Evidence of disease in other body systems may be associated with inflammatory, metabolic, toxic, or metastatic neoplastic disorders of the nervous system. Infections of the CNS may not have any signs other than neurologic. External signs of trauma or toxic exposure may support these mechanisms of disease.
The neurologic examination consists of evaluation of the following: 1) the head, 2) the gait, 3) the neck and thoracic limbs, and 4) the trunk, pelvic limbs, anus, and tail. Initially, an attempt should be made to relate all deficits to one focal anatomic lesion.
If abnormalities are found on evaluation of the head, then an initial attempt should be made to explain all limb abnormalities by a lesion above the foramen magnum. If no abnormalities are found on evaluation of the head, but thoracic limb abnormalities are present, then an attempt should be made to explain the abnormalities by a cervical lesion (C1 to T2). Paralysis or paresis of all four limbs with loss of all spinal reflexes (with or without cranial nerve deficits) is often associated with diffuse peripheral nerve or neuromuscular junction disease (see Diseases of the Peripheral Nerves and Neuromuscular Junction).
Knowledge of specific diseases within a certain mechanism for a given species, age, breed, and sex of animal enables an accurate list of differential diagnoses and a diagnostic plan to be formulated after the history and physical and neurologic examinations are completed. Toxic, metabolic, and nutritional mechanisms rarely produce asymmetric neurologic deficits. The other mechanisms of disease may result in symmetric or asymmetric deficits.
Mentation, head posture and coordination, and cranial nerve functions are observed during evaluation of the head. Abnormal findings are due to lesions above the level of the foramen magnum in the cerebrum, the brain stem (diencephalon, midbrain, pons, or medulla oblongata), or the cerebellum. Dementia, compulsive pacing, or other behavioral abnormalities and seizures are frequently due to lesions in the cerebrum or diencephalon. Stupor, obtundation, semicoma, or coma may be due to lesions of the cerebrum, diencephalon, or midbrain. A head turn or compulsive circling without a head tilt is also associated with a cerebral or diencephalic lesion on the side toward which the animal turns. A head tilt is due to vestibular system disease (CN VIII, rostral medulla oblongata, or cerebellum). Abnormal head coordination, bobbing, and tremors result from cerebellar dysfunction.
The cranial nerves consist of 12 pairs located in specific brain-stem segments; they are simple to test, and test results can help localize disease to that segment. Abnormal findings are produced by lesions of the peripheral cranial nerve or cranial nerve nuclei. If a brain-stem lesion is present, abnormalities are seen in the gait, thoracic or pelvic limbs, and at times mental status. If only a peripheral cranial nerve is affected, there are no changes in gait, the thoracic or pelvic limbs, or mentation. Cranial nerve lesions of one side produce ipsilateral deficits except for lesions of the trochlear nerve (CN IV), which crosses in the midbrain.
The olfactory nerves transmit smell.
The optic nerves are necessary for vision and also carry the afferent fibers of the pupillary light reflex to the midbrain.
Cotton balls can be dropped and the animal observed watching them fall to the floor. The menace response is tested by making a threatening gesture toward each eye, causing the animal to blink. The animal sees the menacing motion (CN II) and blinks the eye (CN VII). In foals and calves this reflex will be evident by 7–10 days of age, whereas in puppies and kittens it may not be present until 10–12 wk. Excessive air currents or touching the eyelashes should be avoided, because this will test response to touch (CN V) rather than vision. Obstacle testing may be necessary when visual acuity is in doubt. It is useful to blindfold one eye at a time to detect blindness of either eye.
Unilateral optic nerve dysfunction results in a decrease or loss of vision and decreased pupillary light reflexes on the affected side. Consensual pupillary constriction of the affected eye should still occur when the other eye is stimulated with light. Unilateral lesions of the optic tract, lateral geniculate nucleus, optic radiation, thalamus, or occipital cortex usually produce a contralateral visual deficit with normal pupillary light reflexes (see above).
