Table 2 Possible causes of loss of consciousness or ‘Blackout’ (on the opposite side to the cerebral lesion) and
there may be a loss of speech or slurred speech
Vaso-Vagal Syncope Simple faint when the CVA affects the left side of the brain.
‘Situational’ Syncope Cough TIA’s comprise a sudden onset of focal CNS
Micturition signs or symptoms due to a temporary occlu-
Carotid sinus hypersensitivity sion of part of the cerebral circulation. They are
Epilepsy frequently associated with partial or complete
Hypoglycaemia stenosis of the carotid artery system. The symp-
Transient Ischaemic Attack toms resolve in less than 24 hours (usually
Orthostatic Hypotension On standing from lying much more quickly). They are harbingers of a
Signifies inadequate vasomotor CVA and the known patient will usually be tak-
reflexes eg elderly patients on ing prophylactic aspirin.
tablets to lower blood pressure Patients with Multiple Sclerosis have a
‘Drop attacks’ Sudden weakness of legs usually diverse condition comprising neurological signs
and symptoms that are disseminated in both site
Stokes-Adams Attacks Transient arrhythmia
and time. A viral aetiology has been postulated
Anxiety but the cause is not known. Onset is variable but
Menieres Disease Vertigo, tinnitus, hearing loss optic neuritis can lead to visual disturbance or
Choking blindness, which may be a presenting feature.
Weakness or paralysis of a limb can occur.
Nystagmus (jerky, oscillating movement of the
present. This is an emergency situation which eyes — which can also be physiological) may
requires urgent intervention with a benzodi- occur, as may ataxia (uncoordinated move-
azepine eg intravenous diazepam. ments) and dysphagia. Loss of sphincter control
Absence seizures or ‘Petit Mal’ tend to occur leading to urinary incontinence may occur. The
in children who may suddenly arrest speech, diagnosis should be considered in a young
attention and movement. So-called ‘partial’ patient presenting with trigeminal neuralgia or a
seizures may be simple or complex. Simple facial palsy. Enquiry in such cases should be
seizures consist of clonic movements of a group directed towards other areas to check for neuro-
of muscles or a limb. Complex seizures may logical signs or symptoms elsewhere.
involve hallucinations of hearing, sight or taste.
Febrile convulsions are common in infancy FACIAL PAIN
and do not predict progression to later epilepsy. Facial pain is common and may affect up to 50%
Keeping the child cool with fans, paracetamol of the elderly population.1 A paroxysm of excru-
and sponging with tepid water are the mainstays ciating stabbing pain lasting only seconds, in
of treatment. the trigeminal nerve distribution suggests
Stokes-Adams attacks describe losses of con- trigeminal neuralgia,2 particularly in patients
sciousness occurring as a result of cardiac over 50 years of age. In the vast majority of
arrhythmias. These may happen with the patient cases it is unilateral and most commonly affects
Status epilepticus in any position and may occur with no warning the mandibular and maxillary divisions. Often a
except for an awareness of palpitations. Recov- ‘trigger area’ may be identified from the history
This is a medical ery is usually within seconds. Other potential that is stimulated by washing or shaving for
causes of ‘blackouts’ are shown in Table 2. example. Talking may be enough to stimulate
emergency and The patient may give a history of a stroke the pain. Usually the trigger is easily identified.
practitioners should (Cerebrovascular Accident — CVA) or a so- Carbamazepine or phenytoin are the mainstays
have a benzodia- called mini-stroke (Transient Ischaemic Attack of treatment.
