2 The neurological examination
Examination of nervous system function is achieved by observation, palpation and inducing reflexes and responses. The following section will explain the significance of the tests and how to perform them.
Mental alertness is sustained by a network of neurons within the brainstem (ARAS: ascending reticular activating system) that project to the cerebrum. Damage to either alters alertness. Systemic illness commonly causes decreased alertness in the absence of primary structural neurological disease. Voluntary actions originate from the cerebrum and are influenced by the patterns of behaviour of that species and learnt behaviour imposed by domesticity; it is therefore important that the clinician is aware of normal species behaviour and the level of training (if any) of the animal. Inappropriate responsiveness to the environment indicates cerebral malfunction, or a psychological disturbance (Fig. 2.2).
A depressed mental state can alter responses. A response, used in a neurological sense, is an action which requires a degree of input from the cerebrum (cf. a reflex action). The menace response, proprioception and pain perception may be absent or inconsistently present with a decreased alertness.
Observe the animal. Notice its interaction with other animals and humans in the waiting room. Once in the examination room, remove any leads and allow the dog to wander around the examination room unrestricted unless there is a loss of balance, history of trauma, paralysis, or any possibility of aggression. This can be done while the history is being taken. Most dogs investigate new surroundings and then either rest, return to the owner for attention, or try and escape out of the examination room. If the latter occurs, ask the owner to restrain the dog. If the dog appears abnormally quiet, or is excessively timid, it is useful to walk the dog outdoors and see if its mental state changes. Ask the owner if the behaviour witnessed is the normal reaction of the animal at the veterinary practice or at home.
Most cats will refuse to exit their cat baskets. Once removed from this shelter, the normal cat usually seeks refuge under chairs, tables or behind waste bins, and refuses to move. Some normal cats do wander about the room and investigate and may or may not voluntarily return to the basket. It is a good idea to keep the cat confined until one’s full attention can be given to observation of both the mental state and the gait. This is to prevent the cat from jumping until the balance and strength have been assessed. It is also because of the fact that many cats will walk a little initially and then refuse to budge.
Notice if, and how, the animal responds to its name, noise and visual stimuli. Does it walk about the room without taking note of distractions? Does it bump into objects, get stuck in narrow places and have problems reversing out, or turn a particular way when changing direction? Does it stop and appear to stare into space, at a wall or into a corner? None of these behaviours are normal (Fig. 2.3).
Describe the abnormal mental state (see page 47) stating what is abnormal about the level of alertness or the appropriateness of the animal’s response to its surroundings. This will act as a better comparison with subsequent examinations than a simple, bald statement of ‘dull’. The clinician will need to decide if the evidence from the history and the examination supports a neurological cause of the altered mental state or not.
The position of body parts is notably influenced by balance, proprioception, coordination, strength and painful stimuli. The significance of an abnormality will only become obvious once the entire examination is complete.
When sitting, the weak or paralysed hindlimbs may extend straight out between or amongst the forelimbs. The paretic animal is often slow to rise from a sitting position and the hindlimbs may not be fully extended when standing, or could be further apart than normal (abducted) (Fig. 2.5).
Note the spontaneous movement of the neck. If the animal shakes its head or body, is the neck moved as vigorously as normal, or at all? Does the head turn when the animal changes direction or is the whole body, head-neck-trunk, moved as a unit? Is the head elevated into a normal position or is the spine held in one straight line? Restriction of neck movement is a sign of pain. Ventroflexion of the neck in cats is usually a sign of weakness. It may not be noticed if the cat is always lying down resting its head on the forepaws or ground. The neck may be lowered and the back may be arched in an effort to shift weight to the forelimbs in cases of hindlimb or back pain.
Watch for tremors of the trunk and the head at rest and during movement. Offer the animal something to smell and notice if there is any intention tremor of the head. Record the position of the head and if it is turned or tilted or both, and to which side (Fig. 2.7).
If the animal is recumbent, is it able to lift its head from the floor? And its forequarters? An animal in lateral recumbancy needs to lift its head before rising. If the neck is painful, or the animal is tetraparetic, it may not be able to rise unaided. Does it roll? Rolling is a sign of vestibular disease.
It is not necessary to perform the righting reflex by which an animal is held upside down off the ground by its pelvis. The normal response is for the animal to automatically assume a 45° angle to the horizontal with the forelimbs outstretched toward the ground. The sensory stimuli are from visual and vestibular input. If blindfolded, the normal animal will still assume the same posture. If vestibular dysfunction is present, the animal will curl up or writhe about.