These nerves carry efferent parasympathetic fibers from the pupillary light reflex center of the midbrain to the fibers of the ciliary ganglion, which innervate the constrictor muscle of the pupils. They are also efferent to the levator palpebrae muscles; the dorsal, medial, and ventral rectus muscles; and the ventral oblique muscles of the eye.
These are the motor nerves to the dorsal oblique muscles of the eye.
These nerves have three branches. The mandibular branch is the motor nerve to the muscles of mastication and the sensory nerve to the floor of the oral cavity, ventral dental arcade, and the skin of the ventrolateral head. The ophthalmic and maxillary branches are sensory to the skin of the dorsolateral head; mucous membranes of the roof of the oral cavity, the dorsal arcade, and the nasal cavity; and the eyeball, including the cornea (pain).
Jaw tone and masticatory movements should be evaluated, and the masseter and temporalis muscles should be palpated for atrophy to evaluate the motor component of the trigeminal nerve. The sensory function can be evaluated by touching the medial and lateral canthi of the eyelid, which elicits the palpebral reflex and closure of the eyelids (trigeminal [CN V] primary afferent and facial [CN VII] efferent). Stimulation of the cornea causes both eyes to blink (trigeminal [CN V] primary afferent and facial [CN VII] efferent). In stoic animals, sensation is tested by a pinprick to the nasal mucosa (an avoidance response, turning the head away, will be seen).
These are the motor nerves to the lateral rectus and retractor bulbi muscles of the eye.
These are the motor nerves to the muscles of facial expression (ear, eyelids, nose, and mouth). The sensory part of CN VII is for taste on the rostral third of the tongue. The parasympathetic portion of CN VII innervates the tear glands.
The menace and palpebral reflexes should be elicited to test orbicularis oculi muscle function. The nose should be examined for deviation (with unilateral lesions). The lip should be pinched to see whether it retracts. The ear should be tickled to see whether it moves. Atropine or another bitter substance may be placed on the distal tongue to test taste. A Schirmer tear test should be performed to evaluate parasympathetic innervation of tear glands.
There are two main divisions of these nerves. The first division, the cochlear nerve, transmits auditory stimuli. The second division, the vestibular nerve, functions to maintain posture, muscle tone, and equilibrium.
Deafness is detected when loud noises do not evoke a response from an awake or sleeping animal. Unilateral deafness is best detected with electrodiagnostics, ie, a brain-stem auditory evoked response (BAER) test. (In puppies, this evaluation should not be performed before 6 wk of age, because results may be erroneous.) Head tilt, dysequilibrium, and a tendency to circle, fall, or roll to one side develop with unilateral or asymmetric vestibular lesions. The animal should be examined for the presence of spontaneous nystagmus with the head held in a normal position and in a deviated position (positional nystagmus), as well as for abnormal eye position (ventral strabismus) on the affected side when the nose is elevated. Normal vestibular nystagmus (physiologic nystagmus) is seen as a few beats to the left as the head is turned to the left, and to the right as the head is turned to the right.
Unilateral lesions of the vestibulocochlear nerves produce dysequilibrium with a head tilt toward the side of the lesion. A spontaneous positional, horizontal, or rotary nystagmus is often present. A positional nystagmus (one in which the character of the nystagmus changes with changes in the animal’s position) or a vertical nystagmus are almost always seen with central vestibular disease. A bilateral vestibular lesion results in dysequilibrium on both sides, wide side-to-side excursions of the head (often with no head tilt), loss of normal vestibular nystagmus, and possible deafness. Occasionally, a cerebellar or cerebellar peduncle lesion will result in a head tilt away from the lesion (paradoxical head tilt), but conscious proprioceptive deficits and hemiparesis will be ipsilateral with hypermetria of limbs on the ipsilateral side.
The glossopharyngeal and vagus nerves provide sensory and motor control of the pharynx and larynx, and the vagus nerves provide sensory and motor control of the viscera.
These nerves innervate the trapezius, sternocephalic, and brachycephalic muscles.