— TIA). A CVA may be haemorrhagic (sub- Other neurological causes of facial pain
zepine in the arachnoid, cerebral), thrombotic or embolic in include post-herpetic neuralgia and atypical
emergency drug origin. A subarachnoid haemorrhage results facial pain. In post-herpetic neuralgia the
kit to treat this from rupture of a Berry aneurysm of the Circle patient complains of a burning pain (often in the
of Willis (which lies at the base of the brain). ophthalmic division of the trigeminal nerve),
condition Subarachnoid haemorrhages tend to affect a which may become chronic. There is no really
younger age group than the other types of CVA successful treatment, transcutaneous nerve sec-
and typically patients give a history of a sud- tioning and LA infiltration in the painful area
den onset of excruciatingly severe headache. has been tried as has carbamazepine. Tricyclic
The prognosis is poor, but has been improved antidepressants have also been used.
by surgical and radiological obliteration of the When all other causes (including non-neuro-
aneurysm. Hypertension and atherosclerosis logical causes of facial pain) have been exclud-
are contributory factors to other types of CVA. ed, some patients may still complain of facial
Cerebral thrombosis deprives the brain of part pain — usually unilateral. The pain is described
of its blood supply and is the most common as severe, constant and not relieved by anal-
type of stroke. Emboli leading to stroke can gesics. This type of pain is more common in
arise on the wall of an atrium that is fibrillating young females and many are prescribed antide-
or from the wall of a heart damaged after a pressants (although not always to curative
myocardial infarction. Typical results of a CVA effect). Atypical facial pain is the term applied to
are a sudden loss of consciousness, hemiplegia this type of facial pain.
20 BRITISH DENTAL JOURNAL VOLUME 195 NO. 1 JULY 12 2003
OTHER DISORDERS Table 3 Some possible causes of facial weakness
Parkinson’s Disease results from degeneration of (mostly unilateral)
the pigmented cells of the substantia nigra lead-
Idiopathic Bell’s Palsy
ing to dopamine deficiency. The incidence is
equal in males and females. The disease may also
result from previous head injury or cerebrovas- Infection Ear infections
cular disease. Clinically the patient may have TB
tremor in the arms and hands (the latter being Ramsay Hunt Syndrome
described as ‘pill-rolling’). A so-called ‘cog- Glandular Fever
wheel’ type of rigidity may be seen on move- AIDS
ment. Slow movements (bradykinesia) and rest- Trauma Facial lacerations/bruising
lessness (akathisia) may also be noted. The in the region of the facial nerve
patient may have an expressionless face and a Penetrating parotid injuries
stooped posture. Impaired autonomic function Post-parotid surgery
may lead to a postural drop in blood pressure and Neoplastic Primary or secondary cancers
hypersalivation resulting in drooling of saliva. Neuroma of facial nerve
Motor Neurone Disease comprises a group of Acoustic neuroma
disorders that affect motor neurones at various Metabolic Diabetes Mellitus
levels. There is no sensory loss and this helps dif- Pregnancy
ferentiation from multiple sclerosis. The aetiolo-
gy is unknown, but a viral agent is thought pos-
sible. Oral hygiene may be difficult in these
patients and dysphagia and drooling may occur.
Tumours may arise in various components of Looking for ‘forehead sparing’ is thus a way of
the CNS and may be primary or metastatic, the differentiating between upper and lower motor
latter being more common in the brain. Benign neurone causes of facial weakness.
brain tumours are still a significant problem as Bilateral facial paralysis is rare. It may be
they may cause pressure effects and may not be seen in sarcoidosis or the Guillain Barre Syn-
amenable to surgery due to their site. Headaches drome (idiopathic polyneuritis) or posterior cra-
are characteristically worse in the morning. nial fossa tumours. The rare Melkersson-Rosen-
Tumours from which cerebral metastases arise thal Syndrome is a condition comprising tongue
include lung, breast, GIT and kidney. fissuring, unilateral facial palsy and facial
Impairment of vision may occur and this swelling. The lesions are histologically similar to
may vary from mild disability to complete those of Crohn’s Disease.
blindness. Diplopia or double vision may occur A summary of other cranial nerve lesions is
after a ‘blowout’ fracture of the orbital floor3 given in Table 4. Nerves may be affected by a
or injury to cranial nerves III, IV and VI. Tran- systemic cause eg diabetes mellitus, MS or
sient visual disturbance may occur secondary there may be a local cause. Multiple cranial
to local anaesthetic that has tracked to the nerve palsies may occur in Bulbar Palsy that
inferior orbital fissure. comprises palsy of the tongue, muscles of Fig. 1 A patient with Bell’s Palsy. The
ipsilateral forehead is affected also
Myasthenia Gravis (MG) is an antibody- chewing/swallowing and facial muscles due to
indicating a lower motor neurone
mediated autoimmune disease with a deficiency loss of function of motor nuclei in the brain- lesion. Bell’s sign (see text) is also
of functioning muscle acetylcholine receptors stem. The onset may be acute eg in infection demonstrated
that leads to muscle weakness. The disorder such as polio, or may be chronic eg in tumours
more commonly affects young women. The of the posterior cranial fossa.
