Can A Lesion On The Pons Cause Hyperacusis And Opthalmoplegia

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The motor nucleus of VII lies in the lower pons and its fibres initially pass posteriorly and medially to loop around the VI nucleus before turning forwards and emerging from the lateral pontomedullary junction (see Fig. 6.19).

Pons LesionsPyramidal Signs

Fig. 6.19 Lesions of the pons. Lesions at 1. (e.g. haemorrhage) cause ipsilateral VI and/or VII nerve palsies and contralateral pyramidal signs. Lesions at 2. (e.g. basilar thrombosis) cause ataxia on the side of the lesion (damage to the cerebellar peduncles). There may also be impaired sensation on Ihe ipsilateral side of the face (spinal tract and n udeus of V nerve) and on the contralateral side of the body (spinothalamic tract) and xcasionally a VII nerve lesion. Lesions in the pons often cause internuclear ophthalmoplegia (p. 202) and ataxic nystagmus.

Vf nerve VII nerve

Superior cerebellar peduncle

Inferior cerebellar peduncle

Spinal tract and nucleus of V nerve

VII nerve nucleus

Spinothalamic tract

Medial lemniscus

Corticospinal (pyramidal) tract

Fig. 6.19 Lesions of the pons. Lesions at 1. (e.g. haemorrhage) cause ipsilateral VI and/or VII nerve palsies and contralateral pyramidal signs. Lesions at 2. (e.g. basilar thrombosis) cause ataxia on the side of the lesion (damage to the cerebellar peduncles). There may also be impaired sensation on Ihe ipsilateral side of the face (spinal tract and n udeus of V nerve) and on the contralateral side of the body (spinothalamic tract) and xcasionally a VII nerve lesion. Lesions in the pons often cause internuclear ophthalmoplegia (p. 202) and ataxic nystagmus.

The nervus intermedins contains parasympathetic fibres from the superior salivatory nucleus and taste libres, which have their cell bodies in Ihe geniculate ganglion and synapse centrally in the gustatory nucleus or nucleus solitarius. It emerges from the pons in close proximity to VII, and the two nerves pass through the pontomedullary CSF cistern in close relationship to the vestibular and cochlear (VIII) nerves. All these nerves enter the internal acoustic meatus. The facial nerve and the nervus intermedins then pass through Ihe facial canal of the temporal bone. The facial nerve emerges from the stylomastoid foramen, passes through the parotid gland and subdivides into several branches which innervate the muscles of the face, the corneal reflex and (he other reflexes. Within the temporal bone and distal to the geniculate ganglion the facial nerve has branches to the stapedius muscle (which dampens down tympanic vibrations), to the pterygopalatine ganglion (from which arises the greater petrosal nerve, which is secretomotar to the lacrimal gland) and to the tongue (chorda tympani which conveys taste).

Examination

Examination of the VII nerve depends largely on inspection to assess facial asymmetry.

Taste sensation is rarely tested in clinical practice: electrical stimulation of the tongue with a small current is more reliable and practical (electrogustometry). Secrctornotor function of the lacrimal gland is usually only tested by ophthalmologists doing a Schirmer test.

Testing for decreased saliva production owing to denervation of the submandibular gland is not performed in clinical practice.

Examination sequence

Inspection

□ Observe the face for any asymmetry which may be related to paresis of the facial muscles.

□ Observe the symmetry of blinking and eye closure and the presence of any tics or spasms of the facial musculature.

□ Observe spontaneous movement of the face, particularly the upper and lower facial musculature during such actions as smiling.

Motor function

□ Test the facial muscles by asking the palient to raise the eyebrows, wrinkle the forehead (this can be achieved by asking the patient to look upwards at the examiner's hand), close the eyes as strongly as possible, to show the teeth (even if these arc false), to blow out the cheeks against the closed mouth, to purse the mouth and to whistle (Fig. 6.20A-D).

O Check the strength of eye closure for paresis of asymmetry.

Taste sensation

□ Instruct the patient not to speak during the test because this will cause the tongue to retract and dissipate the substance into ihe contralateral side of Ihe tongue as well as its posterior one-third.

□ Gently hold the protruded tongue with a swab.

□ Place a test substance (e.g. sweet, salt, bitter or sour substances) on the anterior two-thirds of each side of the tongue in turn.

D Ask the patient to identify the substance by pointing to the appropriate word wrillen on a card.

Schirmer's test

□ Put a piece of special blotting paper under the lower eyelid and remove it after 5 minutes. Normally at least l() mm of the blotting paper will be dampened by evoked tear sccrction.

Common abnormalities

Upper motor neurone lesions affecting the corticonuclear libres will cause facial paresis that is worse in the lower facial muscles with relative sparing of the upper face (because of bilateral cortical innervation of the upper facial

Motor Pathway For Smiling
Fig. 6.20 Testing the motor function of the facial nerve. Ask the patient to E OS blow out the cheeks.

muscles). The corner of the mouth will droop and saliva may dribble, the nasolabial fold will be flattened, but eye closure, although paretic, is usually well preserved. Smiling may also be preserved because emotional facial movements employ additional neural pathways. Taste is normal. The commonest cause of [his type of unilateral facial dysfunction is a vascular lesion involving the contralateral rolandic cortex or its subcortical pathways. Usually there will also be weakness of the ipsilateral upper limb (faciobrachial paresis).

With lower motor neurone lesions affecting the facial nucleus or its nerve, there is unilateral paresis of both upper and lower facial muscles with inability to close the eye and impaired blinking, loss of the nasolabial fold and forehead wrinkles (Fig. 6.21). Taste to the anterior two-thirds of the tongue is impaired if the chorda tympani is also damaged. The commonest cause is idiopathic Bell's palsy (see Table 6.16), A frequent feature in such patients is Bell's phenomenon. This is an upward rotation of the eye on trying to contract the paretic orbicularis oculi.

The location of the VII lesion can be deduced from the clinical findings. Taste and lacrimation will be preserved in those lesions distal to the stylomastoid foramen. A lesion involving the nerve to the stapedius will cause hyperacusis

Eyebrow Lesion

raise the eyebrows, E show the teeth, El close the eyes against resistance and

(e.g. sounds appearing lintder than normal). A lesion involving the greater petrosal nerve will cause a dry eye.

Bilateral facial weakness can be due to the upper or lower motor neurone lesions as well as disorders of the muscles and neuromuscular junctions. Progressive supra nuclcar paresis will cause a bilateral facial paresis associated with a lability of emotional expression and a disassociation between emotional (well preserved) and voluntary (poorly preserved! movement. Such patients may exhibit an obvious snout reflex, Causes of bilateral lower motor neurone facial type paresis (Tabic 6.16) arc relatively uncommon and may he difficult to detect.

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