Normal gait in the dog and cat depends on the functional integrity of the cerebral cortex, the brainstem, cerebellum, spinal cord (ascending and descending pathways), peripheral nerves (sensory and motor), neuromuscular junctions and muscles. A voluntary movement is initiated by nerve impulses generated in the cerebral cortex or brainstem. The cerebellum co-ordinates these voluntary movements and the vestibular system maintains balance during the performance of the movement. The nerve impulses from the brain to the peripheral nerves and, therefore, to the muscles, travel along the descending tracts of the spinal cord. Information on the position of the limbs during movements arrives at the cerebellum and the forebrain from the periphery through the ascending tracts of the spinal cord and brainstem. For educational purposes it can, therefore, be said that voluntary movements are the outcome of synergism between motor functions (descending pathways) and sensory functions (ascending pathways).
Motor function
As a gross simplification it can be said that the descending motor tracts are formed by two types of motor neurones. The upper motor neurones, whose cell bodies are located in the encephalon, are the neurones which initiate a voluntary movement: the axons leaving these cells run down the central nervous system forming the descending bundles of the spinal cord and synapse with the lower motor neurones, bulky cells in the ventral horn of the spinal cord. The axons of the lower motor neurones exit from the spinal cord and, uniting, form the spinal roots of the nerves, then the spinal nerves and, when appropriately grouped, the peripheral nerves. It is these axons that connect to the striated muscle through the neuromuscular plaque (Fig. 1; with kind permission from Elsevier).
Traditionally the descending motor pathways are divided into the pyramidal and extrapyramidal tracts. These latter are formed of a series of interconnected and functionally related structures that run from the neurones of the forebrain to the lower motor neurones in the ventral horn of the spinal tract (in the brainstem for the cranial nerves) (Fig. 2; with kind permission from Elsevier). In the dog and the cat the direct contribution of the forebrain (pyramidal pathways) to the control of gait is much less important than it is in anthropomorphic primates. In the dog and the cat lesions to the forebrain often cause modest or barely perceptible changes in gait, while lesions to the brainstem or spinal cord provoke fairly obvious abnormalities of gait. Animals with lesions in the frontal or prefrontal cortex of the forebrain can have normal or almost normal gait as far as concerns co-ordination and strength of movements (sometimes there can be a mild hemiparesis on the opposite side of the lesion), but the gait can be compulsive in that the animal tends to walk without ceasing and without a destination, until it encounters an obstacle (Video 1). Often the animal tends to stop and push its head against the obstacle; this particular anteropulsive behaviour is described as “head pressing”.
Sensory function (proprioception)
Kinaesthesia is the awareness of the position and movement of one’s own body and, in particular, the limbs. Kinaesthetic information is detected and conveyed by neurones dedicated to general proprioception. The general proprioception system is, for teaching purposes, traditionally divided into the conscious proprioception system, which projects into the somatosensory cortex, and the unconscious proprioception system, which arrives at the cerebellum. The general proprioceptive system is schematically formed of a peripheral receptor, part of the sensory component of the peripheral nerve, the ascending bundles that carry information to the cerebellum or, through the medial lemniscus, to the cerebral cortex (Fig. 3; with kind permission from Elsevier). General proprioception, by providing continuous information on the position of the limbs during movement, is essential for the co-ordination of the movement itself. Other information inputs necessary for the co-ordination of movement arrive from the vestibular system (special proprioception system) and the visual system, with integration from the cerebellum.
Evaluation of gait
The gait of an animal (Video 2) must be evaluated by observing the animal from the side, from the front and from behind while it walks on a non-slippery surface in a straight line and in a circle, while it goes up and down stairs and while it walks on a slope. For dogs, it is advisable to carry out the examination in the open air and, if necessary, in a room in which the animal can move freely. Evaluating the gait of a cat can be much more difficult: a useful strategy can be to release the animal in the centre of the consulting room and observe its movements as it tries to reach the transport container, deliberately placed at a certain distance, or any other shelter. It is important to be familiar with the normal gait of different species, breeds and age groups of animals. Subjects that have difficulty in remaining in a standing position and walking should be supported if necessary. Obviously it is essential to ensure adequate immobilisation of the spine in patients that could have an unstable lesion of the vertebral column, until vertebral dislocations/fractures have been excluded.
