Thursday, September 23, 2010

9.12 The Cranial Nerves - Smell/Vision/Eye/Face/Visceral/Taste

Physician's Notebooks 9 - - See Homepage

12. The Cranial Nerves, Update 22 April 2018
(This is one of several chapters that because packed with much new information is best read slowly, in short segments, and re read as needed, and supplemented by internet Wikipedia when clarification needed)
The following headings in descending order as they appear should help orient readers and also, by search & find or scroll down, help a reader locate a particular subject of interest
What Are the Cranial Nerves?
CN I: Olfactory (Smell) Nerve
CN II: Optic Nerve
Dark & Color Vision
Critical Period for Eye Vision Deprivation
Cranial Nerves III, IV and VI
CN V: Trigeminal Nerve
CN VII: Facial Nerve
CN VIII: Vestibulocochlear (hearing & balance)
CN IX: Glossopharyngeal (Tongue and Throat) Nerve
CN X: Vagus Nerve
The Taste Sense
CN XI: Spinal Accessory (Shrug Shoulder) Nerve
CN XII: Hypoglossal (Tongue Movement)

What Are the Cranial Nerves? They are peripheral nerves of the head and neck. They originate in nerve nuclei in the brainstem and exit the cranium (cranium is the full skull consisting of all the bones in the head) from its base. They send commands to muscles in head and neck, and innervate the body's glands, and they receive sensory signals to and from the periphery and the inner organs and head. The cranial nerve cords are mixed nerves; muscle, gland, sensory and autonomic. Essentially the cranial nerves are a continuation (in the head), of the 31 pairs of the spinal nerves. Their functions are focused on the head and its contents. 
       Cranial nerves II, III, IV, V, and VI exit the skull at the base of the brain. The optic (CN II) nerve enters the optic foramen (See diagram just below), and the oculomotor (III), trochlear (IV), and abducens (VI) nerves, and the first division of the trigeminal (V) nerve leave through the superior orbital fissure. The second and third divisions of the trigeminal nerve exit the cranium through the round and oval foramina, respectively.
     In the posterior fossa (compartment), the facial (VII) and vestibulocochlear (VIII) nerves exit through the internal auditory canal, whereas the glossopharyngeal (IX), vagus (X), and accessory (XI) nerves leave it through the jugular foramen. The hypoglossal nerve (XII) has its own foramen. 

The Figure shows the origin and exit points of the cranial nerves at the base of the skull.

Image not available.
Because of common exit canals in the lower part of the skull, in basal skull fractures, the cranial nerves are easily damaged in groups of 2 or 3, giving a particular syndrome of signs and symptoms, and because of being bathed in cerebral spinal fluid they are liable to spread infection to the brain and be damaged by increased pressure inside the brain. 

The figure just below contains a ventral and lateral view, and locates the cranial nerves as they emerge from and exit the brainstem. Particularly note the trochlear nerve (CN IV) because of its exceptional dorsal exit from the brainstem.

Image not available.