muscle weakness is progressive and develops Tics or involuntary facial movements may
rapidly. Some cases are associated with the occasionally be seen in patients. These may be
Eaton-Lambert Syndrome that may occur in habitual, particularly in children or may be drug
some patients with lung or other cancers. In the induced or they may have a more organic cause.
Eaton-Lambert syndrome, however, the muscles Drug induced dyskinesias are common in the
get stronger rather than weaker with activity. elderly on long-term phenothiazine (anti-psy-
A facial palsy may have a known cause or be chotic) medication which is usually reversible on
idiopathic (Table 3). If the cause is not known the stopping the drug. Intracranial nerve compres-
name Bell’s Palsy (Fig. 1) is applied. Other caus- sion may result in blepharospasm (contraction
es must be excluded before this term is used. In of both eyelids). Hemifacial muscle spasm may
Bell’s Palsy the onset is rapid, unilateral and occur and suggests a lesion eg of the cerebello-
there may be an ache beneath the ear. The weak- pontine angle compressing the facial nerve.
ness worsens over one to two days. If presenta- Whenever a facial tic is found, consideration
tion is early, most clinicians give prednisolone should be given to referral for investigation
for 5 days, the aim being to reduce neuronal since an underlying cause may often be treated.
oedema. An eye patch is of value to protect the In the Ramsay-Hunt Syndrome, a profound
cornea. The paralysis is of a lower motor neu- facial paralysis is accompanied by vesicles in the
rone type in which all the facial muscles are pharynx on the same side and in the external
affected on that side. In an upper motor neurone auditory meatus. It is thought that the geniculate
lesion eg stroke, the forehead is spared since this ganglion of the facial nerve is infected with her-
region is bilaterally represented in the cortex. pes zoster.
BRITISH DENTAL JOURNAL VOLUME 195 NO. 1 JULY 12 2003 21
Table 4 Cranial nerve dysfunction and signs arising from it infective endocarditis which should be specifi-
cally asked about. Signs and symptoms resulting
Cranial nerve Possible problem Sign
from a brain abscess depend on its location and
I Olfactory Trauma, Tumour Decreased ability to smell CT and MRI scanning are useful in localisation
II Optic Trauma, Tumour Blindness, visual field and diagnosis. Urgent surgical drainage is
MS, Stroke defect required.
III Oculomotor Diabetes, increased intra- Dilated pupil Cerebral Palsy is primarily a disorder of
cranial pressure Ptosis
motor function secondary to cerebral damage,
IV Trochlear Trauma Diplopia
most frequently associated with birth injury or
V Trigeminal Sensory — idiopathic, None, sensory hypoxia. It is the most common cause of a con-
trauma, IDN/Lingual deficit on testing
nerve damage genital physical handicap, the patterns of which
are variable. There are three main subtypes —
Motor — Bulbar palsy Signs in IX, X, XI, XII
spastic, ataxic and athetoid varieties. In the
Acoustic Neuroma May be decreased facial sensation. spastic type the muscles are contracted and there
Affects VIII also
may be associated epilepsy. In the ataxic type, a
VI Abducens MS, some strokes Inability of eye to look cerebellar lesion is responsible for a disturbance
Eye deviated towards nose of balance. Writhing movements characterise
VII Facial LMN — Lower motor neurone Total
the athetoid type of cerebral palsy.
