Skull base tumors
Michael Y. Wang, Andrea L. Strayer, Odette A. Harris, Cathy M. Rosenberg, Praveen V. Mummaneni in Handbook of Neurosurgery, Neurology, and Spinal Medicine for Nurses and Advanced Practice Health Professionals, 2017
In contrast to these general symptoms, another subset of symptoms is specific to tumor location; if cranial nerve deficits are present, they can help localize the tumor. (Refer to Chapter 9 for a review of the cranial nerve exam.) Lesions of the anterior skull base such as olfactory groove meningiomas can present with anosmia, or lack of a sense of smell. Involvement in the orbit or along the optic nerves, chiasm, or tract can produce specific visual field defects depending on the location. Tumors of the orbital apex or cavernous sinus may result in diplopia due to compromise of the nerves controlling the extraocular movements (CN III, IV, VI). Involvement of the cavernous sinus is more likely if facial sensation is impaired. Facial sensation (CN V) can be altered by lesions interrupting any or all of the three branches (V1, V2, V3) of the trigeminal nerve. Lesions of the cerebellopontine angle (CPA) can alter facial sensation, abduction of the eye, hearing, vestibular function, and/or facial movement. More extensive lesions of this region, or lesions arising closer to the jugular foramen and hypoglossal canal, can cause significant difficulties swallowing or with vocal cord function or tongue movement due to compression of the lower cranial nerves (CN IX, X, XI, XII).
Cancer pain syndromes
Nigel Sykes, Michael I Bennett, Chun-Su Yuan in Clinical Pain Management, 2008
Involvement of the hypoglossal nerve (XII) indicates involvement of the neighboring hypoglossal canal. An associated Horner’s syndrome indicates extracranial involvement of the sympathetic nerves in proximity to the jugular foramen: ipsilateral ptosis;constricted pupil;enophthalmos;reduced facial sweating.
Clinical Neuroanatomy
John C Watkinson, Raymond W Clarke, Christopher P Aldren, Doris-Eva Bamiou, Raymond W Clarke, Richard M Irving, Haytham Kubba, Shakeel R Saeed in Paediatrics, The Ear, Skull Base, 2018
The final group of cranial nerves are not only anatomically bunched at their major exit, the jugular foramen, but share common nuclear origins. They also have peripheral cross-connections for final distribution that make for poor physiological distinction of function, as well as complex anatomy. Only the hypoglossal nerve with its discrete nuclear origin and separate hypoglossal canal can be discussed in isolation. Even then, its peripheral course brings it into close anatomical relationship with the other three nerves.
Type 2 persistent primitive proatlantal intersegmental artery, a rare variant of persistent carotid-vertebrobasilar anastomoses
Published in Baylor University Medical Center Proceedings, 2019
Gagandeep Choudhary, Narendra Adhikari, Jad Chokr, Nishant Gupta
The ProA is an important blood supply to the posterior fossa structures until the seventh and eighth weeks before VA development. Persistent ProAs can be divided into two types based on their origin. Type 1 (∼57%) corresponds to the first segmental artery, arises from the ICA, and joins the V4 segment of VA, and type 2 (43%) corresponds to the second segmental artery, arises from the external carotid artery or rarely from the common carotid artery, and joins the V3 segment of VA.4,5 Irrespective of their origin, the vessels enter the skull through the foramen magnum. The hypoglossal and ProA are similar but can be differentiated by their course and skull entry site. The hypoglossal course can have a higher origin at the C1 vertebra or the C1 to C2 interspace, is vertically oriented, and enters the skull through the hypoglossal canal. In contrast, the ProA typically arises from the C2 or C3 vertebral level, has a suboccipital horizontal course similar to the V3 segment, and enters the skull through the foramen magnum.5 Proximal VAs are absent or hypoplastic in half of the individual with persistent ProA.6
A rare cause of unilateral hypoglossal nerve palsy: case report of intraneural ganglion cyst of the hypoglossal nerve and review of the literature
Published in Case Reports in Plastic Surgery and Hand Surgery, 2019
Jeremie D. Oliver, Antonio J. Forte
A 56-year-old male presented to our department with a history of seven years of left tongue weakness and progressive atrophy. The patient noted, in the context of eating, that he seemed to be biting his tongue more on the left-hand side. Previous magnetic resonance imaging (MRI) studies performed at an outside institution revealed a cystic structure with T2 hyper intense signal centred on the hypoglossal nerve and hypoglossal canal. No intervention was performed at that time. Follow-up imaging several years later clearly demonstrated a progressively enlarging lesion in the left hypoglossal foramen being T2 hyperintense with no gadolinium contrast enhancement (Figure 1). Ultimately MRI studies one-year later showed substantial expansion of the lesion to approximately 2.5cm (Figure 2). Further CT imaging at that time demonstrated widening of bone in the region of the hypoglossal canal. Brainstem compression was notable, as well as hypoglossal and cerebellar tonsillar compression. At the time of meeting the patient, surgery was offered.
Resolution of hypoglossal nerve palsy after coil embolization of an anterior condylar confluence fistula
Published in British Journal of Neurosurgery, 2021
Donald K. E. Detchou, Gregory Glauser, Omar A. Choudhri
Here, we present the case of a 69-year-old female with a 2-year history of slurred speech, left-sided pulsatile tinnitus, and a left-sided hypoglossal nerve palsy, with tongue deviation and atrophy (Figure 1(A)). MRI and CT Angiography imaging demonstrated increased vascularity at the left hypoglossal canal. Cerebral angiography showed a left anterior condylar confluence fistula, supplied bilaterally by the ascending pharyngeal artery, as well as the posterior meningeal artery (Figure 1(B,C)). For this patient, the treatment plan included a transvenous coil embolization of the left condylar fistula pocket (Figure 2). Subsequent to receiving therapeutic endovascular treatment, the patient had complete resolution of her symptoms (Figure 3).