The neurons that are the final station in a cranial nerve are located in ganglia (singular, ganglion) just before or after exit from cranium. The controlling neurons of each cranial nerve, except CN 1 and CN II (Smell & vision), are in the floor of the brainstem in groups called nuclei (Singular, nucleus).
The functional types are: Special sensory; CN I (smell), CN II (vision), CN VIII (hearing & balance), and also there is taste (by branches of CN V, CN VII, CN IX and CN X).  Eye movement and pupil constriction and dilation; CN III, CN IV & CN VI. Head and neck, brow and face sensory and chewing muscles (CN V). Face muscles (CN VII) and throat control (CN IX). Visceral organ functions; body visceral function and lung and heart action (CN X). Shoulder shrugging, neck turning (CN XI). And tongue control (CN XII). Note that the sense of taste is carried in 4 cranial nerves, but its primary neurons are all in one nucleus in the brainstem called the solitary nucleus. It will be dealt with under taste and not as a single cranial nerve.
 CN I: Olfactory (Smell) Nerve. The receptor smell-bodies are extensions of smell neurons embedded in the upper nostrils and are in the nostril mucous membrane. These smell-bodies are the first neuron part to contact the chemicals that make a smell and each smell-body is in the end-part of a single fiber that starts the chemical signal back to its neuron, and the neuron sends the signal on, in an axon, that synapses (connects & transmits) with a neuron in the olfactory bulb at the underpart of the front base of the brain behind the eyebrow bone. Already, at the entry into the olfactory bulb, the various smells are sorted out. Each basic smell come from a pure chemical compound like ethyl alcohol, which is sharp and distinctive. There are a number of basic smells and each smell-body is coded for one or a very few basic smells. The usual smells of our life are mixtures - in food, body materials, etc. - and how we respond to them comes from our psychological conditioning as well as inborn factors, learned by the species through millions years of evolution. In the olfactory bulb, the smells of a substance are combined and their signals pass back in the olfactory tract to the brain's olfactory cerebral cortex which makes us conscious of what we smell and how we react to a smell. (Smell is the only one of the senses that initially goes directly from its peripheral receptor to the cerebral cortex, bypassing the brain's thalamus) So, the sense of smell is very direct and can be sharp.
 The sense of smell is represented bilaterally (both left & right nostril source in each left and right brain) because there is bridging of fibers going to the cerebrum from right and left olfactory bulbs. Thus, a tumor or artery blockage in one side of brain will not result in one-sided smell loss or much smell loss at all. The consciousness of smells is in the right and left frontal lobe cerebral cortex neurons inside and at bottom inside (median aspect) of each hemisphere in a structure - the Uncus. Epileptic seizures from the Uncus give the afflicted patient a sense of a weird smell. (The famous American musical composer, George Gershwin, first discovered his deadly brain tumor by having a strange smell from his uncus epileptic seizure while giving a piano recital in 1939. By the way, this proves that our perception of smells comes from inside our brain rather than from the outside air where the chemical that makes the smell is coming from).
Smell affects on food taste. Without smell we are unable to taste coffee, chocolate, wine and other fragrant foods. To best enjoy food, one should do a clearing of the nose by blowing one's nose out just before eating. 
The olfactory receptors and the smell fibers get replaced every 60 days but in old age they gradually get less replaced, so an old person has a less keen sense of smell and a poorer sense of food taste than when young, and it explains the increasing desire, as one gets older, to spice food and the aging desire for kinkier smell-connected pleasure.
 Because the millions of olfactory nerve fibers and the main nerves are direct outgrowths from the brain, they are encased in brain membrane sheath with cerebrospinal fluid. The nerve fibers extend to less than a millimeter from the nasal mucus membrane in the nostrils and so the bacteria in nose may easily spread back into the brain causing meningitis and brain abscess. Especially picking in or pressing on the nostrils can push infectious bacteria back into the brain. Despite this, most persons do not get brain infections because of a good immune system but in old age or in immune-weakening diseases like HIV-AIDS this is high risk. So, try to get out of habit of touching your nose and if you get a nasal local infection (boils and raw ulcers) treat it by strong antibiotic. 
Special note- pheromones and smell:  In almost all higher animals but to a lesser extent in humans, a class of chemical secretions called pheromones interact with the sense of smell to affect behavior, especially sexual behavior. Such pheromones have been detected in underarm sweat and vaginal secretions and stimulate sexual desire in males. The pheromone chemical from a woman's underarm or vagina interacts with nasal mucous membrane cells in men and these cells release chemical into the blood - bypassing the nervous system - that is one source to motivate lust in a man towards the woman. Cultural conditioning has made the affects of these pheromones minor in humans but still their effect has some affect on sexual behavior. The perfumes and colognes make use of this effect.

CN II: Optic Nerve: (Note: Also refer to  5.8 Eyes and Vision)The eye retina is the inside surface of the rear cup of the eyeball. The below figure shows a hemisphere view of the cup. It is what the eye doctor sees through an ophthalmoscope. Actually, the retina is not flat but concave with maximal depth at the central point, where the macula lutea is labeled below.

