Cranial nerves
Facial nerve (VII) Anatomy:The motor nucleus of VII lies in the lower pons and its fibers initially pass posteriorly and medially to loop around the VI nucleus before turning forwards and emerging from the lateral pontomedullary junction.
The nervus intermedius contains parasympathetic fibers from the superior salivary nucleus and taste fibers. Which have their cell bodies in the geniculated 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 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 intermedius then pass through the facial canal of temporal bone. The facial nerve emerges from the stylomastoid foramen. Passes through the parotid gland and subdivides into several branches which innervate the muscle of the face. These branches are:
1- Temporal branches: travel superiorly and anteriorly to supply facial muscle situated above zygomatic arch including the orbit and forehead. 2- Zygomatic branches: travel transversely across the face to supply the muscles zygomatic, orbital and infra orbital areas. 3- Buccal branches: supply muscle of the cheek. 4- Marginal mandibular branches: supply muscle of the chin and lower lip 5- Cervical branches: descends to the neck to supply the platysma muscle.
Function: 1- It is efferent limb of the corneal reflex and also the palmomental reflex (a contraction of the ipsilateral mentalis muscle in response to scratching the thenar eminence). The pout or snout reflex (a bilateral pursing of the lips following a brisk tap on the lips). The nasopalpebral reflex (glabellar tap) and the efferent limb of the stapedius reflex. 2- it innervates the muscle of facial expression.
3- It supplies taste sensation to the anterior two-third of the tongue through the chorda tympani branch. 4- Through the nervous intermedius (sensory and parasympathetic fibers) it supplies parasympathetic secretomotor fibers to the lacrimal gland (producing tears) and submandibular gland (producing saliva).
Examination:
Inspection: Observe the face for any asymmetry which may be related 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 patient 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 eye as strongly as possible, to show the teeth(even if these are false). To blow out the cheeks against the closed mouth, to purse the mouth and to whistle. Check the strength of eye closure for paresis or 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 the contralateral side of the tongue as well as its posterior one-third. Gently hold the protruded tongue with a swap. Place a test substance(e.g. sweet, salt bitter or sour substance) on the anterior tow-third of each side of the tongue in turn. Ask the patient to identify the substance by pointing to the appropriate word written 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 10 mm of blotting paper will be dampened by evoked tear secretion.
Common abnormalities:
Upper motor neurone lesions affecting the contriconuclear fibres 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 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 movement employ additional neural pathways. Taste is normal. The commonest cause of this 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 ).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. Test 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. A frequent feature in such patients is Bell's phenomenon. This is an upward rotation of the eye on trying 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 ( e.g. sounds appearing louder 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-nuclear paresis will cause a bilateral facial paresis associated with a labiality 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 are relatively uncommon and may be difficult to detect.
Some myopathies
Skull base tumorGeneralized polyneuropathies (Guillain-Barre syndrome)
Head injuries
Myasthenia gravis
Consider parotid tumor
Neurosarcoidosis
Usually Bell’s palsy Lower motor neuron type weakness
Multiple sclerosis
Consider motor neuron dis.
Cerebral tumor
Often vascular
Usually vascular
Upper motor neuron type weakness
Bilateral
Unilateral
Vestibulocochlear nerve (VIII):
Anatomy: The cochlear branch subserve hearing. The fibers arise from the end organs in the inner ear. They pass centrally along the internal acoustic meatus and across the cerebellopontine CSF cistern to enter the lateral brain stem at the pontomedullary junction. The fibers then synapse in the in the cochlear (dorsal, ventral) and vestibular (inferior, superior lateral and medial) nuclear complexes. From the cochlear nucleus second order fibers ascend to the superior olivary and trapezoid nuclei. Central fibers then ascend up the lateral lemniscus, and synapse in the inferior colliculus and medial geniculated body (MGB) before entering the primary auditory cortex in the superior temporal gyrus. The ascending auditory pathways decussate at several levels so that each cortical region receives impulses from both ears.The inferior and superior vestibule branches and the associated vestibular pathway are very important in the maintenance of correct posture, eye coordination and movement. The vestibular part of the VIII is also afferent limb of both the oculocephalic (doll's eye reflex) and oculovestibular (caloric) reflexes. The oculocephalic reflex involve conjugate movement of the eyes in response to changes in head position. The oculovestibular reflex involves elicitation of eye movements following irrigation of the external ear canal by either cold or warm water.
