Evaluating the Cranial Nerves

Tagged:  

INTRODUCTION

A thorough neurological examination includes the evaluation of a patient's mental status and speech, motor system, sensory system, reflexes, and cranial nerves. Part I of this series, "Evaluating the Cranial Nervies," will give an overview of cranial nerves I and II. The twelve pairs of cranial nerves were classified by a German medical student, Samuel Soemmering, nearly two centuries ago. In general, the numbering of cranial nerves is determined by the order in which the nerves exit the cranium, from front to back.

Some cranial nerves contain only sensory fibers; others contain both sensory and motor fibers called mixed nerves. Sensory fiber cell bodies are located in ganglia outside the brain, and motor fiber cell bodies are in nuclei within the brain.

Virtually every anatomy student has had to memorize the following mnemonic for the cranial nerves: "On Old Olympus's Towering Tops A Finn and German Viewed Some Hops." The first letter of each word corresponds with the first letter of the cranial nerve (Table 1). The physician should, of course, memorize the name of each cranial nerve and be able to define the function of each nerve in a few words. The root of the name gives a clue as to what each nerve actually does or where it is distributed (see "Name Significance" under Table 1). After learning the significance of each name, it is then an easy leap to remember each nerve's actual function (Table 1).

CRANIAL NERVE I

Olfactory Nerve and Tract (Sensory)

Cranial nerve I is not a true nerve, but a fiber tract of the brain. It is wholly sensory and conveys the sense of smell to the brain. Olfactory cells in the nasal epithelium of the superior nasal cavity have olfactory hairs that are exposed to any odor molecules entering the nostrils. Olfactory fibers from the hairs travel through the cribriform plate into the olfactory bulb and pass through the olfactory tract into the primary olfactory area of the cerebral cortex.

It has been said that smell is the most primitive of all senses. Indeed, an unexpected whiff of a familiar odor can instantly transport a person miles away or years back in time to where that odor was previously smelled. The sense of smell is not routinely tested unless the patient complains of changes in smell or taste. Disorders of the sense of smell may be caused by any of a number of lesions, traumatic accidents, infections, intoxications, psychoses, neuroses, and congenital defects.

Disorders of Smell

- Anosmia, the total loss of smell, has clinical significance. Bilateral anosmia is commonly related to the common cold or rhinitis but can be caused by head trauma such as a cribriform fracture that has sheared the olfactory fibers. Unilateral anosmia without nasal disease suggests a lesion in the frontal lobe of the brain.

- Hyposomia, a decrease of smell, may be a result of an anterior lobe lesion or merely the result of chronic rhinitis or aging.

- Hyperosmia, a marked increase in smell, is found in some hysterias and may be found in chronic cocaine users.

- Parosmia, a perversion of smell, may be found in hysterias, psychoses, and lesions of the uncinate gyrus.

- Cacosmia, literally a bad odor, is usually from tissue decomposition and is noted by the patient on expiration.

- Hallucinatory olfaction may be a result of a lesion of the uncus, one of the cortical receptive areas for smell. The hallucinations, usually of disagreeable odors, coincide with strong feelings of déjà vu (an illusion of repetition of a previous situation) or déjà pensé (an illusion of repetition of a previous thought).

Clinical Examination

Inform the patient that you will place some familiar-smelling substances under his nose for identification. First, test the patency of the patient's nostrils by compressing one side of the nose and asking the patient to sniff through the other side. Second, ask the patient to close his eyes. Third, occlude one nostril and hold a bottle of a non-irritating substance, such as peppermint, oil of cloves, citron, etc., under the other nostril. Don't use irritating substances like ammonia or vinegar.

Ask the patient what is smelled and note it. Test the opposite nostril with a different smell. If the patient correctly identifies the smell, that's fine, but the test is more designed to demonstrate the sense of smell, not the accuracy. If the patient can smell something, even without identifying it, they at least don't have anosmia. To verify patients' responses, occasionally ask what they are smelling while holding an empty bottle or nothing at all below their noses.