Bell's Palsy, Skull fracture Facial weakness In spina bifida, the vertebral arches fail to
Parotid tumour fuse, possibly due to a deficiency of folic acid
during foetal development. The condition may
UMN — Upper motor neurone Forehead sparing lead to significant physical handicap such as an
Stroke, Tumour weakness
inability to walk, epilepsy or learning difficul-
VIII Vestibulo- Excess noise;
cochlear Paget's, acoustic neuroma Deafness
ties. There may be an association with hydro-
cephalus which often requires decompression
IX Glosso- Trauma, Tumour Impaired gag reflex
pharyngeal using a shunt. This is discussed further in the
X Vagus Trauma, brainstem lesions Impaired gag reflex paediatric paper (Part 10 of this series).
Soft palate moves to Patients with syringomyelia have a condi-
‘good’ side on saying tion in which cavitation of the central spinal
'aah'. cord occurs leading to a loss in pain and temper-
XI Accessory Polio, stroke Weakness turning head ature sensibility. Syringobulbia is the term used
away from affected side if the brain stem is affected — facial sensory loss
Weakness shrugging may occur, as may tongue weakness.
shoulders (trapezius) An acoustic neuroma is a benign tumour
XII Hypoglossal Trauma Tongue deviated to occurring at the cerebello-pontine angle on the
Brainstem lesions affected side on vestibular part of the vestibulocochlear nerve.
protrusion Cranial nerves V, VII, IX and X may also be
involved leading to tinnitus, deafness and verti-
go. Facial twitching, weakness or paraesthesias
Infections affecting the nervous system may may occur. Other causes of facial sensory loss
be bacterial or viral in origin. The possibility of (innervated by the trigeminal nerve except over
bacterial meningitis should be borne in mind the angle of the mandible which is innervated by
with maxillofacial injuries involving the middle cervical nerves) are given in Table 5.
third of the face. Prompt treatment with antimi- Other neurological disorders that may be
crobials (prophylactically in trauma cases) encountered include Huntington’s Chorea,
should be undertaken. The viral type of menin- which is an autosomal dominant disorder where
gitis is usually mild and self-limiting. The there is progressive dementia with marked invol-
patient with meningitis has a severe headache, untary movements. The signs do not begin to
feels sick or actively vomits and is often drowsy.
The painful, stiff neck and aversion to light are
Table 5 Potential causes of facial sensory loss
well known. In meningitis caused by the bacteri-
um Neisseria meningitidis, a purpuric rash may
be seen on the skin and can progress to adreno- • Neoplasm — Cerebral Tumour
cortical failure as a result of bleeding into the • Inflammatory — MS
adrenal cortex. Granulomatous conditions eg sarcoid TB
Connective tissue disorders
Herpetic encephalitis is rare, but should be
treated promptly with aciclovir. In HIV associat- • Other : Paget’s Disease (nerve compression)
ed neurological disease, a wide variety of infec- Cerebrovascular Disease
tions and tumours are seen, for example lym- Extracranial
phomas. Neurological effects of such lesions
• Neoplasm — Cancer, Metastatic Cancers
vary from fits to limb weakness.
• Inflammatory — Osteomyelitis
Brain abscess is a condition that may be sec- — Pressure from adjacent lesions
ondary to oral sepsis4 or infection elsewhere eg • Trauma — Maxillary/mandibular fractures
the middle ear or paranasal sinuses. A patient Iatrogenic eg removal of mandibular
with congenital heart disease is also at increased third molars
risk. Such abscesses can be a complication of
22 BRITISH DENTAL JOURNAL VOLUME 195 NO. 1 JULY 12 2003
appear until middle age. Friedreich’s Ataxia is
an autosomal recessive or sometimes sex-linked
cord degeneration of unknown cause. Severe
ataxia and deformity occur and there may be
associated cardiac disease with arrhythmias.
The patient’s gait may give an immediate clue to
an underlying neurological condition, for exam-
ple the shuffling gait of Parkinsonism. A spastic
gait is demonstrated by stiff limbs that are often
swung around in a circular motion as the for-
ward movement proceeds.
