.

The APOEε4 polymorphism has no major influence on risk of aSAH, the occurrence of CVS or long-term neurological outcome after aSAH 12).

References

1)

Friedman G,Froom P,Sazbon L,et al. Apolipoprotein E-e4 Genotype Predicts a Poor Outcome in Survivors of Traumatic Injury. Neurology. 1999; 52:244– 248
2)

Nicoll JAR, Roberts GW, Graham DI. Apolipoprotein Ee4 Allele is Associated with Deposition of Amyloid ß-Protein Following Head Injury. Nature Med. 1995; 1:135–137
3)

Mayeux R, Ottman R, Tang MX, et al. Genetic Susceptibility and Head Injury as Risk Factors for Alz- heimer’s Disease Among Community-Dwelling Elderly Persons and Their First Degree Relatives. Ann Neurol. 1993; 33:494–501
4)

Roberts GW, Gentleman SM, Lynch A, et al. ß Amyloid Protein Deposition in the Brain After Severe Head Injury: Implications for the Pathogenesis of Alzheimer’s Disease. J Neurol Neurosurg Psychiatry. 1994; 57:419–425
5)

Mayeux R, Ottman R, Maestre G, et al. Synergistic Effects of Traumatic Head Injury and Apolipoprotein-e4 in Patients with Alzheimer’s Disease. Neurology. 1995; 45:555–557
6)

Greenberg SM, Rebeck GW, Vonsattel JPV, et al. Apolipoprotein E e4 and Cerebral Hemorrhage Associated with Amyloid Angiopathy. Ann Neurol. 1995; 38:254–259
7)

Lin B, Dan W, Jiang L, Yin XH, Wu HT, Sun XC. Association of APOE polymorphism with the change of brain function in the early stage of aneurysmal subarachnoid hemorrhage. Acta Neurochir Suppl. 2011;110(Pt 1):39-42. doi: 10.1007/978-3-7091-0353-1_7. PubMed PMID: 21116912.
8)

Wu HT, Zhang XD, Su H, Jiang Y, Zhou S, Sun XC. Association of apolipoprotein E polymorphisms with cerebral vasospasm after spontaneous subarachnoid hemorrhage. Acta Neurochir Suppl. 2011;110(Pt 1):141-4. doi: 10.1007/978-3-7091-0353-1_24. PubMed PMID: 21116929.
9)

Wan X, Gan C, You C, Fan T, Zhang S, Zhang H, Wang S, Shu K, Wang X, Lei T. Association of APOE ε4 with progressive hemorrhagic injury in patients with traumatic intracerebral hemorrhage. J Neurosurg. 2019 Jul 19:1-8. doi: 10.3171/2019.4.JNS183472. [Epub ahead of print] PubMed PMID: 31323634.
10)

Marini S, Crawford K, Morotti A, Lee MJ, Pezzini A, Moomaw CJ, Flaherty ML, Montaner J, Roquer J, Jimenez-Conde J, Giralt-Steinhauer E, Elosua R, Cuadrado-Godia E, Soriano-Tarraga C, Slowik A, Jagiella JM, Pera J, Urbanik A, Pichler A, Hansen BM, McCauley JL, Tirschwell DL, Selim M, Brown DL, Silliman SL, Worrall BB, Meschia JF, Kidwell CS, Testai FD, Kittner SJ, Schmidt H, Enzinger C, Deary IJ, Rannikmae K, Samarasekera N, Salman RA, Sudlow CL, Klijn CJM, van Nieuwenhuizen KM, Fernandez-Cadenas I, Delgado P, Norrving B, Lindgren A, Goldstein JN, Viswanathan A, Greenberg SM, Falcone GJ, Biffi A, Langefeld CD, Woo D, Rosand J, Anderson CD; International Stroke Genetics Consortium. Association of Apolipoprotein E With Intracerebral Hemorrhage Risk by Race/Ethnicity: A Meta-analysis. JAMA Neurol. 2019 Feb 6. doi: 10.1001/jamaneurol.2018.4519. [Epub ahead of print] PubMed PMID: 30726504.
11)

Cheng C, Jiang L, Yang Y, Wu H, Huang Z, Sun X. Effect of APOE Gene Polymorphism on Early Cerebral Perfusion After Aneurysmal Subarachnoid Hemorrhage. Transl Stroke Res. 2015 Sep 14. [Epub ahead of print] PubMed PMID: 26370543.
12)

Csajbok LZ, Nylén K, Öst M, Blennow K, Zetterberg H, Nellgård P, Nellgård B. Apolipoprotein E polymorphism in aneurysmal subarachnoid haemorrhage in West Sweden. Acta Neurol Scand. 2015 Sep 16. doi: 10.1111/ane.12487. [Epub ahead of print] PubMed PMID: 26374096.