CRANIAL NERVE II

Optic Nerve and Tract (Sensory)

Cranial nerve II is also not a true nerve, but a fiber tract of the brain that terminates in the retina of the eye. Rods and cones found in the retina transmit visual impulses through the optic nerve into the optic chiasm where the nerve fibers from the nasal half of each retina cross; the nerve fibers from the temporal half of each retina do not cross. Exiting the chiasm, the fibers pass through the optic tracts and finally into the visual areas of the brain (Fig. 1).

The more numerous rods found in the retina react to low-intensity light and are useful in twilight and night vision. The cones, found in greater numbers near the center of the retina, react to higher intensity light and are responsible for color and sharp vision.

Knowledge of this neuroanatomy can be useful for discerning objects in dim light or darkness. Looking slightly to one side of an object will excite the more numerous rods located in the peripheral area of the retina. An object that is otherwise virtually invisible when directly stared at may then become visible.

Visual Disorders

- Amaurosis is hereditary or acquired total blindness.

- Nyctalopia (night blindness) is associated with vitamin A deficiency.

- Hemeralopia (day blindness) is defective vision in bright light.

- Amblyopia is defective, dim vision.

- Scotomas are abnormal blind spots found in the visual fields. Positive scotomas appear as dark spots; negative scotomas appear as blank or blind spots that may exist without the patient's knowledge. Scintillating scotomas are experienced as bright, colorless, or colored patterns of light.

- Color blindness includes achromatopia (total color blindness), monochromatism (ability to discern only one of the three primary colors: red, green, blue), and dichromatism (ability to discern two of the three primary colors). Standardized color blindness test cards are used for testing, but color blindness is not usually tested in a routine examination. Colored yarns can also be used if test cards are not available.

Clinical Examination

First, ask the patient whether there has been any change in eyesight. Visual acuity is tested in each eye in turn. Near vision is tested by having the patient read a card with a standard type size at a comfortable reading distance. Far vision is tested by reading a Snellen card at a distance of 20 feet. For patients with markedly poor visual acuity, finger counting and finger movement tests are used.

The visual fields are then tested. The patient and physician face each other about two feet apart. The patient covers one eye; the physician covers his directly opposite eye, i.e., if the patient covers the right eye, the physician covers his or her left eye. The patient is asked to look directly into the physician's uncovered eye.

The physician slowly brings a pencil, finger, or other small object from a peripheral distance into the patient's field of view. The patient is asked to respond when the object appears. At that time, the physician notes and compares with his own normal field of view. The visual field test is repeated from eight directions (Fig. 2). The central area of vision must be included. The test is duplicated on the other eye. Figure 3 shows types of field deficits.

Observe the alignment of the eyes by having the patient focus on a distant object. Compare the relative positions of a penlight or ophthamaloscopic light reflected on the patient's corneas.

Test the pupillary reflex by asking the patient to look into the distance. Dim the lights and shine a bright light on each pupil in turn. First, observe the pupil with the light shining on it; direct pupillary reflex will constrict that pupil. Remove the light and move your attention to the opposite pupil. Once again, shine the light on the original pupil; consensual pupillary reflex should constrict the opposite pupil. Repeat the procedure with the other eye (Fig. 4). In a darkened room, the patient's ocular fundus is examined with an ophthalmoscope. The detailed procedure is beyond the scope of this article, but the general procedure follows.

The ophthalmoscope is adjusted to 0 diopters and the large, round beam of white light. (Some physicians like to use the small, round beam of white light for smaller pupils.)

Note the red reflex. Move closer to the pupil from about 15ø laterally until the optic disc comes into view. Adjust the ophthalmoscope until the optic disc comes into sharp focus. Adjust the lens disc counterclockwise (into the red numbers) for nearsighted patients and clockwise (into the black numbers) for farsighted patients.

Examine the sharpness of the edge of the optic disc. A blurred optic disc may indicate papilledema. Note that the nasal portion of the disc may be slightly blurred when normal.

The disc is normally creamy pink; the center of the disc, called the cup is paler; the retina itself is pinkish red. The cup should not be greater than about half the diameter of the disc, otherwise glaucoma is suspected.