These are the motor nerves to the tongue and geniohyoid muscles.
The gait is observed while the animal walks, trots, gallops, turns, sidesteps, and backs up. In large animals, ambulation up and down a grade, on and off a curb, and while blindfolded may accentuate subtle gait deficits. Evaluation of gait is especially important in ambulatory large animals because postural reactions are difficult to obtain because of size and because spinal reflexes usually are not tested unless the animals are recumbent. In small animals, subtle deficits may be detected by postural reaction testing of the limbs (see Evaluation of the Neck and Thoracic Limbs) and by hemistanding and hemiwalking (standing or walking on one side). Animals with chronic lesions in the cerebral cortex and diencephalon usually have a relatively normal gait but may circle compulsively. Animals with lesions of the midbrain, pons, and medulla oblongata have paresis or paralysis of the limbs, with deficits often more severe on the side of the lesion. Cerebellar lesions produce ataxia and dysmetria. Vestibular dysfunction causes ipsilateral falling, rolling, or circling. If no abnormalities are found on evaluation of the head, but the gait is abnormal, a lesion most likely is located in the spinal cord, peripheral nerves, or muscles.
The neck is examined for pain and, in large animals, atrophy and desensitization to pinprick, which indicate a lesion of the cervical spinal cord. Wheelbarrowing, tonic neck and eye, conscious proprioceptive positioning, placing, hopping, and righting are postural reactions that detect subtle lesions.
The pelvic limbs of small animals are lifted slightly off the ground while keeping body posture as normal as possible, and the animal is evaluated while walking on the thoracic limbs. This test is used to detect subtle deficits of the thoracic limbs. Normal animals should not stumble or knuckle over on the toes as they walk.
With the dog or cat standing, the nose is elevated and the eyes observed to see whether they coordinately adjust to the center of the palpebral fissures. In vestibular dysfunction, the eyeball on the affected side rotates downward (positional strabismus or eye drop). Simultaneously, the thoracic limbs should extend with no tendency to knuckle or collapse, and the pelvic limbs should flex.
Small animals may be carried toward a table top; on seeing the table, a normal animal anticipates placing its forepaws on the surface. If blindfolded, the animal should place the forepaws on the table only when the limbs contact the edge of the table. A loss of placing response may be present in subtle dysfunction even when the gait is normal.
In small animals, three legs can be held off the ground with normal posture maintained, and the animal forced to move or hop (by being pushed laterally and forward) on the fourth limb. For large dogs and other large animals, one pelvic or thoracic limb opposite the side to be tested is held off the ground. When the animal is pushed toward the side to be tested, it should hop on the limb. Animals will not hop when pushed in a medial direction. Motor and proprioceptive loss, cerebellar incoordination, and cerebrocortical deficiency may be detected.
The animal is observed to see whether it can right itself from lateral recumbency. A small animal suspended upside down by the hips attempts to hold its head up when the trunk is rotated from side to side and extends its forelimbs to support weight when lowered to the ground. With vestibular dysfunction, the animal twists toward the side of the lesion or curls its head under (bilateral vestibular lesions).
The spinal reflexes are tested with the animal in lateral recumbency and the limbs relaxed. When the toes or skin of the distal thoracic limb are pinched, that limb should withdraw and the opposite limb usually does not move. This is the flexor or withdrawal reflex; it is present if spinal cord segments C6 to T2 and nerves of the brachial plexus are intact. Intramedullary spinal cord lesions at C6 to T2 usually depress or abolish the reflex, but mild extramedullary lesions may produce no change. With lesions cranial to C6, a simultaneous extension of the opposite limb (the crossed extensor reflex) may occur when the tested limb flexes. The crossed extensor is a normal reflex; however, an exaggerated response is interpreted as an upper motor neuron (UMN) sign indicating loss of inhibition from the UMN. The Babinski reflex is elicited by stroking the palmar surface of the paw in either a carpus to toe or toe to carpus direction. A positive (abnormal) response would be dorsiflexion of the toes, which is interpreted as a UMN sign.
