Ординатура / Офтальмология / Английские материалы / Clinical Medicine in Optometric Practice_Muchnick_2007

Consultation with neurology specialist may be necessary to rule out lesion

Infer nature of lesion from history, signs, and symptoms

No lesion found

Follow patient routinely

Consult with specialist for further diagnosis and treatment plan

Once location is approximated, retest any neurologic structures that pass near lesion

to rule out neuro involvement

Follow patient

for visual prognosis

the clinician should perform a routine examination. (Figure 3-1 is a flow chart for the neurologic evaluation of the eye care patient.)

Symptoms Without Clinical Signs

If no clinical signs are present in a symptomatic patient (Box 3-1), the clinician must rule out the presence of disease. This goal is accomplished by consultation with the family physician, neurologist, ophthalmolo-

gist, neuro-eye specialist, internist, or endocrinologist. For example, if a patient complains of headache and the ocular examination and neurology screening reveal no significant findings, one must decide whether to refer the patient for further evaluation or to monitor the patient oneself.

Radiographic studies and laboratory work may be necessary to establish a diagnosis. Psychogenic symptoms and malingering can be ruled out in this way.

BOX 3-1

SIGNIFICANT NEUROLOGIC SYMPTOMS

Headache

Confusion

Unsteadiness

Visual problems

Speech problems

Tremors

Numbness

Weakness

Visual Defects With No Obvious Neurologic Problems

If a visual pathway deficit is discovered but no neurologic problem is found, further neurologic testing is warranted to rule out the effects of a lesion on neurologic structures passing near the suspected site.

First, the location of the lesion is determined by its effect on the patient’s visual field. With an intimate understanding of neuroanatomy, the optometrist can identify nearby neurologic structures and infer what neurologic deficits would occur if these nearby nerves

were damaged. Finally, the optometrist should perform the neurologic evaluation, paying particular attention to any deficits that would occur given the lesion’s suspected location. The examiner should be careful to elicit only findings that are truly present.

Ocular and Neurologic Defects

A patient may have both ocular and neurologic defects. Whether the patient is symptomatic or asymptomatic, the examiner must correlate these findings with the relevant neuroanatomy to localize the lesion. The nature of the lesion may be tentatively inferred at this point on the basis of the patient’s history, symptoms, and signs, and the approximate location of the lesion.

The differential diagnosis can be narrowed down by radiographic findings. Conventional radiography, CT scan, MR imaging, and color Doppler ultrasonography all help in determining the diagnosis (see Chapter 5).

In most cases the clinician will want to consult with a specialist, who will oversee the advanced diagnostic and treatment options available to the patient. Referral to a neurology specialist helps in pinpointing a more generalized problem. Treatment is determined by the cause of the lesion. Surgery or other forms of treatment may be recommended by vascular specialists or neurosurgeons. Eventually, low vision adaptations may be necessary.

BOX 3-2

THE NEUROLOGIC SCREENING

Mental status

Motor function

Sensory function

Cerebellar function

Reflex function

Cranial nerve function

TABLE 3-1 LOCALIZING VALUE OF MENTAL STATUS EVALUATION

THE NEUROLOGIC SCREENING

For practical purposes, the neurologic examination is divided into six areas that affect optometric practice: evaluation of the patient’s mental status, motor function, sensory function, cerebellar functions, reflexes, and cranial nerve functions (Box 3-2).

Evaluation of Mental Status

Table 3-1 and Box 3-3 discuss the evaluation of mental status.

While talking with the patient, the optometrist should judge from his or her responses whether the patient seems alert and aware. Does the patient seem confused? Is he or she acting in a rational manner? Is the patient oriented to time and place? If the patient is disoriented, does he or she have short-term or longterm memory loss?

The examiner can test memory loss by presenting a set of three common words to the patient and asking him or her to repeat them minutes later. Memory loss may be caused by a temporal lobe lesion.

Is the patient speaking clearly and using vocabulary appropriately? A dysfunction in speech can help to localize a lesion. A patient who vocalizes meaningless

BOX 3-3

EVALUATION OF MENTAL STATUS

Consciousness

Orientation

Memory

Speech

Appropriate affect

Object recognition

Praxis

words has dysphasia, which may indicate a brain lesion of the left hemisphere.

If a patient talks sensibly but has difficulty in producing sound, a disruption exists in the motor function that produces speech. This problem can occur anywhere along the pathway from the brain to the mouth.

Is the patient exhibiting inappropriate emotions, such as sudden laughter or crying? This type of emotional display may be the result of bilateral cerebral damage.

