2 Jun 2008
ROB PETTITT discusses conditions affecting the spine in small animals and examination methods for the practitioner, in the first of a two-part article
SPINAL and vertebral column disease is common in small animals but the chondrodystrophic breeds of dogs are over-represented (Figure 1).
Knowledge of functional anatomy of the vertebral column and spine is essential for a logical and efficient approach. Very applicable anatomical knowledge can be gained from King (1987).
Spinal segment s def ine regions of the spinal cord that are functionally distinct. These are grouped in the following way:
• cervical one to eight;
• thoracic one to 13;
• lumbar one to seven;
• sacral one to three; and
• caudal – variable.
It is important to remember that the spinal segments do not match up exactly with the vertebrae of the same name. The spinal cord itself terminates at the approximate level of L5, although there is some variation between breeds of dog, with dachshunds having cords that terminate further caudally than GSDs (Figure 2). This is because the growth of the spinal cord terminates before growth of the vertebral bodies. The spinal nerves, however, exit from their respective intervertebral spaces. In the cervical region, this is at the cranial aspect of the vertebral body, whereas all other nerves exit at the caudal end.
Variations in the axial skeleton are common. Those most often seen include an abnormal number of ribs, one extra or one less lumbar vertebra and abnormal articulations with the ilium (sacralisation of L7, or lumbarisation of S1).
Anatomy of meninges
The arachnoid and pia mater are termed the leptomeninges. Between these two layers is the subarachnoid space – it is this space that is filled with cerebrospinal fluid (CSF) and with contrast medium during myelography (Figure 3). In most dogs the dural sac ends some distance caudal to the termination of the spinal cord, usually in the sacrum (in about 15 per cent of dogs the dural sac ends at L7). The dura mater is a tough layer and one can feel a spinal needle penetrate this during CSF collection or myelography.
Many spinal cord diseases involve compression of the cord. This may be acute or chronic, but a general rule is that the first neurons to suffer loss of function are the fast-conducting, largediameter, myelinated neurons of the ascending pathways involved with proprioception. They travel in the gracile and cuneate fascicles of the dorsal funiculus.
The next most susceptible are the motor fibres, of which some are myelinated. The most resilient neurons are the smalldiameter, slow-conducting neurons involved with deep pain sensation. Therefore, loss of deep pain, or conscious pain, is an indicator of extreme cord damage and carries a much more guarded prognosis.
Conscious proprioception is gathered from the peripheral nervous system via sensory neurons (type-A fibres). These may project on to interneurons forming part of a reflex arc (Figure 4). In addition, conscious proprioception is transmitted cranially to the brain in the gracile (pelvic limb) and cuneate (thoracic limb) fascicles within the dorsal funiculus.
The lower motor neuron (LMN) is the effector neuron of the reflex arc. Inhibitory neurons project on to the alpha motor neuron from descending tracts from higher centres. Therefore, interruption of these descending tracts causes lack of inhibition of the alpha motor neurons.
For clinical purposes, spinal lesions are classified as either upper motor neuron (UMN) or LMN. LMN lesions give clinical signs consistent with failure of reflex arcs and alpha motor neurons, such as hypo or areflexia hypotonia and rapid atrophy of muscles. UMN lesions give signs consistent with lack of inhibition of alpha motor neurons, such as hyper-reflexia, hypertonia.
With spinal cases in particular it is important to progress in a systematic and logical manner to arrive at an appropriate diagnosis. Failure to progress in such a way will lead to a confused and substandard investigation, which may have serious effects for the patient and its owner.
Signalment, history and clinical signs will often be very suggestive of a specific diagnosis (for example, Hansen type-one disc extrusion in a middle-aged paraplegic dachshund) but care must be taken to consider other causes to avoid potentially disastrous outcomes.
• Patient examination
The aim of patient examination is to determine whether the presenting complaint is spinal in origin. Therefore, the following should be assessed:
– the approximate location of the lesion;
– the severity of the neurological deficit;
– the most likely disease process;
– the most appropriate form of treatment; and
– the prognosis.
