Truncal ataxia

59 Truncal ataxia



INTRODUCTION


Inflammatory CNS disease is a very common cause of neurological signs in small animals, more so in the young to middle-aged. Peripheral leukocytes invade the brain, cord and meninges in response to tissue injury. In the majority of cases, the aetiology remains elusive and the disease is described in histopathological terms. Vasculitis may clinically mimic CNS inflammation.


Involvement of other systems (skin, lung, GIT, eye, haematopoietic system or blood vessels) and structures adjacent to the CNS (sinus, ear, nose, pharynx or intervertebral disc), the possibility of haematogenous spread (bite wounds, dental disease or endocarditis), predisposing conditions (immune-compromised, young, FeLV, FIV or CDV) and exposure (rabies, fungal, tick-borne pathogens or parasites) should be considered.





Clinical diagnosis of infectious disease requires



• Clinical signs referable to the agent

• Serological evidence of exposure to the agent

• Exclusion of other causes

• Demonstration of the agent or a response to treatment.


A recent or active infection is suggested by



• The presence of IgM

• An increasing antibody titre over 2–3 weeks

• Seroconversion from negative to positive.


Presenting signs



• Meningitis: spinal pain, blepharospasm

• Encephalitis. A variety of signs which may not reflect all the sites of disease which may be focal or multifocal. Balance loss is common

• Acute or chronic onset/progression

• Fever and neutrophilia are not consistently present.

The presentations of infectious and non-infectious meningoencephalitis are similar. Certain patterns can be recognized but it is a good idea to approach every case as potentially infectious. Be aware of the endemic parasites, vector-borne infections and fungal diseases in your area. This will increase the chances of a timely diagnosis.



SIGNALMENT 1


A 4-year-old neutered female West Highland white terrier.



CASE HISTORY


Hindlimb ataxia was first noted 6 months prior to referral. A high serum titre for Neospora was found (>1600) and the dog improved after receiving clindamycin for 3 weeks. The problem recurred 1 month after treatment ceased and a 10-day course of clindamycin improved the dog again. Two months later, hindlimb ataxia recurred again and the dog improved on 14 days of clindamycin. The Neospora serum titre at the time of referral was unchanged at >1600. The dog improved to normal on clindamycin after each recurrence of signs but had not improved with treatment for the current return of hindlimb ataxia.



CLINICAL EXAMINATION


The dog was alert with a truncal ataxia at rest and a hindlimb ataxia when walking. Hopping was normal on the left side but slow to initiate movement on the right. Placing was slow in the right fore and hind.

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  4. Idiopathic facial paralysis

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Sep 3, 2016 | Posted by in SMALL ANIMAL | Comments Off on Truncal ataxia

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