The neurological examination and lesion localisation

Chapter 13 The neurological examination and lesion localisation





In veterinary medicine the primary aims of the clinical neurological examination are to establish whether a neurological disease exists and, if it does, to localise the lesion.


Localising the lesion is done by assessing the results of the neurological examination. Lesion localisation is essential as diseases are often region-specific and determining which region(s) is involved permits the clinician to establish a list of possible causes and then pursue appropriate diagnostic tests.


For example, a different region of their nervous system will need to be evaluated diagnostically in an animal that has proprioceptive deficits, paresis and normal cranial nerve function, compared with one that has proprioceptive deficits, no paresis, but has vision deficits in one eye. The former is probably a spinal cord lesion and the latter is probably a forebrain lesion. To localise the lesion, it is just as important to identify the neural functions that are NORMAL as well as those neural functions that are ABNORMAL.


To localise the lesion, the clinician observes the animal closely and performs specific, neurological tests that evaluate the function of different neural systems.


Note that a full physical examination including assessment of the ocular fundus must be performed for the clinician to diagnose and treat appropriately the animal’s condition. Many neurological conditions are associated with diseases elsewhere in the body. Tumours (multicentric or metastatic), metabolic and nutritional diseases, trauma, intoxications and vascular conditions are just some of the examples of systemic diseases that can cause neurological signs.


The following describes the neurological examination in a domestic cat or dog but the general principles are similar for large animals. Specific comments are given to modify the examination for large animals. This chapter represents the culmination of all the functional neuroanatomy described in chapters 112. Please see specific chapters for further details of structure and function.


During the examination, tests are performed that evaluate the following neural functions:



From the results of the tests, the clinician determines:



Using their knowledge of where those neural functions are situated in the CNS and PNS, the clinician should then be able to localise the lesion. Only when the lesion is localised can the clinician devise a sensible list of differential diagnoses and plan appropriate diagnostic tests. All this has to be done before appropriate treatment can be prescribed. Note: sometimes it can be quite difficult to localise a lesion and the neurological examination may need to be repeated several times to confirm results.


For example, if an animal is dysmetric and ataxic but is alert with good motor strength and cranial nerve function, then the lesion is unlikely to be in the spinal cord (i.e. no paresis), the forebrain or brainstem (normal arousal and cranial nerve function). However, a cerebellar lesion would account for the dysmetria and ataxia (incoordination) with preservation of the other neural functions.


It matters little where a lesion is located on a pathway (origin, midway along the pathway, or termination), it will still produce similar signs of dysfunction. This is analogous to a battery (origin), connecting wire (the pathway) and a light (end of pathway). Dysfunction in any one of those sections will cause the same outcome (clinical sign), that is, the light will not work. Most regions of the nervous system are associated with a number of functions either because a neural pathway begins or ends in that region, or is passing through it. The key to localising the lesion is based on having knowledge about which neural functions are associated with that region, and, conversely, which functions are not.


If a lesion is in a particular region, then it could damage pathways in that region and cause signs of dysfunction. However if a pathway does not pass through that region, then it will not be affected. Identifying the neural pathways that are functioning normally indicates to the examiner that the lesion is NOT located in the region that those systems occupy.


For example, if the lesion is in the thoracolumbar spinal cord, then pathways passing through that part of the cord may be damaged (see Fig. 13.15), such as proprioception and UMN tracts to the pelvic limbs causing proprioceptive deficits (conscious and subconscious) and either paraparesis or paralysis. But the lesion will not affect the cranial nerves, arousal or the function of the thoracic limbs, as those neural systems are not associated with the thoracolumbar spinal cord (Fig. 13.1).



An applied example of this diagram would be the animal that has conscious proprioception deficits on the right side of the body and blindness in the right eye (see Fig. 4.10). The conscious proprioceptive pathway (e.g. ‘B’ in Fig. 13.1) begins in the sensory receptors in the forepaw, travels via spinal nerves into the spinal cord, travels cranially in the ipsilateral cervical spinal cord, into the brainstem, crosses over and passes rostrally on the contralateral side to the somatosensory cortex. The lesion could be anywhere along that long pathway. ‘A’ represents the cranial nerves that attach to the brainstem (III–XII) and the UMN centres in the brainstem and ‘C’ represents the visual pathway. As there are no other cranial nerve deficits, or paresis, then the lesion is unlikely to be in region ‘X’. But both the right-side visual pathway (C) and right side proprioception are associated with the left side of the forebrain. Thus the lesion is in region ‘Y’.



The neurological examination


To find out as much information as possible about a patient requires both keen observation before handling it, and then doing hands-on testing of neural functions. Begin with observation, then move to hands-on testing to assess function of the long tracts (proprioception, motor function), the cranial nerves, spinal reflexes, muscle tone and bulk and, finally, spinal hyperpathia. This order of testing is from the most benign to the most noxious. A full physical examination must also be performed.