Examination:
Hearing: Mask hearing in the non tested ear by either rubbing the forefinger and thumb together over the external acoustic meatus or gently massaging the patient's external acoustic meatus with examiner forefinger. Test hearing in each ear by asking the patient to repeat whispered numbers or words.Rinne's test:
By placing a vibrating tuning fork (256 or 512 Hz) on the mastoid process (to assess bone conduction of sound) then just lateral to the external ear. Ask the patient which of the two sounds appear louder.Weber's test:
By placing the strongly vibrating tuning fork to the middle of forehead. Ask the where the sound is heard loudest (in the midline or preferentially to one side). Examine external acoustic canal using an auroscope. Visualize the tympanic membrane and note any abnormal vascularity of the membrane or retrotympanic fluid level.Introduction of positional nystagmus (Hallpihe's test):
Support the patient's head, with eyes open, and lower it briskly below the horizontal plane of the couch, turning the head to one side. Sit the patient up again, and repeat the test, turning the head to the other side. Note the response o the eyes to head movement.Oculovestibular reflex:
Oculocephalic reflex:Perform the test with the patient lying down. Stand above and behind the patient at the head of the bed. Slightly flex and support the patient's head. Briskly rotate the head from one side to the other and note lateral movements of the eyes.
Common abnormalities:
If impaired hearing is unilateral it should be determined whether it is either conductive ( i.e. due to disease of the tympanic membrane or ossicular chain ) or sensorineural ( e.g. involving the organ of Corti or the cochlear nerve ) in origin. If bone conductive is better than air conduction in Rinne's test this indicates a conductive defect. In Weber's test, a patient with sensorineural deafness will perceive the sound as arising from the better ear. In conduction deafness, however, the sound appears to arise from the deaf side; this is because of the improved efficiency of bone conduction in the presence of middle ear damage.Acute abnormalities of the vestibular nerves and labyrinth will usually evoke phasic nystagmus, positional nystagmus or impairment of the caloric response. There are two main types of positional nystagmus and vertigo: 1- Peripheral lesions (usually calcific deposits in the otolith organ ) cause vertigo and nystagmus after a latent period of a few seconds: the nystagmus declines if the position is maintained.
2- nystagmus due to rare " central"-type lesions has no latency, does not show fatigue and is less likely to cause vertigo. Following acute labyrinthine damage or vestibular nerve lesions (fractured petrous temporal bone after head injury, acute vestibular neuritis, etc.) the patient will complain of severe nausea, vertigo or dizziness and disturbance of balance. These symptoms are all aggravated by head movements. In such cases there is frequently phasic nystagmus with the fast phase towards the side of the lesion.
Positional nystagmus will not be elicited in normal subjects. However, where there is a disorder of the labyrinth or its vestibular connection, the patient may complain of vertigo and develop nystagmus within 10 seconds of head movement. The oculocephalic reflex is primarily of value in testing for brain stem death. If the patient is unconscious there will be no nystagmus but on irrigated of one ear with cool water the eyes deviate to the irrigated side. Conversely, if the ear of the unconscious patient is irrigated with warm water, the eyes will deviate to the contralateral side. Bilateral irrigation with either cool or warm water induces vertical eye movement. The reflex is absent in brain stem death.
Chronic lesions of the vestibular nerve ( e.g. acoustic neuroma ) are not normally accompanied by vertigo or nystagmus. Many patients who complain of vertigo and tinnitus ( a subjective awareness of noise such as hissing in the ear ) may have entirely normal clinical examinations, and require detailed audiometry and vestibular tests for diagnosis.
The glossopharyngeal (IX) and
vagus (X) nerves: These nerves are considered together, being related anatomically, functionally and in terms of clinical examination. Anatomy: Both nerves arise as a series of rootlets from the post-olivary sulcus of the lateral medulla. They pass antero-laterally across the cerebellomedullary CSF cistern and exit the skull through the jugular foramen. They traverse the CSF cistern in close relationship to the vertebral artry and posterior inferior cerebellar artery. The motor component of both of these nerves arises from the nucleus ambiguous in the medulla.
Glossopharyngeal nerve:
The motor component is small and innervates the stylopharyngeus muscles. It sometimes contributes to the innervation of the palatal and upper pharyngeal muscles. The large sensory component innervates the mucosa of the pharynx and tonsillar region, conveys taste for the posterior third of the tongue and sensation for part of lining of the tympanic cavity and Eustachian tube. Secretomotor parasympathetic fibers supply the parotid gland.Vagus nerve:
It innervates the muscles of the upper pharynx and soft palate, as well as the intrinsic muscles of the larynx and the cricothyroid. It conveys sensory sensation from the dura mater of the posterior cranial fossa and from part of the skin of the external auditory meatus. It has extensive afferent and efferent connections with the heart, lungs and intestines.The IX and X are also involved in severalreflex:
The gag reflex involves constriction and elevation of the pharynx and palate ( X efferent limb ) in response to tactile stimulation of the upper pharynx and tonsils ( IX afferent limb ). The oculocardiac reflex ( slowing of the heart rate after orbital compression ). The carotid sinus reflexExamination sequence:
Observe movements of the palate and uvula by asking the patient to say 'aah'. Assess tonsillar, palatal and upper pharyngeal tactile sensation using a dampened swab stick and tongue depressor. The gag reflex may be elicited by touching either the tonsil or pharynx. Test each side separately. Testing for the gag reflex is unpleasant. It should be performed only if there is other evidence of nerve paresis.Assess the volume and quality of the patient's speech, noting if the voice is hoarse or has a nasal quality. Ask the patient to cough to determine whether this is more nasal or bovine than normal. Ask the patient to puff out the cheeks, to test palatal closure of the nasopharynx.