 Retina of left eye: The optic disc is off center to your left. The macula lutea is located at central axis of incoming visual image and contains no visual rod neurons and is very sparse in blue color cone neurons. It is the point of best red-yellow, near-vision focus, and its center point, a depression is called the fovea (Not labeled above).
  Below, a micro section of layers of retina. The surface (inner, closest to incoming light ray) is its top here. The neuron fibers, axons, that will form the optic nerve are running horizontally at top after extending out of the retina-ganglion cell bodies. The image light rays must penetrate between the surface fibers and all the layers down to the outer layer rods and cones.
   The layers of the retina cup (Layer number or letter on your left in the figure): At the very bottom (page orientation) part of the outer layer is the P-layer. Just above it, are the neurons whose downward extensions are the solid black rods or thin black-outlined white cones (in layer 1). The rods and cones are light-sensitive pigmented bodies. 
   The origin of the light signal in images formed in your eyes starts with a minimum light ray (a photon) falling on the smallest segment of retina, and exciting a rod cell. Interestingly, of all the sensory receptor cells, the light-sensitive rods and cones in the retina are the only sensory modality (cf. hearing, touch balance) whose electrical apparatus is constantly in a turned-on state. That is, in the dark the electrical apparatus of the cone or rod cell is in a turned-on state, ie, it has open Na+ channels allowing Na+ to enter the cell and depolarize the inner membrane which results in the release of neurotransmitter glutamate. But as soon as a ray of light penetrates the cell, it energizes the closure of the Na+ channels resulting in a reversal of Na+ entering the cell and a hyperpolarization and a stopping of glutamate release which then triggers the retinal ganglion cell action potential that moves along its axon that forms the optic nerve, as a light-on signal. The reason for this opposite to the usual sensory receptor state, ie, the turned-on state in the dark, seems to be the need for a very speedy response to light signals. It is just as if you kept your car engine turned on and purring in order to make a very quick getaway in your car. The light causes a hyperpolarization electric impulse that is turned into a light signal in the rod or the cone, and the signal gets passed up to a connected bipolar cell and then in the next layer cells, the ganglion cells, the signal spikes an action potential (AP) that passes on along its fiber, and the many fibers of which you see in the above form the optic nerve (See in Figure, running parallel along the surface to the optic disc where they combine to start the optic nerve of the eye).
  The rods are extremely sensitive to very low light so they are what we depend on for night vision while the cones pick up strong light and express color wavelengths.
   Also shown in layer 3 (black) and layer 4 (green) are interneurons with horizontal running fibers that inhibit or excite the electrical impulses from the rods and cones at the levels of the bipolar and retina-ganglion cells.
   The light-impulse signals are a multiple, complex type called "center-surround." For each receptive field light-on impulse there is a light-off impulse for the contiguous visual fields surrounding the one spot of the image that is illuminated by the minimal spot of light. This is known as lateral inhibition and makes a contrast for the image. Also there are different kinds of receptive visual fields, eg, for color, for motion, etc.
The figure below shows the visual field pathway: At leisure a reader should study this figure and its explanations. (The below schematic)

Image not available.

Each eye sees most of the visual field, with the exception of a portion of the peripheral visual field labeled in the above as the monocular crescent. The axons of retinal neurons (ganglion cells) carry information from each visual hemifield along the optic nerve up to the optic chiasm, where fibers from the nasal hemiretina cross to the opposite hemisphere. Fibers from the temporal hemiretina stay on the same side, joining the fibers from the opposite side nasal hemiretina to form the optic tract. The tract carries information from the opposite visual hemifield and projects into the lateral geniculate nucleus in the thalamus...Cells in this nucleus send their axons along the optic radiation to the primary visual cortex.
Lesions along the visual pathway produce specific visual field deficits, as shown on the reader's right: in the Figure.
1. A lesion of an optic nerve causes a total loss of vision in the same-side eye.
2. A pressure lesion (eg, tumor) at the optic chiasm causes a loss of vision in the temporal half of each visual hemifield (bitemporal hemianopsia).
3. A complete lesion of the optic tract causes a complete loss of vision in the opposite-side half of the visual hemifield (the side of you that sees in opposite direction to the side of the lesion; contralateral hemianopsia).
4. A lesion of the optic radiation fibers that curve into the temporal lobe causes loss of vision in the upper quadrant of the contralateral visual hemifield in both eyes (upper contralateral quadrantic anopsia).
5,6. Partial lesions of the visual cortex lead to deficits in portions of the contralateral visual hemifield. For example, a lesion in the upper bank of the calcarine sulcus (5) causes a partial deficit in the inferior quadrant, while a lesion in the lower bank (6) causes a partial deficit in the superior quadrant. The central area of the visual field tends to be unaffected by cortical lesions because of the extent of the representation of the fovea and the duplicate representation of the vertical meridian in the hemispheres.

