PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “HYPOGLOSSAL NERVE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources
PubMed1998

Regenerative process after experimental injury of hypoglossal nerves in guinea pigs.

The nerve regenerative process has been investigated by many studies. However, the quantification of the degree of crush of peripheral nerves has not yet been performed. The aim of this study was to determine and standardize the ligature intensity and crush level of the hypoglossal nerve of guinea pigs. The compound action potentials evoked by electric stimulation were used as an index of the degree of nerve crush. To demonstrate nerve regeneration after ligating and crushing of the right hypoglossal nerve, fluorescein isothiocynate conjugated cholera toxin-B subunit (CTb-FITC) was injected into the intact fiber of the left hypoglossal nerve, and the central side from the crushed region of the right hypoglossal nerve fiber. The total cross sectional area of the retrograde-labeled hypoglossal motoneurons was investigated under a confocal laser scanning microscope. The results of the evaluation using CTb-FITC indicated that the nerve regeneration occurred from two weeks after crush and recovered in six weeks.

Action Potentials↗
PubMed1998

The forgotten condyle: Delayed hypoglossal nerve palsy caused by fracture of the occipital condyle.

Fracture of the occipital condyle is a rare injury that can be easily overlooked. Palsies of lower cranial nerves can be the only symptom of the fracture. We report a patient with isolated post-traumatic hypoglossal nerve palsy who developed hypoglossal nerve palsy within 2 months after a car accident, indicating that the acute trauma itself did not damage the hypoglossal nerve. Most likely the palsy is caused by pressure to the nerve prior to the entry or within the hypoglossal canal. Since, in the present case, the fracture was stable and the patient showed only moderate neurological deficits, the operation was deferred.

Cranial Nerve Diseases↗
PubMed1998

A rare case of hypoglossal nerve palsy complicating a head injury.

Hypoglossal nerve palsy (HNP) may follow fracture of the base of the skull. Of the various aetiologies described, trauma is one of the least frequent. HNP can easily be missed at the time of injury and awareness of this rare complication may assist in early diagnosis. A case of HNP after a head injury associated with the loss of taste sensation on the paralysed side of the tongue and aerocoele is reported.

Adult↗
PubMedDate not supplied

Response of respiratory-related hypoglossal nerve activity to capsaicin-induced pulmonary C-fiber activation in rats.

This study was designed to examine respiratory-related hypoglossal nerve activity in response to activation of pulmonary C-fibers by capsaicin. Rats were anesthetized with urethane (1.2 g/kg, i.p.). Tracheostomy was performed. Catheters were introduced into the femoral vein and artery. Another catheter was placed near the entrance of the right atrium via the right jugular vein. Rats were paralyzed with gallamine triethiodide (5 mg/kg, i.v.), and ventilated artificially. Activities of the phrenic nerve (PNA) and the hypoglossal nerve (HNA) were recorded simultaneously. Varied doses of capsaicin (0.625, 1.25, and 5 microg/kg) were delivered into the right atrium to activate pulmonary C-fibers. Before bilateral vagotomy, apnea, decreases in PNA and HNA were observed in response to pulmonary C-fiber activation by the low and moderate doses of capsaicin. The high dose of capsaicin evoked an increase in PNA, an immediate tonic discharge of the hypoglossal nerve, and a decrease in phasic HNA. The onset time of HNA preceding PNA was abolished and replaced by a time lagged pattern as pulmonary C-fibers were activated. Raising CO(2) concentration did not attenuate the inhibitory effect of pulmonary C-fiber activation upon PNA and HNA. After bilateral sectioning of the vagi, administration of the moderate dose of capsaicin to activate non-vagal C-fibers produced increases in PNA and HNA. These results suggest that pulmonary vagal C-fiber activation may narrow the diameter at the oropharyngeal level by a decrease in phasic HNA, which may be disadvantageous for the maintenance of a patent upper airway.

Animals↗
PubMed1988

Bilateral hypoglossal nerve injury after bilateral carotid endarterectomy.

A case of severe bilateral injury to the hypoglossal nerves after two-stage carotid endarterectomy is described. Injury to the hypoglossal nerve occurs in up to 20% of patients undergoing carotid endarterectomy and may result in mild or unnoticed deficits. These injuries must be carefully searched for in patients who will undergo a similar procedure on the opposite side since a bilateral deficit of the hypoglossal nerve is poorly tolerated, causing potentially serious impairment of speech and risk of aspiration.

Aged↗
PubMed1990

Surgical reneurotization of the tongue after unilateral paralysis of the hypoglossal nerve.

