Hypoglossal Nerve
Hypoglossal Nerve Diseases
Tongue
Hypoglossal nerve injury as a complication of anterior surgery to the upper cervical spine. (1/35)
Injury to the hypoglossal nerve is a recognised complication after soft tissue surgery in the upper part of the anterior aspect of the neck, e.g. branchial cyst or carotid body tumour excision. However, this complication has been rarely reported following surgery of the upper cervical spine. We report the case of a 35-year-old woman with tuberculosis of C2-3. She underwent corpectomy and fusion from C2 to C5 using iliac crest bone graft, through a left anterior oblique incision. She developed hypoglossal nerve palsy in the immediate postoperative period, with dysphagia and dysarthria. It was thought to be due to traction neurapraxia with possible spontaneous recovery. At 18 months' follow-up, she had a solid fusion and tuberculosis was controlled. The hypoglossal palsy persisted, although with minimal functional disability. The only other reported case of hypoglossal lesion after anterior cervical spine surgery in the literature also failed to recover. It is concluded that hypoglossal nerve palsy following anterior cervical spine surgery is unlikely to recover spontaneously and it should be carefully identified. (+info)Prevention of the death of the rat axotomized hypoglossal nerve and promotion of its regeneration by bovine brain gangliosides. (2/35)
We have examined the time course of the neuronal death and regeneration of rat axotomized hypoglossal nerve with various conditions of the nerve resection, and established a useful system to measure neurotrophic activities of bioactive substances. In this system, neuronal death can be evaluated by counting surviving neurons in the nucleus of hypoglossal neuron at the brain stem, and the degree of the regeneration can be measured by counting horseradish peroxidase-positive cells at the same region after injection of horseradish peroxidase into tongue. Using this system, the effects of brain gangliosides on rat hypoglossal nerve regeneration following 5 mm transection were examined. The addition of a ganglioside mixture from bovine brain as well as the autograft strongly prevented the death of neurons and promoted the regeneration of the lesioned nerve at 10 weeks after the operation. Further analyses on the dose effects and injection sites of gangliosides were performed. Although the mechanisms of the neurotrophic effects of the gangliosides are unknown, the therapeutic application of gangliosides for neuronal degeneration is a promising approach. (+info)Akt/protein kinase B prevents injury-induced motoneuron death and accelerates axonal regeneration. (3/35)
Motoneurons require neurotrophic factors for their survival and axonal projection during development, as well as nerve regeneration. By using the axotomy-induced neuronal death paradigm and adenovirus-mediated gene transfer, we attempted to gain insight into the functional significances of major growth factor receptor downstream cascades, Ras-extracellular signal-regulated kinase (Ras-ERK) pathway and phosphatidylinositol-3 kinase-Akt (PI3K-Akt) pathway. After neonatal hypoglossal nerve transection, the constitutively active Akt-overexpressing neurons could survive as well as those overexpressing Bcl-2, whereas the constitutively active ERK kinase (MEK)-overexpressing ones failed to survive. A dominant negative Akt experiment demonstrated that inhibition of Akt pathway hastened axotomy-induced neuronal death in the neonate. In addition, the dominant active Akt-overexpressing adult hypoglossal neurons showed accelerated axonal regeneration after axotomy. These results suggest that Akt plays dual roles in motoneuronal survival and nerve regeneration in vivo and that PI3K-Akt pathway is probably more vital in neuronal survival after injury than Ras-ERK pathway. (+info)Neuronal MCP-1 expression in response to remote nerve injury. (4/35)
Direct injury of the brain is followed by inflammatory responses regulated by cytokines and chemoattractants secreted from resident glia and invading cells of the peripheral immune system. In contrast, after remote lesion of the central nervous system, exemplified here by peripheral transection or crush of the facial and hypoglossal nerve, the locally observed inflammatory activation is most likely triggered by the damaged cells themselves, that is, the injured neurons. The authors investigated the expression of the chemoattractants monocyte chemoattractant protein MCP-1, regulation on activation normal T-cell expressed and secreted (RANTES), and interferon-gamma inducible protein IP10 after peripheral nerve lesion of the facial and hypoglossal nuclei. In situ hybridization and immunohistochemistry revealed an induction of neuronal MCP-1 expression within 6 hours postoperation, reaching a peak at 3 days and remaining up-regulated for up to 6 weeks. MCP-1 expression was almost exclusively confined to neurons but was also present on a few scattered glial cells. The authors found no alterations in the level of expression and cellular distribution of RANTES or IP10, which were both confined to neurons. Protein expression of the MCP-1 receptor CCR2 did not change. MCP-1, expressed by astrocytes and activated microglia, has been shown to be crucial for monocytic, or T-cell chemoattraction, or both. Accordingly, expression of MCP-1 by neurons and its corresponding receptor in microglia suggests that this chemokine is involved in neuron and microglia interaction. (+info)Linear regression of eye velocity on eye position and head velocity suggests a common oculomotor neural integrator. (5/35)
The oculomotor system produces eye-position signals during fixations and head movements by integrating velocity-coded saccadic and vestibular inputs. A previous analysis of nucleus prepositus hypoglossi (nph) lesions in monkeys found that the integration time constant for maintaining fixations decreased, while that for the vestibulo-ocular reflex (VOR) did not. On this basis, it was concluded that saccadic inputs are integrated by the nph, but that the vestibular inputs are integrated elsewhere. We re-analyze the data from which this conclusion was drawn by performing a linear regression of eye velocity on eye position and head velocity to derive the time constant and velocity bias of an imperfect oculomotor neural integrator. The velocity-position regression procedure reveals that the integration time constants for both VOR and saccades decrease in tandem with consecutive nph lesions, consistent with the hypothesis of a single common integrator. The previous evaluation of the integrator time constant relied upon fitting methods that are prone to error in the presence of velocity bias and saccades. The algorithm used to evaluate imperfect fixations in the dark did not account for the nonzero null position of the eyes associated with velocity bias. The phase-shift analysis used in evaluating the response to sinusoidal vestibular input neglects the effect of saccadic resets of eye position on intersaccadic eye velocity, resulting in gross underestimates of the imperfections in integration during VOR. The linear regression method presented here is valid for both fixation and low head velocity VOR data and is easy to implement. (+info)Perceptual and instrumental evaluation of voice and tongue function after carotid endarterectomy. (6/35)
OBJECTIVE: Laryngeal and tongue function was assessed in 28 patients to evaluate the presence, nature, and resolution of superior recurrent laryngeal and hypoglossal nerve damage resulting from standard open primary carotid endarterectomy (CEA). METHODS: The laryngeal and tongue function in 28 patients who underwent CEA were examined prospectively with various physiologic (Aerophone II, laryngograph, tongue transducer), acoustic (Multi-Dimensional Voice Program), and perceptual speech assessments. Measures were obtained from all participants preoperatively, and at 2 weeks and at 3 months postoperatively. RESULTS: The perceptual speech assessment indicated that the vocal quality of "roughness" was significantly more apparent at the 2-week postoperative assessment than preoperatively. However, by the 3-month postoperative assessment these values had returned to near preoperative levels, with no significant difference detected between preoperative and 3-month postoperative levels or between 2-week and 3-month postoperative levels. Both the instrumental assessments of laryngeal function and the acoustic assessment of vocal quality failed to identify any significant difference on any measure across the three assessment periods. Similarly, no significant impairment in tongue strength, endurance, or rate of repetitive tongue movements was detected at instrumental assessment of tongue function. CONCLUSIONS: No permanent changes to vocal or tongue function occurred in this group of participants after primary CEA. The lack of any significant long-term laryngeal or tongue dysfunction in this group suggests that the standard open CEA procedure is not associated with high rates of superior recurrent and hypoglossal nerve dysfunction, as previously believed. (+info)Nerve injury reduces responses of hypoglossal motoneurones to baseline and chemoreceptor-modulated inspiratory drive in the adult rat. (7/35)