Cerebellar ataxia (Videos 5 and 6) is caused by disorders of the cerebellum or, more rarely, lesions that selectively affect the spino-cerebellar tracts. This type of ataxia is characterized by an incapacity to regulate the force and range of movements with consequent dysmetria, often manifested as hypermetria (a lengthened protraction phase of gait). This type of ataxia is often associated with other cerebellar symptoms such as a broad-based stance and intention tremors. Cerebellar ataxia, unlike proprioceptive ataxia, is not associated with paresis.
Vestibular ataxia (Video 7) associated with unilateral vestibular lesions is characterized by a tendency to sheer, fall or roll to one side (usually ipsilateral to that of the lesion). This type of ataxia is associated with other vestibular symptoms such as head tilting, spontaneous nystagmus, positional strabismus and the tendency to go round in circles. In the case of a peripheral bilateral vestibular disorder the animal develops symmetrical ataxia with loss of balance on both sides and movements of the head from one side to the other. In order to show defects in co-ordination it can be useful to make the animal walk up and down a flight of stairs (Video 8). Animals with ataxia usually have more pronounced problems descending the stairs, where the imperfect control of the movements can cause the animal to fall.
Paresis can be of varying severity and can be distinguished into ambulatory (when the animal, despite the motor deficit, is able to stand on its four limbs and walk autonomously) and non-ambulatory (when the animal has to be supported in order to be able to stand and walk or at least make an attempt at a few steps). In these latter cases it is very important to take the animal outside, put it at its ease and support it correctly in order to detect evidence of any, even minimal, voluntary motor activity. This enables severe paresis to be distinguished from paralysis, which provides useful prognostic information.
Various different terms are used to define which limbs are affected by the motor deficit: monoparesis/monoplegia (a single limb) (Video 9), paraparesis/paraplegia (both hind limbs) (Video 10), hemiparesis/hemiplegia (the fore limb and hind limb on the same side), (Video 11) tetraparesis/tetraplegia (all four limbs) (Videos 12 and 13). There are two types of paresis/paralysis: spastic paresis/paralysis, the type caused by dysfunction of upper motor neurones (Fig. 4) (Video 14), and flaccid paresis/paralysis, the type caused by dysfunction of lower motor neurones (Fig. 5) (Video 15).
Fig. 4 Fig. 5
This occurs because the upper motor neurones have a modulating effect on the lower motor neurones which, among other functions, maintain muscle tone. A lesion of upper motor neurones causes a deficit in the modulating input to lower motor neurones and, therefore, “frees” these latter from the upper control. The effect is disorganized recruitment of lower motor neurones, with consequent hypertonicity of muscles and spasticity. In contrast, if the lesion affects the lower motor neurones, there is flaccid paresis/paralysis, precisely because those neurones responsible in the first place for maintaining muscle tone are damaged. As already mentioned, most of the gait abnormalities involving the spinal cord are mixed type (sensory and motor), because of the close vicinity of the ascending and descending spinal tracts (video).
In animals with lesions of the peripheral nervous system, such as polyneuropathies, the efferent motor component is particularly affected and can give rise to very severe motor defects. These cases are usually described as paresis (“weakness”) or paralysis with reduced muscle tone and strength, because the lower motor neurone system is affected. A typical sign of paresis due to peripheral nervous system disorders is exercise intolerance (Video 17), characterized by an incapacity to carry out work that would normally not involve any particular effort. In this case the gait initiates almost normally but rapidly changes such that it becomes characterized by an increasingly short stride. Furthermore, the animal develops joint hypometria and hyperflexion, inability to support its own weight, tremor and breathlessness, to the point that it needs to lie down on the ground and rest.
It should be remembered that lesions of moderate entity of the spinal cord give rise to mixed gait disorders, with concomitant paresis and proprioceptive ataxia, given the contiguity of the ascending proprioceptive nerve bundles and the descending motor ones.
The presence of lameness (Video 18) usually suggests an orthopaedic problem, but can also be caused by neurological pathologies involving the nerve roots (for example a lateral extrusion of an intervertebral disc or neoplasia of the nerve sheaths) which give rise to the nerves to the limbs. This type of limping is called “nerve root signature”.
Ataxia and paresis are signs of dysfunction of given structures of the nervous system. In view of this the finding of a gait alteration must be assessed together with any other signs found during the neurological examination in order to identify the site of the lesion. It is on the basis of this anatomical localisation of the lesion that all the clinical differential diagnoses are hypothesised, and the consequent appropriate diagnostic protocol formulated.