The patient with a neurological condition Fig. 2 A patient with Sturge Weber Syndrome
may appear confused. This may be for several
reasons and a summary of potential causes is the cranial nerves in the following groups: ie
given in Table 6. Raised intracranial pressure nerve(s) subserving the sense of smell, eyes, face,
can occur following trauma to the head for mouth, neck and ears. A summary of disorders
example in a patient attending with an injury affecting the cranial nerves and resulting signs
associated with dental trauma. Such patients is given in Table 4.
will complain of headache and may be restless Any changes in the sense of smell may reflect
or vomiting. The classical sign of increased a problem with the olfactory nerve. Colds and
blood pressure and decreased pulse rate occur sinusitis may be the cause but trauma involving
and there is dilation of the pupil on the same side the cribriform plate can also cause the nerve to
as the lesion. Patients with a head injury can be have impaired function. Some operations on the
assessed according to the Glasgow Coma Scale nose may cause injury to the olfactory nerves.
Visual acuity may be roughly assessed by
Table 6 Possible causes of confusion that may be asking the patient to read a printed page. Defects
encountered in a dental patient of the optic nerve may also affect the field of
Hypoxia — Ensure clear airway, care with sedatives
vision. A lesion of the cranial nerve III leads to
complete or partial ptosis (drooping of the upper
eyelid). The external ocular muscles are con-
Infection — Significant oro-facial infection, pneumonia,
trolled by the action of cranial nerves III, IV and
VI. Disruption of the third nerve (which supplies
Metabolic — Hypoglycaemia
all of the extrinsic eye muscles apart from supe-
rior oblique and lateral rectus) causes a paralysis
Vascular — Stroke, MI
of internal, upward and downward movement of
Raised intracranial pressure the eye leading to double vision. The eye points
Nutritional — Deficiency of various B vitamins downwards and outwards except when looking
to the affected side. A fixed dilated pupil may
also be seen. Disruption of IV, the trochlear
(GCS) which involves three scored categories of nerve supplying superior oblique, prevents the Eye signs
assessment — eye opening, muscle responses eye moving downwards and medially. The dou-
and responses to vocal stimuli. ble vision is worse on looking down. Disruption
Horner’s Syndrome comprises the four signs of VI (abducens supplying lateral rectus) causes
Problems with cranial
of a constricted pupil, ptosis (drooping of the an inability to abduct the eye (look to the ipsilat- nerves II, III, IV and VI
upper eyelid), loss of sweating on the ipsilateral eral side). There is deviation of the eye towards affect the eyes
face and enophthalmos. It is caused by interfer- the nose and double vision.
ence with the cervical sympathetic chain eg after The muscles of facial expression are inner-
a radical neck dissection, trauma to the neck or vated by the VII cranial nerve (facial nerve). As
tumour. mentioned previously, upper motor neurone
Patients with cerebral palsy have an lesions affecting the facial nerve eg after a
increased incidence of dental malocclusion and stroke may be differentiated from lower motor
abnormal movement of the oral and facial mus- neurone causes eg Bell’s Palsy since the latter
culature that may cause difficulty in dental causes the whole side of the face to be weak-
treatment provision. ened whereas the forehead is spared in an
The Sturge-Weber syndrome (Fig. 2) describes upper motor neurone lesion due to bilateral
an association between a facial port wine stain representation at the level of the cerebral cor-
(haemangioma) with focal fits on the contralat- tex. The ipsilateral eye moves upwards on
eral side. Exophthalmos and spasticity may also attempted closure of the eyes in Bell’s Palsy —
be evident. The fits are caused by a capillary this is known as Bell’s Sign (Fig. 1).
haemangioma in the brain. In terms of facial sensation the sensory divi-
sion of the trigeminal (V cranial) nerve sub-
CONSIDERATION OF THE CRANIAL NERVES serves this over most of the face. The oph-
A systematic approach is needed for examining thalmic, maxillary and mandibular divisions
the Cranial Nerves. One approach is to consider may be compared by testing skin sensation on
BRITISH DENTAL JOURNAL VOLUME 195 NO. 1 JULY 12 2003 23
either side with a wisp of cotton wool. The treatment under LA, with or without sedation.
corneal (blink) reflex is often the first clinical Ability to protect the airway is also relevant for
deficit to be seen in trigeminal nerve lesions. the provision of GA since all these modes of
The mouth can demonstrate signs of cranial treatment jeopardise the airway to some extent.