(Rejoin main text) The optic nerve (ON) originates in the fibers from the retina-ganglion cell neurons. The light impulse of a retinal receptive field (smallest unit of the visual field that has the part of the image from a single rod or cone cell) starts with a ray (photon) of light stimulating a rod or cone end-body and that causes a change in electrical change leading to a change in neurotransmitter output in the rod or cone retinal cell and that impulse passes on to the connected bipolar cells and then to a connected retina-ganglion cell where an action potential starts the moving signal in its axon. There is much inhibition and excitation and other affects on these retinal neuron connections by the retinal interneurons, and contrast comes from this effect.   
   The retina-ganglion parallel surface fibers all gather together at the optic disc to form the optic nerve of one eye. The optic nerve continues until the optic-chiasm crossing and then it becomes the optic tracts leading to the lateral geniculate nuclei in the thalamus. During this whole passage of the photon signal to the thalamus, each signal from a separate rod or cone type is kept on its own line, aka the labeled line. In the cerebral cortex visual area these lines are combined to make the final vision we experience in our consciousness. Additional to consciousness, the visual signals travel to other midbrain nuclei to make the visual and pupil reflexes, the quick eye movements, and to act as a body clock.
  Concerning the Rods & Cones and High Intensity Light, Low-Light and Dark & Color Vision: There is only one type of rod cell. The rods are all located outside the central vision point macula lutea, or its central pit the fovea, which only contains cones. The rods respond maximally to low-intensity light and do not show color; they are solely for black and white, low-intensity image vision (twilight/night vision).
   An interesting phenomenon, known mostly to astronomers, is the in-the-dark blindspot. Because no rods are in the central vision point of your eyes, a dark object cannot be detected in the central receptive field, ie, if you try to look directly at a star in the sky at night, you will find you have a near central blindspot for it. Note that this spot is separate from the normal blindspot of your optic discs, which is off to the side toward your nose.
   Also, the visual rods are only attached and transmit impulses to retinal-ganglia very small cells (parvocellular) compared to the cones, which attach to a family of much larger cells (magnocellular). As mentioned above, a light impulse from a rod  or from a cone  is separated, starting from each one's very origin and each type impulse runs a parallel course into the brain in what are called labeled lines. The parallel courses of the types of light impulses - the one from the rods passing-on low-intensity light, with contrasts and no colors; and the other from the cones passing-on high-intensity light and the colors - stay separated through the course of the left and right optic nerve back to the great crossing behind the eye (the optic chiasm) and into the first image processing centers in the brain, the left and right lateral geniculate bodies.
Color Vision: Color vision is from the visual cones only.
   The cones which are all in the central retinal area - the macula lutea containing the most central depression, the fovea - are at least 3 types in relation to color-transmission; these types have traditionally been called red-, green- and violet-/blue-sensitive-cones, but, actually each of the 3 types is excited by a range of light wave more accurately denoted as long (L), middle (M) and short (S).
   True color blindness (inability to detect any color) is very, very rare and due to a lack of or defect of the cones. Most so-called color-blindness is due to a failure of the L or M cones to differentiate between shades of red and green and is most obvious to car drivers who need to stop for red lights and to go on green lights, or to painters. It is found mostly in men and passed through the mother.
A test for the most common form of color blindness.
The numerals embedded in this color pattern can be distinguished by people with normal color vision but not by those who are weak in red–green discrimination.

Image not available.

   The visual anatomy in the brain involves the thalamus (Lateral Geniculate Nucleus, or LGN, is part of the thalamus) as a midway connection point between retinal image and occipital cortex image. It starts to integrate position, color, depth, and meaning.
   Also the paired optic nerves, in addition to visual imagery, carry light and dark stimuli that form the first (receptor) part for eye pupil dilation and constriction reflex to dark and light and to pupil change for distant or near visual focus.
   Special non visual retinal ganglion cells (not rods or cones) detect the 24-hour-daylight seasonal variations and feed the info to the suprachiasmatic hypothalamus nuclei that is your mind's time keeper and controller of the time and seasonal rhythms that affect each of your behaviors.
   The appearance of the retina and the optic nerve cup (optic disc) in each eye reveals many diseases, causes of blindness, and increased pressure in brain from tumors, hemorrhage and other brain swelling. The most frequent disease of optic nerve is a sudden, usually temporary blindness in one eye as first sign of multiple sclerosis. 
 The optic nerve, being part of brain, carries with it cerebrospinal fluid; so brain tumors that raise pressure in Brain cause an obvious swelling of the optic discs of both eyes that appears as a blurring of both optic discs. In a first attack of multiple sclerosis, only one disc is affected.
   Critical Period for Eye Vision Deprivation: In lower animals, depriving one eye of vision in the weeks after birth may irreversibly weaken the visual input from that eye (In cats, sewing closed the eyelids of one-side eye between 3 weeks to several months - maximum affect at 4-6 weeks - irreversibly weakens the input from the sewed-over eye after re-opening of the sewn lids. Depriving an eye, for even a few days, during this period is sufficient to cause major changes in ocular-dominance-column anatomy and physiology. Although the exact timing in humans is not known, blockage of vision by, for example, a newborn infant cataract or a severe cross-eyed condition even for a few days during the early critical period may permanently ruin vision from that eye. Thus parents and pediatricians should pay maximal attention to a newborn's eyes and vision; so any abnormality should immediately be treated. 

Cranial Nerves III, IV and VI are dealt with together because they control the eye muscles that move the eyeball and CN III makes eye pupil motions and helps to focus vision and lift the eyelids. 
  Schematic of the CN III, IV and VI controlled muscles that move the right-side eyeball should be referred to in the below descriptions
Image not available.

