Numbness matters: A clinical review of trigeminal neuropathy

Cephalalgia ◽  
2011 ◽  
Vol 31 (10) ◽  
pp. 1131-1144 ◽  
Author(s):  
Jonathan H Smith ◽  
F Michael Cutrer

Aim: Trigeminal neuropathies are a group of clinical disorders that involve injury to primary first-order neurons within the trigeminal nerve. We review the spectrum of etiologies underlying both painful and non-painful trigeminal neuropathies, with attention to particularly dangerous processes that may elude the clinician in the absence of a meticulous evaluation. Complications and management issues specific to patients with trigeminal neuropathy are discussed. Methods: Retrospective literature review. Results: Facial or intraoral numbness, the hallmark of trigeminal neuropathy, may represent the earliest symptomology of malignancy or autoimmune connective tissue disease as sensory neurons are destroyed. Such numbness, especially if progressive, necessitates periodic evaluation and vigilance even years after presentation if no diagnosis can be made. Conclusions: In the routine evaluation of patients with facial pain, the clinician will inevitably be confronted with secondary pathology of the trigeminal nerves and nuclei. The appearance of numbness, even when pain continues to be the most pressing complaint, necessitates clinical assessment of the integrity of all aspects of the trigeminal pathways, which may also include neurophysiologic, radiographic, and laboratory evaluation.

Author(s):  
R. John Leigh ◽  
David S. Zee

This chapter reviews the neural network that temporally integrates premotor, velocity-coded signals to achieve tonic contraction of the extraocular muscles to hold the eyes at an eccentric position in the orbits. The mechanical properties of the eye and its supporting tissues are quantified and related to the pulse-slide-step neural command for a saccadic change in eye position. The anatomical substrate and neuropharmacology of the neural integrator is reviewed, including nucleus prepositus hypoglossi, interstitial nucleus of Cajal and cerebellum. Mathematical and animal models for the neural integrator are discussed, addressing points about how a leaky or unstable integrator may arise. Clinical and laboratory evaluation of gaze holding is summarized. Effects of experimentally inactivating the neural integrator are compared with clinical disorders affecting gaze holding, including a discussion of the pathogenesis of gaze-evoked nystagmus and Alexander’s law. Compensatory mechanisms for a leaky neural integrator are discussed, including centripetal, rebound, and gaze-evoked nystagmus.


Author(s):  
Aydin Gozalov ◽  
Messoud Ashina ◽  
Joanna M. Zakrzewska

Orofacial pain is a complex problem and affects up to 7% of the population. Although trigeminal neuralgia has been considered the prime neuralgic condition in the facial region, other forms of neuropathic pain are now being more frequently recognized and require recognition and a different management approach. Many patients with chronic orofacial pain report numerous comorbidities, such as psychiatric or personality disorders, which significantly affect management. Various pain conditions present in the facial region. Some of them rarely present extra-orally (unless as radiating pain) such as atypical odontalgia or persistent dento-alveolar pain disorder and burning mouth syndrome, whereas others will present in both areas such as classical trigeminal neuralgia, post-traumatic trigeminal neuropathy, trigeminal neuropathy attributed to multiple sclerosis, and persistent idiopathic facial pain. Myofascial pain syndrome related to the muscles of mastication is very common and may also be associated with temporomandibular joint problems. Trigeminal neuralgia and the rarer glossopharyngeal neuralgia are similar in quality and characteristics with specific treatment modalities, but differ in pain location. Trigeminal neuropathic pain is caused most frequently by trauma. If no other diagnostic criteria are fulfilled, a diagnosis of persistent idiopathic facial pain is made. It is crucial for these patients to be managed by multidisciplinary teams.


1980 ◽  
Vol 52 (3) ◽  
pp. 381-386 ◽  
Author(s):  
Stephen J. Haines ◽  
Peter J. Jannetta ◽  
David S. Zorub

✓ The vascular relationships of the trigeminal nerve root entry zone were examined bilaterally in 20 cadavers of individuals known to be free of facial pain. Fourteen of 40 nerves made contact with an artery, but only four of these showed evidence of compression or distortion of the nerve. In addition, the vascular relationships of 40 trigeminal nerves exposed surgically for treatment of trigeminal neuralgia were studied, and 31 nerves showed compression by adjacent arteries. Venous compression was seen in four of the cadaver nerves and in eight nerves from patients with trigeminal neuralgia. These data support the hypothesis that arterial compression of the trigeminal nerve is associated with trigeminal neuralgia.