nerve problems in the case of cranial nerves V Stroke patients may be taking anticoagulants, or
(motor division), IX, X and XII. If the masseter may be hypertensive.
muscles are palpated whilst asking the patient In both multiple sclerosis and motor neurone
to clench the teeth and the motor division of V disease, the degree of compliance achievable for
is inactive, the masseter on that side will not treatment is likely to be impaired. It is best to use
Cranial nerves contract properly. With a unilateral lesion, the LA alone if possible. Limited mobility and/or
mandible deviates to the weak side on opening associated psychological disorders may cause
the mouth (V being motor to the pterygoid difficulties with treatment. Patients are better
Defects in cranial muscles). treated sitting so that respiration is assisted as
nerves V, IX, X and XII Asking the patient to say ‘aah’ will allow an much as possible since it may be impaired.
appraisal of IX and X nerves. The ninth (glos- Patients with MS may be taking corticosteroids,
have intra-oral sopharyngeal) nerve is mainly sensory for the particularly early in the disease. Care of the air-
manifestations pharynx and palate and the tenth (vagus) mainly way may be made more difficult due to muscular
motor. With a unilateral lesion of the vagus, the incoordination.
soft palate is pulled away from the weaker side. Patients with Parkinson’s disease suffer from
Lesions of both nerves lead to an impaired gag excess salivation, which can cause difficulties
reflex. The twelfth (hypoglossal) nerve may be with visibility leading to problems not only pro-
tested by asking the patient to protrude the viding the treatment itself but also for the safe
tongue. The tongue deviates to the weaker side. provision of an anaesthetic. Anti-muscarinic
To test the accessory (eleventh) cranial nerve drugs will reduce the salivation and degree of
the patient should be asked to put their chin tremor. The autonomic insufficiency often found
towards the left or right shoulder against resist- in these patients makes them liable to postural
ance by the examiner. The sternocleidomastoid hypotension and poor candidates for general
muscle (supplied by XI) does not function when anaesthesia.
XI is affected. In myasthenia gravis, local anaesthesia is
The eighth (vestibulocochlear) nerve has two the option of choice. Doses should be kept to a
components — the vestibular (appreciation of minimum. Muscle fatigue appears to increase
position and movements of the head) and the during the day and therefore treatment is best
cochlear (responsible for hearing). Lesions of the carried out early. Intravenous sedation should
nerve may cause hearing loss, vertigo or ringing not be given in a dental practice setting6 since
in the ears (tinnitus). Special tests are needed to respiratory impairment may be worsened.
test the balance and positional functions of the A small oral dose of a benzodiazepine is
nerve. acceptable if the patient is very anxious about
their treatment. For similar reasons general
GENERAL AND LOCAL ANAESTHESIA, anaesthetics are also not advised if possible. In
SEDATION AND MANAGEMENT addition, some of the agents used with GA eg
CONSIDERATIONS IN THE DENTAL PATIENT the muscle relaxant suxamethonium or opioids
WITH NEUROLOGICAL DISEASE eg fentanyl may have their effects potentiated
Patients prone to syncope should be treated with in these patients.
regard to avoidance of known precipitating fac- Patients with visual problems may be per-
tors as far as possible. Treatment in the supine manently disabled or the disorder may be tran-
position has obvious advantages. sient. It is important that a ‘tell-do’ approach is
Epileptic patients referred for GA should used for these patients to minimise anxiety. It is
not be given methohexitone or enflurane since worth bearing in mind in these patients that
these are epileptogenic. It is important to other senses eg hearing may be heightened.
ensure that an epileptic patient has taken their Diplopia can be a transient complication of LA
normal medication on the day of the proce- as mentioned earlier. Other cranial nerve
dure. Intravenous sedation is useful in manag- lesions of relevance include those affecting
ing epileptic patients. The benzodiazepines cranial nerves IX and X since the gag reflex
have anticonvulsant properties and anxiolysis may be impaired leading to potential airway
should decrease the chances of a fit. When compromise, particularly if sedation or GA are
treating epileptic patients with sedation sup- being used.
