THE CRANIAL NERVES

There are twelve bilaterally paired cranial nerves. The cranial nerves are numbered according
to the nerve’s position along the longitudinal axis of the brain. The first two cranial nerves
attach directly to the forebrain while the rest attach to the brainstem.

Olfactory Nerve

The olfactory nerve [I] carries special sensory fibres for the sense of smell. They are purely
sensory and are concerned with smell. The olfactory cells reside in the mucosa of the superior
nasal concha & the upper part of the nasal septum. Nerve fibre arising in this mucosa collect
bundles that together constitute an olfactory nerve. The axons of these cells pass through the
sieve like cribriform plate of the ethmoid bone, pierces the duramater and arachnoid of the
brain to reach the overlying olfactory bulb to the medial surface of the cerebral hemisphere
and the temporal lobe.
Test:

Both perception and identification is tested using aromatic non irritant materials that avoid
stimulaton of the trigeminal nerve fibres in the nasal mucosa. Check that the nasal passages
are clear. Ask the patient to close his eyes and shut one nostril with a finger. Present
commonly available odours such as coffee, chocolate, soap, tobacco or orange peel and ask
the patient to sniff.

Optic Nerve

The optic nerve carries visual information from the retina. The nerves pass through the optic
canals of the sphenoid bone. Then they converge at the ventral anterior margin of the
diencephalon, at the optic chiasma. At the optic chiasm approximately half of the fibres from
each optic nerve cross the midline and exit the chiasm in the opposite optic tract. The fibres
of the optic tracts continue posteriorly around the cerebral peduncles of the midbrain with
most synapsing in the lateral geniculate nucleus of their respective thalamus. A small
portion of the fibers enter the pretectal region of the midbrain and participate in the pupillary
light reflex. Cells of the lateral geniculate nuclei are tertiary sensory neurons which project to
the primary visual cortex in the occipital lobe via the optic radiation

Test

Examination of the optic nerve involves visual acuity, visual field, pupillary examination,
ophthalmoscopy.

Visual acuity

Ask patients to use their appropriate glasses when you measure visual acuity. Use good
ambient lighting and a Snellen chart.A Snellen visual acuity of 6/60 indicates that at 6 metres
the patient can only see letters they should be able to read 60 metres away. Normal vision is
said to be 6/6. If 6/6 vision is not obtained, then a pinhole placed directly in front of the
patient's glasses may correct additional refractive errors. It allows only central rays of light to
enter the eye and can correct for about 4 diopters of refractive error.If patients cannot see the
top line of the chart at 6 metres, bring them forward till they can and record that vision (e.g.
1/60 - can see top letter at 1 metre). If patients still cannot see the top letter at 1 metre, then
check whether they can count fingers, see hand movements or just see light. For children use
different-sized objects instead of letters. For patients complaining of central blurred vision
record the near vision in each eye using reading glasses and Jaeger type card.

Visual Fields

The normal visual field extends 160° horizontally and 130° vertically. The blind spot is
located 15° to the temporal side of the point of visual fixation and represents the optic nerve
head. At the bedside, test visual fields by confrontation. More accurate assessments use
perimetry and visual field analysers.

Confrontation
Compare the patient’s fields of vision by advancing a moving finger or a red 5mm pin from
the extreme periphery towards the fixation point. This map out ‘cone’ vision. A 2mm pin will
define central field defects which may only manifest as a loss of colour perception. In the
temporal portion of the visual field the physiological blind spot may be detected. A 2mm
object should disappear here. The patient must fixate on the examiners pupil.

Goldmann Perimeter
Peripheral visual fields are more sensitive to a moving target and are tested with a Goldmann
Perimeter. The patient fixes on a central point. A point of light is moved centrally from the
extreme periphery. The position at which the patient observes the target is marked on a chart.
Repeated testing from multiple directions provides an accurate record of visual fields. Central
fields are charted with either a Goldmann Perimeter using a small light source of lesser
intensity or a tangent screen.

Ophtalmoscopy
Ask the patient to fixate on a distant object away from any bright light. Use the right eye to
examine the patient’s right eye and the left eye to examine the patient’s left eye. The
ophthalmoscope lens needs to be adjusted until the retinal vessels are in focus and trace these
back to the optic disc. Ask the patient to look at the light of the ophthalmoscope. This brings
the macula into view.
Note for:
• clarity of disc edge
• width of blood vessels and look for arteriovenous nipping at cross over points
• haemorrhages or white patches of exudates (focal ischaemia)
If small pupil size prevents fundal examination, then dilate pupil with a quick acting
mydriatic (homatropine). This is contraindicated is an acute expanding or glaucoma is
suspected.

Pupillary Examination

Examine the shape, size (miosis or mydriasis). Also pupillary reaction to light should be
examined; both pupils should constrict when light is shone in either eye. A lesion of the optic
nerve will abolish papillary response to light on the same side as well as in the contralateral
eye. When light is shone in the normal eye, it and the contralateral pupil will constrict.
Examine pupils’ reaction to accommodation and convergence; pupil constrict when gaze is
transferred to a new point object.

Occulomotor Nerve

The occulomotor nerve consists of two components with distinct functions. Firstly, the
somatic motor component of occulomotor nerve plays a major role in controlling the muscles
responsible for the precise movement of the eyes for visual tracking or fixation on an object.
Secondly, the visceral motor component is involved in the pupillary light and accomodation
reflexes.
There are six extraocular muscles in each orbit. The somatic motor component of CN III
innervates the following four extraocular muscles of the eyes:
• Ipsilateral inferior rectus muscle
• Ipsilateral inferior oblique muscle
• Ipsilateral medial rectus muscle
• Contralateral superior rectus muscle
The remaining extraocular muscles, the superior oblique and lateral rectus muscles, are
innervated by the trochlear nerve and abducens nerve, respectively.
The somatic motor component of occulomotor nerve also innervates the levator palpebrae
superioris muscles bilaterally. These muscles elevate the upper eyelids.
The motor neurones serving the extraocular muscles have their cell bodies in the oculomotor
nucleus, which lies at the base of the periaqueductal grey of the midbrain at the level of the
superior colliculus. Preganglionic parasympathetic neurones arise from the nearby Edinger-
Westphal nucleus. Fibres from both sources course ventrally through the midbrain
tegmentum, many of them traversing the red nucleus, to exit on the medial aspect of the crus
cerebri, within the interpeduncular fossa . The oculomotor nerve passes between the posterior
cerebral and superior cerebellar arteries, then runs anteriorly, lying in the wall of the
cavernous sinus, before gaining access to the orbit through the superior orbital fissure.

