Page 547 - ONLINE PROCEEDING BOOK WSAVA 2017
P. 547

An Urban Experience
Decerebellate rigidity
Cerebellar lesion (rostral cerebellum)
Opistotonus + extension of front limbs
Mentation is normal Hips may be  exed
Schiff-Sherrington syndrome
Acute severe (transverse) T3-L3 spinal cord lesion causing a sudden loss of axons coming from inhibitory neurons situated in L1-L5 spinal cord gray matter on front limb lover motor neurons. Causing disinhibition of the front limb extensor muscles
Extensor hypertonia of front limbs & paralysis of hind limbs
Patient have preserved voluntary movements and proprioceptive placing is normal if tested while the patient is supported
Evaluation of gait
The animal should be evaluated while walking, running
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 sys-
tem (the peripheral vestibular component including the vestibular nerve or the central component – the vestib- ular nuclei situated in the brainstem) is most commonly caused by unilateral disease. The main clinical sign is head tilt accompanied with dif culties with keeping bal- ance. 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 de ned by a dysfunction of the information travelling in the ascending propriocep- tive pathways going to be processed in the brain. The general proprioceptive ascending pathways includes (distal to central) proprioceptors in joints, tendons and muscles, the peripheral nerve, the dorsal root of the spi- nal nerves and from here proprioceptive myelinated  bers traveling in the spinal cord dorsal columns though the brainstem to  nally reach the somatic sensory area in the brain. The paws may be positioned in non-physiological positions (e.g. knuckling over) and proprioceptive de cits
and turning in calm surroundings and on a non-slippery surface. This part of the neurological examination evalu- ates gait abnormalities as well as ataxia.
are present when tested. When observing the animal walking and running, there will typically be an abnormal gait pattern displaying an extended  oating stride. Gen- eral 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 cere- brum 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 compro- mised 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  occulonodularis are present).
Test
CNS/PNS structures involved
Gait
Examine the patient, walking, running and turning
Observe for ataxia (proprioceptive, vestibular or cerebellar)
All parts of the CNS and PNS
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