PEDIATRIC DENTISTRY/Copyright ©1985 byThe American Academy of Pediatric Dentistry

Volume 7 Number 4

Neuropathologic chewing in comatose children

Peter W. H. Ngan, DMD Linda P. Nelson, DMD, MScD

AbstractThis paper reviews the etiology and management of

neuropathologic chewing in 16 comatose children. Thesepatients exhibited ruminant chewing and bruxism thatoften resulted in self-inflicted oral soft tissue trauma. Thesuccess of using various dental appliances was found tobe associated with the neurologic status of these patients.Variables such as etiology, depth and duration of coma,and age of patient can influence the medical prognosisand hence the success of using these appliances. In caseswhere the use of dental appliances were not successful,other managerial techniques are discussed.

Patients in corna, from whatever cause, may de-

velop chewing movements presumably similar to thoseseen in healthy people during sleep. If coma is pro-longed, these chewing movements may be so pow-erful and persistent as to cause self-inflicted traumato the soft tissues of the oral cavity (Fig 1) and attri-tion of the teeth.1 Guyton has termed this conditionneuropathologic cb.ewing.2

The literature concerning neuropathologic chewingis scarce. The exact mechanism of the coordinationof tongue and jaw movements during mastication isstill unclear. Hanson et al. designed an intraoral den-tal appliance based on the neurophysiology of jawmovement in comatose patients. 3 Others fabricatedtongue stents4 and removable appliances5 for adultsto prevent self-inflected trauma to the tongue. Freed-man et al. reported success in managing a 2-year-oldpatient with neuropathologic chewing with a remov-able bite block.6 Peters et al. reported success in man-aging an 8-year-oht patient with a tongue stent andcircummandibular wires.7

Dental services in hospitals frequently are calledupon to assist in the management of comatose pa-tients who exhibit bruxism. Some of these cases arecomplicated by severe intraoral soft tissue laceration

as a result of the uncoordinated movement of thetongue and jaw. Thus, it is desirable for dentists tounderstand this condition and develop effectivemethods for managing these patients in a hospitalsetting.

A retrospective study was made on a series of 16comatose patients with neuropathologic chewing whowere referred to the dental service of the Children’sHospital of Philadelphia between 1979 and 1984. Ap-pliances were made for 10 of these patients. The cri-teria for fabrication of an appliance and the successof using different appliances are discussed in this pa-per. A standard methodology is proposed for man-aging hospitalized patients with neuropathologicchewing.

The Comatose Patient

Coma is a symptom closely related to the integra-tion of functions of the cerebral cortex and the retic-ular activating system. It can be caused by any agentchemical, physical, or biological that is capable of in-terrupting the integrity of the arousal system. Func-tionally, the state of coma originates either from brainstem injury (e.g., herniation) or diffuse cortical in-jury, such as toxicity, anoxia, or metabolic imbalance.The various causes can be classified into supraten-torial, subtentorial, or metabolic,s

Evidence suggests that meningitis, encephalitis,hypoxia, epilepsy, and metabolic insults are the mostcommon causes of coma in children. 9 The outcomeof coma is either recovery, which can be complete orincomplete, or brain death. If recovery is incomplete,the remaining disability can be termed moderate, se-vere, or a form of vegetative state. The outcome ofnontraumatic coma is more favorable in the child thanit is for the adult, with almost 60% of patients eitherrecovering completely or having only a mild handi-cap.9

302 NEUROPATHOLOGIC CHEWING: Ngan and Nelson

FIG 1. (fop) Typical self-inflicted trauma in a comatose patient.Immediate relief was achieved with a ratchet (Molt) mouthprop,

FIG 2. (bottom) The McKesson rubber bite-block is hygienicand easy to insert.

Neurophysiology

Masticatory movements are normally rhythmic andautomatic. The learning of these movements is as-sociated with the cerebral cortex, the reticular for-mation, and the extrapyramidal system.2 Jaw openingsand closings are coordinated by neurons of the tri-geminal sensorimotor complex in the brain stem re-ferred to as the pattern generator.10 The centralprogramming of this generator may be modified byhigher centers in the brain as well as peripheral in-fluences.

Coordination of tongue and jaw movements is nec-essary during normal mastication and likely to beelaborated by the same generator,11 which is why thetongue or cheek muscles usually are not bitten duringroutine movements of the mouth, chewing, speak-ing, or swallowing.