Preganglionic parasympathetic neurones terminate in the ciliary ganglion. From here

postganglionic neurones run in the short ciliary nerves to innervate the sphincter
(constrictor) pupillae muscle of the iris and the ciliary muscle contained within the ciliary
body. The ciliary muscles control the shape and therefore the refractive power of the lens and
the constrictor pupillae muscle of the iris constrict the pupil.

Trochlear Nerve

The trochlear nerve contains only somatic motor neurones. These arise in the trochlear
nucleus, which lies in the midbrain periaqueductal grey at the level of the inferior colliculus.
Axons pass dorsally, around the periaqueductal grey, and cross the midline. The trochlear
nerve emerges from the dorsal aspect of the brain stem (the only cranial nerve to do so) just
caudal to the inferior colliculus. The nerve courses round the cerebral peduncle to gain the
ventral aspect of the brain, passing between the posterior cerebral and superior cerebellar
arteries, as does the oculomotor nerve. It then runs anteriorly, lying in the lateral wall of the
cavernous sinus and enters the orbit through the superior orbital fissure. It supplies just one
muscle, the superior oblique, which moves the eyeball downwards and medially.
 Trigeminal Nerve

The trigeminal nerve has both sensory and motor components. It is the main sensory nerve
for the head and, additionally, innervates the muscles of mastication.

The trigeminal nerve exits from the anterolateral surface of the pons as a large sensory root
and a small motor root. These roots continue forward out of the posterior cranial fossa and
into the middle cranial fossa by passing over the medial tip of the petrous part of the temporal
bone .
In the middle cranial fossa the sensory root expands into the trigeminal ganglion which
contains cell bodies for the sensory neurons in the trigeminal nerve and is comparable to a
spinal ganglion. The ganglion is in a depression (the trigeminal depression) on the anterior
surface of the petrous part of the temporal bone, in a dural cave (the trigeminal cave). The
motor root is below and completely separate from the sensory root at this point. Arising from
the anterior border of the trigeminal ganglion are the three terminal divisions of the
trigeminal nerve, which in descending order are:

• ophthalmic nerve (ophthalmic division [V1]);

• maxillary nerve (maxillary division [V2]);

• mandibular nerve (mandibular division [V3]).

Ophthalmic nerve [V1]

The ophthalmic nerve [V1] passes forward in the dura of the lateral wall of the cavernous
sinus, leaves the cranial cavity, and enters the orbit through the superior orbital fissure.
The ophthalmic nerve [V1] carries sensory branches from the eyes, conjunctiva, and orbital
contents, including the lacrimal gland. It also receives sensory branches from the nasal cavity,
frontal and ethmoidal sinuses, upper eyelid, dorsum of the nose, and the anterior part of the
scalp.

Maxillary nerve [V2]

The maxillary nerve [V2] passes forward in the dura mater of the lateral wall of the cavernous
sinus just inferior to the ophthalmic nerve [V1] , leaves the cranial cavity through the foramen
rotundum, and enters the pterygopalatine fossa.
The maxillary nerve [V2] receives sensory branches from the dura in the anterior and middle
cranial fossae, the nasopharynx, the palate, the nasal cavity, teeth of the upper jaw, maxillary
sinus, and skin covering the side of the nose, the lower eyelid, the cheek, and the upper lip.

Mandibular nerve [V3]

The mandibular nerve [V3] leaves the inferior margin of the trigeminal ganglion and leaves
the skull through the foramen ovale.
The motor root of the trigeminal nerve also passes through the foramen ovale and unites with
the sensory component of the mandibular nerve [V3] outside the skull. Thus, the mandibular
nerve [V3] is the only division of the trigeminal nerve that contains a motor component.
Outside the skull the motor fibers innervate the muscles of mastication, including the
temporalis, the masseter, and the medial and lateral pterygoid muscles, as well as the tensor
tympani, the tensor veli palatini, the anterior belly of the digastric, and the mylohyoid
muscles.
The mandibular nerve [V3] also receives sensory branches from the skin of the lower face,
cheek, lower lip, the ear, the external acoustic meatus and the temporal region, the anterior
two-thirds of the tongue, the teeth of the lower jaw, the mastoid air cells, the mucous
membranes of the cheek, the mandible, and dura in the middle cranial fossa.

Test:

Test for pain sensation (pin prick), temperature (using a cold object or hot cold tubes) and
light touch over the whole face. Each side should be compared and the sensory deficit should
be mapped out testing from the abnormal to the normal region. Note whether the distribution
involve a root or division pattern or a brain stem onion skin pattern.

Corneal reflex

Test the corneal sensation by touching with wisp of wet cotton wool. A blink response should
occur bilaterally. This test is the most sensitive indicator of trigeminal nerve damage.
Motor examination

Observe for wasting and thinning of temporalis muscle- hallowing out of the temporalis
fossa. Ask the patient to clamp jaws together. Feel temporalis and masseter muscles. Attempt
to open patient’s jaws by applying pressure to chin. Ask patient to open mouth. If pterygoid
muscles are weak the jaw will deviate to the weak side, being pushed over by the unopposed
pterygoid muscles of the good side.

Jaw Jerk

Ask the patient to relax jaw. Place finger on chin and tap with hammer. A slight jerk is
normal. An increased jerk implies a bilateral upper neurone lesion.

I- Abducens Nerve

The abducens, like the trochlear nerve, contains only somatic motor neurones. The cell bodies
of origin are located in the abducens nucleus, which lies beneath the floor of the fourth
ventricle in the caudal pons. Fibres pass ventrally through the pons and emerge from the
ventral surface of the brain stem at the junction between the pons and the pyramid of the
medulla. The nerve then passes anteriorly, through the cavernous sinus, enters the orbit
through the superior orbital fissure and supplies the lateral rectus muscle, which abducts the
eye.

Test for the III, IV, VI cranial nerves

A lesion of the III nerve produces impairment of the eye and lid movement as well as
disturbance of pupillary response

Pupil
The pupil dilates and becomes fixed to light. When a torch is shone in the affected eye,
contralateral pupil constricts. There is absent or impaired response in the illuminated eye.
When light is shone into the normal eye, only the pupil on that side constricts.

Ptosis

Ptosis is present if the eyelid droops over the pupil when the eyes are fully open. Since the
levator palpebrae muscle contains both skeletal and smooth muscle, ptosis signifies either a
III nerve palsy or a sympathetic lesion and is more prominent with the former.