Signalment is often useful in the initial assessment, but care should be taken to avoid relying only upon this information when making a diagnosis. A complete orthopaedic and neurological examination can be carried out relatively quickly and can, with practice, give a reliable diagnosis. It should be remembered, however, that the neurological examination will only localise any lesion to certain distinct regions – and not to specific disc spaces.
Further ancillary aids, such as MRI and myelography, are needed to precisely determine the location of any lesion. Advanced imaging is mandatory for cranial lesions.
• History
A full history is mandatory for any suspected spinal case and can often lead to a provisional diagnosis. Particular notice should be given to evidence of trauma, progression, or otherwise, of the condition, previous bouts of lethargy or pain, and presence of pain and urinary function.
• Physical examination
A thorough physical examination should be performed. Medical conditions such as polyarthritis, liver disease and hypokaaemi a may mimic spinal disease, as do some orthopaedic conditions, such as bilateral cranial cruciate ligament ruptures. Careful examination should identify these problems. Particular care should be given to the assessment of joint pain and effusions, as they are routinely present in dogs misdiagnosed with neurological disorders.
The presence of femoral pulses, especially in paralysed cats, should be determined.
A brief neurological survey examination can easily be performed as part of a complete physical examination (Table 1). If any abnormalities are detected, a more thorough neurological examination can be performed.
• Neurological examination
The neurological examination is carried out to determine the location of any lesion and its severity. The initial part of the examination is conducted with the animal standing before it is placed into lateral recumbency.
The examination starts with an observation of the animal’s stance and gait (often more rewarding in cats than other parts of the exam). Listening to the animal walk on a hard surface may alert the examiner to proprioceptive deficits, such as if scuffing of the claws is heard.
Posturale reactions are assessed next. Unilateral weakness and subtle deficits may be revealed by the patient hopping, hemiwalking or hemistanding. Wheelbarrowing with the head lifted can reveal hypermetria or thoracic limb paresis in some cases. The extensor postural thrust is performed by lifting the animal off its hindlimbs. A normal animal should extend the hindlimbs as its feet are lowered to the ground. This can reveal pelvic limb deficiencies.
Conscious proprioception, often the first neurological sign to be noticed by owners, can be tested by the paw position (knuckling) and reflex step tests. With the body supported, the foot is turned over to bring the dorsal surface into contact with the ground. Healthy animals will return the paw to its normal correct position within one to two seconds.
The reflex step test assesses proprioception more proximally in the limb (the paw position test assesses the distal limb) and is performed by placing the foot on a piece of paper and gradually sliding the paper laterally. A normal animal should step off the paper and return the foot to its natural position. If conscious proprioception is normal, it is unlikely that a spinal lesion is present.
Palpation of the abdomen will determine the degree of bladder filling and the ease with which it can be expressed. Bladder function may be affected in spinal patients. One can often glean information from the owner, such as whether the dog leaked urine when lifted. The striated muscle of the urethral sphincter mechanism is innervated by the pudendal nerve arising from S1-S3. A LMN bladder is easy to express because the urethral sphincter mechanism is hypotonic and the bladder feels large and flaccid. Conversely, a UMN bladder is more difficult to express and characteristically tense due to the hypertonic sphincter. UMN bladders are seen with lesions cranial to the sacral segments – typically, those affecting T3-L3. The importance of determining bladder function is twofold: firstly, so appropriate drug therapy can be determined, and also the prognosis for recovery. LMN lesions have a poor prognosis, whereas those with UMN bladder signs have a more reasonable prognosis.
The panniculus reflex is not entirely reliable but can be used to localise some spinal lesions. The reflex is elicited by pinching the skin of the dorsum between the caudal edges of the scapulae to the iliac crests. This should cause contraction of the cutaneous trunci muscle, mainly on the ipsilateral side, but also on the contralateral side, due to decussation (crossing over) of the pathways.
The sensory innervation is segmental via dermatomes. The motor innervation is via the lateral thoracic nerve, which arises from C8 and T1. Therefore, a thoracolumbar lesion may cause a bilateral cut off because of loss of sensory input, whereas a caudal brachial plexus lesion may cause a complete ipsilateral loss of panniculus. The dermatomes lie caudal to their respective vertebrae, with the L1 dermatome at the level of the tuber coxae. The reflex is only normally useful in localising lesions in dogs that are paraplegic.