Observation versus hands-on testing


The functioning of the majority of the nervous system can be assessed by close observation (Fig. 13.2). This is particularly useful if the animal cannot be handled; for example if it is fractious or wild. For animals that you can handle, then observation is still critical for getting an overall impression of neural function and is an excellent opportunity to assess arousal and behaviour. Physical contact usually stimulates the animal and subtle deficits in mental alertness may be missed. Assessing the animal’s arousal level is done best by observing its interaction with the environment. Answering the following questions provides useful information.



Does it respond normally to environmental stimuli? These may include visual, auditory, olfactory, tactile and possibly gustatory stimuli. Does it seem bright, alert and responsive or dull and somnolent? (see Figs. 11.3 and 11.4)


Is the posture of its head, body, limbs and tail normal at rest and during locomotion? (See Fig. 6.2) Does it move normally or are there signs of proprioceptive deficits (stumbling, postural abnormalities), ataxia, stiffness, pain or paresis? If so, which limbs and which joints are functioning normally and which are dysfunctional? Is there any change in muscle bulk?


Observe the head closely. Is the head posture normal? Is there any asymmetry of the face (drooping, muscle wasting)? (see Fig. 10.12) Do the ears, eyelids, eyes and nose move normally? Is it blinking? Is it sniffing at objects? Is it observing things or does it bump into them? Do both eyes track in a coordinated manner? Is there any strabismus, anisocoria or nystagmus? Does it respond to auditory stimuli? Is it swallowing normally or is there any evidence of respiratory stridor or change in voice? Is it licking its lips? Does it prehend food or drink normally?


Are there any signs of autonomic dysfunction such as anisocoria, sweating, faecal or urinary incontinence? (see Fig. 12.6) Spinal reflexes are difficult to assess by observation, but the animal may show a skin twitch if an insect lands on it, or a perineal reflex after defecating or urinating. If the animal has normal posture and gait, then the spinal reflexes are likely to be normal.


The horse in Fig. 13.2 has a left-sided facial nerve paresis. This was due to accidental compression of the facial nerve by the head collar buckle while the horse was recumbent under anaesthesia (see Fig. 10.14B). What do you observe in the horse in Fig. 13.3?




Proprioception and motor function


Normal gait requires both intact proprioception (limbs, trunk, head) and normal motor function (UMN and LMN). Similarly, for an animal to perform normally the proprioceptive tests used in the neurological examination, they require intact motor function. Therefore an animal with a purely motor problem could appear to have faulty proprioception, as it may not have the strength to place the limb in the correct position.


Assessing both proprioception and motor function is done by observing posture (trunk, limbs and head) and gait, and noting the positioning of the limbs under the centre of gravity, both at rest and during locomotion. Are the limbs base-wide or base-narrow? Are the animal’s feet placed too far to the side or do they get crossed underneath while ambulating? Note also whether the animal bears weight on the correct part of the foot or has it knuckled over and is bearing weight on the dorsal aspect.


If only the subconscious proprioception is compromised, then the limbs are often not placed under the centre of gravity either at rest or during locomotion. This results in base-wide or -narrow stance and ataxia with failure of the limbs to track under the centre of gravity when the animal is walking in a straight line. Deficits are often exaggerated when the animal turns. In horses this is seen particularly by excessive circumduction of the outside pelvic limb during tight turns.


The horse in Fig. 13.3 has proprioceptive deficits when turning in both the thoracic and the pelvic limbs. Note excessive circumduction of the left pelvic limb and the delayed movement of the left thoracic limb leaving the foot rotated inappropriately inwards.


If only conscious proprioception is compromised the animal may stand and walk with the limbs placed under the centre of gravity, but it may stand on top of the paw, or scuff the paw along the ground during the protraction phase, resulting in stumbling. Large animals, with their poorly developed corticospinal tracts, may have a remarkably normal gait with a forebrain injury; thus more complex manoeuvres are required to expose any deficit. What do you observe in the animals in Fig. 13.4?




Cranial nerve function


Testing cranial nerve function by observation is outlined in Tables 10.2 and 13.1. Note that as cranial nerves are bilaterally paired, both sides of the head need to be checked (see Chapter 10).