Note the four main arteries with accompanying veins. Carefully examine the arteriovenous crossings. The veins should not be indented by the arteries or hypertension or arteriosclerosis is suspected. Veins may be identified as darker red and larger than the arteries, and having little or no light reflection.

Finally, the macula, which is crucial for central vision, is examined with the patient looking directly at the ophthalmoscope. The macula is slightly darker than the retina and is somewhat difficult to examine. Look for any hemorrhages, exudates, cysts, and patchy holes.

As mentioned in the last article, a thorough neurological examination includes evaluation of a patient's mental status and speech, motor system, sensory system, reflexes, and cranial nerves. Part I dealt with Cranial Nerves I and II; this article will present an overview of Cranial Nerves III, IV, and VI, which innervate the ocular muscles. Some cranial nerves contain only sensory fibers; those contain that contain both sensory and motor fibers are called mixed nerves.

CRANIAL NERVE III

Oculomotor Nerve (Mixed)

The motor portion of the oculomotor nerve (III) originates in the midbrain and branches to the pupilloconstrictor muscle, ciliary muscle of the lens, levator palpebrae superioris muscle of the upper eyelid, and four of the extrinsic eyeball muscles: superior rectus, medial rectus, inferior rectus, and inferior oblique.

The sensory portion of the oculomotor nerve conveys a sense of proprioception; its afferent fibers arise from proprioceptors in the above muscles and terminate in the midbrain.

CRANIAL NERVE IV

Trochlear Nerve (Mixed)

The motor portion of the trochlear nerve (IV) originates in the midbrain and terminates in the superior oblique, an extrinsic eyeball muscle. Not only is the trochlear nerve the smallest of the twelve cranial nerves, but the muscle it innervates is the only one to use a trochlea (pulley).

The sensory portion of the trochlear nerve conveys a sense of proprioception; its afferent fibers arise from proprioceptors in the superior oblique muscle and terminate in the midbrain.

CRANIAL NERVE VI

Abducens Nerve (Mixed)

The motor portion of the abducens nerve (VI) originates in the pons and terminates in the lateral rectus, an extrinsic eyeball muscle. The sensory portion of the abducens nerve conveys a sense of proprioception; its afferent fibers arise from proprioceptors in the lateral rectus muscle and terminate in the pons.

ACTION OF THE OCULAR MUSCLES

There are eleven ocular muscles. Two of the eleven, the pupillodilator and the superior tarsal, are controlled by the autonomic nervous system (ANS). The remaining nine ocular muscles are innervated by Cranial Nerves III, IV, and VI. Two of the ocular muscles are intraocular muscles: the ciliary muscle and the pupilloconstrictor muscle. Both are smooth muscles. The final seven are skeletal muscles.

The ciliary muscle, a smooth muscle that surrounds the lens, adjusts the shape of the lens to change its refractive power for near and far vision accommodation. The iris of the eyeball consists of circular and radial smooth muscles surrounding the pupil, the black opening through which light is admitted into the eye. When light stimulates the eye, the size of the pupil is reduced by the circular pupilloconstrictor muscle, which is controlled by Cranial Nerve III; conversely, when light is dim, the radial, ANS-controlled pupillodilator muscle enlarges the size of the pupil.

The superior tarsal muscle, an extraocular smooth muscle located in the upper eyelid is a small supplement to the levator palpebrae superioris muscle, itself a skeletal muscle. The slowly responding tarsal muscle changes the diameter of the palpebral fissure (eye opening).

Because visceral smooth muscles in the bowel, bladder, blood vessels, bronchi, etc. adjust the diameter of apertures, they can be generalized as sphincter muscles. The intra- and extra-ocular muscles may also be considered sphincters because they similarly adjust apertures.

The seven remaining ocular muscles are all extraocular skeletal muscles. Five of those, the inferior oblique, internal rectus, medial rectus, superior rectus, and the levator palpabrae superioris of the upper eyelid are innervated by Cranial Nerve III. The levator palpabrae superioris quickly responds under voluntary activity to adjust the diameter of the palpebral fissure. Of the final two muscles, the superior oblique and lateral rectus are innervated by Cranial Nerves IV and VI, respectively.