CN III the Oculomotor Nerve controls 4 of the 6 eyeball movement muscles - the medial rectus with which you look toward your nose, the superior rectus with which you look up and which helps you to turn or rotate the eye(ball) inward, the inferior rectus with which you look down and which helps you to turn your eye inward or to rotate it outward, and the inferior-oblique with which rotate your eye away from your nose and which helps you to look away from your nose and to look up.
   Note that like all cranial nerves, except the CN IV trochlear, the CN III affects the same side of the body as its nerve motor nucleus in the brainstem.
   When either left or right CN III nerve trunk is disabled (Usually by hemorrhage in brain or pressure from local tumor) a syndrome results where the eye on the side of CN III damage deviates outward (away from nose) and downward because of unopposed actions of the intact CN VI and CN IV muscles; also its same side eye pupil appears widely dilated and there is loss of near vision clarity because of unopposed iris radial muscle dilator of sympathetic innervation and loss of eye lens control. In the one-sided CN III damage when the patient tries to look straight ahead, the eyes appear to be looking in different directions, with the normal side looking straight ahead.
The pupil response to light is mediated by the CN III parasympathetic innervation of the iris. When the nerve is damaged, the pupil cannot dilate, which should be demonstrated in very low light.
Retinal ganglion cells acting as luminance detectors send their axons through the optic tract to the olivary pretectal nucleus, at the junction of the midbrain and the thalamus. Neurons in this nucleus project through the posterior commissure to left and right parasympathetic preganglionic neurons in and around the Edinger-Westphal nucleus. The axons of the preganglionic cells exit the cranium with the oculomotor (III) nerve and contact the ciliary ganglion cells, which control the pupilloconstrictor muscle in the iris. (LGN, lateral geniculate nucleus; MLF, medial longitudinal fasciculus.)

Image not available.

Other effects of complete one-sided loss of CN III nerve trunk are a weak upper eyelid (involuntary permanent partial wink) on same side due to loss of eyelid lifting assist of CN III.

CN IV Trochlear Nerve controls the superior oblique muscle that rotates the eyeballs toward the nose (intorsion) and helps pull the eye downward and outward. (The comedian of the 1930s/40s, Eddie Cantor, famous for his revolving eyes, could not have succeeded without his superb trochlear nerves) It is the only pair of cranial nerves whose action is on the opposite side from its brainstem nucleus because of the emerging nerves crossing on the dorsum (rear surface) of brainstem. This leads to striking effects. For example, a brain stroke in left brainstem can paralyze the superior oblique muscle in the opposite side right, eye at the same time as the left eye feels the affects of (C III and C VI) oculo-motor and abducens nerves paralysis. 
  What happens to the eye with damage to one trochlear nerve? Victims have trouble with downward glance in the affected eye on one side and when they try to look down and even a little to side, they see disturbing double images. This badly interferes with going down stairs. The victim of a trochlear nerve-trunk-origin paralysis tilts head downward and toward his body. Because of this apparent sad look of trochlear paralysis, it was called the pathetic nerve. The trochlear nerve trunk is damaged sometimes in head trauma.

CN VI: Abducens Nerve controls the lateral rectus eye-movement muscle which does what its name says in Latin: it abducts (Pulls eyeball in horizontal plane outward, to one side away from your nose). The Abducens only innervates one eyeball muscle of each eye but the effect is dramatic because the muscle pulls its eye sidewards-outwards, and even at rest the damaged nerve's unbalancing of one eye leads to cross-eye squint and when the person tries to look to the affected side he sees double.
   Abducens nerve paralysis is not rare because the left and right nerve each runs a long course in the unprotected cranial cavity from exit site in brainstem and so one or both can easily be damaged by trauma, viral infection, tumors, brain hemorrhage or increased brain fluid pressure as in malignant hypertension and hydrocephalus and causes, in worst cases, inwardly crossed eyes and double vision.

CN V, Trigeminal Nerve: The three sensory divisions of the trigeminal (V) nerve innervate face and scalp. Herpes zoster virus often invades the ophthalmic division of the nerve causing a one-sided shingles rash of the upper face that dangerously may involve the eye and cause it to be blinded.