Table 13.1 Observing cranial nerve function. Note that blinking is a reflex action. The afferent stimulus is corneal drying stimulating CN V, ophthalmic branch to the brainstem and the efferent fibres travel in CN VII to the eyelids











































Testing by observation CNN being evaluated
Watch as the animal interacts with its environment Many
Head position – tilted, the eyes are in a different plane compared with lateral rotation (torticollis) in which the eyes are in the same plane Tilt – CN VIII (a), Vestibular
(Torticollis may be due to cervical or forebrain lesions)
Facial symmetry, blinking, nostril and ear movement CN VII
Blinking – due to stimulus of corneal drying Ophthalmic branch of CN V (a), blinking due to CN VII (e)
Pupil size Parasympathetic CN III (e) for miosis, or sympathetic (e) for mydriasis
Eyeball position CNN II or VIII (a), CNN III, IV, VI (e)
Olfaction, vision, hearing, CN I, II, VIII (a)
Masticatory muscle bulk, chewing CN V (e)
Tongue movement, e.g. licking lips or nose CN V (a) maxillary branch
CN XII (e)
Swallowing CN IX, X (a) and (e)
Laryngeal noise – phonation and stridor CN X, XI (e)

The cat has a dilated pupil in the left eye, subtle ventrolateral strabismus and loss of tone in the upper eyelid. This cat had CN III deficit causing loss of tone in the levator palpebrae superioris muscle (elevator of the upper eyelid), medial and dorsal rectus muscles (strabismus) and the iridal constrictor smooth muscle causing mydriasis. This was due to a tumour in the floor of the cranial vault.


The dog’s neurological deficits were readily detectable by observation. Clinically, the dog’s gait was ataxic (incoordinated) and paretic. It had marked atrophy of specific shoulder muscles, especially the supraspinatus muscle. In this particular case it was due to hypertrophied ligamentous tissue in the spinal canal compressing primarily the C6 spinal cord segment. The C6 spinal nerve arising from this segment is a key component of the suprascapular nerve innervating the supraspinatus muscle. LMNs supplying the suprascapular nerve and innervating the supraspinatus muscle (see Fig. 4.7). Functionally, loss of supraspinatus muscle function compromises shoulder extension resulting in hypometria (shortened strides) in the thoracic limbs. It also compressed sensory tracts and UMN tracts passing through the region supplying both the thoracic and pelvic limbs (see Fig. 4.8). Clinically the dog’s pelvic limb gait was ataxic (incoordinated – ‘wobbly’) and paretic, while the thoracic limb gait was short and stiff. This case was an example of ‘Wobbler syndrome’ (see Fig. 6.3).



Hands-on testing


With respect to the hands-on neurological testing, every clinician has their own approach, but here is an example of an approach that is generically useful for most animals. More detailed information on the neurological examination of large animals is given in books such as Large Animal Neurology, by Ian G. Mayhew, Blackwell Publishing, 2009, or Veterinary Neuroanatomy and Clinical Neurology, by deLahunta A and Glass E, 3rd edition, Saunders, 2009.




Hopping


This test is good for evaluating subconscious and conscious proprioception and may be performed, with care, in some large animal patients. In small animals, one leg is held flexed, e.g. the left thoracic limb, and the animal is pushed gently to the right. As the centre of gravity moves laterally over the right thoracic limb, this changes the subconscious proprioceptive input from the muscle spindles (stretching of muscles), joint angle receptors and Golgi tendon organs. It also changes conscious proprioceptive input by stimulating tactile receptors in the feet. In the normal animal, this will induce a lateral hop to replace the limb back under the centre of gravity. In small animals, it is useful to have the animal still bearing weight on the limb girdle that is not being tested. For example, if testing the thoracic limb, let the animal bear weight on its pelvic limbs. Thus the animal pivots in an arc around the supporting limbs; that is around the pelvic limbs when testing the thoracic limbs and vice versa. This makes testing easier for the clinician as they don’t have to try to lift the animal clear of the floor. Animals hop better laterally then medially, so only hop them laterally. Count the number of hops the animal makes on that leg, then test the other leg of the same girdle, through a similar size arc. Counting the number of hops, helps the clinician identify asymmetry between the limbs. The number of hops to cover a certain distance will depend on the size of the animal; a tall dog like a Labrador retriever takes bigger steps than a little dog like a Dachshund. An increase, or decrease, in the number of hops may indicate reduced motor or sensory function, respectively. Thus, the clinician can try to differentiate reduced proprioception from reduced motor function. An animal that has purely motor deficits resulting in reduced motor strength (e.g. myopathy) may not be able to hop properly, even though it has intact proprioception by which it can sense that its feet are not in a good weight-bearing position. Supporting the animal, by holding one hand underneath it, reduces the motor effort required to move the limb and the animal will move, or attempt to move the limb as soon as it senses abnormal limb position, but being weak, the hops will be shorter. Comparatively, if the animal has a proprioceptive deficit, it will not attempt to move the limb as soon as it is no longer in a good weight-bearing position under the body. The centre of gravity must be shifted further, creating a stronger proprioceptive stimulus to finally induce a hop. Thus the hop, if it occurs, will be bigger.


Aug 26, 2016 | Posted by in INTERNAL MEDICINE | Comments Off on The neurological examination and lesion localisation

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