Movement is initiated by the upper motor neuron (UMN), a collective name for the nerve cell bodies within the cerebrum and brainstem and their axons which form the descending motor tracts (fasciculi) of the brainstem and spinal cord. The UMN initiates and maintains normal movement and influences extensor muscle tone to support the body against gravity (Fig. 2.8).
The UMN terminates on interneurons within the spinal cord which have an excitatory or inhibitory effect on the lower motor neuron (LMN). The LMN is the collective name for the motor neurons and their axons which directly connect to muscle. The term LMN encompasses the motor neurons of the cranial nerves as well as the peripheral and spinal nerves, their neuromuscular junctions and the muscles themselves. It also applies to the autonomic nervous system although the LMNs in that case may be referred to as preganglionic or postganglionic.
UMN and LMN lesions both cause weakness. Weakness may be observed by a slowness to rise from sitting, inability to support the body weight or an inability to initiate and sustain movement. Weakness is a diminution of voluntary movement. Paralysis is an absence of voluntary movement.
UMN lesions are differentiated from LMN lesions by the quality of spinal reflexes and muscle tone. UMN lesions result in a loss of descending inhibition and a subsequent increase in muscle tone and spinal reflexes is observed. LMN lesions remove innervation to the muscles and a decrease in muscle tone and spinal reflexes is seen.
Observing the gait alone does not provide sufficient information for the clinician to assign the lesion to a specific part of the nervous system (i.e. LMN vs. UMN). Spinal reflexes must be tested and muscle tone must be assessed (Table 2.1).
|UMN lesions||LMN lesions|
|Paresis or paralysis||Yes||Yes|
|Spinal reflexes||Normal to increased||Decreased or absent|
|Muscle tone||Normal to increased||Decreased or absent|
|Atrophy||Gradual (disuse)||Rapid (denervation)|
It is also important to note that certain orthopaedic diseases can change the gait in a way that suggests neurological disease. Equally, lameness may result from certain neurological diseases. Thus, while observation is crucial, the clinician must actually touch the animal in order to differentiate orthopaedic from neurological causes of abnormal gait.
Strength is only one aspect of the gait. Balance and coordination change the direction and extent of limb movement. Cerebral lesions can result in circling, pacing, head pressing; movements which appear normal in execution but apparently purposeless in function, with a propulsive, relentless quality. The circling is towards the side of the cerebral lesion (Fig. 2.9).
Proprioception is the perception of the body in space. Position and movement of the head is chiefly detected by the vestibular apparatus in both inner ears (special proprioception). Receptors in muscles, tendons and joints project sensory information into the CNS (general proprioception). This is then transmitted to the cerebrum (conscious proprioception) and to the cerebellum (unconscious proprioception) by ascending pathways. Projections to the cerebellum enable it to regulate the gait. Cerebellar lesions do not cause weakness. Reduced or absent proprioception causes ataxia. Associated deficits found on examination help localize the lesion to the vestibular system, the cerebellum, the spinal cord, or the cerebrum. (Lesions of the special proprioception receptors are common. Lesions of the general proprioception receptors are rare.) Ataxia is a sensory phenomenon.
Observe the animal’s ability to move. Normal animals are able to rise and walk unaided on floors with no grip (linoleum, floorboards). Weak and ataxic animals should ideally be examined on a non-slip surface. If the animal is paraparetic, support it under the abdomen so that any movement of the hindlimbs can be seen. If the animal is unable to rise, enlist assistance to hold the animal in a normal standing position and slowly move or coax it forward without releasing support. This is to determine if the animal is ambulatory tetraparetic (weak but able to walk unaided) or non-ambulatory tetraparetic (unable to walk without assistance). Sometimes paraparetic animals will not move the hindlimbs when a sling supports their abdomen. Remove the sling, and support the hindquarters with a hand under the inguinal area, or with a hand on either flank. Have an assistant coax the animal forward and watch for any hindlimb movement.
Do not confuse muscle tone with voluntary movement. UMN paralysis increases muscle tone and such an animal may be ‘propped’ up into an upright, standing, position. Rigor mortis also increases muscle tone, and there is no way that a dead animal could be said to possess voluntary movement.
Neurological deficits are noticeable when the animal is walking. Lameness shows up at faster gaits. Observe the gait from the side, front and from the rear. Squat down to observe the footfall of smaller dogs and cats (Figs 2.10, 2.11).
Walk the dog in small-radius circles: ask the owner to stay in the centre of the circle and lead the dog in a clockwise then anticlockwise direction. Watch for circumduction of the outer hindlimb; the limb on the periphery of the circle may swing out to the side in an arc when advanced. This indicates either a proprioceptive deficit, restricted movement of the joints, or increased muscle tone. If the dog will not cooperate by walking in tight circles, watch the limbs when the animal turns and changes direction in the examination room when off the lead.