Can the patient recognize common objects? Inability to do so is called agnosia. If the patient cannot identify an object by touching it with eyes closed,

30 DIAGNOSTIC PROCEDURES

he or she may have a lesion in the nondominant parietal lobe.

Can the patient carry out simple instructions? Inability to do so is called dyspraxia and may be the result of a deep frontal lobe lesion.

Finally, can the patient copy a simple drawn figure? Inability to do so may be caused by a posterior parietal lobe lesion.

Evaluation of Motor Functions

Muscle weakness is a fairly nonlocalizing finding, because it can be caused by disturbances in the nerves, muscles, cerebrum, brainstem, spinal cord, or neuromuscular junction. To screen for muscle weakness, the examiner should ask the patient to flex and extend both arms and legs against resistance (Figure 3-2). Note any weakness of one limb when comparing the two.

FIGURE 3-3 ■ Evaluation of tactile sense. The patient is asked to close his or her eyes. His or her fingers and toes are lightly touched with a tissue. A significant finding is a marked decrease in sensitivity.

Evaluation of Sensory Functions

Neurologic evaluation should include tests for the senses of touch, pain, and vibration. Loss of these senses may indicate a spinal cord lesion. The following tests are performed with the patient’s eyes closed. To test for the sense of touch, stroke the patient’s fingers with a tissue after asking him or her to tell you when he or she feels the stroke of the tissue (Figure 3-3). Repeat the test on the patient’s toes.

To test for pain sensation, touch the patient on the fingers and hand with the point of a safety pin. Begin touching the fingers and hand, alternating the sharp tip with the blunt end, and determine whether the patient can discern the difference between sharp and dull sensations (Figures 3-4 and 3-5). Repeat this test on the patient’s toes.

FIGURE 3-2 ■ Evaluation of motor function. To test the forearms for flexion and extension, the patient exerts force against the examiner, who holds the patient by the wrist. This procedure tests roots C5-C6 (flexion) and C6-C8 (extension).

FIGURE 3-4 ■ Evaluation of pain sense. The patient is asked to close his or her eyes. With the sharp end of a safety pin the fingers and toes are lightly pricked.

Finally, test vibration sense using a 128-Hz tuning fork. Strike the tuning fork with your hand and place it over the base of the nail bed on the patient’s index finger. Place your index finger under the patient’s fingertip so you can feel the vibration also (Figure 3-6). Ask the patient to report when he or she no longer feels the vibration.

Evaluation of Cerebellar Functions

To test for cerebellar disorders, perform a “finger- to-nose” test. Hold your finger at arm’s length from the patient. Ask the patient to touch his or her nose with his index finger and then touch your index finger. Repeat this several times with the patient’s eyes open and then closed (Figure 3-7). A patient with a disorder

FIGURE 3-5 ■ Evaluation of pain sense. The procedure described in Figure 3-4 is repeated with the dull end of the pin. The examiner alternates the sharp and dull ends of the pin, and the patient is asked to compare sharp and dull sensation while the examiner moves proximally.

FIGURE 3-6 ■ Evaluation of vibration sense. A 128-Hz tuning fork is tapped to produce a vibration. The base of the fork is placed on the base of the patient’s fingernail. The patient closes his or her eyes and reports when he or she can no longer feel the vibration. A significant finding is a reduced vibration sense.

of the cerebellum tends to overshoot the target. This response is called past pointing.

Another convenient test for cerebellar function is the Romberg test. Have the patient stand in front of you with heels and toes together. Then, ask the patient to close his or her eyes and attempt to maintain balance. Be prepared to catch the patient if he or she falls off balance. This test assesses the posterior columns.

You may also ask the patient to raise his or her arms palms up while balancing with eyes shut (Figure 3-8). Patients with a hemiparesis will drop one arm and flex the fingers. This condition is called pronator drift.

A

B

FIGURE 3-7 ■ A and B, Evaluation of cerebellar function (“finger-to-nose” test). The examiner holds his or her finger outstretched at arm’s length from the patient. With eyes open, the patient first touches his or her nose and then touches the examiner’s finger. This sequence is repeated several times. Next, it is repeated with the patient’s eyes shut. Cerebellar disease causes overshooting of the target and digital tremor.

The most important cerebellar function test is examination of gait (Figure 3-9). First, observe the patient as he or she walks away from you. Next, have the patient walk toward you on his or her toes. Finally, have the patient walk away from you, putting heel to toe. Loss of this ability can occur in cerebellar dysfunction caused by such diseases as syphilis.

Watch for normal posture and proper arm movement. Cerebellar ataxia is heightened by gait testing. Lower extremity muscle weakness may also be evaluated in this way.