plemental oxygen should be provided via a Patients with cerebral palsy may not be able
nasal cannula.5 The use of the benzodiazepine to tolerate treatment under LA, and GA may be
reversal agent flumazenil should be avoided in the only way of achieving it. In the athetoid
patients with epilepsy as this drug can precipi- type, potential epilepsy should be borne in mind.
tate convulsions. Anxiety will often worsen the effects of the cere-
Patients who have had a CVA should have bral palsy and therefore premedication e.g. with
treatment only when their condition has been diazepam is often wise. Patients with spina bifi-
optimised if possible. There may be a loss of da have increased incidence of latex allergy.
reflexes such as swallowing or the gag reflex, Such patients may be prone to postural hypoten-
which has implications for the safe provision of sion and are therefore best treated sitting up.
24 BRITISH DENTAL JOURNAL VOLUME 195 NO. 1 JULY 12 2003
Epilepsy and renal anomalies may also be asso- immune complexes. The antigens can be as
ciated. In Friedreich’s Ataxia, possible arrhyth- diverse as microorganisms or drugs.
mias should be remembered. The anti-muscarinic anti-Parkinsonian drugs
such as orphenadrine and benzhexol can pro-
EFFECTS OF DRUGS USED IN NEUROLOGICAL duce dry mouth, which may increase caries inci-
DISORDERS ON ORO-DENTAL STRUCTURES dence. In addition, the dopaminergic drugs such
Drugs used to treat neurological conditions can as levodopa and co-careldopa may produce taste
produce unwanted effects in and around the disturbances.
mouth. Anticonvulsants have a number of
unwanted effects of interest to dentists. Gingival SUMMARY
overgrowth is a recognised side effect of pheny- As with disorders of other systems, neurological
toin7 but may also occur with sodium valproate diseases impact on dental treatment provision,
and ethosuximide. In addition, phenytoin causes both in terms of the treatment itself and the pro-
taste disturbance and may produce Stevens- vision of safe methods of anaesthesia/analgesia
Johnson syndrome. This drug may also affect to facilitate it.
the teeth. It has been implicated in producing
1. Madland G, Newton-John T, Feinmann C. Chronic idiopathic
hypercementosis and shortening of the roots.8 Orofacial pain: I: What is the evidence base? Br Dent J 2001;
Sodium valproate may produce parotid gland 191: 22-24.
enlargement. Lamotrigine may cause dry mouth 2. Nurmikko T J, Eldridge P R. Trigeminal neuralgia –
pathophysiology, diagnosis and current treatment. Br J
and Stevens-Johnson syndrome. Ethosuximide Anaesth 2001; 87: 117-132.
may produce Stevens-Johnson syndrome and 3. Courtney D J, Thomas S, Whitfield P H. Isolated orbital
gingival bleeding. Carbamazepine may produce blowout fractures: survey and review. Br J Oral Maxillofac
xerostomia, glossitis and oral ulceration. Surg 2000; 38: 496-502.
4. Corson M A, Postlethwaite K R, Seymour R A. Are dental
Stevens-Johnson syndrome is the name given to infections a cause of brain abscess? Case report and review
a severe form of erythema multiforme. The latter of the literature. Oral Diseases 2001, 7: 61-65.
predominantly affects young males and is char- 5. Meechan J G, Robb N D, Seymour R A. Pain and Anxiety
Control for the Conscious Dental Patient. pp287-290. Oxford:
acterized by mucosal lesions with or without Oxford University Press, 1998.
skin lesions. The typical skin lesion is described 6. Malamed S F. Sedation: a Guide to Patient Management. 3rd
as looking like a target as it consists of concen- ed. p595 – 596. St Louis: Mosby, 1995.
tric erythematous rings. The rashes may appear 7. Hassell T M. Epilepsy and the Oral Manifestations of
Phenytoin Therapy. Basle: Kruger, 1981.
differently however, hence the name ‘multi- 8. Seymour R A, Meechan J G, Walton J G. Adverse Drug
forme’. The aetiology of erythema multiforme is Reactions in Dentistry. 2nd ed. p 121. Oxford: Oxford
not known but is thought to be a disorder of University Press, 1996.
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