Jaw jerk or Masseter or Mandibular reflex

Theory: Sensory fibers → mesencephalic nucleus → reflex center in pons → motor nucleus → motor fibers

Normal Minimal or absent response

Limb hyperreflexia due to cervical spinal lesion Normal jaw reflex

Generalized hyperreflexia Exaggerated jaw reflex

Note: Exaggerated reflex is due to lesion in the bilateral corticobulbar tracts above motor

nucleus, e.g. pseudobulbar palsy or amyotrophic lateral sclerosis.

Fig. 6D(iii).46: Illustration showing examination of jaw jerk.

Testing [Fig. 6D(iii).47]:

Examiner places the index finger or thumb over the middle of patient’s chin, holding the

mouth open about midway with jaw relaxed and then taps the finger with reflex hammer.

The response is upward jerk of mandible.

Other methods:

For bilateral response:

Tapping chin directly

Placing the tongue blade over the tongue or lower incisor and tapping the protruding

end.

For unilateral response:

Tapping the angle of the jaw

Placing the tongue blade over the lower molar teeth of one side and tapping the

protruding end.

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Fig. 6D(iii).47: Examination of jaw jerk.

Sternutatory/Nasal/Sneeze Reflex

Primary clinical use is to cross check the corneal reflex.

Method: Stimulation of nasal mucous membrane with cotton, a spear of tissue or similar

object → wrinkling of nose, eye closure, and often a forceful exhalation resembling a feeble

sneeze.

Theory: The ophthalmic division of trigeminal innervates the nasal septum and anterior

nasal passages.

Afferent limb Center Efferent limb

V1 Brainstem and upper spinal cord V

VII

IX

X

Corneal Reflex

Elicited by lightly touching the cornea with wisp of cotton or tissue [Fig. 6D(iii).48].

Stimulus is ideally delivered to upper cornea because the lower cornea may be

innervated by CN V2 in some individuals.

Stimulus should be ideally brought in from the side so that patient cannot see it.

Stimulus must be delivered to cornea but not sclera

Afferent limb Efferent limb

V1 VII

Conjunctival Reflex

Same as corneal reflex [Fig. 6D(iii).48]

However, the sensitivity of corneal reflex is more.

Trigeminal lesion (complete)

Direct reflex Consensual (indirect) reflex

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Stimulus to involved eye Absent Absent

Stimulus to opposite eye Present Present

Facial nerve lesion (complete)

Direct reflex Consensual (indirect) reflex

Stimulus to involved eye Absent Present

Stimulus to opposite side Present Absent

Fig. 6D(iii).48: Demonstration of corneal/conjunctival reflex.

Disorders of V Nerve Dysfunction

1. Motor Dysfunction

Unilateral UMN lesion—generally no weakness observed.

Bilateral UMN lesion—pseudobulbar palsy—marked weakness seen with exaggerated

jaw jerk.

Myasthenia gravis—masticatory fatigue (not to be confused with claudication pain of giant

cell arteritis)

ALS: Jaw drop with diminished jaw jerk—dysphagia and difficulty in swallowing their own

saliva.

Involuntary movements include—dystonia (extrapyramidal symptoms of antipsychotic

drugs), Meige syndrome (oromandibular dystonia with blepharospasm), and trismus.

Causes of trigeminal nerve involvement

Supranuclear—bilateral (pseudobulbar) palsy

Nuclear—syringobulbia

Nerve root—cerebellopontine angle tumor

Gasserian ganglion—Gradenigo syndrome, otitis media, meningitis, and aneurysms of internal carotid artery

Cavernous sinus—thrombosis/tumor

Superior orbital fissure—Tolosa–Hunt

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Individual branches involvement

2. Sensory Dysfunction

Site of lesion Disease Manifestation

Parietal lobe or sensory radiation

(supranuclear lesion)

Stroke/tumors May raise the sensory threshold of

contralateral face

Thalamic lesion Stroke/tumors Facial hypoesthesia with

hyperpathia or allodynia

Principal sensory nucleus:

Pressure

Touch

Vibration

Stroke/tumors Diminished tactile sensation of skin

and mucous membrane of that side

Spinal nucleus Lateral medullary or pontine

lesion/tumors

Pain and temperature loss

Intramedullary lesion Syringomyelia/syringobulbia/tumors Dissociative loss of sensation

Figs. 6D(iii).49A and B: (A) Balaclava helmet and (B) Dejerine onion skin distribution seen

in syringobulbia.

Trigeminal Neuralgia (Also known as Fothergill’s disease Tic douloureux)

Most common disorder to involve trigeminal sensory function.

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Paroxysms of fleeting but excruciation unilateral facial pain—usually involves II and III

division and rarely I division.

Pain lasts for few seconds but may occur many times per day.

Trigger for pain may be talking, chewing, brushing, exposure to cold or by wind on face.

Most common cause for compression of sensory root by ecstatic arterial loop of the

basilar artery (AICA or superior cerebellar artery)

Other causes include MS, tumors of CP angle—bilateral is suggestive of MS.

3. Postherpetic Neuralgia

Acute herpes zoster is extremely painful.

Usually in CN V1—pain in vesicles in forehead, eyelid, and cornea but may affect other

division also.

Persistent neuralgic pain syndrome after 1 month of acute eruption is appropriately

labeled as postherpetic neuralgia. It is a dysesthetic with burning component, constant

but with superimposed paroxysm of lancinating pain that may be provoked by touching

certain spots with affected area.

There may be hypo- or hyperesthesia.

4. Facial Numbness

Numb chin syndrome: In distribution of mental nerve—due to metastatic process in

mental foramen.

Numb cheek syndrome: Involvement of infraorbital nerve.

5. Other Trigeminal Nerve Disorders

Marcus-gunn

phenomenon or

jaw winking

phenomenon

Seen in congenital ptosis: Opening the mouth, chewing or lateral jaw movements cause an

exaggerated reflex elevation of the ptotic lid due to proprioceptive impulses form the

pterygoid muscles being misdirected to the oculomotor nucleus

Reversed Gunn

phenomenon or

inverse jaw

winking or MarinAmat sign

Synkinesis due to aberrant regeneration of facial nerve where there is involuntary closure of

one eye on mouth opening

Frey syndrome Flushing, warmness, and excessive perspiration over the cheek and pinna on one side

following ingestion of spicy food—due to misdirection of secretory fibers to parotid gland to

the sweat glands and vasodilator ending in the auriculotemporal nerve distribution—usually

follows trauma or infection of parotid gland or local nerve injury

Sturge–Weber or

Weber–Dimitri

disease

Congenital nevi or angiomas over the side of face in the trigeminal distribution with

associated ipsilateral leptomeningeal angiomas and intracortical calcification with attendant

neurologic complications

Raeder’s

paratrigeminal

syndrome

Unilateral oculosympathetic paresis (differential diagnosis with Horner)

Ipsilateral trigeminal involvement

Gradenigo’s

syndrome

Damage to V1 division of trigeminal nerve

Ipsilateral 6th nerve palsy

Cavernous sinus

syndrome

3, 4, 6 nerves with V1 and V2 (less often)

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