Evaluation of Body Posture

Alterations of body posture can result from central nervous system (CNS) and peripheral nervous system (PNS) lesions causing a regulatory loss of body control, but can certainly also be caused by pain. Such discomfort associated alterations of body posture may originate from CNS or PNS disease (for example disc herniation and brachial plexus neoplasm associated pain) or from conditions outside the CNS/PNS such as for example acute trauma with fracture or cruciate ligament rupture, organ disease such as acute pancreatitis and acute neuromuscular disease and metabolic non-neurological disease can cause general weakness and associated alterations of body posture.

Certain body postures are strong indicators of involvement of specific neuroanatomical structures. One very common change of body posture is head tilt which is associated with vestibular disease (central or peripheral). A number of very characteristic abnormal body positions are listed below in table 1.

Table 1. Abnormal body positions

Evaluation of Gait

The animal should be evaluated while walking, running and turning in calm surroundings and on a non-slippery surface. This part of the neurological examination evaluates gait abnormalities as well as ataxia.

Ataxia

The word ataxia comes from Greek, with A meaning without and TAXIA meaning order. Ataxia describes a lack of coordination. Three main categories of ataxia will be described here:

Vestibular Ataxia

Ataxia arising from dysfunction of the vestibular system (the peripheral vestibular component including the vestibular nerve or the central component - the vestibular nuclei situated in the brainstem) is most commonly caused by unilateral disease. The main clinical sign is head tilt accompanied with difficulties with keeping balance. The animal may circle (in small circles), lean, fall or roll - with few exceptions towards the affected side - and express other vestibular signs, such as, e.g., pathological nystagmus.

General Proprioceptive Ataxia

General proprioceptive ataxia is defined by a dysfunction of the information travelling in the ascending proprioceptive pathways going to be processed in the brain. The general proprioceptive ascending pathways include (distal to central) proprioceptors in joints, tendons and muscles, the peripheral nerve, the dorsal root of the spinal nerves and from here proprioceptive myelinated fibers traveling in the spinal cord dorsal columns through the brainstem to finally reach the somatic sensory area in the brain. The paws may be positioned in non-physiological positions (e.g., knuckling over) and proprioceptive deficits are present when tested. When observing the animal walking and running, there will typically be an abnormal gait pattern displaying an extended floating stride. General proprioceptive ataxia can, for example, be observed in animals suffering from wobbler’s syndrome where the proprioceptive pathways in the cervical spinal cord are compressed.

Cerebellar Ataxia

The cerebellum acts as a coordinator and regulator of motor activity (whereas the motor cortex of the cerebrum initiates movements). The cerebellum controls the speed, direction and force of movement. The cerebellum regulates equilibrium and tonus and thereby supports a normal positioning of the body.

Cerebellar ataxia is observed in animals with a compro­mised cerebellar function and may arise from a variety of causes including congenital cerebellar abiotrophy, in utero virus-induced cerebellar abiotrophy, space occupying lesions, stroke and trauma. Cerebellar ataxia is characterized by incoordination and dysmetria (most often hypermetria) with preserved strength, head (and sometimes body) tremor, lack of menace response and vestibular signs (if lesions of lobus flocculonodularis are present).

Evaluation of Postural Reactions

General proprioception is concerned with the ability to sense stimuli arising within the body and extremities regarding position, motion, and equilibrium. Such stimuli are registered by sensors located in tendons, muscles and joints, from where signals are transported to the brain through ascending proprioceptive pathways. After being consciously processed, the efferent pathways originating from upper motor neuron cell bodies situated in the cerebral motor cortex send their axons to descend through the midbrain, brainstem and spinal cord to influence spinal cord lower motor neurons. From the spinal cord, peripheral nerves (formed from several nerve roots) travel peripherally to connect with and finally cause an adequate response from the skeletal effector muscles.

