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The ataxic dog - is it neurological or orthopaedic? - part 1

Alejandro Artiles, DVM

Introduction

Ataxia may be defined as “loss of coordination of gait” and gait can be defined as “the movements made when an animal moves from one place to another, or the continuous posture changes implicated in movement” (1). From a neurological point of view, ataxia refers only to the malfunction of sensory pathways, while paresis (which presents as a broadly similar clinical picture) involves malfunction of efferent motor pathways. Ataxia and paresis are often confused; altered locomotion can actually involve changes in both sensory and motor pathways (2). The proprioceptive neurons form the sensory system that collects the state of position and movement of muscles and joints (3) and a proprioceptive deficit indicates neurological damage, although it is non-specific as to where the lesion is. Ataxia is a symptom rather than a disease, and can be divided into proprioceptive, vestibular and cerebellar forms.

Clinical presentation and approach

Clinical signs depend on the type of ataxia, although common presentation is a lack of coordination of movements combined with a broadbased stance, crossed limbs at walk, or very short or exaggerated steps (4). Movement - normal or ataxic - requires musculoskeletal, neurological, cardiovascular and endocrine systems to be fully functional and coordinated. While problems in any of these systems can produce gait abnormalities, neurological or orthopaedic pathologies are the main causes of lameness and abnormal movement in dogs and cats (Figure 1). figure 1 - the dog presented with knuckling of the right hindlimb and a reluctance to bear weight on the left forelegThe increased longevity of companion animals means that the clinician is frequently presented with elderly patients where changes in one or more of the major systems listed above can present as gait disorders. It can be challenging to identify which condition is causing the presenting signs. A radiograph may demonstrate severe hip dysplasia, leading to assume this must be the cause of the problem and to treat accordingly. However it is imperative to decide if the hip dysplasia is actually the cause of the abnormal locomotion - otherwise treatment may not solve the problems. With the interrelated nature of the body’s systems, decisions must be based on pathophysiology to obtain the most accurate diagnosis with a uniform, systematic approach to the clinical examination. Emergency trauma patients can disrupt this approach, but the clinician should aim to stabilize the patient as first priority and still achieve a simultaneous neurological/orthopaedic evaluation.

How do I approach the ataxic patient?

My preferred method is to follow a systematic protocol, as follows:

• Past medical history
• History of present illness
• Physical examination
• Orthopaedic examination
• Neurological examination
• Location of injury or injuries
• Differential diagnosis
• Ancillary tests
• Diagnosis
• Prognosis, treatment and follow-up

Medical records must be as complete as possible.

The first three points are critical in setting diagnostic priorities while sometimes history and physical examination will point to the final diagnosis. As the major systems involved in gait disorders are neurological and orthopaedic, the first and most reliable test for ataxia is the physical examination. Subsequent complementary tests can be performed after answering these questions:

Where is the injury? Locations can be focal, multifocal or diffuse. If we know that our patient suffers from ataxia, then we need to establish the neurologic location of the injury.

• What are the possible differential diagnoses? The mnemonic VITAMIN D is useful, as a reminder to consider vascular, inflammatory, traumatic, anomalies, metabolic/toxic, idiopathic, neoplastic and degenerative causes.

Fully developing these two points will indicate which complementary diagnostic tests are preferred and ultimately assist an accurate diagnosis.

How do I conduct an orthopaedic examination?

The physical orthopaedic examination starts by observing how the patient walks. We should assess the patient's gait from different perspectives, walking it on both flat and moderately inclined non-slip surfaces. If a neurologic injury is suspected, gait should be examined on a flat surface followed by a ramp or stairs. Orthopaedic injuries are best seen when the dog is moving quickly as the lameness is usually more obvious. A dog with a neurological problem may tend to walk slowly as it tries to compensate for imbalance or weakness. Step length can be normal or increased in upper motor neuron (UMN) lesions (spinal motor efferent pathways), while orthopaedic or muscular injuries usually show short steps. For uncooperative patients, ask the owner to film their pet at home.