Diffusion tensor imaging for trigeminal neuralgia

Diffusion tensor imaging for trigeminal neuralgia

Trigeminal neuralgia (TN) is often classified as type 1 (TN1) when pain is primarily paroxysmal and episodic or type 2 (TN2) when pain is primarily constant in character. Diffusion tensor imaging (DTI) has revealed microstructural changes in the symptomatic trigeminal root and root entry zone of patients with unilateral TN.

Noninvasive DTI analysis of patients with TN may lead to improved trigeminal neuralgia diagnosis of TN subtypes (e.g., TN1 and TN2) and improve patient selection for surgical intervention. DTI measurements may also provide insights into prognosis after intervention, as TN1 patients are known to have better surgical outcomes than TN2 patients 1).


As diffusion tensor imaging (DTI) is able to assess tissue integrity, Leal et al., used diffusion to detect abnormalities in trigeminal nerves (TGN) in patients with trigeminal neuralgia (TN) caused by neurovascular compression (NVC) who had undergone microvascular decompression (MVD).

Using DTI sequencing on a 3-T MRI scanner, we measured the fraction of anisotropy (FA) and apparent diffusion coefficient (ADC) of the TGN in 10 patients who had undergone MVD for TN and in 6 normal subjects. We compared data between affected and unaffected nerves in patients and both nerves in normal subjects (controls). We then correlated these data with CSA and V. Data from the affected side and the unaffected side before and 4 years after MVD were compared.

RESULTS: Before MVD, the FA of the affected side (0.37 ± 0.03) was significantly lower (p < 0.05) compared to the unaffected side in patients (0.48 ± 0.03) and controls (0.52 ± 0.02), and the ADC in the affected side (5.6 ± 0.34 mm2/s) was significantly higher (p < 0.05) compared to the unaffected side in patients (4.26 ± 0.25 mm2/s) and controls (3.84 ± 0.18 mm2/s). Affected nerves had smaller V and CSA compared to unaffected nerves and controls (p < 0.05). After MVD, the FA in the affected side (0.41 ± 0.02) remained significantly lower (p < 0.05) compared to the unaffected side (0.51 ± 0.02), but the ADC in the affected side (4.24 ± 0.34 mm2/s) had become similar (p > 0.05) to the unaffected side (4.01 ± 0.33 mm2/s).

CONCLUSIONS: DTI revealed a loss of anisotropy and an increase in diffusivity in affected nerves before surgery. Diffusion alterations correlated with atrophic changes in patients with TN caused by NVC. After removal of the compression, the loss of FA remained, but ADC normalized in the affected nerves, suggesting improvement in the diffusion of the trigeminal root 2).


Herveh et al. studied the trigeminal nerve in seven healthy volunteers and six patients with trigeminal neuralgia using the diffusion tensor imagingderived parameter fractional anisotropy (FA). While controls did not show a difference between both sides, there was a reduction of FA in the affected nerve in three of six patients with accompanying nerve-vessel conflict and atrophy. Reversibility of abnormally low FA values was demonstrated in one patient successfully treated with microvascular decompression 3).


3T MR diffusion weighted, T1, T2 and FLAIR sequences were acquired for Multiple sclerosis related trigeminal neuralgia MS-TN, TN, and controls. Multi-tensor tractography was used to delineate CN V across cisternal, root entry zone (REZ), pontine and peri-lesional segments. Diffusion metrics including fractional anisotropy (FA), and radial (RD), axial (AD), and mean diffusivities (MD) were measured from each segment.

CN V segments showed distinctive diffusivity patterns. The TN group showed higher FA in the cisternal segment ipsilateral to the side of pain, and lower FA in the ipsilateral REZ segment. The MS-TN group showed lower FA in the ipsilateral peri-lesional segments, suggesting differential microstructural changes along CN V in these conditions.