Patients in coma may have sustained injuries to thecerebral cortex, the reticular or pyramidal system, thetrigeminal nucleus, or the hypothalamus, and the finecoordinated movements of the jaw and tongue mayhave been lost. Jackson states that the placement ofa bolus between the teeth perpetuates myotactic mas-ticatory reflex.4 In comatose patients, the tongue canbecome juxtapositioned between the teeth resultingin this chewing reflex.

Management of Comatose Children withNeuropathologic Chewing

Several important factors need to be considered be-fore initiating dental treatment for a comatose pa-tient. A careful history should be taken which wouldinclude the etiology of coma (Table 1), the age of thepatient, the depth and duration of coma, and howrapidly the patient was resuscitated in instances dueto anoxia. These are all important factors in predict-ing the outcome of the comatose patient. The designof any dental appliance also depends on the prog-nosis of the patient, the neurologic status, and theseverity of chewing and/or bruxing.

When examining the patient, dentists should befamiliar with the clinical findings in stupor and coma9

(Table 2). A rapid neurologic assessment should beperformed to establish the severity of injuries to thebrain.12 The rapid neurologic assessment is a system-atic way to examine the airway, motor functions, andcranial nerves of patients who encounter injuries tothe head and neck. The protocol is complete and yetsimple enough to be performed by dental practition-

TABLE 1. Common Etiologies of Unconsciousness

SupratentorialTraumaCerebral vascular accidentCerebral venous thrombosisSubdural empyemaIntracerebral tumor

SubtentorialTumorsTraumaPrimary hemorrhage

MetabolicAnoxiaHypoglycemiaDiabetic ketoacidosisElectrolyte abnormalitiesExogenous poisoningsMeningitisEncephalitisReye's syndromeHepatic encephalopathy

From Packer RJ, Berman PM: Coma, in Textbook of PediatricEmergency Medicine, Fleischer G, Ludwig S, eds. Baltimore; TheWilliams and Wilkins Co, 1983.

PEDIATRIC DENTISTRY: December 1985/Vol. 7 No. 4 303

TAIILI~ 2. Clinical Findings in Stupor and Coma

Level of Damageor Depression Respirations Pupils

None (psychogenic Eupnea or 2-3 mm, reactiveunresponsiveness hyperventilation

Cerebral Sighing, eupnea, 2 mm, reactivehemisphere Cheyne-Stokes (CSR)

Diencephalon Eupnea or CSR 1.5-2 mm,reactive

Uncal herniation Eupnea or central Ipsilateralneurogenic dilationhyperventialation(CNH)

Midbrain CSR or CNH

Oculovestibular(caloric) Responses

Pons Apneustic, cluster or Pinpoint, oftenataxic temporarily fixed

Nystagmus ~bilaterally

Tonic conjugatedeviation

Tonic conjugatedeviation

Incipient III nerveweakness

Midposition 4-6 Sluggish ormm, fixed, suggestive ofirregular internuclear

ophthalmoplegia

Absent

MotorResponse

Medulla Ataxic or apnea Small (2 mm), Unaffectedreactive

Voluntary orabsent

Paratonia,paretic

Paretic ordecorticate

Ipsilateral orcontralateralparasis,paratonia

Decorticate ordecerebrate

Decerebrate orlower extremityflexor responseFlaccid or lowerextremity flexorresponse

From Plum F, in Scientific Foundations of Neurology, Critchley M, O’Leary JL, Jennett B, eds. Philadelphia; DavisCo, 1972.

ers in their offices. Teasdale and Jennett developedthe Glasgow Coma Scale that correlates the level of

consciousness and severity of injury to the head.13

The neurosurgeon then should be consulted to learnthe neurologic status and prognosis of the patient.An oral examination should be performed to detectthe presence of ruminatory movements of the jaw,bruxism, and the severity of self-inflicted trauma tointraoral soft tissues. The anesthesia team should beconsulted as to the risk of sedating and/or paralyzingthe patient if impressions must be obtained for thefabrication of dental, appliances.