2009 ◽  
Vol 110 (4) ◽  
pp. 627-632 ◽  
Author(s):  
Jonathan P. Miller ◽  
Feridun Acar ◽  
Bronwyn E. Hamilton ◽  
Kim J. Burchiel

Object Neurovascular compression (NVC) of the trigeminal nerve is associated with trigeminal neuralgia (TN), but also occurs in many patients without facial pain. This study is designed to identify anatomical characteristics of NVC associated with TN. Methods Thirty patients with Type 1 TN (intermittent shocklike pain) and 15 patients without facial pain underwent imaging for analysis of 30 trigeminal nerves ipsilateral to TN symptoms, 30 contralateral to TN symptoms, and 30 in asymptomatic patients. Patients underwent 3-T MR imaging including balanced fast-field echo and MR angiography. Images were fused and reconstructed into virtual cisternoscopy images that were evaluated to determine the presence and degree of NVC. Reconstructed coronal images were used to measure nerve diameter and crosssectional area. Results The incidence of arterial NVC in asymptomatic nerves, nerves contralateral to TN symptoms, and nerves ipsilateral to TN symptoms was 17%, 43%, and 57%, respectively. The difference between symptomatic and asymptomatic nerves was significant regarding the presence of NVC, nerve distortion, and the site of compression (p < 0.001, Fisher exact test). The most significant predictors of TN were compression of the proximal nerve (odds ratio 10.4) and nerve indentation or displacement (odds ratio 4.3). There was a tendency for the development of increasingly severe nerve compression with more advanced patient age across all groups. Decreased nerve size was observed in patients with TN but did not correlate with the presence or extent of NVC. Conclusions Trigeminal NVC occurs in asymptomatic patients but is more severe and more proximal in patients with TN. This information may help identify patients who are likely to benefit from microvascular decompression.


2006 ◽  
Vol 64 (4) ◽  
pp. 983-989 ◽  
Author(s):  
Manoel J. Teixeira ◽  
Silvia R.D.T. Siqueira ◽  
Gilberto M. Almeida

OBJECTIVE: To determine the outcomes of 354 radiofrequency rhizotomies and 21 neurovascular decompressions performed as treatment for 367 facial pain patients (290 idiopathic trigeminal neuralgia, 52 symptomatic trigeminal neuralgia, 16 atypical facial pain, 9 post-herpetic neuralgia). METHOD: Clinical findings and surgery success rate were considered for evaluation. A scale of success rate was determined to classify patients, which considered pain relief and functional/sensorial deficits. RESULTS: Radiofrequency rhizotomy was performed in 273 patients with idiopathic trigeminal neuralgia and in all other patients, except for trigeminal neuropathy; neurovascular decompression was performed in 18 idiopathic trigeminal neuralgia patients; 100% idiopathic trigeminal neuralgia, 96.2% symptomatic trigeminal neuralgia, 37.5% atypical facial pain and 88.9% post-herpetic neuralgia had pain relief. CONCLUSION: Both techniques for idiopathic trigeminal neuralgia are usefull. Radiofrequency rhizotomy was also efficient to treat symptomatic facial pain, and post-herpetic facial pain, but is not a good technique for atypical facial pain.


Cephalalgia ◽  
2018 ◽  
Vol 39 (2) ◽  
pp. 316-322 ◽  
Author(s):  
Samantha Bobba ◽  
Manisha Narasimhan ◽  
Alessandro S Zagami

Background Chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids (CLIPPERS) is an inflammatory central nervous system disorder, typically presenting with subacute symptoms referable to brainstem and cerebellar pathology. This is the first report of CLIPPERS presenting with a painful trigeminal neuropathy. Case report We report an unusual case of CLIPPERS presenting with facial pain and sensory symptoms, in the absence of other brainstem or cerebellar signs. Perivascular enhancement of peri-pontine structures on neuroimaging, lymphocytic infiltrate on histopathology and rapid clinical and radiological responsiveness to glucocorticosteroids were key to diagnosis. Extensive investigations excluded various differential aetiologies. Conclusion The pathogenesis of CLIPPERS is poorly understood, and the diagnostic criteria are yet to be validated. In this case, facial pain was not associated with other brainstem or cerebellar signs, broadening current understanding of how CLIPPERS may present. This has clinical implications in guiding future investigations for patients presenting with painful trigeminal neuropathy.


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