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Case reports A rare case of hypoglossal nerve palsy complicating a head injury A M Shweikh, S AL-Atrakchi Abstract Hypoglossal nerve palsy (HNP) may fol- low fracture of the base of the skulil. Of the various aetiologies described, trauma is one of the least frequent. HNP can easily be missed at the time of injury and aware- ness 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. (7Accid Emerg Med 1998;15:427-429) Keywords: hypoglossal (XIIth) cranial nerve palsy; aerocoele; fracture base of skull Unilateral hypoglossal (XIIth) nerve palsy (HNP) is a rare complication after trauma to the base of the skull in the region of the occipi- tal condyles. This can follow significant decel- erative head injuries usually associated with road traffic accidents. There is a difficulty in diagnosing fractures of the base of the skull using conventional radiography. In the case presented here and other documented cases,1 although the XIIth nerve palsy was permanent, near normal clinical function returned within one year, suggesting a good prognosis for these cases of HNP. Case report A 44 year old driver of a vehicle was involved in a head on collision with another car in Decem- ber 1994. He was brought to the accident and emergency (A&E) department in a very confused state with a Glasgow coma score of 12/15. He sustained a head injury with a deep laceration in the occipital area with exposure of skull and a small laceration in the right upper eyelid. There was no documentation of bleed- ing or cerebrospinal fluid leak from the nose or ears. The airway was clear and the vital signs were normal. Apart from swelling and tender- ness around his right shoulder there were no associated injuries and no reported neurologi- cal deficit. Radiography of the skull showed a long linear fracture of the left occipital bone extending upwards from the base of the skull (fig 1), and also a collection of air in the frontal area (aerocoele) (fig 2). Computed tomogra- phy revealed numerous locules of intracranial air, the largest being on the frontal lobes (figs 3 and 4), and also confirmed the presence of a linear fracture extending from the foramen magnum up to the level of the internal occipi- tal protuberance. The patient was treated conservatively in a neurosurgical unit and eight days later he was transferred back to Grimsby Hospital and noticed to have a slurred speech. Examination of the oral cavity revealed the presence of wasting with fasciculation of the left side of the tongue with a bite mark on the weak side of the tongue. The patient was able to move the tongue but it deviated to the left side on protruding from the mouth (fig 5). Taste sensation (sweet, sour, and salt) was lacking on the left, wasted, side of the tongue but normal on the opposite side. Protective sensation was normal on both sides of the tongue. The patient did not experience any difficulty with swallowing. The patient was treated conservatively and within six months of the injury he had regained a near normal speech in spite of the persistent wasting of the left side of his tongue and his Figure 1 Linear fracture of the left occipital bone. Figure I Linearfracture of the left occipital bone. Figure 2 Aerocoele on lateral view of skull. Accident and Emergency Department, North East Lincolnshire NHS Trust, Grimsby Hospital, Scartho Road, Grimsby DN33 2BA A M Shweikh S AL-Atrakchi Correspondence to: Mr Shweikh, Consultant. Accepted for publication 27 June 1998 427 on March 29, 2020 by guest. Protected by copyright. http://emj.bmj.com/ J Accid Emerg Med: first published as 10.1136/emj.15.6.427 on 1 November 1998. Downloaded from

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Page 1: Case hypoglossal complicating head injury · (HNP) is a rare complication after trauma to thebaseoftheskull intheregionoftheoccipi-tal condyles. This canfollow significant decel-erative

Case reports

A rare case of hypoglossal nerve palsycomplicating a head injury

A M Shweikh, S AL-Atrakchi

AbstractHypoglossal nerve palsy (HNP) may fol-low fracture ofthe base ofthe skulil. Ofthevarious aetiologies described, trauma isone of the least frequent. HNP can easilybe missed at the time ofinjury and aware-ness of this rare complication may assistin early diagnosis. A case of HNP after ahead injury associated with the loss oftaste sensation on the paralysed side ofthetongue and aerocoele is reported.(7Accid Emerg Med 1998;15:427-429)

Keywords: hypoglossal (XIIth) cranial nerve palsy;aerocoele; fracture base of skull

Unilateral hypoglossal (XIIth) nerve palsy(HNP) is a rare complication after trauma tothe base of the skull in the region of the occipi-tal condyles. This can follow significant decel-erative head injuries usually associated withroad traffic accidents. There is a difficulty indiagnosing fractures of the base of the skullusing conventional radiography.

In the case presented here and otherdocumented cases,1 although the XIIth nervepalsy was permanent, near normal clinicalfunction returned within one year, suggesting agood prognosis for these cases of HNP.

