Neurology
Fazal-I-Akbar Danish in Essential Lists of Differential Diagnoses for MRCP with diagnostic hints, 2017
Trigeminal neuralgia (episodic facial pain):1 No sign present; just pain: a Idiopathic (ophthalmic branch is not involved).2 Sign/s present: a Postherpetic neuralgia (scarring and sensory loss over the forehead).b Tumour involving the 5th nerve.c Multiple sclerosis.
Pain in neurological disease
Peter R Wilson, Paul J Watson, Jennifer A Haythornthwaite, Troels S Jensen in Clinical Pain Management, 2008
Trigeminal neuralgia occurs in multiple sclerosis approximately 300 times more often than in the general population. It is generally similar in its presentation to the idiopathic condition, but tends to occur at a younger age and is more likely to be bilateral (which is extremely rare in the idiopathic disorder). It is generally responsive to treatment along similar lines to idiopathic tic douloureux,13 although microvascular decompression (in a small series) appeared less effective,14 and there also appears to be relative refractoriness to neurolytic surgical procedures.15 A 1994 study7 suggests a prevalence in the order of 5 percent (rather higher than formerly believed). Unlike most pain syndromes in MS, trigeminal neuralgia may be a presenting symptom of the disease, and the underlying diagnosis should therefore be considered particularly in a young patient or one with bilateral symptoms. The clinical manifestations and treatment of trigeminal neuralgia are discussed at greater length in Chapter 35, Facial pain.
Geriatric headache
Stephen D. Silberstein, Richard B. Upton, Peter J. Goadsby in Headache in Clinical Practice, 2018
The diagnosis of trigeminal neuralgia is established by its typical clinical features. The physical examination is normal except for positive trigger points. Diagnostic studies are generally normal. Impaired sensation in the distribution of the Vth nerve suggests a structural, demyelinating, or compressive trigeminal nerve lesion (Table 17.6). The initial evaluation should include MRI, with special attention to the region of the cerebellopontine angle and the exit foramen of the trigeminal nerve. Majoie et al54 assessed the diagnostic yield of MRI in patients who had symptoms and signs related to the trigeminal nerve. A normal examination and trigeminal neuralgia symptoms alone were highly correlated with a negative MRI study. Impaired sensation, subjective feelings of facial numbness, other positive neurologic signs and symptoms, progression of symptoms and signs, and symptoms that had been present for less than lyear correlated with an abnormal MRI. Trigeminal evoked potentials may also be a valuable diagnostic aid in the search for underlying compressive lesions of the trigeminal nerve. Sundaram et al55 demonstrated abnormal trigeminal evoked potentials in all patients with trigeminal neuralgia resulting from known intracranial mass lesions, suggesting that trigeminal evoked potentials should be considered in the normal work-up of patients who have trigeminal neuralgia and negative MR imaging. If the evoked potential responses are abnormal, then nerve compression is still the most likely cause of the patient’s trigeminal neuralgia symptoms.
The expression of voltage-gated sodium channels in trigeminal nerve following chronic constriction injury in rats
Published in International Journal of Neuroscience, 2019
Mingxing Liu, Jun Zhong, Lei Xia, Ningning Dou, Shiting Li
Trigeminal neuralgia is a form of neuropathic pain usually described by the patients as an unbearable, excruciating discomfort, sometimes severe enough to lead to suicidal thoughts. As early in 1932, Dandy found vascular compression of the trigeminal root was the cause of the disorder [1]. Today, this etiology has been widely verified by successful microvascular decompression surgery [2, 3]. However, its underlying pathogenesis has been still unclear up to now. Jannetta had hypothesized the ‘peripheral theory’ which believed that the ephaptic impulses spread at compression sites induced the neuralgia [4]. While, others introduced the ‘central theory’ which believed that the autorhythmicity of trigeminal ganglion (TG) was the main reason [5–7]. Regardless of the peripheral or central theories, there has been few findings concerning the mechanism of trigeminal neuralgia have been reported except the demyelination in the trigeminal root [8–10]. Nevertheless, so far it has been acceptable that the substantiality of the disorder is a sort of hyperexcitability manifested by abnormal discharges or ectopic action potentials [11–13].
The pharmacological management of dental pain
Published in Expert Opinion on Pharmacotherapy, 2020
Joseph V. Pergolizzi, Peter Magnusson, Jo Ann LeQuang, Christopher Gharibo, Giustino Varrassi
Cluster headaches and migraine headaches are neurovascular events that may sometimes present with dental pain. Neurovascular headaches may refer pain to the teeth and the patient may present with headache or toothache or both together; these are known as neurovascular toothaches. The headache causes neuropeptides to be released from the trigeminal nerve endings in the intracranial blood vessels to dilate and the resulting inflammation and pressure cause pain. In cases of a suspected referred toothache, it may be useful to ask the patient about headache status. Treatment of the headache may relieve pain and an NSAID can be used to reduce the dental inflammation [73]. Cluster headache is often treated with oxygen and migraine may be treated with any of several pharmacological treatments (calcitonin gene-related peptide inhibitors, Botox, opioids, acetaminophen/caffeine, and others). If dental pain resolves with headache treatment, it suggests that the toothache was neurovascular. In the same way, trigeminal neuralgia may present with excruciating sharp or shooting pains in the teeth or oral cavity. Treatment of the trigeminal neuralgia (carbamazepine) may improve symptoms, but dental blockade will not [66].
Trigeminal schwannoma: a single-center experience with 43 cases and review of literature
Published in British Journal of Neurosurgery, 2021
Mingchu Li, Xu Wang, Ge Chen, Jiantao Liang, Hongchuan Guo, Gang Song, Yuhai Bao
Among the 43 patients, the tumor was totally removed in 39 patients (90.7%) and near-totally removed in three patients (7.0%). In one patient (2.3%), the tumor was only partially removed, because the ICA was injured, and the patient died after the operation. The abducens nerve was damaged in two patients (4.7%), and the nerve function achieved a significant improvement during the follow up. One patient developed mild facial paralysis and two patients developed intracranial infection after the operation. However, all of them achieved complete recovery before discharge. All four patients with trigeminal neuralgia achieved total recovery. However, the facial numbness got relief in only four patients, and this still continued in 24 patients (85.7%). In two patients, facial numbness even aggravated after the operation. For the nine patients with preoperative trigeminal motor impairment, the symptom did not achieve relief in any patient. Patients with oculomotor nerve paralysis, abducent paralysis and hearing decrease also achieved significant improvement during the follow-up. At a median of 45.3 ± 25.5 months (6–84 months) of follow up, the tumor recurred in only one patient, and this patient received a second operation via FTSA. The surgical results and follow-up results are shown in Table 4.
Related Knowledge Centers
- Atypical Trigeminal Neuralgia
- Brainstem
- Chronic Pain
- Suicide
- Stroke
- Trigeminal Nerve
- Blood Vessel
- Myelin
- Depression
- Multiple Sclerosis