Diagnostic Approach to Neurologic Disease

Chapter 125 Diagnostic Approach to Neurologic Disease



William R. Fenner, Philip A. March



PRINCIPLES OF NEUROLOGIC EXAMINATION



Objectives



• Confirm that neurologic disease is present.

• Localie the site of any lesion(s).

• Determine the extent to which the nervous system is involved.

• Guide the choice of diagnostic aids.

• Determine the prognosis.


Approach



• Perform the examination in a logical, methodical, and consistent manner.

• Develop a consistent sequence and follow it with all patients.

• Begin with the general and advance to the specific.

• Perform painful portions of the examination last.


PROCEDURES FOR THE NEUROLOGIC EXAMINATION



General Observations



Mental Status


Mental status is regulated by the brain stem and cerebrum and consists of level and content of consciousness.



• Begin by evaluating the level of consciousness. A normal animal is alert; an abnormal animal is depressed, stuporous, or comatose, depending on the severity of the mental depression. Abnormal levels of consciousness may result from lesions of the brain stem or diffuse cerebral disease.

• In addition to the level of consciousness, evaluate the patient for mentational disorders. Behavior of a normal animal is described as appropriate; an animal with abnormal behavior is considered demented.
• A demented animal is unaware and unconcerned with its surroundings. It may head-press, walk off tables, and in other ways show a complete disregard for its own safety and well-being.

• Dementia is a sign of a cerebral disorder.


Head Posture


Head posture is regulated by the vestibular system and the strength of neck muscles.



• A normal animal holds its head in a plane parallel to the ground.

• If an animal holds one ear closer to the ground than the other ear, it is described as having a head tilt, which suggests a vestibular injury.

• In some animals, the chin is tucked under or pulled tightly toward the sternum; this postural abnormality (ventroflexion) may be seen in cats with polymyopathies (e.g., hypokalemia) or thiamine deficiency and in dogs with cervical vertebral malformations.


Coordination of Head Movement


This is regulated primarily by the cerebellum. Disturbances of head coordination appear as head tremors.



Circling


Circling is a nonspecific finding in animals with brain disease.



• A lesion in any part of the brain may cause circling; the animal usually circles toward the diseased side.

• Circling in brain stem and cerebellar injury usually is a result of a vestibular dysfunction; therefore, circling is accompanied by a head tilt.

• Animals with cerebral injury circle, but they rarely have head tilts.


Gait and Stance



Gait


A normal gait requires integration of almost the entire nervous system; therefore, abnormal gaits may result from injury to almost any part of the nervous system.



• Sensory disturbances, such as loss of proprioception, usually result in ataxia or loss of coordination of limb movements. Signs of loss of coordination of the limbs include swaying, veering, crossing over of the limbs, and scuffing of the toes.



Key Point


Ataxia may be seen with disease or injury of the cerebellum, brain stem, spinal cord, and injuries to cranial nerve 8 (vestibular nerve). Cerebral and peripheral nerve lesions rarely cause ataxia.



• Cerebellar lesions cause ataxia in most patients.

• Cerebral lesions may produce mild weakness characterized by intermittent stumbling, tripping, and reluctance to initiate or sustain activity. More obvious signs of weakness may be caused by an injury to the brain stem, spinal cord, or peripheral spinal nerves. When classifying the weakness, also consider the resting muscle tone in the limbs.
• Spasticity is an increase in muscle tone resulting in decreased flexion of the limbs during movement. The resultant gait is rigid and choppy.

• Spasticity may be seen with injuries to the cerebrum, the brain stem, and some levels of the spinal cord.


Stance


Normal animals stand with their limbs at about shoulder or hip width, with the weight equally distributed on all four limbs.



• Abnormal posture may be caused by diminished position sense (proprioception), weakness, or pain.

• Many animals present with abnormal posture as a result of pain from orthopedic disorders rather than neurologic disturbances.


Tests of Postural Reactions


Attitudinal and postural (A-P) reactions test the integrity of the interconnecting pathways that regulate posture and movement as an extension of the evaluation of gait and stance. These tests evaluate the proprioceptive fibers of peripheral nerve, spinal cord, brain stem, cerebrum, and cerebellum. Some tests also evaluate special proprioception. The upper motor neurons and their connections to lower motor neurons are also evaluated.


Because so many portions of the nervous system are evaluated, A-P reactions are good screening tools for detecting nervous system disorders but are not very helpful with specific localization.



• With lesions of the cerebrum, the postural deficit normally is seen in the limbs on the opposite side of the body (contralateral) from the diseased hemisphere.

• With brain stem lesions, the clinical signs usually are bilateral but are worse on the same side (ipsilateral) as the brain stem injury.

• With lesions of the cerebellum, spinal cord, and peripheral nerves, the clinical signs are almost always on the same side of the body as the nervous system injury.

• With cerebellar injuries, A-P reactions usually are present but are ataxic.

• With peripheral vestibular injuries, A-P reactions are preserved, but the animal tends to lean, fall, and roll to the diseased side when the maneuvers are performed. Hemihopping may be slightly delayed on the same side as the vestibular lesion.


Proprioceptive Positioning


Abnormally abduct or adduct a limb, or turn the paw so that the animal bears weight on the dorsal surface of its paw (stands knuckled over). If A-P reactions are intact, the animal briskly brings the limb back to a normal resting position.



Hemihopping


Hold the limbs on one side off the ground while the patient is hopped sideways on its other two limbs. A normal animal has no trouble initiating a brisk hopping response without buckling or collapsing on the limb if conscious proprioception and strength are normal in that limb. Hemistanding the animal on one or two limbs can also be used to assess limb strength.



Wheelbarrowing


Hold the thoracic or pelvic limbs off the ground while the patient is walked forward and then backward on its other two limbs. A normal animal has no trouble maintaining itself and walking normally during this test.



Other Attitudinal and Postural Reactions


Additional A-P reactions include the extensor postural thrust reaction, the righting reaction, visual placing reactions, tactile placing reactions, and tonic neck reactions. All these tests evaluate the same basic pathways, although each may test one portion of the nervous system more completely than another. These tests are well described in standard neurology texts.



Cranial Nerve Examination


The cranial nerve (CN) examination tests the function of each CN. Often a CN deficit confirms the presence of a lesion above the foramen magnum. The CN examination allows precise localization of intracranial diseases in many cases. Because many CNs supply only the motor or the sensory component of a CN reflex, the testing of a CN reflex generally involves testing more than one nerve. This is unlike spinal reflexes in which generally the sensory and the motor components of a reflex are carried by the same nerve.


Many of the CN reflexes also are under higher control. Therefore, a CN reflex evaluates the following:


• Two peripheral CNs (one motor and one sensory)

• A central connection (usually the brain stem)

• A higher regulatory center (usually the cerebrum)

A lesion in any one of these sites may cause loss or depression of the reflex being tested. For a more complete review of the neuroanatomy of CNs, consult a neuroanatomy textbook.



Menace Response (see also Chapter 141)


The menace response tests CN2 (sensory) and CN7 (motor) and their central connections in the cerebrum, brain stem, and cerebellum. The test is performed by making a menacing gesture toward an animal. The normal response is an avoidance response (e.g., an eye blink or turning of the head).



• Loss of the menace response normally indicates a lesion in one of the following sites: retina (ipsilateral), optic nerve (ipsilateral), optic tract (contralateral), cerebrum (contralateral), brain stem (ipsilateral), cerebellum (ipsilateral), or facial nerve (CN7) (ipsilateral).

• False-positive menace responses also occur, most commonly when the movement of the hand produces air currents that stimulate the corneal reflex.

• Sounds and other distractions may make the menace response difficult to evaluate. Animals (especially cats) in a stressful environment may have an absent menace (false-negative finding).