Case reportA 44 year old driver of a vehicle was involved ina head on collision with another car in Decem-ber 1994. He was brought to the accident andemergency (A&E) department in a veryconfused state with a Glasgow coma score of12/15. He sustained a head injury with a deeplaceration in the occipital area with exposure ofskull and a small laceration in the right uppereyelid. There was no documentation of bleed-ing or cerebrospinal fluid leak from the nose orears. The airway was clear and the vital signswere normal. Apart from swelling and tender-ness around his right shoulder there were noassociated injuries and no reported neurologi-cal deficit. Radiography of the skull showed along linear fracture of the left occipital boneextending upwards from the base of the skull(fig 1), and also a collection of air in the frontalarea (aerocoele) (fig 2). Computed tomogra-phy revealed numerous locules of intracranialair, the largest being on the frontal lobes (figs 3and 4), and also confirmed the presence of alinear fracture extending from the foramenmagnum up to the level of the internal occipi-tal protuberance.The patient was treated conservatively in a

neurosurgical unit and eight days later he wastransferred back to Grimsby Hospital andnoticed to have a slurred speech.

Examination of the oral cavity revealed thepresence of wasting with fasciculation of theleft side of the tongue with a bite mark on theweak side of the tongue. The patient was ableto move the tongue but it deviated to the leftside on protruding from the mouth (fig 5).Taste sensation (sweet, sour, and salt) waslacking on the left, wasted, side of the tonguebut normal on the opposite side. Protectivesensation was normal on both sides of thetongue. The patient did not experience anydifficulty with swallowing.The patient was treated conservatively and

within six months of the injury he had regaineda near normal speech in spite of the persistentwasting of the left side of his tongue and his

Figure 1Linearfracture of the left occipital bone.

Figure I Linearfracture of the left occipital bone.

Figure 2 Aerocoele on lateral view of skull.

Accident andEmergencyDepartment, NorthEast Lincolnshire NHSTrust, GrimsbyHospital, ScarthoRoad, Grimsby DN332BAAM ShweikhS AL-Atrakchi

Correspondence to:Mr Shweikh, Consultant.

Accepted for publication27 June 1998

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Case reports

Figure 3 Computed tomography, sagittal scan, showingfree air between frontal bones andfrontal lobe of brain.

Figure 4 Computed tomography, axial scan, showing locules of intracranial air, mainly onthe frontal lobes.

Figure 5 Paralysis of the left side of the tongue withwasting; the tongue deviates to the left (paralysed) side onprotrudingfrom the mouth.

taste sensation in the left side of the tongue hadnot recovered.

DiscussionUnilateral HNP is a rare complication aftertrauma to the base of the skull in the region ofthe occipital condyles. Such a complication hasbeen observed after significant decelerativehead injuries usually associated with road traf-fic accidents. This complication can be missed

at the time of injury and may even present upto several months after injury.'There are many causes of isolated HNP and

associated muscle wasting is a feature of lowermotor neurone lesions. Common causes in-clude carotid endarterectomy (usually tempo-rary), tonsillectomy, tooth extraction, adenoidcystic carcinoma of the tongue, metastaticmalignant tumours of the middle and posteriorcranial fossae, syringomyelia, neck tumours,and surgery. Vertical subluxation of the odon-toid process in rheumatoid arthritis has alsobeen reported to cause HNP. Cranial basetrauma in the region of the occipital condylesas a result of sudden deceleration head injuriesmay also result in HNP. In many of these acci-dents, there may be other significant braininjury and HNP may be bilateral. These bilat-eral palsies have poorer prognoses for func-tional rehabilitation compared with the unilat-eral palsy.'When the sole clinical deficit is an isolated

unilateral HNP of late onset, the existence ofposterior cranial base fracture often goes unde-tected.

Bilateral HNP is very rare and of the variousaetiologies described, trauma is one of the leastfrequent. The diagnosis can easily be missed inthe initial assessment of traumatised patientsafter severe decelerative injuries in road trafficaccidents and subsequently noted after extuba-tion and discharge from the intensive care unit.The hypoglossal nerve emerges from the

medulla oblongata as a series of rootletsbetween the pyramid and olive, passes laterallyand superior to the vertebral artery leaving thecranial cavity through the hypoglossal canal ofthe occipital bone superior to the occipitalcondyle. The hypoglossal nerve innervates allthe ipsilateral intrinsic and extrinsic muscles ofthe tongue except the palatoglossus.' Intrauma, the forces involved in high speeddeceleration head injuries can cause fracture ofthe occipital condyle, thereby injuring thehypoglossal nerve. In the case reported here, afracture line was demonstrated running fromthe foramen magnum on computed tomogra-phy and is thought to have caused damage tothe hypoglossal nerve, although the fractureline was not seen running through thehypoglossal canal. Posterior cranial base frac-tures are extremely difficult to demonstrate onplain radiographs and computed tomographyis essential to confirm the diagnosis.2The XIIth nerve may have also been injured

indirectly at the time of impact. Severe neckhyperextension at the time of injury can causetraction and elongation of the nerve (producedby subluxation of the atlantoaxial articulationor occipital condyle trauma) but this mech-anism of injury is unlikely because the patientdid not have any symptoms suggestive of neckinjury.To explain the late onset of some HNP it is

thought that the healing process and subse-quent callus formation may play a part in oblit-erating the hypoglossal canal.