Evaluation of Reflexes

The neurology tests should include an evaluation of deep tendon reflexes. A loss of these reflexes may occur in some cerebellar disorders. Of the many reflex

tests to choose from, the patellar tendon reflex test is most important.

Have the patient sit on the edge of a table or chair and dangle his or her feet. Place your hand on the quadriceps muscle of one leg and strike the patellar tendon with a reflex hammer. You should feel the quadriceps contract and see the knee extend (Figure 3-10).

Loss of deep tendon reflexes occurs in 50% to 90% of patients with Adie’s syndrome. Bilateral Adie’s tonic pupils, which are typically mid-dilated, may be confused with bilateral Argyll Robertson tonic pupils caused by syphilis, although these are typically constricted. Deep tendon knee reflexes help the examiner to confirm the presence of Adie’s pupil, because this reflex is not lost in patients with Argyll Robertson pupil.

CRANIAL NERVE TESTING

The cranial nerves control the five senses, allowing the patient to interact with the environment, to feel it, move through it, experience it, and alter it. These twelve pairs of nerves, which extend from the brain to vital organs throughout the body, are necessary for the patient’s everyday activities.

The cranial nerves may be affected by a wide range of conditions, including trauma, infection, demyelination from multiple sclerosis, cerebrovascular ischemia from stroke, intracranial inflammation from meningitis, and development of space-occupying lesions (such as tumors or aneurysms). The cranial nerves receive sensory (afferent) input from internal organs and from the skin, as well as special sensory input from the eyes, ears, and nose. The motor (efferent) innervation is supplied through the cranial nerves to voluntary and involuntary muscles throughout the body.

The functioning of each cranial nerve should be tested and evaluated. All of the following tests can be performed in the optometrist’s office (Table 3-2).

First Cranial Nerve—Olfactory Nerve

The olfactory nerve is a special afferent cranial nerve composed of sensory fibers only. The sole function of this nerve is olfaction, the ability to discern smells. To test the olfactory nerve, the examiner should ask the patient to shut his or her eyes and occlude one nostril. The patient’s open nostril is presented with a variety of vials, each containing a concentrated extract such as coffee, vanilla, or peppermint. The patient is asked to sniff

FIGURE 3-10 ■ Evaluation of deep tendon reflexes. The patellar tendon reflex is tested by positioning the patient on the edge of the examination chair or table so that his or her legs dangle freely with no obstruction. The examiner lightly places one hand on the quadriceps muscle. The patellar tendon is struck firmly by the base of the hammer. Extension of the knee should occur, and contraction of the quadriceps should be felt. This procedure tests the nerves at roots L2 to L4.

and identify each smell (Figure 3-11). The loss of olfactory ability is called anosmia and can be caused by viral infection, trauma to the skull, or frontal lobe masses or seizures. Olfactory nerve testing is rarely performed, because it is an unreliable test of cranial disease.

Nasal polyps are the most common cause of anosmia. The loss of smell on one side is more ominous than bilateral anosmia, because it indicates a possible lesion affecting the ipsilateral olfactory nerve or tract.

Second Cranial Nerve—Optic Nerve

Like the olfactory nerve, the optic nerve contains only special sensory afferent fibers. The optic nerve functions to convey visual information from the retina to the occipital lobe through the visual pathway. The optic nerve is tested in the office by visual acuity measurement, color testing, pupil testing, visual fields testing, and optic nerve head evaluation with an ophthalmoscope or stereo biomicroscopy.

Visual fields testing has great localizing value when an intracranial lesion affects the visual pathway. Prechiasmal lesions usually cause monocular field defects. Chiasmal lesions produce heteronymous hemianopsia, and postchiasmal lesions produce homonymous hemianopsia. The more posterior the lesion, the more congruous (alike) the two fields appear.

Third Cranial Nerve—Oculomotor Nerve

The oculomotor nerve contains only motor fibers, of which there are two types. Somatic efferent fibers innervate the medial rectus, inferior rectus, superior rectus, levator palpebral superioris, and the inferior oblique muscles of the eye. Visceral efferent motor fi- bers innervate the constrictor pupillae and ciliary muscles with parasympathetic fibers from the ciliary ganglion.

Because the third nerve innervates four of the six extraocular muscles, testing is performed by having the patient’s eyes follow a near target while the examiner draws out a physiologic “H” pattern, causing adduction (medial rectus), depression while abducting (inferior rectus), and elevation (superior rectus and inferior oblique). Pupillary constriction is tested by the light reflex, and accommodation can be tested on a near target. Loss of third-nerve function may cause diplopia and an eye that is “down-and-out” with ptosis and mydriasis.