Image not available.
CN V: Trigeminal Nerve has a large sensory trunk for what you feel over chin, face and front of scalp and a motor trunk for jaw and muscles. Its 3 sensory branches (Shown above in the Figure) are; the Ophthalmic, for nose and eye surface, and forehead and scalp; the Maxillary for cheek, mustache area, upper jaw including upper set of teeth and gums; and the Mandibular for lower jaw continuing up the strip of skin in front of and above ear lobe. It also controls a muscle that affects hearing and when the muscle's nerve branch gets disabled one gets hypersensitive to sound volume (ie, a condition, hyperacusis). The sensory fibers for CN V come together inside the cranium, at its base just in front of and beneath the under-brain surface in the large right and left trigeminal ganglia but the neuro-muscle fibers are from neurons in the brain stem. Its worst disease is trigeminal neuralgiatic douloureux (one-sided shooting facial & mouth pains) due to irritation of the ganglion neurons by trauma, blood vessel, tumor or Multiple Sclerosis. An infection of CN V by recurrent chickenpox virus in adults causes terrible trigeminal herpes zoster (shingles) on one side of face, the level depending on which of the 3 branches  is affected. It may cause blisters on one or the other eye cornea that can make one blind in that eye. So immediate care needed.
The motor component of CN V innervates muscles of chewing and the one pair of hearing muscles. Final motor neurons of muscle fibers are located in neuron nucleus in the brainstem Pons.
All the muscles controlled by CN V receive bilateral innervation in the cerebral cortex (upper brain motor control). It means that a brain stroke of one side of the cerebral cortex will not show in the chewing and hearing muscles.
CN VII: Facial Nerve controls the muscles of facial expression - right and left side. In its most famous disease, Bell's palsy, half the face on one side loses strength, causing a queer leer to one's expression when trying to smile with the teeth showing. As with all cranial nerves except CN IV, the lower fibers (from the brainstem nerve nucleus down) of the nerve do not cross sides so the side of the palsy is the same side as the lower nerve lesion.
 The upper-motor (above brain stem) facial nerves innervate, bilaterally, each facial nerve affecting the upper face but in the lower face the innervation is contralateral. It means that a facial palsy coming from one side of brain spares the brow, an important sign of non-Bell's facial palsy in contrast to Bell's, or lower facial nerve palsy, which involves the full half of the face from brow to chin. 
The path of the facial nerve after it exits from the brainstem and before it divides into its 3 external branches is important because in this space interval it runs alongside the body of the CN VIII vestibulcochlear nerve that gives us hearing and balance and in a bony (temporal facial) canal in the base of the cranium. Not infrequently the canal gets damaged in head trauma leaning to a syndrome of mixed CN VII and CN VIII paralysis on one side (loss of hearing, balance and occurrence of a facial palsy on one side). It should always be suspected in skull fractures and especially followed by bloody discharge from an ear, and special basal fracture x-rays or MRI or CT should be done to rule it out. Clinically too, the examiner should look for one sided paralysis of the functions.
 Additionally, three quirks of CN VII that help in diagnosis of facial palsy are: 1) A sensory branch that joins the nerve late in its course transmits each side's front and side of tongue taste; 2) another late branch controls a key muscle to one ear bone that filters out too loud sounds that could hurt or damage your hearing; and 3) the lower motor neuron nucleus of CN VII in the brainstem's Pons is almost touching the nucleus of CN VI, the Abducens nerve whose damage causes cross-eyes. So if your facial weakness has painful hearing or double vision or altered taste, it exactly locates the damage to the nerve and may help treatment for returning normal function.
Since the lifetime chance - Dear Reader - of your getting a facial paralysis is a rather high 1 in 60 - here is very practical information for you if you wake up one morning and look in the mirror and find one side of your face droopy, unable to close that side's eye, and saliva dribbling from that side's corner of mouth. First, you know you got a case of facial palsy. But while you are looking in the mirror try to wrinkle your brow and try to squeeze shut your eyes. In the usual type of facial palsy known as Bell's Palsy one complete half of your face from brow will be weak while the other half is OK. But if your facial palsy is coming from higher up in the brain, the side of brow on the side of the lower facial palsy should retain some strength. That would be bad news because upper facial palsy is more serious - being due to brain tumors or strokes. And, if your one-sided, lower-half-of-face facial palsy is combined with an acute cross-eyed stare on the same side as the face, you got nuclear facial palsy, very bad news. If you have Bell's palsy (full half side of face; no cross-eyes), test your front of tongue taste. If you lose it on same side as the facial loss, it locates the disease to a small area around the parotid gland. Similarly if you notice sounds that normally do not bother you, causing pain in same side ear, it locates the disease very specifically in the ear canal. Bell's Palsy is facial paralysis from damage or disease to the lower motor CN VII facial nerve. It is usually due to virus infection or trauma but its cause may not be evident. It also can occur with mumps because the facial nerve runs in the parotid gland. Facial palsies that are unusual, bilateral or serial on one side after the other should get an MRI of brain and its base looking for Multiple Sclerosis (MS) or Sarcoidosis. By the way, both MS and sarcoidosis affect multiple cranial nerves together or serially and ought to be on your list if you get a cranial nerve palsy.
