What kind of mri for trigeminal neuralgia

The specifics will vary depending on MRI hardware and software, radiologist's and referrer's preference, institutional protocols, patient factors e. Please Note: You can also scroll through stacks with your mouse wheel or the keyboard arrow keys. Updating… Please wait. Unable to process the form. Check for errors and try again. Thank you for updating your details.

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About Recent Edits Go ad-free. To better characterize the anatomical patterns of NVC in patients with TN, high resolution anatomical scans, combined with other non-conventional methods e. In contrast, nerve dislocation or distortion occurs frequently at the affected trigeminal nerve, suggesting that NVC associated with TN is more severe than at the unaffected nerve or in asymptomatic individuals Lorenzoni et al.

Moderate and severe NVC may result in compression or distortion of the trigeminal nerve Figure 1 , bottom panels. NVC of the affected trigeminal nerve tends to be severe in patients with TN, whereas NVC at the unaffected nerves of patients or in healthy individuals are mostly of the simple contact form Satoh et al. TN is also associated with atrophy of the affected trigeminal nerve Erbay et al.

High-resolution MR has demonstrated that the mean diameter and cross-sectional area of the trigeminal nerve on the symptomatic side of TN patients is smaller compared to the asymptomatic side. It was proposed that atrophy is likely secondary to structural abnormalities of the trigeminal nerve, including axonal loss and demyelination that result from NVC Erbay et al.

Corroborating these findings, a recent study reported that trigeminal NVC as detected by MRI is likely to be symptomatic when it is accompanied by anatomical nerve changes including nerve atrophy Antonini et al.

Anatomically, myelinated axons at the REZ are primarily associated with CNS myelin produced by oligodendrocytes, which transitions to peripheral myelin produced by Schwann cells Peker et al. In this study, trigeminal nerve roots of patients with trigeminal pain syndromes were obtained during autopsy. At this location, various changes in the central myelin were observed including deformation and demyelination. The notion that CNS myelin is primarily disrupted at the REZ of TN patients is consistent with peripheral myelin being significantly more resistant to compression and damage.

This provides the rationale for why vascular contact more distally along the trigeminal nerve can occur in individuals without any history of TN Nurmikko and Eldridge, Immunohistochemical studies rely on trigeminal nerve biopsy samples extracted during surgical procedures for TN or during autopsy.

However, DTI provides a noninvasive means for examining trigeminal nerve microstructure in vivo. DTI involves fitting a tensor, which is an ellipsoid shaped mathematical model, at each brain voxel of a diffusion MR scan. There are several measures of tissue microstructure that can be derived from these eigenvalues, the most widely used being fractional anisotropy FA; Figure 2A.

FA ranges from zero i. Diffusion varies for different tissue types because the structural barriers innate to certain tissues hinder diffusion.

These variations are reflected by the shape of the tensor derived from a voxel of that tissue type. For example, the shape of a tensor derived from a voxel within the CSF would be roughly spherical in shape, indicating that diffusion is not hindered and molecules can flow equally in all directions.

In this case, diffusion is said to be isotropic. In contrast, there are several barriers to diffusion in white matter bundles making diffusion along the length of the axis greater than across it.

Diffusion is said to be anisotropic when this occurs and the shape of the tensor is less spherical. Figure 2. Schematic representation of diffusion tensor images DTI -derived metrics.

Figure is adapted from DeSouza et al. This has motivated a handful of studies to examine structural abnormalities in the trigeminal nerves of patients with TN using FA as measure Herweh et al. In these studies, FA was extracted from the trigeminal nerves of patients and healthy control participants, with the majority of the studies Herweh et al.

These studies demonstrated that a noninvasive in vivo measure of trigeminal nerve microstructure could be used to detect abnormalities in the trigeminal nerves of TN patients. However, the studies did have some limitations. First, the data were acquired using resolutions that may not have been sufficient to reveal all abnormalities.

In DTI, multiple images are collected so that the signal can be sensitized to diffusion in different directions, building up multiple measurements for each voxel in the brain Johansen-Berg and Rushworth, In these aforementioned studies, a relatively low number of diffusion gradient-directions were used i.

While only six noncollinear directions are required to estimate the diffusion tensor, many more images are usually required to boost the signal intensity-to-noise ratio Mukherjee et al. The rationale for sampling more directions is that it reduces orientational dependence and increases the accuracy and precision of estimating tensor-derived parameters such as FA Mukherjee et al.