The effects of peripheral nerve lesions on the membrane and synaptic properties of motoneurones have been extensively studied. However, minimal information exists about how these alterations finally influence discharge activity and motor output under physiological afferent drive. The aim of this work was to evaluate the effect of hypoglossal (XIIth) nerve crushing on hypoglossal motoneurone (HMN) discharge in response to the basal inspiratory afferent drive and its chemosensory modulation by CO(2). The evolution of the lesion was assessed by recording the compound muscle action potential evoked by XIIth nerve stimulation, which was lost on crushing and then recovered gradually to control values from the second to fourth weeks post-lesion. Basal inspiratory activities recorded 7 days post-injury in the nerve proximal to the lesion site, and in the nucleus, were reduced by 51.6% and 35.8%, respectively. Single unit antidromic latencies were lengthened by lesion, and unusually high stimulation intensities were frequently required to elicit antidromic spikes. Likewise, inspiratory modulation of unitary discharge under conditions in which chemoreceptor drive was varied by altering end-tidal CO(2) was reduced by more than 60%. Although the general recruitment scheme was preserved after XIIth nerve lesion, we noticed an increased proportion of low-threshold units and a reduced recruitment gain across the physiological range. Immunohistochemical staining of synaptophysin in the hypoglossal nuclei revealed significant reductions of this synaptic marker after nerve injury. Morphological and functional alterations recovered with muscle re-innervation. Thus, we report here that nerve lesion induced changes in the basal activity and discharge modulation of HMNs, concurrent with the loss of afferent inputs. Nevertheless, we suggest that an increase in membrane excitability, reported by others, and in the proportion of low-threshold units, could serve to preserve minimal electrical activity, prevent degeneration and favour axonal regeneration. (+info)Regulation of stearoyl-CoA desaturase-1 after central and peripheral nerve lesions. (8/35)
BACKGROUND: Interruption of mature axons activates a cascade of events in neuronal cell bodies which leads to various outcomes from functional regeneration in the PNS to the failure of any significant regeneration in the CNS. One factor which seems to play an important role in the molecular programs after axotomy is the stearoyl Coenzyme A-desaturase-1 (SCD-1). This enzyme is needed for the conversion of stearate into oleate. Beside its role in membrane synthesis, oleate could act as a neurotrophic factor, involved in signal transduction pathways via activation of protein kinases C. RESULTS: In situ hybridization and immunohistochemistry demonstrated a strong up-regulation of SCD at mRNA and protein level in regenerating neurons of the rat facial nucleus whereas non-regenerating Clarke's and Red nucleus neurons did not show an induction of this gene. CONCLUSION: This differential expression points to a functionally significant role for the SCD-1 in the process of regeneration. (+info)Hypoglossal nerve injuries refer to damages or impairments to the twelfth cranial nerve, also known as the hypoglossal nerve. This nerve is primarily responsible for controlling the movements of the tongue.
An injury to this nerve can result in various symptoms, depending on the severity and location of the damage. These may include:
1. Deviation of the tongue to one side when protruded (usually away from the side of the lesion)
2. Weakness or paralysis of the tongue muscles
3. Difficulty with speaking, swallowing, and articulation
4. Changes in taste and sensation on the back of the tongue (in some cases)
Hypoglossal nerve injuries can occur due to various reasons, such as trauma, surgical complications, tumors, or neurological disorders like stroke or multiple sclerosis. Treatment for hypoglossal nerve injuries typically focuses on managing symptoms and may involve speech and language therapy, exercises to strengthen the tongue muscles, and, in some cases, surgical intervention.
The hypoglossal nerve, also known as the 12th cranial nerve (CN XII), is primarily responsible for innervating the muscles of the tongue, allowing for its movement and function. These muscles include the intrinsic muscles that alter the shape of the tongue and the extrinsic muscles that position it in the oral cavity. The hypoglossal nerve also has some minor contributions to the innervation of two muscles in the neck: the sternocleidomastoid and the trapezius. These functions are related to head turning and maintaining head position. Any damage to this nerve can lead to weakness or paralysis of the tongue, causing difficulty with speech, swallowing, and tongue movements.