Fourth Cranial Nerve—Trochlear Nerve

The trochlear nerve supplies only somatic efferent motor fibers to the superior oblique muscle of the eye. The superior oblique is tested, as previously described, by having the patient’s eyes follow a near target while the examiner traces an “H” pattern. The trochlear nerve causes superior oblique contraction, which rotates the eye inward, downward, and outward. To best isolate this nerve, the examiner should have the patient adduct and look down toward the nose.

The trochlear nerve is the only cranial nerve to exit from the dorsal aspect of the brain, and it has the longest intracranial course of any cranial nerves. Lesions that affect the fourth nerve include injury, inflammatory disease, compression from an aneurysm of the posterior cerebral and superior cerebellar arteries, and cavernous sinus entities. A lesion that affects the trochlear nerve causes diplopia and torticollis (twisted neck).

Fifth Cranial Nerve—Trigeminal Nerve

The trigeminal nerve supplies both sensory and motor fibers to the face and periorbital area. The afferent sensory fibers supply sensation to the face, scalp, tongue, teeth, conjunctiva, tympanic membrane, and mucous

FIGURE 3-11 ■ Testing the olfactory nerve. One nostril is occluded by the examiner. The patient is asked to sniff extracts of vanilla, coffee, and peppermint, and attempts to identify each of them.

membranes of the paranasal sinuses. Motor efferent fibers function to innervate several facial muscles, including the muscles of mastication.

Three tests are used to evaluate the trigeminal nerve: the corneal reflex test, the sensory division test, and the motor division test. The examiner evaluates the corneal reflex by gently touching the temporal side

of the cornea with a thin sterile braid of cotton while the patient looks down and toward his nose. Normally, the patient immediately shuts his eyes. This procedure tests both the sensory fifth nerve and the motor portion of the seventh, or facial, nerve, which is responsible for lid closure (Figure 3-12, A).

To test the sensory division of the fifth nerve, the examiner should ask the patient to close his or her eyes, and then lightly touch one side of the patient’s forehead with a tissue. Next, the examiner should touch the other side and ask the patient to compare sensations. A reduced sensation of touch on one side may indicate a hemiparesthesia. The test is repeated on the cheeks to test the second division of the trigeminal and on the chin to test the third division (Figure 3-12, B).

To test the motor component of the trigeminal nerve, the examiner should ask the patient to clench his or her teeth to produce a prominence of the masseter muscle. The examiner should palpate both masseters and compare the muscle tone of both (Figure 3-12, C).

One of the most common causes of sensory loss of the fifth nerve is fracture of a facial bone, especially a blow-out fracture of the orbital floor. This trauma may cause ipsilateral reduction or loss of feeling on the cheek. Vascular damage, tumors of the pons, and trauma may cause damage to the motor neuron or its axons.

C

A blow-out fracture can cause numbness to the gum behind the incisor. To test this, the examiner should push the wooden end of a sterile, cotton-tipped applicator gently into the patient’s gum behind the incisor tooth of the uninvolved side. The procedure is repeated on the involved side, and the patient is asked to compare the sensations on both sides. A blow-out fracture of the orbital floor can cause a reduced sensation to this area of the gum on the ipsilateral side.

Sixth Cranial Nerve—Abducens Nerve

The abducens nerve supplies only somatic efferent motor fibers to the lateral rectus muscle of the eye. This muscle functions to abduct the eye.

To test the abducens nerve, have the patient’s eyes follow a near target through the physiologic “H” pattern. An inability to abduct the eye indicates a possible abducens deficit. Patients with abduction deficit may complain of diplopia and may appear esotropic. Causes of abducens deficit include trauma, meningitis, cerebellar tumors, increased intracranial pressure, and cavern-

ous sinus pathology, and aneurysms of the posterior cerebellar or basilar arteries or internal carotid arteries.

Seventh Cranial Nerve—Facial Nerve

The facial nerve supplies efferent motor innervation to the muscles of facial expression and lacrimal gland (and others), and sensory afferent fibers from the anterior two thirds of the tongue for taste. Testing of the facial nerve involves examination of the muscles it innervates. Four tests can easily evaluate the seventh nerve. First, the examiner should ask the patient to smile or bare his or her teeth without laughing, and look for any asymmetry of the cheeks that might indicate a hemiparesis of the nerve (Figure 3-13, A). Next, the clinician should push in on the patient’s cheeks with the fingers while the patient attempts to puff out both cheeks. Then, the patient should attempt to wrinkle his or her forehead. A weakness on one side of the forehead causes a diminution in the wrinkling on the affected side (Figure 3-13, B). Finally, the patient should tightly shut his or her eyes while the examiner

36 DIAGNOSTIC PROCEDURES

A

B

C

FIGURE 3-13 ■ Testing the facial nerve. A, The patient bares his or her teeth and the nasolabial folds on either side of the face are compared. B, The patient wrinkles his or her forehead and the wrinkling of the two sides is compared. C, The examiner attempts to pry open the patient’s tightly shut eyelids.

attempts to pry the eyelids open. A weakness of the facial nerve allows for a relatively easy parting of the lids (Figure 3-13, C).