Ocular movement

Steady the patient’s head and ask him to follow an object held at arm’s length. Observe the
full range of horizontal and vertical eye movements. Note any misalignment or limitation of
range. Examine each eye movements in the six different directions of gaze representing
maximal individual muscle strength.

1. looking up and out- superior rectus

2. looking up and in- inferior oblique

3. medial movement( adduction)- medial rectus

4. lateral movement( abduction)- lateral rectus

5. looking down and in- superior oblique

6. looking down and out- inferior rectus

Conjugate movements

Note the ability of the eyes to move together in horizontal or vertical direction or tendency
for gaze to fix in one particular direction

Nystagmus

Note for the direction of the fast phase and the gaze direction where nystagmus is maximal

Facial Nerve

The facial nerve is the seventh (VII) of twelve paired cranial nerves.
The facial nerve contains sensory, motor and parasympathetic components. It joins the brain
stem at the ventrolateral aspect of the caudal pons , near the pontomedullary junction, in a
region known as the cerebellopontine angle. The nerve consists of two roots, the more
lateral (sometimes called the nervus intermedius) containing sensory and parasympathetic
fibres, the more medial root being composed of motor axons.

The sensory fibres of the facial nerve supply taste sensation from the anterior two-thirds of
the tongue, the floor of the mouth and palate, and also cutaneous sensation from part of the
external ear. The cell bodies of primary afferent neurones lie in the geniculate ganglion
within the facial canal of the petrous temporal bone. The central processes of taste fibres
terminate in the rostral part of the nucleus solitarius of the medulla. Ascending fibres from
the nucleus solitarius project to the ventral posterior nucleus of the thalamus, which in turn
sends fibres to the sensory cortex of the parietal lobe. Afferent facial nerve fibres that carry
cutaneous sensation terminate in the trigeminal nucleus.

Motor fibres of the facial nerve originate in the facial motor nucleus of the caudal pontine
tegmentum. The axons initially pass dorsally, looping over the abducens nucleus beneath the
floor of the fourth ventricle before leaving the brain stem in the motor root of the facial nerve.
Motor fibres are distributed to the muscles of facial expression, platysma, stylohyoid, the
posterior belly of the digastric muscle and the stapedius muscle of the middle ear.

The facial motor nucleus receives afferents from other brain stem areas for the mediation of
certain reflexes and also from the cerebral cortex. Reflex connections are established that
mediate protective eye closure in response to visual stimuli or tactile stimulation of the
cornea (corneal reflex) through fibres from the superior colliculus and trigeminal sensory
nucleus, respectively. In addition, fibres from the superior olivary nucleus, a part of the
central auditory pathway, subserve reflex contraction of the stapedius muscle in response to
loud noise.

Corticobulbar fibres from motor cortical areas innervate the facial motor nucleus. Those
controlling motor neurones that supply the muscles of the upper face (frontalis, orbicularis
oculi) are distributed bilaterally. Those which control the motor neurones supplying the
muscles of the lower face are entirely crossed. Unilateral upper motor neurone lesions,
therefore, give rise to paralysis of the lower facial muscles.
Preganglionic parasympathetic fibres of the facial nerve originate in the superior salivatory
nucleus of the pons. Fibres leave the brain stem in the sensory root of the facial nerve (nervus
intermedius). From here they pass to parasympathetic ganglia, namely the submandibular and
pterygopalatine ganglia, where they synapse with postganglionic neurones. Those from the
submandibular ganglion innervate the submandibular and sublingual salivary glands.
Postganglionic fibres from the pterygopalatine ganglion innervate the lacrimal gland and the
nasal and oral mucous membranes

Branches

Inside the facial canal

• Greater petrosal nerve- provides parasympathetic innervation to lacrimal gland,

sphenoid sinus, frontal sinus, maxillary sinus, ethmoid sinus, nasal cavity, as well as
special sensory taste fibers to the palate via the Vidian nerve.
• Nerve to stapedius - provides motor innervation for stapedius muscle in middle ear
• Chorda tympani - provides parasympathetic innervation to submandibular gland and
sublingual gland and special sensory taste fibers for the anterior 2/3 of the tongue.
• branch to the tympanic plexus

Outside skull (distal to stylomastoid foramen)

• Posterior auricular nerve - controls movements of some of the scalp muscles around
the ear
• Branch to Posterior belly of Digastric and Stylohyoid muscle
• Five major facial branches (in parotid gland) - from top to bottom:

1. Temporal (frontal) branch of the facial nerve

2. Zygomatic branch of the facial nerve
3. Buccal branch of the facial nerve
4. Marginal mandibular branch of the facial nerve
5. Cervical branch of the facial nerve

Test

Observe patient as he talks and smiles, watching for:

 • eye closure
• asymmetrical elevation of one corner of the mouth
• flattening of nasolabial fold

The patient is then instructed to

• wrinkle the forehead by looking upwards (frontalis)

• close the eyes while the examiner attempts to open them (orbicularis oculi)
• purse the lips while the examiner presses cheeks (buccinator)
• show teeth (orbicularis oris)

Taste may be tested by using sugar, tartaric acid or sodium chloride. A small amount of each
substance is placed anteriorly on the appropriate side of the protruded tongue.

Vestibulocochlear nerve

The vestibulocochlear nerve is a sensory nerve that conveys impulses from the inner ear. It
has two components.

1. the vestibule nerve which carries information related to position and movement of
head

2. the cochlear nerve which carries auditory information

The vestibulocochlear lies posterior to the origin of the facial nerve. This nerve reaches the
sensory receptors of the inner ear by entering the internal acoustic canal in company with the
facial nerve. Each vestibulocochlear nerve has 2 distinct bundles of sensory fibres.

1. The vestibular branch originates at the receptors of the vestibule ( portion of the inner
ear concerned with balance sensations). the sensory neurones are located in an
adjacent sensory ganglion and their axons target the vestibular nuclei of the pons and
medulla oblongata

2. The cochlear branch monitors the receptors in the cochlea (portion of the inner ear
that provides the sense of hearing). The cell bodies of the sensory neurones are
located within a peripheral ganglion- spiral ganglion. Their axons synapse within the
cochlear nuclei of the pons and medulla oblongata.
Test

Test by whispering numbers into one ear while masking hearing in the other ear by occluding
and rubbing the external meatus. If hearing is impaired, examine external meatus and the
tymphanic membrane with auroscope to exclude wax or infection.

Differentiate conductive (middle ear) deafness from perceptive deafnesss (nerve) Weber’s
and Rinne’s test.