Second, many of these studies primarily assessed the DTI metric FA, that does not fully describe the tensor shape. Therefore, information important for a full interpretation of the findings was limited because other DTI metrics such as mean, radial and axial diffusivities MD, RD, AD were not collected. These other measures of tissue microstructure have been linked to specific pathophysiological mechanisms such as demyelination, neuroinflammation and edema Alexander et al.

While reduced FA has been reported across a broad spectrum of disorders Alexander et al. Figure 3. The yellow box highlights the pons of the brainstem and the cisternal portions of the left and right trigeminal nerves. B A zoomed-in version of this box reveals the location of the REZ masks white squares, highlighted with circles used to extract each of the four examined DTI metrics in TN patients and controls. Between-group comparisons revealed that TN patients had abnormalities in all four metrics examined.

The chart shows the direction of these abnormalities in patients relative to controls. Panels A,B were adapted from DeSouza et al. Brain gray matter abnormalities have been identified in patients with chronic pain Davis and Moayedi, The most common location of gray matter abnormalities include regions implicated in the multidimensional experience of pain such as the prefrontal cortex PFC , insula, anterior and mid-cingulate cortices ACC, MCC , thalamus, primary and secondary somatosensory cortices S1, S2 , basal ganglia, amygdala and brainstem Davis and Moayedi, These abnormalities are commonly found for many types of chronic pain including those affecting the trigeminal system such as migraine Rocca et al.

Since some abnormalities are common across most chronic pains e. However, the direction of the gray matter abnormalities in other brain regions varies across patient populations. Differences in the direction of abnormality may reflect specific symptomology e.

For example, mechanisms pertaining to gray matter underlying MR-detectable differences in brain structure may include changes in neuronal size or number, synaptogenesis, dendritic branching, axon sprouting, synaptic pruning, neuronal cell death, alterations in vasculature and the size or numbers of glial cells Blumenfeld-Katzir et al. We recently employed high-resolution T1-weighted scans of patients with TN and examined subcortical and cortical brain gray matter using voxel-based morphometry and CT analyses, respectively DeSouza et al.

Compared to healthy controls, we identified widespread abnormalities in regions that contribute to sensory-discriminative and cognitive-affective dimensions of pain, pain modulation, and motor function. Specifically, TN patients had greater gray matter in the thalamus, contralateral S1 putative face area , amygdala, frontal pole FP , periaqueductal gray PAG , primary motor cortex M1 and basal ganglia, and cortical thinning in the orbitofrontal cortex OFC , pregenual anterior cingulate cortex pgACC and insula DeSouza et al.

These findings may reflect unique symptomatology because TN is characterized by paroxysmal pain triggered by innocuous stimuli or movements, and is without major sensory loss.

The findings may be a consequence of the pain or be pre-existing and contribute to the development of TN Figure 4C. Figure 4. Widespread gray matter abnormalities in patients with TN. A CT analysis revealed several cortical gray matter abnormalities in TN patients. Compared to controls, patients had thinner cortex red clusters in the pgACC bilaterally, the right ins including the dorsal posterior insula and the ventral anterior insula vAI , and the ventral OFC bilaterally.

TN patients had thicker cortex blue clusters in the bilateral FP and M1, and left S1 putative face area, contralateral to their side of pain. B Patients also had several subcortical gray matter abnormalities as determined using voxel-based morphometry. Compared to controls, TN patient had larger volumes blue clusters in the sensory thalamus, including the MD and VPM thalamus bilaterally, the right amygdala, the posterior putamen bilaterally, PAG green box shows magnified region , and regions of the right NAc, anterior putamen, and caudate.

C Prior to surgery, CT abnormalities compared to healthy controls in the pgACC, the OFC and M1, were more pronounced in the TN patients who had significant pain relief after effective Tx blue bars compared to those in which treatment was ineffective red bars.

These pre-treatment baseline CT levels were significantly different between the groups of patients that achieved effective vs. While it remains unknown as to whether these abnormalities are a consequence of the pain or are pre-existing and contribute to the development of TN, these preliminary data suggest that certain abnormalities may have predictive value to identify patients that will benefit from treatment.

CT, cortical thickness; Tx, treatment. Panels A,B have been reproduced from DeSouza et al. A handful of other studies have examined gray matter in patients with trigeminal pain syndromes including TN. Similar to our findings, less gray matter in the ACC, anterior insula, and OFC were reported in these patients compared to healthy controls Gustin et al.

However, in contrast to our findings, the patients also had decreased gray matter in the S1, thalamus Gustin et al. The differences in these findings with our own may be due to the mixed trigeminal pain patient groups that were examined and the different methodology used to assess gray matter. For example, in one study, the patient group included those with either trigeminal neuropathic pain or TN Gustin et al.