Indications for the need of fabricating dental ap-pliances should be based on the following criteria:

1. The presence of persistent ruminatory move-ments of the jaw or bruxism which is usually ofmore than 24-hr duration

2. The presence of intraoral soft tissue lacerations.

If either of the above criteria is absent, the fabri-cation of appliances is not immediately necessary.

Numerous metho.ds had been tried to prevent self-inflicted trauma by comatose patients including acrylicbite-blocks, ratchet mouth props, padded tongueblades, and intermaxillary fixation. The use of anydental appliance should be based on the neurophys-iology of neuropathologic chewing with modifica-tions based on the special needs of a particular patient.

Patients who had mild ruminatory movementstreated by the authors responded well to a taped mouth

propa or a rubber bite-block b (Fig 2). These are hy-gienic appliances, easy to insert, and no laboratorypreparation is necessary. These appliances also areindicated in cases where immediate relief is neededand can be used temporarily until further treatmentdecisions are made.

The removable custom-made appliance with a pos-terior bite-block is the next most hygienic appliancefor patients with mild ruminatory movements (Fig 3).The detailed fabrication of this appliance is well de-

scribed and allows tongue movement, but preventsthe tongue from acting as a bolus which causes reflexchewing patterns. 6 The amount of mandibular open-ing is controlled by the height of the posterior bite-blocks. Retention is usually adequate if most of theprimary or permanent dentition is present. The dis-advantages of using this appliance are the necessityof paralyzing the patient in order to obtain theimpression and the extensive laboratory work re-quired.

In patients with powerful chewing movements, theuse of removable appliances usually fails because ofproblems of retention. A fixed tongue depressing stentmay be necessary to temporarily depress the tongueand prevent it from being traumatized.7

Another method of preventing self-inflicted oral

Molt mouth prop -- Hu Friedy: Chicago, IL.McKesson rubber bite-block -- Silverman: Plymouth Meeting,PA.

304 NEUROPATHOLOGIC CHEWING: Ngan and Nelson

Fic 3. The removable custom appliance with a posterior bite-block allows free range of movements but prevents the tonguefrom acting as a bolus. This appliance requires laboratory fab-rication.

trauma is the fabrication of a soft acrylic custom tray(Fig 4). The custom tray can be fabricated by moldingvinyl mouthguard materialc on the impression modelsusing the dental molding machine. This appliancedoes not control the height of the posterior opening

c Buffalo Dental Mfg Co, Inc: Syosett, NY.

Fic 4. The soft acrylic custom tray is easy to insert but doesnot control the height of the posterior opening.

and is not as rigid an appliance as the posterior bite-block, but it is easy to fabricate and insert and doesnot require extensive laboratory work.

The authors do not recommend intermaxillary fix-ation because it is very difficult to maintain good oralhygiene and removable appliances are eventuallynecessary if and when the fixation is removed.

Finally, for patients who have mild chewing move-ments with no apparent intraoral damage, fabricationof appliances should be delayed since in some casesneuropathologic chewing may be a self-limiting phe-nomenon. These patients are observed daily for anysigns of intraoral traumatic injuries and if necessaryan appliance is fabricated and employed.

A Retrospective Study of SixteenComatose Children

A retrospective study of 16 pediatric comatose pa-tients with neuropathologic chewing was carried out(Table 3). These patients ranged in age from 11 monthsto 16 years and were comatose due to a variety ofcauses including anoxia, metabolic disorders, men-ingoencephalitis, multiorgan failure, and hypogam-maglobulinemia.

Dental appliances were fabricated for 11 of the pa-tients who met the criteria for appliance fabrication.Eight patients were managed successfully with bite-block therapy. These patients exhibited healing of thelacerated soft tissues. In addition, due to the concom-itant improvement in neurologic status, 6 of the 8patients did not have clenching or chewing move-ments after wearing the appliance a few months.