Weber’s test

Hold base of tunning fork against the vertex and ask patient if sound is heared more loudly in
one ear. Normally, the sound should be equal in both ears. In conductive deafness, the sound
is louder in the affected ear since distraction from external sounds is reduced in that ear.
However, in nerve deafness the sound is louder in the normal ear.

Rinne’s test

Hold the base of a vibrating tuning fork against the mastoid bone. Ask the patient if note is
heard. When note disappears, hold tuning fork near the external meatus. Patient should hear
sound again since air conduction via ossicles is better than bone conduction. It should be
noted that in conductive deafness, bone conduction is better than air conduction. In nerve
deafness, both bone and air conduction is impaired.

Glossopharyngeal Nerve

The glossopharyngeal nerve is principally a sensory nerve, although it also contains

preganglionic parasympathetic and a few motor fibres. It attaches to the brain stem as a linear
series of small rootlets, lateral to the olive in the rostral medulla.

The afferent fibres of the glossopharyngeal nerve convey information from: receptors for
general sensation in the pharynx, the posterior third of the tongue, Eustachian tube and
middle ear, taste buds of the pharynx and the posterior third of the tongue, chemoreceptors in
the carotid body and baroreceptors in the carotid sinus.
Within the brain stem, afferent fibres for general sensation end in the trigeminal sensory
nucleus. Fibres carrying touch information from the pharynx and back of the tongue are
important for mediating the gag reflex, through connections with the nucleus ambiguus and
the hypoglossal nucleus. Visceral and taste fibres of the glossopharyngeal nerve terminate in
the nucleus solitarius of the medulla.

The motor component of the glossopharyngeal nerve is very small. It arises from cells in the
rostral part of the nucleus ambiguus of the medulla and innervates just one muscle, the
stylopharyngeus, which is involved in swallowing.

Preganglionic parasympathetic fibres in the glossopharyngeal nerve originate in the inferior

salivatory nucleus of the rostral medulla. These synapse with postganglionic neurones in the
otic ganglion, which in turn innervate the parotid salivary gland.

II- Vagus nerve

Rootlets of the vagus nerve attach to the lateral aspect of the medulla immediately caudal to
the glossopharyngeal nerve. The vagus contains afferent, motor and parasympathetic fibres.
The afferent fibres of the vagus convey information from: receptors for general sensation in
the pharynx, larynx, oesophagus, tympanic membrane, external auditory meatus and part of
the concha of the external ear, chemoreceptors in the aortic bodies and baroreceptors in the
aortic arch and receptors widely distributed throughout the thoracic and abdominal viscera.

Within the brain stem, receptors for general sensation end in the trigeminal sensory nucleus,
whilst visceral afferents end in the nucleus solitarius.
The motor fibres of the vagus arise from the nucleus ambiguus of the medulla. They
innervate the muscles of the soft palate, pharynx, larynx and upper part of the oesophagus.
The nucleus ambiguus is, therefore, crucially important in the control of speech and
swallowing. By convention, the most caudal efferents from the nucleus ambiguus are
regarded as leaving the brain stem in the cranial roots of the accessory nerve, but these
transfer to the vagus nerve proper at the level of the jugular foramen.

The parasympathetic fibres of the vagus nerve originate from the dorsal motor nucleus of the
vagus, which lies in the medulla immediately beneath the floor of the fourth ventricle. They
are distributed widely throughout the cardiovascular, respiratory and gastrointestinal systems.
Test for glossoharyngeal and vagus nerve

Note the patient’s voice for any vocal cord paresis which would manifest as a high pitched
voice. Ask the patient to open mouth and say ‘Ah’. Note any asymmetry of palatal
movements which indicate vagus nerve palsy.
Note any swallowing difficulty or nasal regurgitation of fluids.

Gag reflex

Depress patient’s tongue and touch palate, pharynx or tonsil on one side until the gags.
Compare sensitivity on each side and observe asymmetry of palatal contraction. Absent gag
reflex implies loss of sensation and/ or loss of motor power.

XI: Accessory nerve

The accessory nerve is purely motor in function. It consists of two parts: cranial and spinal.
The cranial part emerges from the lateral aspect of the medulla as a linear series of rootlets
that lie immediately caudal to the rootlets of the vagus nerve. The cranial root of the
accessory nerve carries fibres that have their origin in the caudal part of the nucleus ambiguus
of the medulla. At the level of the jugular foramen these fibres join the vagus nerve and are
distributed with it to the muscles of the soft palate, pharynx and larynx.
The spinal root of the accessory nerve arises from motor neurones located in the ventral horn
of the spinal grey matter at levels C1-C5. The axons leave the cord not through the ventral
roots of spinal nerves but via a series of rootlets that emerge from the lateral aspect of the
cord midway between the dorsal and ventral roots. These rootlets course rostrally, coalescing
as they do so, and enter the cranial cavity through the foramen magnum. At the side of the
medulla, the spinal root of the accessory nerve briefly joins the cranial root, but the
component fibres separate once again as the nerve leaves the cranial cavity through the
jugular foramen. Here the fibres of the cranial root of the accessory, which are derived from
the nucleus ambiguus, join the vagus and are distributed with it. The fibres of the spinal root
pass to the sternomastoid and trapezius muscles, which serve to move the head and shoulders.

Test

Sternomastoid
Ask patient to rotate head against resistance. Compare power and muscle bulk on each side.
Also compare each side with patient pulling head foward against resistance.

Trapezius

Ask patient to shrug shoulders and to hold them in this position against resistance. Compare
on each side. Patient should manage to resist any effort to depress shoulders.

XII: Hypoglossal nerve

The hypoglossal nerve is purely motor in function. It innervates both the extrinsic and
intrinsic muscles of the tongue and, therefore, serves both to move and to change the shape of
the tongue. The axons originate in the hypoglossal nucleus, which lies immediately beneath
the floor of the fourth ventricle, near the midline. Axons course ventrally through the medulla
and emerge from its ventrolateral aspect as a linear series of rootlets located between the
pyramid and the olive. The hypoglossal nucleus receives afferents from the nucleus solitarius
and the trigeminal sensory nucleus. These are involved in the control of the reflex movements
of chewing, sucking and swallowing. It also receives corticobulbar fibres from the
contralateral motor cortex, which subserve voluntary movements of the tongue such as occur
in speech.