In this study, the authors reported that only patients with trigeminal neuropathic pain and not patients with TN contributed to the decreased thalamic volume result in patients. In another study, patients with classical TN and TN with concomitant facial pain were compared to healthy controls Obermann et al.

While the authors report no differences between the two patient populations, the results reported derive from a mix of both types of trigeminal pain compared to controls. Additionally, the use of different methods to assess cortical gray matter may have contributed to the differences in results. The human cerebral cortex of humans is highly folded with its thickness varying across regions.

CT analysis as implemented by DeSouza et al. In contrast, voxel-based morphometry approaches as implemented by Gustin et al. In addition to widespread gray matter abnormalities, several studies have reported abnormalities in the brain white matter of chronic pain patients, many of which interconnect gray matter regions involved in the multi-dimensional experience of pain.

A popular method used to examine white matter abnormalities in chronic pain patients compared to healthy controls is Tract-Based Spatial Statistics, which makes whole-brain comparisons of white matter DTI metrics Rocca et al. The location of these abnormalities is variable between chronic pains and may be related to factors such as disease duration or pain symptomology Rocca et al.

We found that patients had widespread abnormalities characterized by lower FA in the corpus callosum CC , cingulum, posterior corona radiate pCR and superior longitudinal fasciculus SLF contralateral to their side of pain Figure 5A. These tracts connect some gray matter regions involved in the multi-dimensional experience of pain, attention, and motor functions that we previously showed to be abnormal in TN. Figure 5. Brain white matter abnormalities in TN. Tract-based spatial statistics results showing that TN patients have several regions of abnormal brain white matter, compared to controls.

This figure has been reproduced from DeSouza et al. While in these cross-sectional studies it was not possible to confirm whether the observed brain abnormalities were pre-existing or occurred as a consequence of TN, studies examining how effective treatment impacts these abnormalities are starting to provide valuable insight.

A handful of studies have used structural MRI to demonstrate that some gray matter abnormalities in patients with chronic pain are reversible following effective treatment Gwilym et al. This suggests that they in part arise as a consequence of being in pain and do not necessarily cause the pain.

There are currently several treatment approaches available for the management of TN. Although medications are always the first line of treatment Zakrzewska and Akram, , over time, pain attacks may be longer lasting, occur more frequently, and be less responsive to medications, leading patients to seek neurosurgical intervention for pain relief Nurmikko and Eldridge, Surgical treatments for TN target the trigeminal nerve at different anatomical sites Figure 6 with the goal of displacing the offending vessel at the trigeminal REZ, as in microvascular decompression MVD surgery, or partially injuring the trigeminal nerve distal to the REZ to reduce nociceptive signaling, as in Gamma Knife radiosurgery GKRS; Figure 6 ; Zakrzewska and Akram, Both of these treatments result in a high proportion of patients with good or complete pain relief.

Our results indicated that effective surgical treatment was associated with the resolution of trigeminal abnormalities at both the affected and unaffected REZ Figure 7A. Figure 6. Neurosurgical treatment options for TN. MVD surgery uses a retrosigmoid craniotomy to remove a small piece of skull via a small incision behind the ear. The cerebellopontine angle is then approached, and using microscopic magnification, the location of the trigeminal nerve and offending vessel is identified.

GKRS is a focal radiosurgery technique. Gamma rays are emitted from approximately radioactive cobalt sources precisely focused on the trigeminal nerve using a collimator helmet B, right and a stereotactic frame not shown.

Figure 7. In contrast, pre-treatment REZ abnormalities persisted in patients that had ineffective treatment green box. Arrows indicate direction of abnormalities relative to controls. C The vAI green cluster on inflated brain was the only gray matter region to normalize in patients following effective treatment only. Specifically, prior to treatment patients had significantly thinner vAI thickness compared to controls.

Following treatment, vAI thickness significantly increased to become comparable to control vAI thickness. Panels B,C have been adapted from DeSouza et al. In addition to the REZ normalization, we also found that right ventral anterior insula vAI thinning normalized towards the level of healthy controls following effective neurosurgical treatment for TN DeSouza et al.

The right-lateralization of this finding is consistent with other studies that have reported right-lateralized activations in the context of pain expectation and the emotional modulation of pain Wiech and Tracey, Interestingly, vAI normalization was not associated with pain relief as shown in other chronic pain disorders Seminowicz et al. Since most studies of chronic pain report thinning of the AI, cingulate, and prefrontal cortices, it is possible that these abnormalities reflect pain chronicity in general, or other aspects of pain perception such as negative affect Wiech and Tracey, ; Kurth et al.