The study demonstrates objective differences in CN V microstrucuture in TN and MS-TN using non-invasive neuroimaging. This represents a significant improvement in the methods currently available to study pain in MS 4).


The aim of a study was to evaluate the microstructural tissue abnormalities in the trigeminal nerve in symptomatic trigeminal neuralgia not related to neurovascular compression using diffusion tensor imaging. Mean values of the quantitative diffusion parameters of trigeminal nerve, fractional anisotropy and apparent diffusion coefficient, were measured in a group of four symptomatic trigeminal neuralgia patients without neurovascular compression who showed focal non-enhancing T2-hyperintense lesions in the pontine trigeminal pathway. These diffusion parameters were compared between the affected and unaffected sides in the same patient and with four age-matched healthy controls. Cranial magnetic resonance imaging revealed hyperintense lesions in the dorsolateral part of the pons along the central trigeminal pathway on T2-fluid-attenuated inversion recovery sequences. The mean fractional anisotropy value on the affected side was significantly decreased (P = 0.001) compared to the unaffected side and healthy controls. Similarly, the mean apparent diffusion coefficient value was significantly higher (P = 0.001) on the affected side compared to the unaffected side and healthy controls. The cause of trigeminal neuralgia in our patients was abnormal pontine lesions affecting the central trigeminal pathway. The diffusion tensor imaging results suggest that microstructural tissue abnormalities of the trigeminal nerve also exist even in non-neurovascular compression-related trigeminal neuralgia 5).


DTI analysis allows the quantification of structural alterations, even in those patients without any discernible neurovascular contact on MRI. Moreover, our findings support the hypothesis that both the arteries and veins can cause structural alterations that lead to TN. These aspects can be useful for making treatment decisions 6).


The mean diameter of compression arteries (DCA) in NVC patients with TN (1.58 ± 0.34 mm) was larger than that without TN (0.89 ± 0.29 mm). Compared with NVC without TN and HC, the mean values of RD at the site of NVC with TN were significantly increased; however, no significant changes of AD were found between the groups. Correlation analysis showed that DCA positively correlated with radial diffusivity (RD) in NVC patients with and without TN (r = 0.830, p = 0.000). No significant correlation was found between DCA and axial diffusivity (AD) (r = 0.178, p = 0.077).

Larger-diameter compression arteries may increase the chances of TN, and may be a possible facilitating factor for TN 7).


Fractional anisotropy (FA) value quantitatively showed the alteration of trigeminal nerve (TGN) caused by Neurovascular compression (NVC). It provided direct evidence about the effect of NVC which facilitated the diagnosis and surgical decision of Type 2 trigeminal neuralgia (TN) . Besides, significant reduction of FA value may predict an optimistic outcome of microvascular decompression (MVD) 8).


Sophisticated structural MRI techniques including diffusion tensor imaging provide new opportunities to assess the trigeminal nerves and CNS to provide insight into TN etiology and pathogenesis. Specifically, studies have used high-resolution structural MRI methods to visualize patterns of trigeminal nerve-vessel relationships and to detect subtle pathological features at the trigeminal REZ. Structural MRI has also identified CNS abnormalities in cortical and subcortical gray matter and white matter and demonstrated that effective neurosurgical treatment for TN is associated with a reversal of specific nerve and brain abnormalities 9).


Forty-three patients with trigeminal neuralgia were recruited, and diffusion tensor imaging was performed before radiofrequency rhizotomy. By selecting the cisternal segment of the trigeminal nerve manually, they measured the volume of trigeminal nerve, fractional anisotropy, apparent diffusion coefficient, axial diffusivity, and radial diffusivity. The apparent diffusion coefficient and mean value of fractional anisotropy, axial diffusivity, and radial diffusivity were compared between the affected and normal side in the same patient, and were correlated with pre-rhizotomy and post-rhizotomy visual analogue scale pain scores. The results showed the affected side had significantly decreased fractional anisotropy, increased apparent diffusion coefficient and radial diffusivity, and no significant change of axial diffusivity. The volume of the trigeminal nerve on affected side was also significantly smaller. There was a trend of fractional anisotropy reduction and visual analogue scale pain score reduction (P = 0.072). The results suggest that demyelination without axonal injury, and decreased size of the trigeminal nerve, are the microstructural abnormalities of the trigeminal nerve in patients with trigeminal neuralgia caused by neurovascular compression. The application of diffusion tensor imaging in understanding the pathophysiology of trigeminal neuralgia, and predicting the treatment effect has potential and warrants further study 10).