Two other patients were treated with soft acryliccustom trays because of a poor recovery prognosis.In 1 patient, the remaining teeth were extracted due

PEDIATRIC DENTISTRY: December 1985/Vol. 7 No. 4 305

TABLE 3. Retrospective Study of Sixteen Comatose Patients 1979-84

Patient A~, e Etiolo~, yBB 5 AnoxiaWK 1.5 AnoxiaKB 3 AnoxiaLB 4 Hypogam maglobulinemiaJG 4 TraumaCW 4 Anoxia

encephalopathyKK 2 Anoxia

encephalopathySC 4 AnoxiaCE 16 Multiorgan failureRB 13 MetabolicMT 2.5 MeningoencephalitisAJ 1 MeningitisAS 3 AnoxiaRC 9 AnoxiaCS 2 AnoxiaFA 2.5 Cardiac failure

Pro[~n osis Trea tm en tGood Acrylic bite-blockGood Acrylic bite-blockGood Acrylic bite-blockPoor Acrylic bite-blockFair Acrylic bite-blockGood McKesson bite-block

Fair McKesson bite-block

Poor McKesson bite-blockPoor* Molt mouthpropPoor* Custom trayPoor* Custom tray-ExtractionGood Follow-up observationGood Follow-up observationFair Follow-up observationFair Follow-up observationFair Follow-up observation

* Patient expired during treatment.

to poor retention of the appliance and powerful jawmovements. These 2 patients exhibited soft tissue im-provement, but died within a short period after ini-tiating treatment. In 1 other patient, due to the limitedmouth opening from TMJ disease, treatment was lim-ited to the use of a mouth prop. One patient (LB) wasdiagnosed as having end-stage poliomyelitis withprogressive neurologic deterioration. At age 4 sheshowed evidence of neuropathologic chewing. Dueto her poor prognosis and in anticipation of furtherdeterioration of neurologic status, a bite-block wasfabricated to prevent further trauma to the intraoralsoft tissues. The patient tolerated the appliance wellunder parental supervision until she died from res-

piratory distress.In the other group of 5 patients for which dental

appliances were not indicated, dental treatment in-cluded observation alone. In 4 of the cases, neuro-pathologic chewing was self-limiting. One patientcontinued to have a bruxing and chewing habit butwithout associated intraoral damage.

Dr. Ngan is an assistant professor, orthodontics, The Ohio StateUniversity, College of Dentistry, Columbus, OH. Dr. Nelson ischief of dentistry, Children’s Hospital of Philadelphia, and an as-sistant professor, pedodontics, University of Pennsylvania Schoolof Dental Medicine, 40(11 Spruce St., Philadelphia, PA 19104. Re-print requests should be sent to Dr. Nelson.

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neurological disorders, in Proceedings of a Symposium onthe Clinical and Physiological Aspects of Mastication, An-derson DJ, ed. University of Bristol; John Wright and SonsLtd, 1976 pp 221-24.

2. Guyton AC: Textbook of Medical Physiology, 3rd ed. Phila-delphia; WB Saunders Co, 1966 p 879.

3. Hanson GE, Ogle RG, Giron L: A tongue stent for preventionof oral trauma in the comatose patient. Crit Care Med 3:200-203, 1975.

4. Jackson MJ: The use of tongue depressing stents for neuro-pathologic chewing, l Prosthet Dent 10:309-11, 1978.

5. Piercell MP, Waite DE, Nelson R: Prevention of self-inflictedtrauma in semicomatose patients. J Oral Surg 32:903-5, 1974.

6. Freedman A, Sexton T, Reich C, Berkowitz RJ: Neuropath-ologic chewing in comatose children: a case report. PediatrDent 3:334-36, 1981.

7. Peters T, Blair A, Freeman R: Prevention of self-inflicted traumain comatose patients. Oral Surg 57:367-70, 1984.

8. Packer RJ, Berman PM: Coma, in Textbook of Pediatric Emer-gency Medicine, Fleischer G, Ludwig S, eds. Baltimore; TheWilliams and Wilkins Co, 1983 p 94.

9. Plum F, Posner JB: The Diagnosis of Stupor and Coma, 3rded. Philadelphia; Davis Co, 1980 pp 225-343.

10. Ramfjord SP, Ash MM: Occlusion. Philadelphia; WB Saun-ders Co, 1983 pp 71-127.

11. Dubner R, Sessle BJ, Storey AT: The Neural Basis of Oral andFacial Function. New York; Plenum Publishing Co, 1978 pp311-47.

12. Croll TP, Brooks EB, Schut L, Laurent JP: Rapid neurologicassessment and initial management for the patient with trau-matic dental injuries. JADA 100:530-34, 1980.

13. Teasdale G, Jennett B: Assessment of coma and impaired con-sciousness. A practical scale. Lancet 2:81~4, 1974.

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