Common abnormalities:
lesion of IX and X cause dysphagia ( difficulty in swallowing due to palatal and pharyngeal paresis ), loss of the gag reflex and dysphonia ( altered voice quality usually hoarseness, resulting from weakness of the muscles moving the vocal cords and plate). IX nerve dysfunction is usually seen with other signs of cranial nerve or brain stem dysfunction. An isolated IX nerve lesion is very unusual. It is suggested by unilateral loss of palatal, tonsillar or pharyngeal sensation, together with an absent or depressed gag reflex.Disorders of the X nerve will cause asymmetrical elevation of the soft palate with deviation of the uvula away from the side of the lesion. The voice may have a nasal quality. With lesions to the recurrent laryngeal branch of the vagus nerve the voice will sound hoarse and the cough bovine.
The accessory ( XI ) nerve:
Anatomy: This motor cranial nerve has two nuclei, one of which is intimately related to that of X in the caudal part of the nucleus ambiguous (innervates the intrinsic muscles of the larynx). The much larger spinal element is derived from segments C1-C5. This arises as an extensive series of rootlets from the lateral medulla and spinal cord. Its fibres ascend through the foramen magnum then merge to exit the skull base through the jugular foramen, where the bulbar component rejoins the vagus nerve (see X). the spinal component descends to supply the sternomastoid and the upper half of the trapezius muscles.
Examination sequenc:
Inspect the trapezius muscles from behind. Ask the patient to shrug the shoulders and maintain them in elevation, then apply downward pressure to the shoulders to chech for paresis of the trapezius muscle. Inspect the sternomastoids for hypertrophy or atrophy and palpate to assess tone and bulk. Test the left sternomastoids ny asking the patient to rotate the head to the right side of the chain in an effort to stop this rotatory movement. Examine the right sternomastoids during rotation to the left.Common abnormalities:
Wasting or weakness of the trapezius muscles will produce a flaring of the vertebral border of the scapula, which will be displaced away from the spine in its upper part and rotated towards the spine at its lower end. The point of the shoulder will appear dropped and the arm will appear lower. Isolated paresis of the trapezius can occur if branches of the spinal accessory nerve are cut during surgery in the posterior triangle of the neck. The nerve may be involved with lower cranial nerves in basal skull tumours or following penetrating injury.Upper motor neurone lesions involving the spinal accessory nerve or damage to corticobullar fibers may produces little in the way of clinical signs. Lower motor neurone lesions may occur as part of a progressive bulbar palsy. Paresis of the sternomastoid muscle occur in a range of myopathic disorders, especially dystrophia myotonica.
The hypoglossal ( XII ) nerve:
Anatomy: The XII nerve arises from a motor nucleus located beneath the floor of the fourth ventricle. Its rootlets arise from the pre-olivary sulcus and pass anterolaterally in front of the vertebral and posterior inferior cerebellar arteries. It exits the skull base through hypoglossal canal in the occipital bone. It then passes to the root of the tongue, where it divides into branches that innervate the tongue muscles. Normal tongue movement is essential for articulation adequate chewing and the onset of swallowing.
Examination sequence:
Ask the patient to protrude the tongue; observe the symmetry of movement, bulk and look for wasting and fasciculation. Assess movements of the tongue from side to side. Ask the patient to press the tongue against the cheek and feel the strength of contraction and assess muscle bulk. Assess hypokinesis of tongue movement by asking the patient to say ' lah lah lah ' as quickly as possible, and to make rapid in-and-out and side-to-side movements of the tongue.Common abnormalities:
With unilateral atrophy the tongue becomes wrinkled and thinner on the side and deviates towards that side on protrusion. Spontaneous construction ( fasciculation ) of small parts of the muscles may be apparent and more easily seen when the tongue is protruded. Unilateral XII nerve lesions are usually seen with other cranial neuropathies, and the causes may be neoplastic ( skull base tumour ), vascular medullary infarct, vertebral artery aneurysm or traumatic. Bilateral lower motor neurone lesions may be seen as part of a wider clinical syndrome ( e.g. motor neurone disease or syringobulbia ) and are often component of bulbar palsy.Bilateral lower motor neurone lesions may be seen as part of a wider clinical syndrome ( e.g. motor neurone disease or syringobulbia ) and are often component of bulbar palsy. Unilateral upper motor neurone lesions may produce deviation of the protruded tongue which is not associated with fasciculation or wasting. This is most typically seen immediately after an acute cerebrovascular event; the asymmetry of tongue protrusion tends to resolve after several days. With bilateral upper motor neurone lesions, voluntary movements of the tongue are hypokinetic ( slow ) and the tongue appears small and tends to assume a more conical from. There tends to be dysarthria and dysphagia. Such dysfunction (pseudobulbar palsy) may occur in.