The above may sound complicated, but there is an easy way to remember which ocular muscles each cranial nerve innervates. Parsing the name of Cranial Nerve VI (Abducens) denotes that it abducts; also the term rectus means "straight." What muscle abducts straight out? The aptly-named lateral rectus. Convert the abbreviation of the superior oblique (SO) to a sulfate radical (SO(4)) to remember Cranial Nerve IV. Those are the only two muscles that really have to be memorized. All of the other muscles are innervated by Cranial Nerve III (Table 1).

SOME DISORDERS OF III, IV, AND VI

A number of disorders may affect Cranial Nerves III, IV, and VI, including, but not limited to, syphilis, meningitis, encephalitis, botulism, tumors, cerebral hemorrhage, skull fracture, multiple sclerosis, Circle of Willis internal carotid artery aneurysm, hysteria, and certain drug reactions.

Ophthalmoplegias (paralyses) of the ocular muscles may be acute, chronic, or progressive and may be central or peripheral. Testing for paralysis of six extraocular muscles is discussed below (Testing the Ocular Muscles). Note that ptosis from a paralyzed levator palpebrae superioris is common in myasthenia gravis.

Neurosyphilis commonly causes Argyll Robertson pupil, in which there is a loss of light reflex, retention of accommodation reflex (see Testing the Ocular Muscles), and loss of ciliospinal reflex, a reflex tested by pinching the neck. Normally, the pupil should dilate upon painful stimulation. The syndrome may also be caused by epidemic encephalitis and alcoholism.

Associated Symptoms and Signs of Eye Disorders

Symptoms associated with eye disorders include:

1. Strabismus, or deviation of either or both eyes. Internal strabismus is commonly referred to as "crossed eyes"; external strabismus is commonly referred to as "wall eyes."
2. Diplopia (double vision).
3. Head tilting to compensate for diplopia.
4. Conjugate deviation of the eyes (to the same side). Central lesions are the usual cause.
5. Nystagmus, a rhythmic oscillation of the eyes, may be due to central or labyrinthine lesions, or may be physiologic.
6. Ptosis (lid drop) from paralyzed or weak levator palpebrae superioris muscle.
7. Dizziness often associated with diplopia.
8. Limited eye movement.
9. Loss of eye reflexes.

Actions of Six Extraocular Muscles

Six extraocular muscles control the movement of the eyeball around three axes of rotation: sagittal, horizontal, and vertical. The positions of some of the muscle attachments to the eyeball effect complex, compound movements, and because the muscles work in concert, it is difficult to isolate the movement of an individual muscle (Figure 1).

Actions of the Three Intraocular Muscles

The ciliary muscle changes the shape of the lens for distance accommodation. In addition, the pupilloconstrictor and pupillodilator muscles are paired to act in tonic opposition to each other when controlling the size of the pupil.

Figure 2 shows the neural circuitry that controls direct and consensual pupillary reflex and lens accommodation. Note that Cranial Nerve II also plays a role.

Testing the Ocular Muscles

Finger Following

The best way to test for paralysis of an extraocular muscle is to have the patient's eyes follow the examiner's finger into the six cardinal positions of gaze (see Figure 3). Note that straight up and down are not cardinal positions. If the patient cannot move an eye to the indicated position, it denotes paralysis of that corresponding extraocular muscle. The eye must be tested to the extreme points of gaze to exaggerate any defects and to permit easy recognition.

Accommodation Testing

The patient focuses on the examiner's finger, which is first held at a distance and then brought up close to the eyes. The examiner notes eyeball convergence and pupillary change. Normally, the pupils should constrict when the patient looks at a near object.

Light Reflex and Consensual Light Reflex

In light reflex, the examiner shines a light into one eye and notes any pupillary constriction. Note that this test also depends on an intact Cranial Nerve II. In consensual light reflex, the examiner shines a light into one eye and notes any pupillary constriction in the opposite eye. This test also depends on an intact Cranial Nerve II.