Other tendons (biceps and triceps) and muscles (extensor carpi radialis) may be tapped with a percussion hammer and the response evaluated to test C6 to C7, the musculocutaneous nerve (biceps), and C7 to T2, the radial nerve (triceps, extensor carpi). These reflexes can be difficult to obtain in normal animals, so a reduced response should be interpreted with caution. All reflexes may be normal or exaggerated with lesions above C6.
Conscious perception of superficial (skin) or deep (osseous) pain is tested by applying forceps to the skin or bone, respectively, and observing a behavioral response. Such a response indicates that the peripheral sensory nerve and spinal cord, as well as the pathways through the brain stem to the cortex, are intact.
If the evaluation of the head is abnormal, an initial attempt should be made to explain any thoracic limb abnormalities by a lesion above the foramen magnum. If the thoracic limb abnormalities cannot be explained by a lesion in the head, then a multifocal or diffuse disease process (such as an inflammatory, toxic, metabolic, nutritional, traumatic, or metastatic neoplastic disorder) must be present.
If there are no abnormalities on evaluation of the head, and the thoracic limbs are abnormal, then a lesion of the cervical spinal cord or brachial plexus is present. In lesions of the cervical spinal cord, the gait of the thoracic and pelvic limbs is abnormal, and pelvic limb spinal reflexes are normal or exaggerated.
If no abnormalities are found on evaluation of the head and thoracic limbs, then a lesion must be below the T2 spinal cord segment.
The trunk of the animal is observed for abnormal posture or deviation of the vertebral column, pain, desensitization or hyperesthesia to light pinpricking, and focal muscle atrophy.
This reflex causes contraction of the cutaneous trunci muscle and is elicited by pinching or pricking the skin of the trunk between T2 and L6–7. The reflex arc includes the afferent cutaneous branches of the lumbar and thoracic spinal nerves, C8 to T1 spinal cord segments, and LMNs in the lateral thoracic nerve innervating the cutaneous trunci muscles. A focal spinal cord lesion that interrupts this pathway results in loss of the reflex caudal to the level of the lesion.
Wheelbarrowing, proprioceptive positioning, placing, and hopping are evaluated on the pelvic limbs in a manner similar to that used for the thoracic limbs. As with the thoracic limbs, these tests require complete integrity of the brain, spinal cord, and peripheral nerves; thus, they are useful to localize lesions and to detect subtle deficits that support the presence of a neurologic lesion.
The pelvic limb spinal reflexes are more reliable to localize thoracolumbar lesions than are the thoracic limb reflexes. Spinal reflexes are normal or exaggerated with lesions above the reflex arc (UMN) and are depressed or absent with lesions at the level of the reflex (LMN). Percussion of the patellar tendon should cause the stifle to extend if L4 to L6 spinal cord segments and the femoral nerve are intact. Percussion of the gastrocnemius and cranial tibial muscles causes the hock to extend or flex, respectively, and tests the tibial and peroneal nerves, lumbosacral plexus, and L6 to S2 spinal cord segments. A crossed extensor reflex may be associated with lesions above L6 (UMN sign). When the anus is pinched or pricked with a pin, the sphincter tightens and the tail pulls down if S1 to S3 (anus) and caudal (Cd) tail segments and nerves are intact. An atonic (areflexic) bladder, anus, and tail are seen with lesions affecting S1 to Cd5 or the cauda equina. As an incidental finding, the femoral (patellar tendon) reflex may be absent in some geriatric dogs.
In some animals with acute, severe lesions of the spinal cord between T2 and L3, the pelvic limb paralysis is accompanied by an extensor rigidity of the thoracic limbs when the animal is in lateral recumbency. This occurs because of an interruption of an ascending spinal cord tract from the lumbar intumescence, which inhibits extensors of the forelimb. Although a severe lesion produces this syndrome, the prognosis is probably not hopeless if deep pain sensation can be elicited from the pelvic limbs.