Test

Ask the patient to open mouth and inspect tongue. look for evidence of atrophy (increased
folds and wasting) and fibrillation (small wriggling movements)
Ask patient to protrude and note any difficulty or deviation. Protruded tongue deviates
towards side of weakness.
REVIEW THE STRUCTURE AND FUNCTION OF
NEURONE , SYNAPSE AND SUPPORTING
TISSUES

NEURONE

The neurone is the basic structural and functional unit of the nervous system. The functions
of the neurone are to receive and integrate incoming information from sensory receptors or
other neurones and to transmit information to other neurones or effector organs. Neuronal
structure is highly specialised to fulfil these functions.
There is wide diversity in the shape and size of neurones in different parts of the nervous
system, but all share certain common characteristics. There is a single cell body from which a
variable number of branching processes emerge. Most of these processes are receptive in
function and are known as dendrites. They possess synaptic specialisations, sometimes many
thousands of them, through which they receive information from other nerve cells with which
they make contact. In sensory neurones, the dendrites may be specialised to detect changes in
the external or internal environment. One of the processes leaving the cell body is called the
axon or nerve fibre and this carries information away from the cell body. Axons are highly
variable in length and may divide into several branches or collaterals through which
information can be distributed to a number of different destinations simultaneously. At the
end of the axon, specialisations called terminal boutons occur; here information is
transferred to the dendrites of other neurones.
Information is coded within neurones by changes in electrical energy. The neurone at rest
possesses an electrical potential (the resting potential) across its membrane of the order of
60-70 millivolts, the inside being negative with respect to the outside. When a neurone is
stimulated or excited above a certain threshold level, there is a brief reversal of the polarity of
its membrane potential, termed the action potential. Action potentials are propagated down
the axon and invade the nerve terminals. Transmission of information between neurones
almost always occurs by chemical rather than electrical means. Information is passed
between neurones at specialised regions called synapses where the membranes of adjacent
cells are in close apposition.
 SYNAPSE

There are two major types of synapses: (1) the chemical synapse and (2) the electrical
synapse.

Almost all the synapses used for signal transmission in the central nervous system of the
human being are chemical synapses. In these, the first neuron secretes at its nerve ending
synapse a chemical substance called a neurotransmitter , and this transmitter in turn acts on
receptor proteins in the membrane of the next neuron to excite the neuron, inhibit it, or
modify its sensitivity in some other way. acetylcholine, norepinephrine, epinephrine,
histamine, gamma-aminobutyric acid (GABA), glycine, serotonin, and glutamate are well
known neurotransmitters.

Electrical synapses are characterized by direct open fluid channels that conduct electricity
from one cell to the next. Most of these consist of small protein tubular structures called gap
junctions that allow free movement of ions from the interior of one cell to the interior of the
next. it is by way of gap junctions and other similar junctions that action potentials are
transmitted from one smooth muscle fiber to the next in visceral smooth muscle and from one
cardiac muscle cell to the next in cardiac muscle .

Chemical synapses always transmit the signals in one direction: that is, from the neuron that
secretes the transmitter substance, called the presynaptic neuron, to the neuron on which the
transmitter acts, called the postsynaptic neuron. This is the principle of one-way conduction
at chemical synapses, and it is quite different from conduction through electrical synapses,
which often transmit signals in either direction. presynaptic terminals are the ends of nerve
fibrils that originate from many other neurons.

The presynaptic terminal is separated from the postsynaptic neuronal soma by a synaptic
cleft. The terminal has two internal structures important to the excitatory or inhibitory
function of the synapse: the transmitter vesicles and the mitochondria. The transmitter
vesicles contain the transmitter substance that, when released into the synaptic cleft either
excites or inhibits the postsynaptic neuron-excites if the neuronal membrane contains
excitatory receptors, inhibits if the membrane contains inhibitory receptors. The mitochondria
provide adenosine triphosphate (ATP), which in turn supplies the energy for synethesizing
new transmitter substance.
When an action potential spreads over a presynaptic terminal, depolarization of the synaptic
knob occurs. The depolarization of the synaptic knob opens voltage-gated calcium channels
causing calcium ions to rush into the knob. Their arrival triggers exocytosis and release of the
neurotransmitter into the synaptic cleft. The release of neurotransmitter stop very soon
because the calcium ions that triggered exocytosis are rapidly removed from the cytoplasm
by active transport. They are either pumped out of the cell or transferred into mitochondria,
vesicles, or endoplasmic reticulum. The released transmitter in turn causes an immediate
change in permeability characteristics of the postsynaptic neuronal membrane, and this leads
to excitation or inhibition of the postsynaptic neuron, depending on the neuronal receptor
characteristics.

The membrane of the postsynaptic neuron contains large numbers of receptor proteins. The
molecules of these receptors have two important components: (1) a binding component that
protrudes outward from the membrane into the synaptic cleft-here it binds the
neurotransmitter coming from the presynaptic terminal-and (2) an ionophore component that
passes all the way through the postsynaptic membrane to the interior of the postsynaptic
neuron. The ionophore in turn is one of two types: (1) an ion channel that allows passage of
specified types of ions through the membrane or (2) a "second messenger" activator that is
not an ion channel but instead is a molecule that protrudes into the cell cytoplasm and
activates one or more substances inside the postsynaptic neuron. These substances in turn
serve as "second messengers" to increase or decrease specific cellular functions.

Ion Channels

The ion channels in the postsynaptic neuronal membrane are usually of two types: (1) cation
channels that most often allow sodium ions to pass when opened, but sometimes allow
potassium and/or calcium ions as well, and (2) anion channels that allow mainly chloride ions
to pass but also minute quantities of other anions.
When the cation channels open and allow positively charged sodium ions to enter, the
positive electrical charges of the sodium ions will in turn excite this neuron. Therefore, a
transmitter substance that opens cation channels is called an excitatory transmitter.
Conversely, opening anion channels allows negative electrical charges to enter, which
inhibits the neuron. Therefore, transmitter substances that open these channels are called
inhibitory transmitters. After a neurotransmitter molecule has been recognized by a post-
synaptic receptor, it is released back into the synaptic cleft. Once in the synapse, it must be
quickly removed or chemically inactivated in order to prevent constant stimulation of the
post-synaptic cell and an excessive firing of action potentials.

SUPPORTING TISSUES

Neurones are delicate, highly specialised structures and require support and protection. This
is afforded to them in the nervous system by specialised connective tissue called neuroglia. If
neurones are damaged and destroyed their place is filled by proliferation of neuroglial
material.
The axons are surrounded by a fatty sheath called myelin which has an important effect on
the conduction of impulses. Because of this sheath, bundles of axons give a whitish
appearance and form the white matter of the central nervous system.
Outside the central nervous system nerve fibres are surrounded by a membrane called the
neurilemma. The latter may regenerate if they are destroyed
REVIEW THE ORGANISATION AND FUNCTION OF :
CEREBRAL HEMISPHERES

The cerebral hemisphere is the largest part of the forebrain. Superficially, the cerebral
hemisphere consists of a layer of grey matter, the cerebral cortex, which is highly convoluted
to form a complex pattern of ridges (gyri) and furrows (sulci). This serves to maximise the
surface area of the cerebral cortex.