Diplopia (Double Vision) Testing

Ocular muscles may also be tested through the use of diplopia, or double vision, testing.

Testing for Ocular Deviation

If the patient complains of diplopia or dizziness, it may be from ocular deviation. A paralyzed extraocular muscle may be a cause. An easy way to determine whether there is any ocular deviation is for the patient look directly into a flashlight held directly in front of the examiner. Normally, the light reflection is symmetrically positioned on the cornea over the pupils. Any asymmetric reflection discloses a deviated eye. Figure 4 demonstrates how light reflects from a deviated eye. The examiner can roughly gauge the degree of deviation by noting where the displaced reflection falls.

The cover test may be used to determine deviation of even less than 5ø. The examiner should cover one of the patient's eyes with a card while the patient is looking with both eyes at a flashlight. The examiner should then watch the patient's uncovered eye; if it moves to fix its gaze on the flashlight, it was not straight before the opposite eye was covered. If the eye does not move, then it was originally straight. The examiner should repeat the procedure on the patient's other eye. Normally, both eyes of the patient should test perfectly straight. The next article will continue examining more cranial nerves.

Bibliography

1. Bates B. A guide to physical examination. 3rd ed. Philadelphia: J B Lippincott Company; 1983.
2. Berkow R, editor. The merck manual. 14th ed. Rahway, NJ: Merck & Co, Inc; 1982.
3. Chusid JG. Correlative neuroanatomy & functional neurology. 19th ed. Los Altos, CA: LANGE Medical Publications; 1985.
4. DeMyer W. Technique of the neurologic examination: a programmed text. 3rd ed. New York: McGraw-Hill; 1980.
5. Ferezy JS. The chiropractic neurological examination. Gaithersburg, MD: Aspen Publishers, Inc; 1992.
6. Moore KL. Clinically oriented anatomy. Baltimore: Williams & Wilkins; 1980.
7. Netter FH. The CIBA collection of medical illustrations, nervous system, vol. 1, part 1. West Caldwell, NJ: CIBA Pharmaceutical Company; 1983.
8. Prior JA, Silberstein JS, Stang JM. Physical diagnosis: the history and examination of the patient. 6th ed. St. Louis: The C.V. Mosby Company; 1981.
9. Snell RS. Clinical neuroanatomy for medical students. Boston: Little, Brown and Company; 1980.
10. Tortora GJ, Anagnostakos NP. Principles of anatomy and physiology. 4th ed. New York: Harper & Row, Publishers; 1984.

References

(1.) Bates B. A guide to physical examination, 3rd ed. Philadelphia: J.B. Lippincott Company; 1983.

(2.) Berkow R, ed. The merck manual, 14th ed. Rahway, NJ: Merck & Co., Inc.; 1982.

(3.) Chusid JG. Correlative neuroanatomy & functional neurology, 19th ed. Los Altos, CA: LANGE Medical Publications; 1985.

(4.) DeMyer W. Technique of the neurologic examination: a programmed text, 3rd ed. New York: McGraw-Hill; 1980.

(5.) Ferezy JS. The chiropractic neurological examination. Gaithersburg, MD: Aspen Publishers, Inc.; 1992.

(6.) Netter FH. The CIBA collection of medical illustrations, nervous system, vol 1, part 1. West Caldwell, NJ: CIBA Pharmaceutical Company; 1983.

(7.) Prior JA, Silberstein JS, Stang JM. Physical diagnosis: the history and examination of the patient, 6th ed. St. Louis: The C.V. Mosby Company; 1981.

(8.) Snell RS. Clinical neuroanatomy for medical students. Boston: Little, Brown and Company; 1980.

(9.) Some pathological conditions of the eye, ear and throat: an atlas. North Chicago, IL: Abbott Laboratories; n.d.

(10.) Tortora GJ, Anagnostakos NP. Principles of anatomy and physiology, 4th ed. New York: Harper & Row, Publishers; 1984.

The National College of Chiropractic.

~~~~~~~~

By Larry W. Greenly

Share this with your friends