Hemiglossal paralysis due to lesions of the peripheral hypoglossal nerve leads to marked muscle atrophy with disturbed functioning in a minority of cases. Reinnervation from the unparalyzed, contralateral side may then be desired. In animal experiments on cats, a Z-plasty of the midportion of the tongue was carried out by transposing a portion of the normal tongue musculature into the opposite side following denervation 1 month previously by resection of the hypoglossal nerve. Electromyography was performed 13 months later. The tongue was then examined histochemically in serial sections in search of the motor endplates together with the nerves fibers. However, there was no evidence for reinnervation in the specimens examined. Signs of successful "reanimation" of the tongue by Z-plasty may be caused by mechanical synkinesia due to scar formation rather than by actual reneurotization.

Animals↗
PubMed1999

Chronic recordings of hypoglossal nerve activity in a dog model of upper airway obstruction.

The activity of the hypoglossal nerve was recorded during pharyngeal loading in sleeping dogs with chronically implanted cuff electrodes. Three self-coiling spiral-cuff electrodes were implanted in two beagles for durations of 17, 7, and 6 mo. During quiet wakefulness and sleep, phasic hypoglossal activity was either very small or not observable above the baseline noise. Applying a perpendicular force on the submental region by using a mechanical device to narrow the pharyngeal airway passage increased the phasic hypoglossal activity, the phasic esophageal pressure, and the inspiratory time in the next breath during non-rapid-eye-movement sleep. The phasic hypoglossal activity sustained at the elevated level while the force was present and increased with increasing amounts of loading. The hypoglossal nerve was very active in rapid-eye-movement sleep, especially when the submental force was present. The data demonstrate the feasibility of chronic recordings of the hypoglossal nerve with cuff electrodes and show that hypoglossal activity has a fast and sustained response to the internal loading of the pharynx induced by applying a submental force during non-rapid-eye-movement sleep.

Airway Obstruction↗
PubMed1998

Isolated unilateral hypoglossal nerve palsy: nine cases.

We report nine patients with hypoglossal nerve palsy as the sole neurological manifestation, without simultaneous involvement of other cranial nerves or long-tract signs. In four patients, no cause was found and the outcome was excellent. The next common cause proved to be metastatic disease at the base of the skull in three patients. Two exceptional causes were Chiari malformation in one case and dural arteriovenous fistula of the transverse sinus in another. Although the aetiological importance and ominous prognosis of neoplasia has been emphasized by others, our study suggests that an isolated hypoglossal nerve palsy may be benign and idiopathic.

Adolescent↗
PubMed1998

Dual-isotope SPECT diagnosis of a skull-base metastasis causing isolated unilateral hypoglossal nerve palsy.

We describe a 48-year-old female with an isolated unilateral hypoglossal nerve palsy caused by a skull base metastasis from breast cancer. The patient had a medical history of conservative breast therapy for breast cancer. Although the cause of such a neurological deficit includes various pathologies, the reports focusing on metastatic tumor have been limited in number. Radiologic investigation showed a mass involving both the right hypoglossal canal and the clival edge. Swelling of the hypoglossal nerve was observed in views including its canal. Three-dimensional CT images demonstrated the tumor protruding from the enlarged external orifice of the hypoglossal canal. In the present report we mentioned a nuclear medicine procedure to visualize and characterize the small, abnormal tissue in the skull base. Dual-isotope SPECT confirmed an abnormal uptake of 99mTc-HMDP around the hypoglossal canal and a 201Tl-positive elongated lesion running along the hypoglossal nerve.

Cranial Nerve Diseases↗
PubMed2003

Unilateral spontaneous dissection of the internal carotid artery presenting as hypoglossal nerve palsy.

A rare case of an isolated unilateral hypoglossal nerve palsy in a 61-year-old man is reported. Imaging showed a dissection of the extracranial internal carotid artery. The expansion of the circumference of the artery causes compression of the hypoglossal nerve resulting in a palsy. To the best of our knowledge this disorder has twice been dealt with in the otorhinolaryngological literature.

Carotid Artery, Internal, Dissection↗
PubMedDate not supplied

[Schwannoma of the hypoglossal nerve presenting as a syndrome of Collet-Sicard].

Collet-Sicard is a rare syndrome that consists of the palsy of all the lower four cranial nerves. We describe this entity in relation with a schwannoma of the hypoglossal nerve. A 45 year-old-patient was admitted to the hospital referring hoarseness and difficulty in swallowing for two weeks. On neurological examination, the patient exhibited palsy of the ninth, tenth, eleventh and twelfth nerves. This is a syndrome of Collet-Sicard. The cranial MRI revealed a small intracranial and extracranial tumor adjacent to the hypoglossal foramen. The tumor involved the jugular foramen and was moderately enhanced with gadolinium The patient underwent surgical removal. The pathologic examination of the surgical specimen confirmed the diagnosis of a schwannoma of the hypoglossal nerve. We have carried out a research of the Collet-Sicard syndrome and of its aetiology. Although schwannoma the hypoglossal nerve is a rare disorder we consider that this entity should be included in the differential diagnosis of the Collet-Sicard syndrome.

Accessory Nerve↗
PubMed1994

A bromodeoxyuridine labelling study of proliferating cells in the brainstem following hypoglossal nerve transection.