Bilateral HNP causes dysphagia, dysarthria,and a non-mobile tongue. No tongue move-ments can be made on attempted protrusion.

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Case reports 429

In the case presented by Paley and Wood,2 sen-sation of the tongue was found to be normaland the taste sensation was found to beunaltered, although the tongue was not mobile.Swallowing was found to be difficult andvideofluoroscopy demonstrated abnormality ofthe oral phase of swallowing due to lack oftongue function. The patient could onlymanage fluids and semisolids with the aid ofgravity. Electromyographic studies may be use-ful in showing evidence of bilateral denervationof the tongue compatible with bilateral axonot-mesis of XIIth nerve.3

In our case, only one half of the tongue wasparalysed and this patient was able to use histongue. He could move and protrude histongue and although his tongue tended to bepushed to the paralysed side (by the normalside of the tongue), he did not have any prob-lem with swallowing, although his speech wasslurred. Examination of the tongue alsorevealed a rare finding of loss of taste sensationto sweet, salt, and sour on the paralysed side ofthe tongue after injury.

ANATOMICAL AND PHYSIOLOGICAL BACKGROUNDThe sweet taste is localised principally on theanterior surface and tip of the tongue, the saltyand sour taste on the lateral side of the tongue,and bitter taste on the circumvallate papillas onthe posterior surface of the tongue. Tasteimpulses from the anterior two thirds of thetongue pass first into the lingual branch of themaxillary nerve, which is the third division ofthe trigeminal nerve. Impulses then passthrough the chorda tympani into the facialnerve and then to the tractus solitarius in thebrain stem.4The chorda tympani is given off from the

facial nerve as it passes vertically downwards atthe back of the tympaneum, about a quarter ofan inch before its exit from the stylomastoidferamen. It passes forwards through the cavityof the tympaneum and emerges from that cav-ity through a foramen (canal of Hunguier) andthen descends between the two pterygoid mus-cles and meets the gustatory (or lingual) nerveat an acute angle.

In our patient, there was no facial nervepalsy and so the facial nerve itself was intact.The paralysed half of the tongue had not lostthe protective sensation and so to explain theloss of taste sensation the patient mostprobably had damaged the chorda tympaninerve after it left the facial nerve and beforejoining the lingual nerve.Another interesting feature was the presence

of an aerocoele; the entry of air into the cranial

cavity usually occurs in association withcerebrospinal fluid rhinorrhea and indicates atear of the dura (usually basal) and a fractureinvolving the paranasal sinuses (frontal, eth-moid, or spheroid). This complication occursparticularly if the patient blows his nose.5'6

This unusual combination of cranial nervepalsies was not reported in the case reportsreviewed in this paper. This complication didnot cause any major concern to the patientbecause taste sensation was intact elsewhere inthe tongue. Both tongue paralysis and the lossof taste sensation have not resolved on followup and indicate permanent nerve damage. Inspite of that, functional recovery was satisfac-tory by compensatory mechanisms.

This combination of cranial nerve palsiesrepresents a rare complication of fracture tothe base ofthe skull, which can easily be missedat the initial presentation of these patients toA&E departments when the efforts of traumateams are, quite rightly, focused on the moreserious aspects of injury.

In this case, the presence of slurred speechwas the first indication to examine the oral cav-ity and the tongue in particular. In headinjured patients, examination of the cranialnerves should not be overlooked once theinitial trauma management has been carriedout and awareness of such cranial nerve palsieswould facilitate early diagnosis.There is no specific treatment for XIIth

nerve palsy and the lesion usually improvesspontaneously by compensatory mechanisms.Decompression of the injured cranial nerves

has been suggested, but it seems that there isno indication for this. If the nerve injury doesnot recover, it is likely that the mechanisms ofinjury have been a combination of traction andcrushing which will not be helped by decom-pression and patients often make good func-tional recovery.7

1 Castling B, Hicks K. Traumatic isolated unilateral hypoglos-sal nerve palsy-case report and review of the literature. BrJ Oral Maxillofac Surg 1995;33:171-3.

2 Paley MD, Wood GA. Traumatic bilateral hypoglossal nervepalsy. BrJ Oral Maxillofac Surg 1995;33:239-41.

3 Freixinet J, Lorenzo F, Hernandez Gallero J, et al. Bilateraltraumatic hypoglossal nerve paralysis. Br J Oral MaxillofacSurg 1996;34:309-10.

4 Guyton AC. Textbook of medical physiology. 7th Ed.Philadelphia: W B Saunders, 1986:747-8.

5 Harding Rains AJ, David Ritchie H. Bailey and Love's shortpractice of surgery. London: H K Lewis, 1984: 410, 414.

6 Jennett B, Teasdale G. Management of head injuries. 2nd Ed.Philadelphia: F A Davis, 1981: 203.

7 Bridgman SA, McNab W Traumatic occipital condyle frac-ture, multiple cranial nerve palsies and torticollis. A casereport and review of the literature. Surg Neurol 1992;38:152-6.

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