Pupillary Light Reflex (see also Chapter 141)


This tests the reflex portion of the optic nerve (CN2) and the autonomic function of the oculomotor nerves (CN3). The test is performed by illuminating the eye with a bright light source. The normal response is rapid constriction of both pupils.


The pupillary constriction in the eye being illuminated is called the direct pupillary response. The constriction in the opposite pupil (the one being illuminated indirectly) is called the consensual response. Failure of one or both pupils to constrict is an abnormal pupillary light reflex (PLR).



• A lesion of CN2 produces loss of constriction in both pupils when the affected eye is illuminated; however, when the normal eye is illuminated, both pupils constrict.

• If the lesion is in CN3 or the brain stem, the affected pupil fails to constrict regardless of which eye is being illuminated, but the unaffected eye constricts normally when each eye is illuminated.

• Because ophthalmic diseases such as posterior synechia or severe iris atrophy may also produce loss of pupillary responsiveness, a thorough eye examination is essential in any patient with abnormal pupils.

• Other causes of a misleading PLR are increased sympathetic tone and a weak light source, both of which will slow the PLR.


Pupillary Symmetry


In this test the eyes are observed for equal pupil size.



• If CN3 and the sympathetic nerve to the eye are normal, the two pupils will be equal in size.

• If the pupils are unequal (anisocoria), this indicates possible damage to one of these two nerves.
• If CN3 is abnormal, the large pupil is denervated and the PLR will be absent in that eye.

• If the sympathetic nerve is abnormal, the small pupil is abnormal and the PLR will be normal in both eyes.

• Cats may have mild physiologic anisocoria if one eye is receiving more light than the other. For this reason, ensure that both eyes receive equal illumination when evaluating for anisocoria.

• A number of ophthalmic disorders may produce anisocoria, including glaucoma, iritis, uveitis, and synechia. Because of this, perform a complete ophthalmic examination on all patients with anisocoria.


Pupillary Size


The size of the pupil is determined by the amount of ambient light (CN2) and the integrity of the innervation of the pupillary muscles (CN3 and sympathetic nerve).



• Abnormally large pupils may be caused by excitement (sympathetic stimulation), bilateral optic nerve injury, CN3 paralysis, or ophthalmic disease.

• Abnormally small pupils may be associated with loss of sympathetic tone, excess parasympathetic tone, or ophthalmic disease.


Ocular Position


In normal dogs and cats, both eyes look in the same direction at any given time (normally straight ahead). This normal resting position is determined by the influence of the cerebrum and CN8 on the extraocular muscles (CN3, CN4, and CN6). If one of these portions of the nervous system is not functioning, deviation of one or both of the eyeballs may occur.


Strabismus is deviation of only one globe.



• Medial strabismus may result from an injury to CN6 (abducens nerve).

• Ventrolateral strabismus may result from injury to CN3 or CN8 (vestibulocochlear nerve).

• A lesion to CN4 (trochlear nerve) results in intorsion (a form of rotation) of the eye, which can be recognized only in animals with oval pupils or on ophthalmic examination.

• Passive deviation of both eyes in the same direction (gaze paresis) is sometimes seen in cerebral injuries.


Ocular Motility



Voluntary Eye Movement


Voluntary eye movement is initiated by cerebral stimulation of CN3, CN4, and CN6. As the animal looks around the examination room, observe to see if it appears unable to move the eyes in one or more directions.



• With a cerebral lesion, both eyes are involved, and there is a tendency for the eyes to look toward the diseased cerebral hemisphere.

• With a lesion of the CNs, only one eye is usually involved. The involved eye will tend to have strabismus at rest and lack the ability to move.


Involuntary Eye Movements: Nystagmus


Involuntary rhythmic oscillations of the eyes, termed nystagmus, can be induced by turning the head. This maneuver stimulates CN8, which in turn stimulates CN3, CN4, and CN6, which innervate the extraocular muscles. This involuntary eye movement is called physiologic nystagmus.