The vast majority of those nerve fibres that pass between the cerebral cortex and subcortical
structures are condensed, deep within the hemisphere, into a broad sheet called the internal
capsule. Buried within the white matter lie a number of nuclear masses, most notably the
caudate nucleus, putamen and globus pallidus, known collectively as the basal ganglia.

The two cerebral hemispheres are separated by a deep cleft, the great longitudinal fissure,
which accommodates the meningeal falx cerebri. In the depths of the fissure, the
hemispheres are united by the corpus callosum, an enormous sheet of commissural nerve
fibres which run between corresponding areas of the two cortices.

Certain gyri and sulci on the surface of the hemisphere divide it into four lobes, namely the
frontal, parietal, temporal and occipital lobes.

The lateral fissure separates the temporal lobe below, from the frontal and parietal lobes
above. The central sulcus marks the boundary between the frontal and parietal lobes.
The frontal lobe constitutes the entire region in front of the central sulcus. Immediately in
front of the sulcus, and running parallel to it, lies the precentral gyrus, which is the primary
motor region of the cerebral cortex.

Behind the central sulcus, and above the lateral fissure, lies the parietal lobe. Its most anterior
part is the postcentral gyrus, which is the site of the primary somatosensory cortex. Behind
this region lies the sensory association cortex, which is responsible for the interpretation of
general sensory information.
The temporal lobe lies beneath the lateral fissure. On the superior surface of the superior
temporal gyrus, the transverse temporal gyri mark the location of the primary auditory cortex.
Adjacent lies the auditory association cortex, which is responsible for the interpretation of
auditory information and which, in the left hemisphere, constitutes Wernicke's area. It is
crucial for understanding of the spoken word and has important connections with other
language areas of the brain.

The occipital lobe makes up the posterior part of the hemisphere. On the medial surface, the
calcarine sulcus indicates the location of the primary visual cortex. The rest of the occipital
lobe is the visual association cortex, which is responsible for the interpretation of visual
information.

Beneath the cortical surface lies an enormous mass of nerve fibres, all of which have their
origin or termination, or sometimes both, within the cortex. The fibres are classified into
three types, depending upon their origin and destination:

• association fibres, which interconnect cortical sites lying within one cerebral
hemisphere.
• commissural fibres, which run from one cerebral hemisphere to the other, connecting
functionally related structures.
• projection fibres, which pass between the cerebral cortex and subcortical structures
such as the thalamus, striatum, brain stem and spinal cord.
(A) Lateral aspect of the cerebral hemisphere showing major functional areas.

(B) Median sagittal section of the cerebral hemisphere showing major functional areas.
THE CEREBELLUM

The cerebellum is the largest part of the hindbrain. It originates from the dorsal aspect of
the brain stem and overlies the fourth ventricle. The cerebellum is connected to the brain
stem by three stout pairs of fibre bundles, called the inferior, middle and superior
cerebellar peduncles; these join the cerebellum to the medulla, pons and midbrain,
respectively. The functions of the cerebellum are entirely motor and it operates at an
unconscious level. It controls the maintenance of equilibrium (balance), influences posture
and muscle tone, and coordinates movement. The cerebellum consists of a midline vermis
and two laterally located hemispheres. Anatomically, the cerebellum is divided into
anterior, posterior and flocculonodular lobes.The cerebellum basically consists of an outer
layer of grey matter, the cerebellar cortex, and an inner core of white matter. The
cerebellar cortex is highly convoluted, forming numerous transversely oriented folia.
Within the cortex lie the cell bodies, dendrites and synaptic connections of the vast
majority of cerebellar neurones. The white matter is made up largely of afferent and
efferent fibres that run to and from the cortex and towards which it extends irregular,
branch-like projections . Buried deep within the white matter are four pairs of cerebellar
nuclei, which have important connections with the cerebellar cortex and with certain
nuclei of the brain stem and thalamus.

The cerebellum is often regarded as consisting of three functional subdivisions

• The archicerebellum corresponds to the flocculonodular lobe and fastigial

nucleus. Its principal connections are with the vestibular and reticular nuclei of the
brain stem and it is concerned with the maintenance of equilibrium.
• The paleocerebellum corresponds to the vermis and paravermal area, together
with the globose and emboliform nuclei. It receives fibres from the spinocerebellar
tracts and projects to the red nucleus of the midbrain.
• The neocerebellum corresponds to most of the cerebellar hemisphere and the
dentate nucleus. It receives afferents from the pons and projects to the ventral lateral
nucleus of the thalamus.
• Cerebellar lesions cause incoordination of the upper limbs (intention tremor),
lower limbs (cerebellar ataxia), speech (dysarthria) and eyes (nystagmus).
At the roots of the upper and lower limbs are located the brachial plexus and the
lumbosacral plexus, respectively. Here, the nerve fibres present in spinal nerves
become redistributed to form named peripheral nerves, which then run distally to their
targets. The distribution of peripheral nerves is, therefore, different from that of spinal
nerves.

Each spinal nerve carries the sensory innervation for a part of the body surface. The
area of skin that is supplied by a particular spinal nerve is known as a dermatome.
The group of skeletal muscles innervated by a particular spinal nerve is collectively
known as a myotome. These muscles are usually functionally related and are
responsible for particular patterns of movement.

Classification of peripheral nerve injuries

The Seddon’s classification of nerve injuries is a useful guide where nerve injuries are
categorised as neurapraxia, axonotmesis and neurotmesis.

Neurapraxia

It is a temporary block to conduction and interruption of physiological function without

disturbance of its anatomy or Wallerian degeneration. Neurapraxia affects mainly the
larger myelinated fibres. Some modalities of sensations are spared. Motor fibres are the
largest and the most vulnerable, therefore motor loss is often complete. Distal nerve
conduction is spared. There is absence of fibrillation potentials in paralysed muscles. It
is caused by compression, concussion or traction of the nerve. It may also be caused by
intermittent or short duration ischaemia. Spontaneous recovery is usually rapid and
complete.

Axonotmesis

It is the disruption of axons followed by wallerian degeneration. The connective tissue

sheaths of the nerve remains intact that is the endoneurium and perineurium. There is
complete motor and sensory loss. It is more commonly caused from closed fractures or
dislocations, traction lesions and ischaemic injuries. Recovery is always better in
axonotmesis compared to neurotmesis mainly due to intact connective tissue
framework.