Abnormal gait can present in various ways. Joint ankylosis and stiffness usually present as short steps and, although not exclusive, are typical of non-neurologic pathology. Lameness is mainly a sign of orthopaedic problems (arthrosis, tendinitis, etc.) but care should be taken as nerve root disease (e.g. disc compression, degenerative spinal disease, and nerve root tumors) can sometimes produce frank lameness of non-orthopaedic origin. figure 2 - note how this dog is flexing its hindlimbs to assist weight distribution after a fallWatch for improper distribution of the load at walk. Usually more weight (~60%) is carried on the forelimbs but some pathologies may alter this; e.g. after a fall a dog may have bilateral carpal ligament injury and show hyper-extension of both carpii, and the dog will walk with a compensatory back posture, flexing its hindlimbs to carry more of the load (Figure 2). Muscular weakness can have diverse origins and it can be challenging to decide if it is neurological or not. Myositis may present as both pain and weakened gait. Endocrinemetabolic disturbances which can cause muscle weakness include hypothyroidism, hyper/hypoadrenocorticism, hypoglycaemia and hyper/hypokalaemia.

For patients that remain sitting or lying down, it is imperative to establish if they are not standing because they are in pain (bilateral cruciate ligament rupture, myositis) or because they cannot stand (tetraplegia, vestibular damage).

After assessing gait we palpate the limbs in a set order, from distal to proximal. If there is an evidently painful area, it should be examined last. Be aware of the possibility of referred pain. Note any presence of inflammation/heat which may suggest an acute inflammatory process. Tightening of a muscle/tendon can mean contracture or calcification. Muscle tone is an important clue.

Lower motor neuron (LMN) lesions present with flaccid muscles or loss of tone whilst upper motor neuron (UMN) neurological problems maintain a normal or increased muscle tone. Note that if a problem continues for some weeks, muscle atrophy and loss of tone will eventually develop.

Apophyses and points of muscle insertions should be examined. Patients with chronic paresis tend to have skin ulceration or thickening that may have secondary infection. Examine all joints to ensure they are free of ankylosis or laxity and that flexion/extension movements are of normal range. There are a variety of tests that may demonstrate excessive laxity (e.g. stifle drawer test, hip Ortolani test) and they may be best done under sedation. Joint instability does not cause ataxia, so if a patient shows ataxia, weakness or gait alteration, a complete neurological examination should be performed.

 

This article was kindly provided by Royal Canin, makers of Mobility diet for dogs and cats.  Come back next week for part 2 on how to conduct a neurological exam.  For the full range please visit www.RoyalCanin.co.uk or speak to your Veterinary Business Manager:

Royal Canin Mobility FelineRoyal Canin Mobility

 

References

1. Lorenzo V, Bernardini M. In: Neurología del perro y del gato. 1st ed. Buenos Aires, Intermédica, 2007;42-63.
2. De Lahunta A, Glass E. In: Veterinary neuroanatomy and clinical neurology. 3rd ed. St Louis, Saunders, 2009;222-230.
3. Dietz V. Propioception and locomotors disorders. Nat Rev Neuro2002;3:781-790.
4. Jaggy A, Spiess B. Neurologic examination of small animals. In: Small animal neurology. 2010. Hannover, Schlütersche; 8-9.
5. Cochrane S. A practical approach to the abnormal gait: is it orthopedic or neurologic? In: Proceedings. WSAVA Congress 2007.
6. Cuddon P. The neurologic examination in small animals. In: Proceedings. European Veterinary Conference 2009, Voorjaarsdagen, Amsterdam.
7. Penderis J. Localising spinal cord and peripheral nerve lesions. In: Proceedings. European Veterinary Conference 2010, Voorjaarsdagen, Amsterdam.
8. Cuddon P. Myopathy I-II. In: Proceedings. European Veterinary Conference 2009, Voorjaarsdagen, Amsterdam.
9. Lorenzo V, Bernardini M. In: Neurología del perro y del gato. 1st ed. Buenos Aires, Intermédica 2007;114-116.
10. Lang J, Konar M. MRI of the musculoskeletal system. In: Proceedings WSAVA 2006;286-287.

This article was previously published in 2011.


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