The proliferative activity in the hypoglossal nucleus following hypoglossal nerve injury has been studied with the 3H-thymidine analogue, bromodeoxyuridine (BrdUrd). BrdUrd was injected into cisterna magna of the rat brain 2 h prior to killing and subsequently visualised with immunofluorescence. The peak of BrdUrd labelling in the hypoglossal nucleus occurred at 2 d following nerve transection and a lower level at 4 and 7 d postoperatively. BrdUrd labelled cells were also found outside the anatomical boundaries of the hypoglossal nucleus, conceivably mainly corresponding to the dendritic extension of the axotomised neurons. It is therefore concluded that microglial cells are activated in relation to the entire intramedullary portion of the axotomised neurons and not only in the immediate vicinity of the perikarya. Double labelling experiments with specific markers for astrocytes, oligodendrocytes and microglial cells showed that only microglial cells were BrdUrd positive at all postoperative survival times examined. It is therefore concluded that microglial cells are the only glial cell type which proliferate in the hypoglossal nucleus following peripheral nerve injury.

Animals↗
PubMed1980

Non-selective distribution of hypoglossal nerve fibers after section and resuture: a horseradish peroxidase study in the cat.

The retrograde tracing method of horseradish peroxidase (HRP) was applied to examine the process of regeneration of severed hypoglossal nerve in the cat. After section and resuture of the hypoglossal nerve, the cats were allowed to survive for 4-6 months. In these cats, distribution of neurons labeled with HRP injected into the genioglossus muscle was examined and compared with that in the normal cat. In the operated cats, labeled genioglossus motoneurons were scattered within all subdivisions of the hypoglossal nucleus, indicating non-selective distribution of regenerating hypoglossal nerve fibers to the lingual muscles.

Animals↗
PubMed2001

[Neurinoma of the descending loop of the hypoglossal nerve. Report of a case].

Neurinomata developed from extracranial portion of hypoglossal nerve are very scarce. We report one case of neurinoma originated in the descending branch of hypoglossal nerve and not having found after careful perusal of the literature of this subject another case we consider the ours as the first portraying this type of pathology and its localization.

Cranial Nerve Neoplasms↗
PubMed1983

Synaptic efficacy of inhibitory synapses in hypoglossal motoneurons after transection of the hypoglossal nerves.

In cat hypoglossal motoneurons after axotomy the synaptic efficacy of inhibitory synapses made by the lingual nerve afferent fibers was studied. The amplitude of the short- and the long-lasting inhibitory postsynaptic potential produced in tongue protruder motoneurons 24 days after axotomy by stimulation of the lingual nerve was significantly reduced in size as compared with the control on the unoperated side. In most protruder motoneurons 40 days after axotomy a large excitatory postsynaptic potential and a spike was produced by stimulation of either the ipsilateral or the contralateral lingual nerve. We have demonstrated that the decline of synaptic efficacy of inhibitory synapses for the short-lasting inhibitory postsynaptic potential was more prominent than that for the long-lasting inhibitory potential in the motoneuron 24 days after axotomy. After the cut axons of protruder motoneurons were re-united to tongue muscles, we have demonstrated that the decline of synaptic efficacy of inhibitory synapses for the short-lasting inhibitory postsynaptic potential was less prominent than that in axotomized protruder motoneurons.

Animals↗
PubMed2003

Subacute hypoglossal nerve paresis with internal carotid artery dissection.

OBJECTIVES: To describe a case of an isolated hypoglossal nerve palsy in a patient with a spontaneous internal carotid artery dissection (ICAD). This condition is a well-recognized cause of cerebral ischemic stroke in patients younger than 45 years of age. Isolated cranial nerve neuropathy is a rare presentation. More common manifestations include incomplete hemiparesis, hemicrania, Horner syndrome, cervical bruit, pulsatile tinnitus, and multiple cranial nerve palsies. METHODS: A comprehensive literature search (Ovid, MEDLINE) for the presentation, diagnostic evaluation, treatment, and outcome of patients with internal carotid artery dissection was performed. RESULTS: A 43-year-old man presented with a 3-week history of mild dysarthria. There was no history of craniocervical trauma. The physical examination revealed an isolated left hypoglossal nerve paresis. Magnetic resonance imaging and angiography findings were consistent with a left skull base ICAD. The patient was successfully treated with anticoagulation therapy. The current rate of cranial nerve involvement is estimated at 10% of all ICADs. This is the second report of isolated hypoglossal nerve palsy without hemicrania in a case of atraumatic ICAD. CONCLUSIONS: Patients with an ICAD infrequently present to the otolaryngologist because of its head and neck manifestations. It is crucial to recognize atypical findings and to perform an accurate and prompt diagnostic evaluation. The foundation of treatment is aggressive anticoagulation, with surgical or radiologic intervention reserved for cases demonstrating life-threatening progression.

Administration, Oral↗