References

1)

Willsey MS, Collins KL, Conrad EC, Chubb HA, Patil PG. Diffusion tensor imaging reveals microstructural differences between subtypes of trigeminal neuralgia. J Neurosurg. 2019 Jul 19:1-7. doi: 10.3171/2019.4.JNS19299. [Epub ahead of print] PubMed PMID: 31323635.
2)

Leal PRL, Roch J, Hermier M, Berthezene Y, Sindou M. Diffusion tensor imaging abnormalities of the trigeminal nerve root in patients with classical trigeminal neuralgia: a pre- and postoperative comparative study 4 years after microvascular decompression. Acta Neurochir (Wien). 2019 May 2. doi: 10.1007/s00701-019-03913-5. [Epub ahead of print] PubMed PMID: 31049710.
3)

Herweh C, Kress B, Rasche D, Tronnier V, Tröger J, Sartor K, Stippich C. Loss of anisotropy in trigeminal neuralgia revealed by diffusion tensor imaging. Neurology. 2007 Mar 6;68(10):776-8. PubMed PMID: 17339587.
4)

Chen DQ, DeSouza DD, Hayes DJ, Davis KD, O’Connor P, Hodaie M. Diffusivity signatures characterize trigeminal neuralgia associated with multiple sclerosis. Mult Scler. 2016 Jan;22(1):51-63. doi: 10.1177/1352458515579440. PubMed PMID: 25921052.
5)

Neetu S, Sunil K, Ashish A, Jayantee K, Usha Kant M. Microstructural abnormalities of the trigeminal nerve by diffusion-tensor imaging in trigeminal neuralgia without neurovascular compression. Neuroradiol J. 2016 Feb;29(1):13-8. doi: 10.1177/1971400915620439. PubMed PMID: 26678753; PubMed Central PMCID: PMC4978338.
6)

Lutz J, Thon N, Stahl R, Lummel N, Tonn JC, Linn J, Mehrkens JH. Microstructural alterations in trigeminal neuralgia determined by diffusion tensor imaging are independent of symptom duration, severity, and type of neurovascular conflict. J Neurosurg. 2016 Mar;124(3):823-30. doi: 10.3171/2015.2.JNS142587. PubMed PMID: 26406792.
7)

Lin W, Zhu WP, Chen YL, Han GC, Rong Y, Zhou YR, Zhang QW. Large-diameter compression arteries as a possible facilitating factor for trigeminal neuralgia: analysis of axial and radial diffusivity. Acta Neurochir (Wien). 2016 Mar;158(3):521-6. doi: 10.1007/s00701-015-2673-4. PubMed PMID: 26733127; PubMed Central PMCID: PMC4752583.
8)

Chen F, Chen L, Li W, Li L, Xu X, Li W, Le W, Xie W, He H, Li P. Pre-operative declining proportion of fractional anisotropy of trigeminal nerve is correlated with the outcome of micro-vascular decompression surgery. BMC Neurol. 2016 Jul 16;16:106. doi: 10.1186/s12883-016-0620-5. PubMed PMID: 27422267; PubMed Central PMCID: PMC4947245.
9)

DeSouza DD, Hodaie M, Davis KD. Structural Magnetic Resonance Imaging Can Identify Trigeminal System Abnormalities in Classical Trigeminal Neuralgia. Front Neuroanat. 2016 Oct 19;10:95. Review. PubMed PMID: 27807409; PubMed Central PMCID: PMC5070392.
10)

Chen ST, Yang JT, Yeh MY, Weng HH, Chen CF, Tsai YH. Using Diffusion Tensor Imaging to Evaluate Microstructural Changes and Outcomes after Radiofrequency Rhizotomy of Trigeminal Nerves in Patients with Trigeminal Neuralgia. PLoS One. 2016 Dec 20;11(12):e0167584. doi: 10.1371/journal.pone.0167584. PubMed PMID: 27997548.
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