Postural reactions are tests of strength and coordination. They distinguish the normal from the abnormal limb. Cerebral lesions can leave the gait unaffected, producing contralateral paresis and proprioceptive deficits only noted when performing postural reaction tests. Orthopaedic disease, myopathies and defects in neuromuscular transmission may leave an animal unwilling or unable to weight-bear on a limb, but the proprioception is left unaffected.
The animal is supported under the abdomen by one of the clinician’s hands. The other hand grasps the antebrachium, flexing the limb off the ground. The animal is gently pushed laterally, away from the centre of gravity (Fig. 2.12).
The clinician notes any delay in initiating the hopping movement (a sign of weakness, or a conscious or unconscious proprioceptive deficit) and the degree of lateral movement of the tested limb (reduced by weakness, exaggerated with cerebellar disease). A weak limb may collapse, so the clinician must be ready to prevent the animal falling forward. If the animal cannot support weight on the forelimb being tested without collapsing, the clinician should support the forequarters with a hand under the sternum. Do not allow the owner to hold the head or the lead around the animal’s neck as this removes the animal’s weight from the forelimbs making it easier for the animal to hop (Fig. 2.13).
A similar technique is used. The body weight is supported by a hand under the animal’s sternum; while the examiner’s other hand holds one hindlimb in a flexed position. This is easier to perform with the animal’s head facing the clinician. The point of supporting some or all of the animal’s weight is to ensure that the limb being hopped is weight-bearing. It is very important, whether testing the fore- or hindlimbs, that the animal remains in as normal an anatomical position as possible, with the spine as parallel to the ground as possible (Fig. 2.14).
This is a useful technique for larger, heavier dogs. The clinician stands on one side of the animal, lifts the ipsilateral fore- and hindlimb, and slowly pushes the animal laterally, away from the clinician (Fig. 2.15).
The animal hops on both limbs. This is a useful test for those animals that will not hop on the hindlimbs: normal dogs will sometimes extend the hindlimb and leave it to slide to the side when being pushed by the clinician. When hemiwalking, the animal has to hop or it will fall. This technique should be used with caution in the weak animal as the clinician is poorly positioned to prevent the animal from falling. Hemistanding describes the animal supporting its body weight using the limbs on one side of its body.
It is not physically possible to support the body weight of a giant breed dog while hopping it. This is overcome by leaving the forelimbs on the ground when hopping the hind, and vice versa when testing the forelimbs. Alternately, hemiwalking is used. Long-limbed sighthounds and short-limbed clinicians is another difficult combination which can be resolved with the same technique.
When the body is pushed laterally and the shoulder is no longer vertically aligned with the paw, the limb hops laterally so that the paw is once again ‘under’ the shoulder and weight-bearing is achieved. An abnormal response is a delayed movement of the limb, an exaggerated movement of the limb (hypermetric and overreaches, the paw being placed too far laterally), no movement or collapse of the limb. Slow movement with a decreased range and collapse of the limb indicate weakness of the limb. A delayed onset of movement with preservation of strength is common with cerebellar lesions. A delayed onset with collapse of the limb indicates weakness.
assesses the forelimb gait. It is physically more difficult to perform than hopping. The clinician supports all the weight of the hindquarters by placing a hand under the animal’s abdomen. The animal is then pushed forward. Cats almost uniformly refuse to cooperate and lie down which may be misinterpreted as forelimb weakness. It can be difficult to observe the movement of the forelimbs from one’s position at the rear of the animal. It can be difficult controlling the direction the dog walks, and they may struggle when manipulated in this fashion. One way around this is for the clinician to place the other hand under the dog’s head and dorsiflex the neck; this also removes visual clues and may highlight a proprioceptive deficit. It places an enormous strain on the clinician’s back and the information obtained can be more reliably gained by hopping and proprioceptive testing.
The clinician stands behind the animal and with hands around the thorax, lifts the animal’s forequarters and then the hind off the ground. The suspended animal is lowered to the ground, and its hindlimbs reach out and walk backwards. This is a useful alternative to hopping for testing hindlimb strength in cats. It is not routinely performed in dogs due to their size and weight. The normal response is for the hindlimbs to walk backwards, supporting weight to the same degree. A weak hindlimb is noted by it lagging behind or being dragged (Fig. 2.16).
Each limb, in turn, is tested by flexing the paw so that its dorsal surface becomes the weight-bearing surface. Normal animals will immediately turn the paw back to its natural position. An abnormal response is one in which the movement is delayed, does not occur, or replaces the paw too far forward, caudal, or lateral (abducted).