Neurotmesis

In neurotmesis, the axon, Schwann cell, myelin sheath and connective tissue scaffold of
the nerve are severed. There is complete motor and sensory loss. It is caused by violent
traction force or in open wounds. Recovery is usually poor and requires surgical repair.

1- neurapraxia
2- axonotmesis
3- axonotmesis
4- neurotmesis: discontinuity in perineurium
 5- neurotmesis: transectin injury.

THE PYRAMIDAL SYSTEM

The most important output pathway from the motor cortex is the corticospinal tract,
also called the pyramidal tract. The corticospinal tract originates about 30 per cent from
the primary motor cortex, 30 per cent from the premotor and supplementary motor
areas, and 40 per cent from the somatosensory areas posterior to the central sulcus.
After leaving the cortex, it passes through the posterior limb of the internal capsule
(between the caudate nucleus and the putamen of the basal ganglia) and then downward
through the brain stem, forming the pyramids of the medulla. The majority of the
pyramidal fibers then cross in the lower medulla to the opposite side and descend into
the lateral corticospinal tracts of the cord, finally terminating principally on the
interneurons in the intermediate regions of the cord gray matter; a few terminate on
sensory relay neurons in the dorsal horn, and a very few terminate directly on the
anterior motor neurons that cause muscle contraction.
A few of the fibers do not cross to the opposite side in the medulla but pass ipsilaterally
down the cord in the ventral corticospinal tracts. Many if not most of these fibers
eventually cross to the opposite side of the cord either in the neck or in the upper
thoracic region. These fibers may be concerned with control of bilateral postural
movements by the supplementary motor cortex.
THE EXTRA PYRAMIDAL SYSTEM

The extrapyramidal system is a neural network located in the brain that is part of the
motor system involved in the coordination of movement. The system is called
"extrapyramidal" to distinguish it from the tracts of the motor cortex that reach their
targets by traveling through the "pyramids" of the medulla. The pyramidal pathways
(corticospinal and some corticobulbar tracts) may directly innervate motor neurons of
the spinal cord or brainstem (anterior(ventral) horn cells or certain cranial nerve
nuclei), whereas the extrapyramidal system centers around the modulation and
regulation (indirect control) of anterior(ventral) horn cells.
Extrapyramidal tracts are chiefly found in the reticular formation of the pons and
medulla, and target neurons in the spinal cord involved in reflexes, locomotion,
complex movements, and postural control. These tracts are in turn modulated by
various parts of the central nervous system, including the nigrostriatal pathway, the
basal ganglia, the cerebellum, the vestibular nuclei, and different sensory areas of the
cerebral cortex. All of these regulatory components can be considered part of the
extrapyramidal system, in that they modulate motor activity without directly
innervating motor neurons.

REVIEW THE FACTORS INFLUENCING ALPHA

MOTOR NEURONE ACTIVITY

There are two categories of lower motor neurones of the spinal cord: alpha motor
neurones (α-MNs) and gamma motor neurones. The α-MNs directly trigger the
generation of forces by muscles. One α-MN and all the muscle fibres it innervates
collectively make up the elementary component of motor control; motor unit. Muscle
contraction results from the individual and combined actions of these motor units. The
collection of α-MNs that innervates a single muscle is called a motor neuron pool.

The nervous system uses several mechanisms to control the force of muscle contraction
in a finely graded fashion. The first way the CNS controls muscle contraction is by
varying the firing rate of motor neurones. An α-MN communicates with a muscle fiber
by releasing the neurotransmitter acetylcholine (ACh) at the neuromuscular junction,
the specialised synapse between a nerve and a skeletal muscle. Because of the high
reliability of neuromuscular transmission, the ACh released in response to one
presynaptic potential cause an excitatory postsynaptic potential in the muscle fibre
(endplate potential) large enough to trigger one postsynaptic action potential. By
mechanisms, a post synaptic action potential causes a twitch- a rapid sequence of
contraction and relaxation- in the muscle fibre. A sustained contraction requires a
continual barrage of action potentials. High frequency presynaptic activity causes
temporal summation of the postsynaptic responses, as it does for other types of synaptic
transmission. Twitch summation increases the tension in the muscle fibre and smoothes
the contraction. The rate of firing of motor units is therefore one important way the
CNS grades muscle contraction.

A second way the CNS grades muscle contraction is by recruiting additional synergistic
motor units. The extra tension provided by the recruitment of an active motor unit
depends on how many muscle fibers are in that unit. Muscles with a large number of
small motor units can be more finely controlled by the CNS.

Input to motor neurons from descending neurons and afferent neurons is transferred via
interneurons. Local Interneurons are confined to the general region of the motor neuron
on which they synapse. Some interneurons have processes extending up or down either
short or long distances within the CNS. Longer processes are important in coordinating
actions that involve movement of both an arm and a leg. Shorter processes are involved
in movements of only a smaller region of the body like the shoulder. Local interneurons
integrate information at the local level from higher centers of the motor control
hierarchy, peripheral receptors, and other interneurons. Interneurons can help overcome
a reflex motion i.e.. overriding the local reflex arc involved with dropping a hot object
if it is something of importance. Motor neurons can only cause an excitatory synapse
on a muscle cell. Interneurons can make inhibitory or excitatory synapses on motor
neurons or other interneurons, thus further refining movement.
Local afferent fibers bring information to the interneurons from
1) The muscles controlled by the interneurons
2) Other nearby muscles
3) Tendons, joints, and skin surrounding the muscle

Receptors at the end of the afferent neurons monitor length and tension in muscles,
movement of joints, pressure on the skin.
REVIEW THE NEUROLOGICAL BASIS OF MUSCLE
TONE AND MOVEMENT AND DEMONSTRATE
HYPOTONIA, HYPERTONIA, RIGIDITY, ATAXIA,
ATHETOSIS, CHOREA.

The skeletal system supports the body in an erect posture with the expenditure of
relatively little energy. However, even at rest, muscles normally exhibit some level of
contractile activity. Isolated (i.e., denervated) unstimulated muscles are in a relaxed
state and are said to be flaccid. However, relaxed muscles in the body are
comparatively firm. This firmness, or tone, is caused by low levels of contractile
activity in some of the motor units and is driven by reflex arcs from the muscle
spindles. Interruption of the reflex arc by sectioning the sensory afferent fibers will
abolish this resting muscle tone. Resistance of skeletal muscle to passive stretch
occurs due to viscoelastic properties of muscle and joints and the degree of alpha
motor neuron activity. Increased alertness results in higher alpha motor
neuron activity and increased muscle tone

MOTOR CONTROL BY THE CEREBRAL CORTEX,

CEREBELLUM, AND BASAL GANGLIA

The lateral corticospinal tract is the most important descending pathway for fine
movements that use distal muscles, such as those that control the hand and fingers. A
portion of the corticobulbar tract is important for the control of facial and tongue
movements. However, many other pathways are also engaged to activate more
proximal and axial muscles.