Physiologic Nystagmus

Physiologic nystagmus is characterized by a “slow phase,” in which the eyes move slowly away from the direction in which the head is turning, followed by a “fast phase,” in which the eyes rapidly move in the direction of the head turn. This recurring slow-fast, slow-fast oscillation continues as long as the head is moving.



• A lesion of CN8 or its central connections may result in loss of the ability to initiate physiologic nystagmus so that neither eye will move when the head is turned toward the side of the vestibular lesion.

• A lesion of one or more of the CNs that innervate the extraocular muscles (CN3, CN4, or CN6) paralyzes only that eye, resulting in loss of physiologic nystagmus in the paralyzed eye.


Pathologic Nystagmus

When a normal animal’s head is not moving, it does not display any involuntary eye movements. If nystagmus is present when the head is at rest, this is a sign of nervous system disease and is called pathologic nystagmus. This usually is the result of an imbalance in the special proprioceptive system, which includes CN8, the brain stem, and the cerebellum. A lesion of any of these structures can cause pathologic nystagmus. Features of pathologic nystagmus that may help localize its origin include the direction, method of induction, and persistence of the nystagmus.



• Direction of nystagmus:
• In horizontal nystagmus, the eyes move in a plane parallel to the head (i.e., the eyes move from side to side).



Key Point


Horizontal nystagmus is most commonly seen in peripheral vestibular disease but can occur in central vestibular disease (see Chapter 61). The fast component of the nystagmus usually is away from the diseased side.




• In vertical nystagmus, the eyes move in a plane perpendicular to the head (e.g., the eyes move up and down).



Key Point


Vertical nystagmus is most commonly seen in central vestibular disease. The fast component of the nystagmus is usually away from the diseased side; therefore, brain stem disease causes up-going nystagmus, and cerebellar disease causes down-going nystagmus.




• In rotatory nystagmus, the eyes rotate in a clockwise or counterclockwise direction in the orbit, with components of both horizontal and vertical movement. This type of nystagmus may occur with a peripheral or central vestibular lesion.

• Method of induction of nystagmus:
• Resting nystagmus occurs when the head is at rest and in a normal position. This type of nystagmus is most characteristic of peripheral vestibular disease but can be seen with central vestibular disease.

• Positional or induced nystagmus occurs when the head is still but is in an abnormal position (e.g., on its side or upside down). Positional nystagmus is most characteristic of central vestibular dysfunction (e.g., brain stem and cerebellar lesions). It is also seen during the recovery phase of peripheral vestibular diseases.

• Persistence of nystagmus:
• Permanent nystagmus persists over time. It may have any direction and method of induction, but it is consistently present. Permanent nystagmus is characteristic of most brain stem diseases and of progressive peripheral vestibular and cerebellar diseases.

• Resolving nystagmus disappears over a period of time (days to weeks). It does not recur unless there is new damage to the vestibular system. Resolving nystagmus is characteristic of nonprogressive peripheral vestibular and cerebellar diseases. In the recovery period of these diseases, nystagmus may become positional.


Facial Symmetry


Facial weakness (CN7) may result from injury to the contralateral cerebrum, ipsilateral brain stem, and ipsilateral peripheral nerve.



• Clinical signs include drooping of the lip, deviation of the nasal philtrum, increases in palpebral fissure size (pseudoptosis), and in some animals, drooping of the eyelid (true ptosis).

• Confirm the diminished muscle function by testing the palpebral and/or corneal reflexes.


Palpebral Reflex


This reflex tests CN5 and its brain stem connection to CN7.



• Initiate the reflex by touching the palpebral margins, which produces an eye blink. Loss of the eye blink reflex is usually complete if there is an injury to CN5 or CN7.

• In some animals with contralateral cerebral disease or myasthenia gravis, lagophthalmos or incomplete closure of the palpebral margins is observed.


Corneal Reflex


Like the palpebral reflex, this reflex tests CN5 and its brain stem connection to CN7.