Technique is all important. Begin by supporting the animal’s weight under the abdomen, when testing the hindlimbs, and under the sternum when testing the forelimbs. Weak or painful animals may have normal proprioception but be physically unable to support their body weight and correct the ‘knuckled over’ paw. Some normal animals will only correct the paw’s position when the limb being tested is weight-bearing to some degree. The clinician slightly moves the animal, shifting its weight over to the tested limb to see if this is the case. Proprioceptive testing is a response and can therefore be affected by the animal’s level of alertness. Cats do not tolerate ‘knuckling’ of the hindpaws and it is usually easier to test the hindlimb proprioception with placing responses (Fig. 2.17).
is harder to perform and less consistent results are obtained. The animal’s paw is placed on a sheet of paper, which is then pulled to the side. The animal should return the displaced limb to a normal position. The problem is that a lot of normal dogs do not seem stimulated enough to return the limb to a normal position, and thus allow the limb to remain on the paper sheet. There is some thought that the paper slide test assesses the proximal limb proprioceptors and the ‘knuckling’ tests the distal limb proprioceptors. This is irrelevant in the clinical setting. Proprioceptive deficits occur because of lesions in the sensory nerves, the ascending proprioceptive pathways, the sensory relay nuclei of the thalamus or the sensory cortex of the cerebrum.
is another method of testing proprioception in smaller patients. The animal is held under the sternum and abdomen, picked up, and brought towards the edge of a table. The normal animal reaches for the table and places the forelimbs and hindlimbs on the table top without delay. Technique is very important. The animal must be brought towards the table at a speed which enables the animal time enough to move its own limbs. It must not be held so tightly against the clinician’s body that it is unable to freely move its limbs. For this reason it is good practice to test the animal by holding it on either side. Small animals often get their hindlimbs caught in the clinician’s lab coat pocket. Visual placing is the above technique performed without covering the animal’s eyes. Tactile placing is the above technique performed with a hand over the animal’s eyes (Fig. 2.18).
The animal soon learns to reach for the table, whether the eyes are covered or not. When performing tactile placing, approach the table at a slow, steady pace. Pausing in mid-space will induce the animal to reach for the table; this is a nice demonstration that the animal has learnt what to expect but it is not a measure of proprioception.
Proprioceptive deficits result in abnormal paw position when walking. Scraping, ‘knuckling over’ or dragging the dorsum of the paw against the ground flattens the dorsal surface of the middle two claws, wearing off the overlying fur. Examine all paws. This may not be noticeable if the dog is only walked on grass (Fig. 2.19).
Pain and joint abnormalities affect the gait and posture. Atrophy occurs with disuse, denervation, secondary fibrosis of muscle, generalized weight loss, and in some myopathies. Muscle enlargement may follow ischaemia, local inflammation, trauma, neoplasia, myotonia, and muscular dystrophy. The distal or proximal limb may be selectively involved.
Muscle tone is influenced by both the UMN and LMN. Judging the amount of muscle tone present, as assessed by palpation, contributes to the differentiation of LMN from UMN causes of paresis and paralysis.
The head is examined when the cranial nerve function is assessed. Ear canals should be palpated and smelt for evidence of otitis externa. Lymph nodes and tracheal sensitivity are checked as part of the physical exam.
Apply gradually increasing digital pressure to the dorsal spine and to the lateral spine to detect pain. A normal animal tolerates firm pressure. Hold the muzzle closed with one hand and slowly flex the neck laterally to either side. A normal animal is able to place its nose on its shoulder. An animal with neck pain refuses to move its neck. The clinician is able to feel increased neck tension or spasm and should not force the head laterally. Keep one hand on the neck while the head is dorsiflexed and then ventroflexed. The normal animal is able to look up at the ceiling and down at the floor without resisting neck movement. Do not perform this test in toy breed dogs with tetraparesis or neck pain as C1–C2 subluxation may be present. Fearful or excited normal dogs, or cats, may resist neck manipulation. Observe spontaneous movement of the neck; this is usually limited in range when neck pain is present.
Place one hand under the animal’s abdomen and with the other apply gradually increasing digital pressure to the dorsal spine to detect sites of pain. A normal animal tolerates firm pressure and does not collapse. If the animal resents palpation and struggles, wait until the animal calms down, and repeat the palpation to be sure that pain was the cause of the animal’s reaction. Pressure on a painful thoracic or lumbar spine causes the abdominal wall to tense which can be felt by the examiner. It can be confused with abdominal pain. Acute pancreatitis is usually accompanied by vomiting (cf. acute spinal pain). Weak animals may flex the limbs and collapse when pressure is applied to the spine. Some normal animals sit (Fig. 2.20).