What to do if you get it? If you have the usual facial palsy (Bell's; full half face paralysis not sparing the brow), relax. It may be very inconvenient for your social life but it should be gone after 8 weeks. It is best to quickly consult a neurologist because corticosteroid pills (Better yet high dose IV corticosteroid for 3 days) are shown to speed recovery. If the palsy is due to a virus, the antiviral acyclovir or its like should be added. Protective measures are advised for the eye.
CN VIII: Vestibulocochlear (hearing & balance) These nerve signals originate from 2 special sensory structures of the inner ear (behind and deep to the eardrum), the cochlea and the labyrinth. The cochlea amplifies the sound coming in, and then, by the vibration of its special hairs, starts a signal to the brain through the cochlear branch of CN VIII.   The labyrinth is 3 fluid-filled, coiled, connected tubes at right angles to each other in the 3 planes of our 3-dimensional world (the horizontal width & the length and the vertical height), filled with fluid and having sensory hairs. And at the base of the tubes are 2 gravity-sensitive bodies (utricle and saccule) at right angles to each other and also attached to hair structures and bathed in fluid. The direction of the flows of fluid signals to your brain the spatial orientation of your body in the 3 directions, and the pull of gravity on the weight-bodies signals body orientation with respect to your standing or lying-down position. These signals are all passed through the vestibular branch of CN VIII.
Thus, two nerve branches - the cochlear nerve for hearing and the vestibular nerve for body position, - combine, after picking up each one's primary sense signal, to make up CN VIII, which enters the brain stem then separates to go to nearby neuron groupings (nuclei) in the Pons and from there it relays the data to each cerebral temporal lobe to allow hearing in conscious thought and relays to the cerebellum for giving a sense of body balance and also to the brainstem eye centers to help our eyes and vision keep steady despite changing body position. For hearing, each side of the cochlear nucleus in the brain-stem pons relays predominantly to the opposite cerebral temporal lobe cortex but enough bilateral innervation occurs so that each ear's hearing is bilaterally represented in the brain. That is good because, due to it, a one-sided brain stroke affecting the hearing area of cortex in temporal lobe results in not much loss of opposite-side hearing. 
The diseases of hearing and balance like Meniere's Disease are due to damages, infections and processes affecting CN VIII parts. It should also be mentioned here that the the brain by its unilateral and bilateral representation of sound on a place- and frequency-grid, allows a person to determine where a sound is coming from and how far away and how high it is and whether it is approaching or moving away from the animal. In humans these skills are not developed but are still important to our survival. In lower animals especially night and dark living animals like bats and owls they are crucial to survival.
CN IX: Glossopharyngeal (Tongue and Throat) Nerve is a mixed sensory-motor nerve: It transmits taste from rear of tongue and feeling in back of throat; and for motor, it controls swallowing; and it also carries many autonomic nerve fibers. (Affects arterial blood pressure from carotid sinus & aortic arch reflexes and increases respiration in response to low oxygen in blood via carotid body reflex) An important feature is that its external nerve trunk exits skull in the same bony canal as CN X (the Vagus Nerve) and XI (the Spinal Accessory nerve) so all three nerves may be damaged together by local tumors, head trauma leading to basal skull fracture causing a triple cranial nerve syndrome with highly specific localizing symptoms and signs.
CN X: Vagus Nerve is the most famous cranial nerve because its autonomic nervous system part supplies most parasympathetic nerve fibers - to the heart and blood vessels, the voice box and lungs, most of GI tract and liver, pancreas, and kidneys, bladder and prostate in men and reproductive organs in women. Also it has a branch that innervates taste buds in back of throat and upper esophagus. Its adjectival name (vagal) is an alternative for parasympathetic. A motor nerve component innervates muscles of back of throat (with CN IX) and also larynx. Its recurrent laryngeal nerve damage causes hoarseness or complete voice loss (with 2-branch damage). An external sensory component transmits pain from inner ear canal, coverings in rear brain and taste from parts of tongue while an internal sensory component carries pain from distension or damage of internal organs like stomach, intestines, liver, heart. (Cutting the vagus nerve branches to the heart was an old treatment for relieving severe angina pain of heart) Sometimes the vagus nerve branch to the stomach is purposely cut in an operation against peptic ulcer because it is the route for impulses that cause stomach acid secretion but the side effect of the operation is a sluggish stomach and upper intestine, often complicated by bouts of apparent obstruction.
