China
Africa
Explore chapters and articles related to this topic
Otalgia
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
Geniculate neuralgia, also known as intermediate nerve neuralgia or tic doloureux of the nervus intermedius, is a rare disorder characterized by brief paroxysms of neuralgic pain felt deeply in the ear. The intermediate nerve (of Wrisberg) is a root of the facial nerve containing sensory and parasympathetic fibres. It is considered to be responsible for the sense of taste in the anterior two-thirds of the tongue, floor of the mouth, palate and sensory information from the skin of the external auditory canal as well as the mucous membranes of the nasopharynx and nose. Its cell bodies are located within the geniculate ganglion. The cutaneous field of the nervus intermedius has been described as the zone of Ramsay Hunt (or zoster zone) and consists of the tympanic membrane, auditory meatus, tragus, concha and the groove between the pinna and scalp.43 Although the aetiology is often not clear, symptoms have been ascribed to vascular loops44,45 and previous herpes zoster infection.
Discussions (D)
Published in Terence R. Anthoney, Neuroanatomy and the Neurologic Exam, 2017
Most authors of recent textbooks in basic neuroanatomy at some point describe the nervus intermedius as a part of the facial nerve (e.g., Brod, p. 495; wilk, p. 115, 116 [Fig. 6.13], chus, p. 121, 122 [Fig. 6- 13]; N&F, p. 173, 199; B&K, p. 84–85, 131, 133; W&W, p. 1064, 1070). Many of these same authors, however, describe the nervus intermedius elsewhere as if it is separate from the facial nerve. For example, after stating that the “intermediate nerve” is a “root of the facial nerve,” Martinez Martinez describes its location as “between the facial and the vestibular nerve” (1982, p. 172; see, also, Brod, p. 496, 636; wilk. p. 16 [Fig. 1.11], 72; Chus, p. 124 (Fig. 6–14]; N&F, p. 192–193 [Fig. 78]). This even occurs with some authors who give the non-nervus-intermedius portion of the facial nerve a special name, such as the “motor root of the facial nerve.” For example, Noback and Demarest (1981) describe two components of the “facial nerve”—the “facial nerve proper” and the “nervus intermedius” (p. 258). However, they don’t always include the adjective “proper,” which leads to descriptions of the facial nerve and the nervus intermedius as two separate nerves: “The facial nerve emerges … just anterior to the vestibulocochlear nerve. The nervus intermedius is located between these two nerves. The three nerves pass. …” (p. 258)
The Triple Heater (TH)
Published in Narda G. Robinson, Interactive Medical Acupuncture Anatomy, 2016
Facial nerve (CN VII): The motor root of the facial nerve emerges from the skull at the stylomastoid foramen and courses through the parotid gland. It then divides into six terminal branches: the posterior auricular, temporal, zygomatic, buccal, mandibular, and cervical branches of the facial nerve. These nerve branches supply the muscles of facial expression via the motor root of the facial nerve. The other root of the facial nerve is smaller, called the intermediate nerve (or nervus intermedius). The intermediate nerve carries taste, parasympathetic, and somatic sensory fibers and travels in a distinct fascial sheath from the motor root. While the motor root emerges through the stylomastoid foramen, the intermediate nerve heads elsewhere, supplying visceral motor fibers to the lacrimal, submandibular, and sublingual glands and the mucous membranes of the nose, soft palate, and hard palate. The intermediate nerve also carries sensation from the skin of the concha (the deepest depression in the auricle) and a small area of skin behind the ear. It may assist the mandibular nerve (CN V3) in supplying the wall of the acoustic meatus and external tympanic membrane. The intermediate nerve provides special sensory fibers to the anterior two-thirds of the tongue and palates to carry taste.
Electrophysiological demyelinating features in hereditary ATTR amyloidosis
Published in Amyloid, 2019
Nobuhiko Ohashi, Minori Kodaira, Hiroshi Morita, Yoshiki Sekijima
Abnormal temporal dispersion and conduction block are crucial indices of heterogeneous demyelination in intermediate nerve trunks. Abnormal temporal dispersion, often associated with CMAP reduction (3.3 ± 5.2 mV), was noticeable predominantly in the tibial nerve. However, abnormal temporal dispersion in the tibial nerve (36.6 ± 6.2%) slightly exceeded the upper threshold set to 30% increments of CMAP duration. This mild abnormal temporal dispersion may be due to the following reason: MNCS in the tibial nerve physiologically exhibits temporal dispersion due to CMAP recording from multiple intrinsic muscles of the foot and a wider distance between stimulation and recording sites [24].
The audiologic profile of patients with Charcot-Marie Tooth neuropathy can be characterised by both cochlear and neural deficits
Published in International Journal of Audiology, 2019
Nicholas Giuliani, Lenore Holte, Michael Shy, Tiffany Grider
Charcot-Marie-Tooth (CMT) neuropathy is the most commonly inherited neurodegenerative disorder and affects ∼1:2500 people (NIH 2007). CMT is a heterogeneous condition and is categorised into two major groups: a demyelinating peripheral neuropathy and an axonal peripheral neuropathy. Prior to 1991, clinical differentiation between these classifications was based solely on phenotypic (observable) characteristics but has since expanded to include gene mutations specific to each group (Bird 2016a). Individuals with the demyelinating form of CMT (CMT1) generally exhibit slow nerve conduction velocities (<25 m/s) while individuals with the axonal form of CMT (CMT2) exhibit normal nerve conduction velocities (40–50 m/s). A third form of CMT (CMT-INT) was recently recognised and individuals with this variant exhibit intermediate nerve conduction velocities (25–45 m/s) (Bird 2016a). X-linked CMT (CMT1X) is a common subtype in which females are often mildly affected or asymptomatic while men are typically more severely affected (Bird 2016b). There are also CMT3 and CMT4 classifications, but these conditions are not common (NIH 2007). In fact, CMT3 (now known as Dejerine-Sottas disease) is antiquated nomenclature for severe, early onset types of peripheral neuropathy and is no longer in general usage to classify CMT (Pearce 2006). Through genetic testing, CMT can be further differentiated into subgroups based on the affected gene(s). Mutations in more than 90 genes have been linked to CMT (Timmerman et al. 2014). The genetic determinant of CMT is indicated by a letter following the numerical designation (e.g. CMT1A) (see Fridman et al. 2015 for further information). Generally, CMT onset is insidious and causes progressive degeneration, which in turn leads to motor and sensory impairment (Bähr et al. 1999; Reilly and Shy 2009). Characterising the clinical features of CMT is challenging because there are many genetic causes and each genetic aetiology has the potential for unique features.