• Initiate the reflex by lightly touching the cornea, which produces an eye blink.


Retractor Oculi Reflex


This reflex tests CN5 and its brain stem connection to CN6 (abducens nerve).



• Initiate the reflex by lightly touching the cornea, which produces retraction of the eye into the orbit.

• Lack of the reflex usually is a sign of neurologic dysfunction of CN5 or CN6.

• In some animals with loss of the retrobulbar fat pad, the eye may be enophthalmic and incapable of retraction, whereas in others, a retrobulbar mass may prevent retraction.


Facial Sensory Examination


This tests CN5 and its cerebral connections.



• Lightly stimulate the nasal mucosa, which should produce an avoidance response such as head turning or withdrawal.

• The nasal mucosa is a more reliable site for stimulation than the lips, which are relatively insensitive in some animals.


Gag Reflex


The gag reflex, which is easier to test in dogs than in cats, tests CN9 (glossopharyngeal nerve) and CN10 (vagus nerve) and their brain stem connections.



• To initiate the test, lightly stimulate the oropharynx, which should produce a swallowing reflex. Loss or depression of the reflex usually indicates brain stem or peripheral nerve dysfunction.

• Examine the pharynx for evidence of paralysis of the soft palate, and look at the larynx for evidence of laryngeal paralysis (may be difficult in an awake animal). Either condition may result from brain stem injuries or peripheral nerve injuries to CN9 or CN10.


Tongue Examination



• Look for atrophy of the tongue, which can be produced by brain stem or peripheral nerve injury to CN12.

• Also look for deviation of the tongue, which can be caused by cerebral injuries, as well as brain stem and peripheral nerve injuries. The tongue will deviate toward the side of the lesion.


Spinal Reflex Examination


The spinal segmental reflexes directly test the reflex arcs of the spinal cord. They also indirectly test the higher centers in the brain that regulate the spinal reflexes.




Key Point


If an injury occurs within the reflex arc, it will cause loss or depression of the reflex. Such a reflex loss allows precise localization of a nervous system injury. Because a lesion in the lower motor neuron (LMN) is involved, loss of reflexes is called an LMN sign or an LMN reflex change.




Key Point


If a lesion occurs cranial to a reflex arc, it disconnects the reflex from its higher (brain) regulation. This regulation tends to be inhibitory over specific proprioceptive reflexes such as the patellar and triceps reflexes. Loss of regulation results in exaggeration of these reflexes, especially the patellar reflex. Because this exaggeration reflects a lesion in the central nervous system (CNS) involving upper motor neuron (UMN) pathways, these reflex changes are called UMN signs or UMN reflexes.


UMN changes are not as precisely localizing as LMN reflexes. Spinal reflexes are classified into three groups:



• Proprioceptive reflexes

• Nociceptive reflexes

• Special (released) reflexes

This division is based on the type of sensory stimulation required to elicit the first two reflexes and on the special conditions required to elicit the third reflex.



Proprioceptive Reflexes


These myotatic reflexes are initiated by stretch of tendons or muscle spindles. The patellar reflex is strongly influenced by UMN pathways and, therefore, may be exaggerated with UMN lesions. Other proprioceptive reflexes either are not influenced or are weakly influenced by the UMN system. Increases and decreases in the force of reflex activity are both components of proprioceptive reflexes; thus, be sure to grade the strength of these reflexes. A standard grading scale is as follows:


0 = Absent reflex

1 = Diminished reflex

2 = Normal reflex

3 = Increased reflex

4 = Increased reflex with clonus


Thoracic Limb Proprioceptive Reflexes



Triceps Reflex

This tests the radial nerve that arises from spinal cord segments C7 to T2.



• Elicit by striking the tendon of insertion of the triceps muscle. A normal response is a slight extension of the elbow.

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Aug 27, 2016 | Posted by in SMALL ANIMAL | Comments Off on Diagnostic Approach to Neurologic Disease

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