20: Sensory and motor changes

Sensory and motor changes

INTRODUCTION

Sensory, motor or autonomic neuropathies may affect the orofacial region. The main orofacial sensory and motor lesions are shown in Table 20.1.

Table 20.1

Main orofacial neuropathies

Features	V	VII
Major	Sensory loss in face	Weak muscles of facial expression
Minor	Jaw movements impaired	Reduced sense of taste in anterior ⅔ of tongue

Sensory changes most frequently follow nerve damage from trauma. Weakness of the facial muscles is most commonly seen in neurological disorders and presents with paralysis (palsy) but is also seen in primary muscle disease and neuromuscular junction disorders, is then usually symmetrical, and the uncommon causes include:

myasthenia gravis

dystrophia myotonica

facioscapulohumeral dystrophy.

SENSORY CHANGES

Normal facial sensation, mediated by the trigeminal nerve, is important to protect the skin, mucosae and especially the cornea of the eye from damage. Facial sensory changes, which can be caused by lesions of a sensory branch of the trigeminal nerve or the central connections (Fig. 20.1), may lead to sensory awareness that is:

Fig. 20.1 Causes of sensory loss: (A) intracranial; (B) extracranial

completely lost (anaesthesia)

partially lost (hypoaesthesia)

altered (paraesthesia) – often ‘pins and needles’ or similar discomfort – which may arise during recovery from nerve damage

increased (hyperaesthesia).

Sensory defects may lead to unrecognized damage from trauma or burns (‘trophic lesions’), and are occasionally associated with hyperaesthesia (i.e. the patient has a decreased sensory perception, but when sensation is perceived, it may cause discomfort).

AETIOLOGY AND PATHOGENESIS

Causes of lesions affecting the trigeminal nerve are shown in Boxes 20.1 and 20.2.

BOX 20.1 Main causes of sensory loss

Trauma (e.g. surgical, fractures)

Infections or inflammatory

Disseminated sclerosis

Cerebrovascular disease

BOX 20.2 More advanced list of causes of facial sensory loss

Trauma (e.g. surgical, fractures) to inferior dental, lingual, mental or infraorbital nerves

infections – neurosyphilis, HIV infection, herpesviruses, tuberculosis, leprosy, diphtheria, Lyme disease

carcinoma of antrum or nasopharynx

metastatic tumours

leukaemic deposits

paraneoplastic syndrome

Trauma (e.g. surgical treatment of trigeminal neuralgia)

disseminated sclerosis

connective tissue disorders

cerebral tumours (metastases, glioma, meningioma, acoustic neuroma)

cerebrovascular disease

Drugs: (see Table 54.21)

benign trigeminal neuropathy

idiopathic (connective tissue diseases)

hyperventilation syndrome

Metabolic and endocrine disease:

chronic kidney disease

EXTRACRANIAL CAUSES

Extracranial causes of facial sensory loss are most common and include damage to the trigeminal nerve from the following causes.

Trauma

This is the usual cause of sensory loss – especially after orthognathic or cancer surgery. Ipsilateral hypoaesthesia or anaesthesia usually result. If the nerves are stretched or compressed (neuropraxia), there is often only hypoaesthesia, and recovery of sensation is speedy, typically within days. However, if the nerves are severed (neurotmesis), anaesthesia is profound and recovery is delayed for months accompanied by paraesthesia or hyperaesthesia. Recovery is sometimes not complete: repair may be indicated:

Trauma to the mandibular division can have a variety of causes:

inferior alveolar local analgesic injections

fractures of the mandibular body or angle

surgery (particularly surgical extraction of lower third molars, osteotomies or jaw resections) or even endodontics or implants.

Trauma to the mental nerve can have a variety of causes:

operations in the region

pressure from a denture – the mental foramen is close beneath a lower denture and there is anaesthesia of the lower lip on the affected side.

Trauma to the lingual nerve can arise especially during resections or removal of lower third molars, particularly when the lingual split technique is used.

Trauma to branches of the maxillary division of the trigeminal nerve may be caused by direct trauma or fractures (usually Le Fort II or III middle-third facial fractures) or surgery.

Bone disease

Osteomyelitis in the mandible may affect the inferior alveolar nerve to cause labial anaesthesia.

Osteochemonecrosis.

Neuropathies

Drugs occasionally produce hypoaesthesia (Box 20.1).

Disseminated (multiple) sclerosis may cause sensory loss.

Diabetes may produce a neuropathy.

Infections such as syphilis, leprosy, Lyme disease or herpesviruses are rare causes.

Neoplastic disease

Oral carcinomas may invade the jaws to cause anaesthesia.

Skull base or central malignancies such as osteosarcoma may produce a similar pattern.

Nasopharyngeal carcinomas may invade the pharyngeal wall to infiltrate the mandibular division of the trigeminal nerve, causing pain and sensory loss in the region of the inferior alveolar, lingual and auriculotemporal nerve distributions; invade the levator palati to cause soft palate immobility; and, by occluding the Eustachian tube, cause deafness (Trotter syndrome).

Leukaemia, myeloma or metastases (usually from breast, lung, stomach or colon cancer) may cause deposits in the mandible and labial hypoaesthesia.

Carcinoma of the maxillary antrum may produce ipsilateral upper labial hypoaesthesia or anaesthesia.

Intracranial lesions

Intracranial lesions affecting the trigeminal nerve or connections are uncommon but often serious.

Causes include:

Trauma including surgical treatment of trigeminal neuralgia.

Inflammatory disorders:

disseminated sclerosis

infections (e.g. HIV, syphilis)

connective tissue disorders.

Neoplasms, such as brain tumours (often metastases).

Cerebrovascular disease:

since other cranial nerves are anatomically close, there may be associated neurological deficits in intracranial causes of facial sensory loss. Thalamic strokes in particular can cause facial sensory loss

in posterior cranial fossa lesions, for example, there may be cerebellar features, such as ataxia

in middle cranial fossa lesions there may be associated neurological deficits affecting cranial nerve VI and thus mediolateral eye movements.

Brainstem lesions that may involve the fifth nuclei and central connections include brainstem:

disseminated sclerosis

syringobulbia: this leads to sensory loss spreading from the periphery of the face inwards towards the nose, plus a lower motor nerve lesion of the vagus, hypoglossal and accessory nerves, leading to disturbances of speech and swallowing, and bilateral upper motor neurone lesions affecting all limbs. A ‘syringomyelia-like’ syndrome has been infrequently reported in neurological disorders such as Tangiers disease, lepromatous leprosy and a novel syndrome termed ‘facial onset sensory and motor neuronopathy syndrome’ (FOSMN).

Cerebellopontine angle lesions that can compress the trigeminal nerve and as they enlarge, affect the neighbouring seventh and eighth nerves, producing facial weakness and deafness include:

acoustic neuroma

Petrous temporal bone lesions may cause pain and also affect the sixth nerve (Gradenigo’s syndrome) and include the following.

INFECTION SPREADING FROM THE MIDDLE EAR

Metastases

Cavernous sinus lesions can compress the trigeminal (Gasserian) ganglion and these include:

internal carotid artery aneurysm

cavernous sinus thrombosis

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Tags: Oral and Maxillofacial Medicine The Basis of Diagnosis and Treatment 3e

Jan 9, 2015 | Posted by mrzezo in Oral and Maxillofacial Pathology | Comments Off

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