With the dog in lateral recumbency (examination in both left and right recumbency are required) the spinal reflexes are then tested. The hindlimb myotatic reflexes are reliable in mature dogs and cats. The patellar and withdrawal reflexes are the most useful. The patellar reflex is innervated by the femoral nerve (afferent and efferent) and this emanates from spinal segments L4 and L5.
The withdrawal reflex is innervated by the sciatic nerve (afferent and efferent) and this comes from segments L6, L7 and S1. Pinching the toes causes a reflex withdrawal of the limb involving flexion of the hip, stifle and hock. It is important to realise that this is a local reflex. It does not mean the dog can feel the toes being pinched and is, therefore, not an indication of conscious pain sensation (CPS). However, if the dog turns its head, or tries to bite or bark when the toes are pinched, this is indicative of CPS.
The loss of CPS warrants a guarded prognosis. In some cases a response may not be elicited until the stimulus is increased by using large instruments (such as forceps) across the digit or nail bed.
The forelimb myotatic reflexes are much less reliable. It is important to test and compare left and right responses. The tricep and extensor carpi radialis reflexes test the radial nerve, and the bicep reflex tests the musculocutaneous nerve. They are most useful for identifying hyperactive responses in dogs with UMN lesions.
In dogs, an ascending motor tract originates in the border cells of the dorsolateral grey matter of the lumbar spinal segments. The axons of these cells project cranially in the contralateral proprius fascicle of the lateral funiculus and inhibit the extensor muscles of the thoracic limb. Interference with this pathway is seen occasionally in dogs with severe lumbar spinal injury and is called the Schiff-Sherrington phenomenon (Figure 5). It is characterised by rigid hyperextension of the forelimbs. Be careful not to over-diagnose this as many paraplegic dogs will stretch out their forelimbs in an attempt to prop themselves up. However, they can still use the forelimbs in a voluntary manner and, thus, do not have Schiff-Sherrington.
The final part of the examination with the dog standing is to palpate the vertebral column. The cervical vertebrae are best palpated laterally, while the thoracic and lumbar and sacral vertebrae are best palpated from a dorsal aspect. The occurrence of pain is very useful in prioritising the differential diagnoses.
In most cases the author elects to palpate the spine after completing the lateral recumbency part of the neurological examination. This is because a compliant patient may quickly become less so after pain has been induced.
On the basis of the neurological examination it should be possible to localise the lesion to one of the following (Table 2):
– C1-C5;
– C6-T2 (cervical intumescence);
– T3-L3; or
– L4-S3 (lumbar intumescence).
• Severity assessment
For most patients it is useful to grade the neurological deficits as this acts as a guide for prognosis. In general, those with a LMN lesion have a much poorer prognosis than those with a UMN lesion.
In UMN lesions, the speed of onset, duration and degree of damage to the spinal cord all have a bearing on the clinical signs. For a thoracolumbar lesion, the degree of dysfunction is scored on a scale of one to five as shown in Table 3 below.
Prognosis is also dependent on the aetiology: a disc extrusion carries a very different prognosis from a spinal tumour. Cervical lesions show a similar progression of signs, although loss of CPS in cervical lesions is generally incompatible with life. Severe cervical lesions can cause interruption with pathways of respiration – for example, intercostal function. Thus, there may be paradoxical respiration where the chest wall collapses as the diaphragm contracts.
• In part two of this article I will cover the initial management and work-up of the spinal patient.
Figure 1. Paraplegia is a common presentation in canines, especially those of a chondrodystrophic breed.
Figure 2. Schematic image to show the approximate position of the spinal cord segments within the vertebral canal.
Figure 3. Diagram of the anatomy of the meninges.
Diagrams: courtesy of Professor J F Innes.
Figure 4. Diagram showing a spinal reflex arc.
Diagrams: courtesy of Professor J F Innes.
Figure 5. Schiff-Sherrington syndrome in a Gordon setter.
Table 1. Screening neurological examination as part of physical examination
Table 2. Summary of different combinations of neurological findings
Table 3. Grading scale for thoracolumbar lesions
Rob Pettitt
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