Before any movement occurs, commands carried by descending motor pathways must
first be organized in the brain. The target of the movement is identified by pooling
sensory information in the posterior parietal cerebral cortex. This information is
then transmitted to the supplementary motor and premotor areas, where a motor plan
is developed. The plan includes information about the specific muscles that need to be
contracted, the strength of the contraction, and the sequence of contraction. The motor
plan is implemented by commands transmitted from the primary motor cortex through
the descending pathways. Successful execution of these motor commands, however,
depends on feedback provided to the motor cortex through the ascending pathways to
the somatosensory cortex, as well as through the visual pathway. During the planning
and execution stages of a movement, motor processing is provided by two major
motor control systems, the cerebellum and the basal ganglia

The cerebellum helps regulate movements and posture, and it plays a key role in some
forms of motor learning. Note that removal of the cerebellum affects neither sensation
nor muscle strength. The cerebellum influences the rate, range, force, and direction of
movements. Therefore, damage to the cerebellum disturbs the coordination of
movements.

The cerebellum helps regulate the vestibuloocular reflex, and it participates in the
improvements in motor performances that result from practice of motor skills.
Therefore, the cerebellum is thought to be involved in motor learning.

The cerebellum exerts its motor control on a moment-by-moment basis. It uses

sensory information from various sources, most prominently from the proprioceptive
system, to update its computations of body position, muscle length, and muscle
tension. The cerebellum may be able to compare this sensory feedback with neural
signals that are transmitted to the cerebellum from the motor areas of the cerebral
cortex and that represent the desired motor act. Errors are corrected by output signals
from the cerebellum to other components of the motor system.

The basal ganglia are the deep nuclei of the cerebrum. In association with other nuclei
in the diencephalon and midbrain, the basal ganglia differ from the cerebellum in the
way they regulate motor activity. Unlike the cerebellum, the basal ganglia do not
receive an input from the spinal cord, but they do receive direct input from the
cerebral cortex, unlike the cerebellum. The main action of the basal ganglia is on the
motor areas of the cortex by way of the thalamus. In addition to their role in motor
control, the basal ganglia contribute to affective and cognitive functions. Lesions of
the basal ganglia produce abnormal movements and posture

Hypotonia

It is the reduction in preparedness for action found in the muscles when there are
defects in certain areas of the extrapyramidal part of the central nervous system. The
excitatory influence exerted by the extrapyramidal system upon the motoneurone
pools is diminished and as a result the muscles show a reduction in sensitivity to
stretch. Hypotonia may be confused with muscle paralysis initially because the
muscles appear to be flail. The muscles have a normal motor neurone supply but the
factors exerting an influence upon the motoneurone pools are seriously disturbed. The
stretch reflex mechanism will be slugghish. Hypotonia never affects muscle groups in
isolation because it is not a peripheral problem. The common cause of hypotonia is
disturbance in function of the cerebellum. It may be the result of damage or disease in
the cerebellum itself or in the links between the cerebellum and the brainstem extra-
pyramidal mechanism.

Hypertonia

It is the opposite of hypotonia. There are two types of hypertonia, spasticity and
rigidity. Muscles show a physiological resistance to passive motion. This is called
muscle tone. Spasticity is the increase in this physiological muscle tone. The faster the
passive movement, the greater the resistance of the muscle. The increase in muscle
tone causes loss of trunk balance and difficulty of active movement in the extremities.
The pathogenesis of spasticity is presumed to be an increase in the excitability of the
lower motor neuron. This presents as hyperactive stretch reflexes at clinical
examination. Hhyperexcitability is thought to be due to a change in the balance of
excitatory and inhibitory inputs to the motor neuron pool. When the inhibitory inputs
are reduced, the interneurons send excitatory impulses to the lower motor neurons and
they become hyperexcitable.

Rigidity
It is a type of hypertonicity and is manifested as co contraction of agonist and
antagonist muscles. An increase in the supraspinal system causes an increase in tone
of the agonist and the antagonist.

Rigidity is of two types.

1. leadpipe: when the limb is moved passively, the resistance is present to the

same degree throughout the full range of movement, affecting flexor and
extensor muscle groups equally.

2. cogwheel: this occurs when tremor is superimposed upon rigidity.

Athetosis
It is a disorder of movement because of fluctuation in the level of postural fixation.
The patient adopts a succession of abnormal postures which may be quite grotesque.
The condition is made more severe by excitment and emotional stress. It is thought to
be due lesions within the basal ganglia (putamen). The basal ganglia fail in their
ability to encourage adequate postural fixation and fluctuations therefore occur.

Chorea
This is a series of involuntary movements which occur in the face and limbs. They are
quicker than athetosis and are made worse by voluntary movement. the basal ganglia
are considered to be at fault.
Differentiate between Bell’s palsy and facial
palsy
A LMN lesion of CN VII which occurs at or beyond the stylomastoid foramen is
commonly referred to as a Bell's Palsy. facial palsy occurs a a result of an upper motor
neurone lesion. A unilateral UMN lesion usually spares the forehead as it is also
innervated from the other side of the brain (part of facial nucleus supplying the upper
face principally the frontalis muscle receive the supranuclear fibers from each
hemisphere); however an LMN lesion affects all of one side of the face.

An upper motor neuron lesion causes weakness of lower part only of face on the side
opposite the lesion. The frontalis muscle is spared; the normal furrowing of the brow
is preserved, and the eye closure and blinking are not affected. The earliest sign is
simply slowing of one side of the face, for example on baring the teeth or smiling.
Moreover, in upper motor neuron lesion there relative preservation of spontaneous
'emotional' movement (e.g. smiling) compared with voluntary movement.

A unilateral lower motor neuron lesion causes weakness of all the muscles of facial
expression on the same side. The face, especially the angle of the mouth, falls, and
dribbling occurs from the corner of the mouth. There is weakness of the frontalis and
of eye closure since the upper facial muscles are weak. Corneal exposure and
ulceration occurs if the eye does not close during sleep. The platysma muscle is also
weak.