The hypoglossal nerve, also known as the 12th cranial nerve (CN XII), is primarily responsible for controlling tongue movements. Hypoglossal nerve diseases refer to conditions that affect this nerve and result in various tongue-related symptoms. These disorders can be congenital or acquired, and they may stem from different causes such as trauma, tumors, infections, inflammation, or degenerative processes.
Hypoglossal nerve diseases can present with the following symptoms:
1. Weakness or paralysis of the tongue muscles on one or both sides.
2. Deviation of the tongue towards the affected side when protruded.
3. Fasciculations (involuntary muscle twitches) or atrophy (wasting) of the tongue muscles.
4. Difficulty with speaking, swallowing, and chewing due to tongue weakness.
5. Changes in taste and sensation on the back of the tongue and throat.
Some specific hypoglossal nerve diseases include:
1. Hypoglossal nerve palsy: A condition characterized by unilateral or bilateral weakness or paralysis of the tongue due to damage to the hypoglossal nerve. Causes can include trauma, tumors, stroke, multiple sclerosis, or other neurological disorders.
2. Hypoglossal neuritis: Inflammation of the hypoglossal nerve, often caused by viral infections or autoimmune processes, leading to tongue weakness and atrophy.
3. Congenital hypoglossal nerve anomalies: Abnormal development of the hypoglossal nerve during fetal growth can result in various tongue-related symptoms and difficulties with speech and swallowing.
4. Tumors affecting the hypoglossal nerve: Both benign and malignant tumors, such as schwannomas or neurofibromas, can compress or infiltrate the hypoglossal nerve, causing weakness or paralysis.
5. Hypoglossal-facial anastomosis: A surgical procedure that connects the hypoglossal nerve to the facial nerve to restore facial movement in cases of facial nerve palsy. This connection can lead to tongue weakness as a side effect.
In medical terms, the tongue is a muscular organ in the oral cavity that plays a crucial role in various functions such as taste, swallowing, and speech. It's covered with a mucous membrane and contains papillae, which are tiny projections that contain taste buds to help us perceive different tastes - sweet, salty, sour, and bitter. The tongue also assists in the initial process of digestion by moving food around in the mouth for chewing and mixing with saliva. Additionally, it helps in forming words and speaking clearly by shaping the sounds produced in the mouth.
Peripheral nerve injuries refer to damage or trauma to the peripheral nerves, which are the nerves outside the brain and spinal cord. These nerves transmit information between the central nervous system (CNS) and the rest of the body, including sensory, motor, and autonomic functions. Peripheral nerve injuries can result in various symptoms, depending on the type and severity of the injury, such as numbness, tingling, weakness, or paralysis in the affected area.
Peripheral nerve injuries are classified into three main categories based on the degree of damage:
1. Neuropraxia: This is the mildest form of nerve injury, where the nerve remains intact but its function is disrupted due to a local conduction block. The nerve fiber is damaged, but the supporting structures remain intact. Recovery usually occurs within 6-12 weeks without any residual deficits.
2. Axonotmesis: In this type of injury, there is damage to both the axons and the supporting structures (endoneurium, perineurium). The nerve fibers are disrupted, but the connective tissue sheaths remain intact. Recovery can take several months or even up to a year, and it may be incomplete, with some residual deficits possible.
3. Neurotmesis: This is the most severe form of nerve injury, where there is complete disruption of the nerve fibers and supporting structures (endoneurium, perineurium, epineurium). Recovery is unlikely without surgical intervention, which may involve nerve grafting or repair.
Peripheral nerve injuries can be caused by various factors, including trauma, compression, stretching, lacerations, or chemical exposure. Treatment options depend on the type and severity of the injury and may include conservative management, such as physical therapy and pain management, or surgical intervention for more severe cases.