Bell’s palsy is a common lower motor neuron lesion of the facial nucleus or its axon. All voluntary and reflex muscles ipsilateral to the lesion are affected. The result is facial asymmetry with drooping of the eyebrow, a smooth nasolabial fold, drooping of the corner of the mouth, and a reduced blink reflex on the affected side. All patients who have a new case of Bell’s palsy should have a Lyme titer determination, because Lyme disease can produce hemifacial palsy (see Chapter 6).

Eighth Cranial Nerve—Vestibulocochlear Nerve

The eighth cranial nerve is composed of two special sensory afferent fibers. One fiber controls vestibular function, or balance, and the other controls audition, or hearing. Evaluation of the eighth cranial nerve for audition is covered in Chapter 2. The Rinne and Weber’s tests are easy to perform in the examination room and can help the examiner differentiate conductive deficits from neurosensory lesions (Figure 3-14) (see Chapter 2). No useful screening test currently exists to evaluate balance or vestibular function. Damage to the hearing apparatus or eighth cranial nerve can be caused by tumors, injury, or infection. Damage to the vestibular apparatus is most often caused by a tumor called an acoustic neuroma, which leads to nausea, deafness, dizziness, tinnitus, hearing loss, Bell’s palsy, and loss of balance. These symptoms occur because the eighth and seventh nerves run together along part of their paths.

A

FIGURE 3-14 ■ Testing the vestibulocochlear nerve. A, The Rinne test for audition. A tuning fork is held against the mastoid process until the patient can no longer hear it. The stillvibrating fork is then brought to the ear.

Ninth Cranial Nerve—Glossopharyngeal Nerve

The ninth cranial nerve supplies motor fibers to the parotid gland and the pharynx. It also supplies sensory fibers from the carotid body (to monitor oxygen tension in the blood) and from the posterior third of the tongue, mediating the taste sensation in the posterior tongue. Because the ninth cranial nerve innervates the pharynx, testing the gag reflex evaluates the integrity of the nerve. Light stroking of the wall of the pharynx should cause the patient to gag. A damaged nerve results in an absence of this reflex. The tenth and eleventh cranial nerve pathways are so close to those of the ninth that one rarely sees an isolated lesion of one of these nerves.

For an additional test of the integrity of the ninth and tenth nerves, the examiner should ask the patient to open his or her mouth and say “ahh.” This action raises the soft palate high up in the back of the oral cavity. The uvula, a small, cone-shaped piece of tissue suspended from the back of the throat, should elevate without lateral deviation (Figure 3-15). Paralysis of the ninth nerve causes a pulling of the uvula to the unaffected side.

Tenth Cranial Nerve—Vagus Nerve

The tenth cranial nerve contains both sensory and motor components. The nerve receives sensory afferent fibers from the larynx, trachea, esophagus, pharynx, and abdominal viscera, and sends efferent motor fi- bers to the pharynx, tongue, larynx, and thoracic and abdominal viscera.

FIGURE 3-15 ■ Testing the glossopharyngeal nerve and vagus nerve. The patient sticks out his or her tongue and says “ahh.” This action elevates the soft palate. The uvula should elevate without lateral deviation.

A unilateral lesion that affects the vagus nerve causes a loss of laryngeal function, producing hoarseness and difficulty in swallowing. To evaluate the vagus (and the ninth cranial nerve), the examiner should perform the “ahh” test described in the preceding section on the ninth cranial nerve (see Figure 3-15). Causes of unilateral vagus lesions include trauma from surgical procedures of the neck (such as carotid endarterectomy or thyroidectomy), aortic aneurysm, and metastatic carcinoma, in which enlarged paratracheal lymph nodes can compress the vagus nerve.

Eleventh Cranial Nerve—Accessory Nerve

The accessory nerve carries only efferent motor fibers to supply innervation to the sternomastoid and trapezius muscles. Damage to this nerve causes a drooping of the ipsilateral shoulder and loss of trapezius function on the affected side. The patient may have difficulty turning his or her head to the side that is opposite the lesion.