Upper Motor Neuron (UMN) & Lower Motor Neuron (LMN)

Understanding the UMN and LMN system and the clinical signs arising from dysfunction of UMN/LMN respectively, are essential when trying to localise lesions in the spinal cord.

The UMN acts as an inhibitor of LMN activity, initiates movement and sustain extensor tone. The LMN is the efferent neuron of the peripheral nervous system connecting the CNS with an effector organ (muscle).

UMN (cerebral cortical motor neurons/1. neurons) are primarily situated in the cerebral motor cortex pyramidal system, but also in the diencephalon basal nuclei and in the brainstem extrapyramidal system. The UMN axons travel in their descending tracts through the spinal cord, where they synapse with interneurons to communicate with LMN.

LMN (2.neurons) are situated in all segments of the spinal cord (ventral horn grey matter). LMN axons leave the spinal cord in the ventral (motor) root of the spinal nerves. The peripheral nerves are formed by the union of spinal nerves.

Spinal reflexes are evaluated with the purpose of evaluating spinal cord LMN functionality. Spinal reflexes performed in the front limb evaluate spinal cord segments C6-T2, the brachial plexus (formed by spinal nerves from cervical spinal cord segments C6-T2) and the associated peripheral nerves. Spinal reflexes performed in the hind limb and perineal region evaluate spinal cord L4-S3, the lumbosacral plexus (formed by spinal nerves from cervical spinal cord segments L4-S3) and the associated peripheral nerves.

Evaluation of Reflex Quality

Dysfunction of the UMN-LMN system interaction is reflected in the quality of the spinal reflexes and in muscle tone. With lesions of the UMN pathways the inhibitory effect on the LMN is decreased or lost caudal to the lesion. This is reflected clinically by exaggerated spinal reflexes (hyperreflexia) and muscle hypertonia or spasticity. A spastic paresis or paralyses may be present. With lesions of the LMN in the spinal cord the associated spinal reflexes are decreased to absent, muscle tone may be decreased to lost and flaccid paresis or paralysis may be present. LMN signs are associated directly with the dysfunctional segments of the spinal cord affected by the lesion. Loss of LMN function will cause rapid and pronounced muscle atrophy of the muscles innervated from the damaged spinal cord segments, so-called neurogenic muscle atrophy.

Lesions affecting the above pathways where they are travelling in the thalamus, capsula interna or cortex will result in contralateral deficits of limb function, whereas lesions situated caudally to the thalamus (where these pathways crosses the midline) and in the spinal cord will result in ipsilateral deficits of limb function caudal to the lesion.

Signs of Peripheral Nerve Dysfunction

Lesions of the peripheral nerves are closely related to the structures innervated by the specific nerve (localised muscular dysfunction and muscle atrophy).

Signs of Peripheral Nerve or Neuromuscular Dysfunction

Generalised neuromuscular disease may be episodic or stationary. If the animal can support its own weight, it may express a typical posture with a lowered head and walk with a short stride. The animal appears weak and will preferable sit or lie down. Vocalisation may be weak. Pain sensation is normal. The animal must be supported in order to conduct a proper examination of proprioception and postural reactions.

*Note that the withdrawal reflex is the only consistently reliable reflex in the front limb in normal animals

References

1.  De Lahunta A, Glass EN, Kent M. Veterinary Neuroanatomy and Clinic IJI Neurology. 3rd ed. Saunders Elsevier; 2009:134–167,476–486,487–524.

2.  GarosiL, Lowrie M. The neurological examination. In: Platt SR, Olby NJ, eds. BSAVA Manual of Canine and Feline Neurology. 4th ed. BSAVA British Small Animal Veterinary Association. BSAVA; 2013:1–24.

3.  Garosi L. Lesion localization and differential diagnosis. In: Platt SR, Olby NJ, eds. BSAVA Manual of Canine and Feline Neurology. 4th ed. BSAVA British Small Animal Veterinary Association. BSAVA; 2013:25–35.

4.  The Free Dictionary/Medical Dictionary: www.dictionary.thefreedictionary.com.