Since effective treatment can reverse vAI thinning in TN, our study provided novel evidence that some central abnormalities occur as a consequence of TN pain and likely contribute to the maintenance of this disorder.

While many patients experience excellent outcomes from TN treatments, some experience minimal pain relief. That is, there is individual variability with regard to patient responsiveness to treatment. Since conventional clinical diagnostic measures cannot predict which patients will benefit from a given treatment approach for TN, neuroimaging may be an effective tool to noninvasively provide brain-based biomarkers to support the optimal treatment selection for individual TN patients.

We previously established that TN is associated with subtle, yet widespread abnormalities in brain structure as measured by morphometric and microstructural measures of brain gray matter and white matter DeSouza et al. Furthermore, our preliminary data suggest that some pre-treatment cortical abnormalities differ between patients that achieve good vs.

As such, future studies may determine which of these measures most accurately predict treatment outcome using a machine learning approach.

The application of machine learning algorithms to pain neuroimaging has become a recent topic of interest e. In general, neuroimaging data can be used to train a discriminative classifier, such as a support vector machine, to make predictions about new data. Clinically, it would be highly advantageous to have brain-based biomarkers that can predict outcomes in individual patients based on models that were trained on prior groups to make out-of-sample predictions Lindquist et al.

Knowing in advance which patients may better benefit from a certain treatment type e. While the predictive accuracy of a classification algorithm based solely on morphological measures is cautioned Labus et al. In one study, a combination of structural and resting-state functional MRI measures were shown to accurately predict treatment response in patients with social anxiety disorder Whitfield-Gabrieli et al.

It could also provide insight into the fundamental mechanisms underlying individuality of pain and its alleviation and complement patient self-reports. In this review, we have provided structural neuroimaging evidence to support peripheral theories of TN etiology and pathophysiology, showed a role for the CNS in TN pain, and discussed implications for the use of potential neuroimaging-based biomarkers to predict treatment response.

It is becoming increasingly understood that TN pathophysiology is associated with both trigeminal nerve and brain abnormalities. While future studies are needed to assess the extent to which these abnormalities are the cause or consequence of TN, it is clear that structural MRI methods offer a valuable means to noninvasively examine the trigeminal system in vivo and inform our understanding of trigeminal nerve and brain abnormalities in TN.

DDD: concept and design for manuscript content; critical revision of the manuscript for important intellectual content. Your doctor may recommend laboratory tests to determine if the cause of your pain is a tumor, an abnormal blood vessel, or a condition such as multiple sclerosis. Imaging tests such as a magnetic resonance imaging MRI scan can be very helpful in diagnosing trigeminal neuralgia.

An MRI can help your doctor see if there is pressure on the trigeminal nerve. In our state-of-the-art clinic, our Trigeminal Neuralgia Program brings together neurosurgeons, neurologists, radiologists, psychiatrists, pain management specialists, and other highly trained professionals. They collaborate closely to provide you with the most innovative diagnostic and treatment options as well as the latest research findings.

So, as a Stanford Health Care patient, you may have access to treatment options not available anywhere else. To schedule an appointment, please call: Share on Facebook. Notice: Users may be experiencing issues with displaying some pages on stanfordhealthcare. We are working closely with our technical teams to resolve the issue as quickly as possible. Thank you for your patience. View the changes to our visitor policy » View information for Guest Services ». New to MyHealth? Manage Your Care From Anywhere.

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Team-based treatment planning that brings together orthopaedic surgeons, neurologists and neurosurgeons, pain management specialists, rheumatologists, physiatrists, and others to tailor care to your needs. Advanced treatment options emphasizing noninvasive approaches whenever possible, including exercises and physical therapy , plus medication therapy and, when needed, spine surgery.

Comprehensive support services including care coordination from diagnosis to treatment to follow-up. Active research program to develop new diagnostic and treatment advances. Treatment for Trigeminal Neuralgia. Medication For some patients, medication provides pain relief.

Other medications your doctor may prescribe for trigeminal neuralgia pain relief include:. Surgery Stanford performs the most advanced, minimally invasive surgical procedures to treat trigeminal neuralgia. Surgical options at Stanford include:. Neuromodulation therapy In addition to medication and advanced surgical procedures, we offer neuromodulation therapies that target the brain and nervous system with electrical stimulation to help relieve pain caused by trigeminal neuralgia.

Options include:. Alternative treatments Some people find their trigeminal neuralgia symptoms improve with alternative treatments, such as acupuncture , chiropractic care, vitamin therapy, nutrition therapy , and biofeedback.