The Taste Sense allows us to identify and seek the foods that are most nutritious and to detect and avoid poisons. Its front line is the taste bud, mostly located on the tongue but also on the soft palate (rear of roof of mouth), the epiglottis (structure just behind the tongue that covers the airway when you swallow) and in the upper esophagus. The taste buds contact the chemicals in foods and in other substances we put in mouth, identify and detect the various tastes and at the same time start a process that will cause us to desire or to avoid the food containing the chemical. The signals from the taste buds involve the sensory nerve fibers of four cranial nerves. Most taste buds are on the front of the tongue including its sides and their signals travel in a branch of CN VII, the facial nerve. (A branch of CN V carries the final distal taste nerve fibers but as it runs towards the brain it becomes part of the main trunk of CN VII). The rear of the tongue has taste buds innervated by CN IX while the taste buds of the epiglottis and upper esophagus use CN X (The fact that taste relies on separate cranial nerves, each one serving a different location prevents the loss of this key sense that would happen occasionally if it relied only on a single cranial nerve)  All the sensory taste fibers from the these cranial nerves end in the solitary nucleus on each side in the brain stem. From the right and left solitary nucleus, nerve fibers run unilaterally and cross bilaterally to right and left cerebral cortex where consciousness of taste is effected. So taste is represented on each side by both the left and right upper brain (the cortex) preventing loss of taste from one-sided cerebral cortex brain stroke.
Each taste bud is composed of 50 to 100 (some sources say up to 200) taste cells.
How taste is detected depends on the taste receptors at the tips of the taste cells inside each taste bud. The tips of the taste cells with the receptors project out from the tongue outer cell lining and are bathed in mouth secretions. Each taste cell has only one taste receptor keyed to a basic taste. Humans can perceive 5 basic tastes: sweet, bitter, sour, salty and umami (umami is the taste of the amino acid, glutamate present in most protein foods and best known to us from soy sauce). These are what I call the digital tastes. The tastes of foods are mixtures and are determined by the proportion of the digital tastes, and I call these mixtures the analog  tastes. There is yet another factor in taste - its appreciation, or how we each react upon detecting a particular taste. This is in the taste cell and may be called an on or an off appreciation. A taste cell that is an on will cause you to want to eat whatever taste it detects, even if that taste is bitter (In the natural state no bitter receptors are attached to the on taste cells) Oppositely, an off taste cell tells you to avoid swallowing whatever taste it detects These facts have been proven in genetically engineered mice that have human bitter taste receptors attached to on taste cells and vice versa. This can be important because certain tastes can be inherited. For example, most people (75%) find phenylthiocarbamide intensely bitter and will spit it out immediately on tasting, whereas 25% cannot detect it at all. The points here are that there are genetic variations in taste which may explain why different persons like or dislike sharply different tasting foods.
Salty taste is a measure of the sodium ion (Na+) and not other salts, and sour taste is a measure of the acidity (the hydrogen ion H+)
The purpose of taste comes in here. First to help animals or the primitive or today still uncivilized human find highly nourishing food, the basic tastes, receptors of sweet (find food with sugar) and umami (find food with proteins) are geared to detect only high concentrations. Second to help avoid poisons, the bad taste of bitter detects very low concentrations. In a similar way, animals that need to detect food from far off can sense the taste of amino acids (meat)  like a shark can detect one drop of blood in an Olympic size swimming pool.  In us modern folk, of course, the taste sense allows appreciation of food, a basic happiness of life.
End about taste with advice on enjoying your food: Before eating, blow your nose clear because smell is important for enjoying the taste of food and beverage. Secondly before tasting a food or drink you plan to enjoy, take a drink of water to get rid of all other tastes, especially coffee, alcohol, salts or acids. Thirdly keep aware that both analog (How sweet a sugar) and digital (Is sugar sweet or not) taste senses may individually have an inherited DNA input explaining why what the other person admires is not what you admire (Cats cannot taste sugars as sweet).
CN XI: Spinal Accessory (Shrugging Shoulder) Nerve Actually, the CN XI nerve-trunk originates from the final-spinal motor neurons in the upper spinal cord C1 to C5 and also from final motor neurons in the brain-stem pons. If a surgeon cuts your left CN XI, you lose power to turn head to right side and partly lose power to shrug left shoulder. Isolated lesions of CN XI are rare; more often it is part of the nerve syndrome affecting also CN IX & CN X.
CN XII: Hypoglossal (Tongue Movement) is a pure motor nerve. Its final motor neurons are in brainstem, and the nerve roots come together as CN XII and leave the cranium in the hypoglossal foramen (a bone tunnel). Complete cutting of the nerve will paralyze one side of the tongue, causing a tongue that curves slightly especially when you try to stick it out. Actually it cannot be done; rather, it deviates to the paralyzed side. The CN XII upper motor neurons in cerebral cortex are, like most Upper Motor Neurons contralateral to their target muscles. So a left sided upper brain stroke will paralyze muscles of right side of the tongue and right-sided stroke will paralyze muscles of left side of tongue.
Eventually the paralyzed muscles atrophy, shriveling the tongue on its paralyzed side. Diseases of the CN XII nerve are rare: mostly surgical trauma or accident involving fracture of base of skull or growth of local tumor that compresses the nerve. 
End Note: Fractures and head trauma involving the base of the skull (upper neck area), suspicion of early multiple sclerosis, and conditions that cause high cerebrospinal fluid pressure (brain tumors, meningitis) with headache should always make a suspicion of cranial nerve injuries or disease (Need, first, special skull x-rays; then, CT  or MRI, and neurology consultation). 
  END OF CHAPTER. To read next click 9.13 Growth & Death of Your Brain Through Your Lif...

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