1,721,239 research outputs found
Intracranial stimulation of the trigeminal nerve in man. I. Direct motor responses.
No full textDirect electrical stimulation of the intracranial portion of the trigeminal nerve was performed in 23 subjects undergoing retrogasserian thermocoagulation for the treatment of idiopathic trigeminal neuralgia. In 16 subjects, who were having the operation for the first time, neurological examination was normal, as was neurophysiological testing of trigeminal function. Seven subjects were being operated for the second time, owing to a recurrence of symptoms. In all the subjects being operated for the first time, direct motor responses were obtained from ipsilateral temporalis, masseter and anterior belly of the digastric. The motor conduction velocity was equal for the fibres directed to all three muscles. This was estimated to be 54m/s in the masseteric nerve and 55-68 m/s in the intracranial portion of the trigeminal nerve. Patients who had undergone previous thermocoagulation had a considerably slower conduction velocity. It is supposed that myelin sheaths had been damaged at the first operation
Trigeminal neuralgia
No full textPURPOSE OF REVIEW:
Although trigeminal neuralgia is well known to neurologists, recent developments in classification and clinical diagnosis, new MRI methods, and a debate about surgical options necessitate an update on the topic.
RECENT FINDINGS:
Currently, a worldwide controversy exists regarding the classification, diagnostic process, and surgical treatment of trigeminal neuralgia. This controversy has been caused on one side by the recognition that some 50% of patients with trigeminal neuralgia, apart from characteristic paroxysmal attacks, also have continuous pain in the same territory, which results in greater diagnostic difficulties and is associated with a lower response to medical and surgical treatments. In contrast, recent developments in MRI methods allow differentiation between a mere neurovascular contact and an effective compression of the trigeminal root by an anomalous vessel, which implies more difficulties in the choice of surgical treatment, with the indication for microvascular decompression becoming more restricted.
SUMMARY:
This article proposes that the diagnosis of trigeminal neuralgia, with or without concomitant continuous pain, must rely on clinical grounds only. Diagnostic tests are necessary to distinguish three etiologic categories: idiopathic trigeminal neuralgia (nothing is found), classic trigeminal neuralgia (an anomalous vessel produces morphologic changes of the trigeminal root near its entry into the pons), and secondary trigeminal neuralgia (due to major neurologic disease, such as multiple sclerosis or tumors at the cerebellopontine angle). Carbamazepine and oxcarbazepine (ie, voltage-gated, frequency-dependent sodium channel blockers) are still the first-choice medical treatment, although many patients experience significant side effects, and those with concomitant continuous pain respond less well to treatment. The development of sodium channel blockers that are selective for the sodium channel 1.7 (Nav1.7) receptor will hopefully help. Although all the surgical interventions (percutaneous ganglion lesions, gamma knife radiosurgery, and microvascular decompression) are very efficacious, precise MRI criteria for differentiating a real neurovascular compression from an irrelevant contact will be of benefit in better selecting patients for microvascular decompression
How diagnostic tests help to disentangle the mechanisms underlying neuropathic pain symptoms in painful neuropathies
No full textNeuropathic pain, ie, pain arising directly from a lesion or disease affecting the somatosensory afferent pathway, manifests with various symptoms, the commonest being ongoing burning pain, electrical shock-like sensations, and dynamic mechanical allodynia. Reliable insights into the mechanisms underlying neuropathic pain symptoms come from diagnostic tests documenting and quantifying somatosensory afferent pathway damage in patients with painful neuropathies. Neurophysiological investigation and skin biopsy studies suggest that ongoing burning pain primarily reflects spontaneous activity in nociceptive-fiber pathways. Electrical shock-like sensations presumably arise from high-frequency ectopic bursts generated in demyelinated, nonnociceptive, Aβ fibers. Although the mechanisms underlying dynamic mechanical allodynia remain debatable, normally innocuous stimuli might cause pain by activating spared and sensitized nociceptive afferents. Extending the mechanistic approach to neuropathic pain symptoms might advance targeted therapy for the individual patient and improve testing for new drugs
Topical treatment of peripheral neuropathic pain: applying the evidence
Full text linkPatients with peripheral neuropathic pain (NP) may only achieve partial pain relief with currently recommended first-line oral treatments, which are also associated with systemic adverse events. Topical treatments are currently considered second- or third-line options, but a recent pharmacologic treatment algorithm has called for broader first-line use of these agents. This has highlighted a need to communicate the benefits associated with topical agents, in particular around the efficacy, targeted local action, and limited systemic availability resulting in minimal systemic adverse events and drug-drug interactions
Laser evoked potentials in patients with trigeminal disease: the absence of Adelta potentials does not unmask C-fibre potentials.
Full text link[IF 2.468]
Objective: Although laser stimuli activate both Ad- and C-fibres, the corresponding laser evoked potentials (LEPs) remain restricted to the Ad-fibre input. Previous studies found C-LEPs after limb stimulation only in subjects with block or clinical impairment of Ad-fibres. In this study, we aimed at verifying whether in the trigeminal territory the impairment of Ad-fibres unmasks the C-LEP. Methods: By collecting retrospectively LEPs recorded in 370 patients, we analyzed the results from 150 trigeminal divisions with absent Ad-LEPs.
Results: We found signals that were consistent with the C-fibre input in three patients only. In most patients with absent Ad-LEPs, however, laser stimuli still elicited the Ad-conveyed pinprick sensation. Conclusions: The preserved pinprick sensation suggests that the Ad-fibre volley, though weakened, reached the cortex. The C-LEP absence may be explained according to the first come first served hypothesis: the evoked potential related to an afferent volley reaching the cortex shortly after a preceding input (i.e. a C-fibre volley coming after an Ad-fibre) will be suppressed.
Significance: In clinical studies using the standard laser pulses to evoke the Ad-LEPs, the finding of absent signals does not indicate a concomitant impairment of C-fibres
Painful sensory neuropathy.
No full textThis editorial highlights the role of Laser evoked potentials fo9r assessing neuropathic pai
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