Transcript Neurological Disorders

Neurological Disorders
INAG 120 – Equine Health
Management
November 7, 2011
Photo © UC-Davis, Center for
Equine Health
Overview
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The Equine Central Nervous System
Differentiating between neurological disease and
lameness – The neurological exam
EPM
EMND
EDM
CVM and Vertebral Fractures
Plant Toxicities
Viruses – covered in separate lecture
The Equine Central Nervous System
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Brain, brainstem, spinal cord
Brain
– Enclosed and protected by the cranial cavity
– Horse is amazingly trainable and possesses a remarkable
memory
– Possesses, integrates, and stores sensory information
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Brain Stem
– Also called the lower brain, coordinates and controls respiration,
blood pressure, and many other life processes
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Spinal Cord
– Connects the brain with the peripheral nerves
– Many of the simpler motor responses occur as "spinal reflexes"
without directly involving the higher levels of the nervous
system.
The Neurologic Exam
Goal: establish presence of neurologic
problem and determine location
 Cervical radiography
 Cerebrospinal fluid (CSF) analysis
 Electrodiagnostic testing
 Physical Exam
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– 5 categories
Neurologic Physical Exam
1.
2.
Head and Mental Status
Gait and
Posture
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Postural
reactions
Spinal
reflexes
Gait
abnormalities
Neurologic Exam…Localizing the
problem
Neck and Forelimbs
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Gait abnormalities in all
4 limbs
Trunk and Hindlimbs
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If limited to hind limbs,
damage done caudal to 2nd
thoracic spinal cord segment
Tail and Anus
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Abnormal use  lesion caudal to sacral vertebrae
Video of Horse Suffering from
Neuro-EHV
Neurological Disorders
Nervous tissue does not respond well to
damage
 Capacity for repair is limited
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Equine Protozoal Myeloencephalitis
(EPM)
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Protozoan Parasite
Sarcocystis neurona
Neospora hughesei
Infects spinal cord and
brain
 Infection does not mean
clinical disease!
 Hosts and carriers
 Doesn’t pass horsehorse
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EPM…
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Clinical Signs:
– Asymmetric lameness
– Asymmetric facial
paralysis
– Muscle atrophy
– Weakness
– Ataxia
Photos © UC-Davis, Center for
Equine Health
EPM…
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Risk Factors:
– < 6 years old
– Season (higher in
spring and summer)
– Region
– Opossums
– Previously diagnosed
cases on farm
– Stress
– Racehorses and show
horses
Photo © http://www.yourhorseshealth.com/epm/risk.html
EPM…
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Diagnosis:
– POLITICAL
– MUST BE A CLINICAL DIAGNOSIS with both
clinical signs and changes in
cerebrospinal fluid
– Can show antibodies in CSF from previous
exposure (not necessarily infection)
– Must rule out wobbler and equine
degenerative myeloencephalopathy
EPM…
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Treatment:
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Feasible if damage is not too severe
Marquis
Navigator
Long term therapy with anti-folic-acid drugs such
as TMS (Trimethoprim-sulfadiazine) plus
pyrimethamine
– Vitamin E may be given for antioxidants
– Levamisole may be given to stimulate immunity
– DMSO for anti-inflammatory
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Prognosis depends on severity of symptoms;
horses often show permanent neurological
damage
More on EPM
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Opossum = definitive
host
– Up to 1 billion
sporocysts in one
gram of opossum
feces
Horse = aberrant host
 Raccoons, cats,
armadillos and skunks
= intermediate hosts
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Photo © Dr. Martin Furr, VMRCVM
EPM Prevention
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Keep feed and water sources “clean”
– Make feed unavailable to wildlife
Confine horses
 Limit stress
 Vaccine?
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Equine Motor Neuron Disease
Degenerative disorder of lower motor
neurons
 First described in 1990
 Most likely caused by Vitamin E deficiency
 Affects horses over the age of 2
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EMND – Clinical Signs
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Weight loss
Acute onset of trembling
Constant shifting of
weight in hind legs
Excessive recumbency
Elevated tail +
abnormally low carriage
of head and neck
40% horses deteriorate
and are euthanized
40% respond to
treatment
20% remain debilitated
Photo © Dr. Martin Furr, VMRCVM
EMND – Diagnosis
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Biopsy of tail head
Blood tests:
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Mild-moderate increase in CK and AST
Vit. E consistently low
Selenium normal
Vit. A low-normal
Serum iron = high
Spinal cord
– Copper is increased
– Low Vitamin E
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Glucose absorption impaired
EMND – Treatment
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Horses with EMND = dead motor neurons and
alive but dysfunctional motor neurons
If numbers of dysfunctional > dead  clinical
imrovement
Seems to affect neurons that supply muscles
with highly oxidative type 1 fibers
Feed green forages
Vitamin E supplementation (commercial
concentrates already have added E due to
recent research)
Equine Degenerative
Myeloencephalopathy
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VERY similar to EMND but a distinctly different
disorder
Most commonly seen in sucklings and
weanlings; very rarely after the age of 2
Loss of neurons in the brain stem and spinal
cord
Vitamin E deficiency, along with a familial
component
Vitamin E has a protective effect against
oxidative damage in the spinal cord of horses
with the neuroanatomical site differing based on
age?
Vertebral Fractures
Treatment possibilities depends on nature,
extent and stability of fracture
 Each case must be observed individually
 Forelegs unstable  located in neck or
front of thoracic spine
 Mild cases may resolve on their own
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Cervical Vertebral Malformation
“Wobbler” Syndrome
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Leading cause of non-infectious spinal cord
ataxia
Especially seen in rapidly-growing well-nourished
horses
Male > Female
Highest incidence in Thoroughbreds
Evidence that it’s due to aberrations of bone
development
Excess forces and trauma may predispose the
animal to deformities
Wobblers…
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Cervical Vertebral Instability (CVI)
– 6-12 months old
– Instability of cervical joint  excess
movement  pressure on spinal cord
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Cervical Static Stenosis (CSS)
– Older horses, usually 1-4 years
– Degenerative joint disease of less mobile
joints of neck
– Excess bone impinges on spinal cord
Wobblers…
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Clinical Signs/Diagnosis:
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History of recent trauma
Signs of ataxia
“Hindlimbs affected worst and first”
Weakness
Spinal cord lesions usually symmetrical
Treatment:
– NSAIDS, steroids, or DMSO to reduce inflammation
– Stall rest
Wobblers Video
http://www.youtube.com/watch?v=XQSlN9t
Yudc&feature=related
Sudan Grass Toxicity
Consumption of sudan grass (Johnson
grass, shattercane)
 Urinary incontinence (no bladder control)
 Ataxia and paresis
 Treatment usually unsuccessful once signs
are prominent
 Early cases recover when removed from
pasture
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Johnsongrass, Sudangrass
Brackenfern
Pteridium aquilinum
Moderately toxic
 Plant contains thiaminase
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– All plant parts, especially roots
– Causes Thiamin deficiency
Blindness, depression, weight loss,
staggering
 Rx: Thiamin supplementation, blood
transfusion for bone marrow destruction
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Brackenfern