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Clinical Neuroanatomy
Published in John C Watkinson, Raymond W Clarke, Christopher P Aldren, Doris-Eva Bamiou, Raymond W Clarke, Richard M Irving, Haytham Kubba, Shakeel R Saeed, Paediatrics, The Ear, Skull Base, 2018
This is probably the most painful condition known, the cause of which seems to be due to ageing changes in the nerve or seemingly trivial irritation by adjacent aberrant arteries. From a practical, anatomical point of view, the very strict localization of the pain in Vth nerve territory is a vital diagnostic feature. There is no such thing as atypical trigeminal neuralgia and it is not acceptable to allow the pain to radiate behind the ear, onto the neck or across the midline, and the anatomically precise distribution is the linchpin of diagnosis. The pain is usually described in two characteristic distributions. The first runs from the lower canine tooth along the lower jaw to just in front of the ear and sometimes round into the upper jaw (i.e. it involves both V3 and V2). The second less frequent type runs from the upper incisor or canine, up the side or inside the nose and encircles the eye, involving both V2 and V1. It is probably this spread over two divisions that makes simple surgical section of the peripheral branches unsuccessful in managing the condition long term, although triggering is occasionally reduced. Although it is claimed that transient sensory deficit may follow a spasm of pain, any evidence of sensory loss, impaired corneal reflex or Vth motor weakness should invalidate the diagnosis. Although trigeminal neuralgia may complicate multiple sclerosis, it is very rare as a presenting symptom of this disease.
Trigeminal Neuralgia
Published in Gary W. Jay, Clinician’s Guide to Chronic Headache and Facial Pain, 2016
The most well-known procedure is the Janetta procedure (microvascular decompression) which involves an occipital craniotomy. Any vascular contacts with the fifth cranial nerve (trigeminal roots) are decompressed, with long-term benefit found in 80% to 100% of patients. Recurrence rates vary from 1% to 6%. Surgical mortality can be 1% and serious morbidity is seen in 7% (hemorrhage, hearing loss, or hematoma, CSF leak, infection). The procedure appears to be more effective when treating “typical” versus atypical trigeminal neuralgia (34-40).
Craniofacial Pain
Published in John W. Scadding, Nicholas A. Losseff, Clinical Neurology, 2011
‘Atypical trigeminal neuralgia’ is sometimes used to describe pain that has some but not all the diagnostic features of the condition. However, a diagnosis of trigeminal neuralgia should be resisted unless the pain fulfils the diagnostic criteria, and ‘atypical trigeminal neuralgia’ is a term best avoided.
The effect of conditioning stimulus intensity on conditioned pain modulation (CPM) hypoalgesia
Published in Canadian Journal of Pain, 2021
Alexia Coulombe-Lévêque, Yannick Tousignant-Laflamme, Guillaume Léonard, Serge Marchand
Pain perception is modulated by various intrinsic mechanisms, such as the diffuse noxious inhibitory controls described in animal models by Le Bars et al.,1 wherein a noxious stimulus induces widespread hypoalgesia. This phenomenon is studied in humans under the umbrella term “conditioned pain modulation” (CPM),2 and its dysfunction has been implicated in the development, maintenance, and exacerbation of many chronic pain conditions,3 including fibromyalgia, osteoarthritis, irritable bowel syndrome, temporomandibular disorder, and atypical trigeminal neuralgia.4–8 CPM response can be hyperalgesic (i.e., resulting in more intense pain sensations) or hypoalgesic (i.e., resulting in milder pain sensations); a hypoalgesic response is more common3 and is the focus of the present study.