1. EQUINE DYSAUTONOMIA/
GRASS SICKNESS
-> is a polyneuropathy affecting the central, peripheral and enteric nervous systems.
->The majority of visible clinical signs are related to paralysis within the digestive tract although nerve damage
occurs throughout the body. There are three forms of grass sickness:
 acute grass sickness (AGS) - horses display signs of colic and require euthanasia or die within 48 hours
 subacute grass sickness (SAGS) - horses display clinical signs similar to AGS but with less severity and may
survive up to 7 days
 chronic grass sickness (CGS) - horses present with severe and rapid weight loss and a selected portion of
these cases may survive.
 ETIOLOGY:
 unknown but the causative agent is thought to be associated with grazing
( Clostridium botulinum toxin type C may be involved)
 Seen at any age after weaning
 Highest incidence in spring in horses 2-7 years old
 Death occurs within 24 hours, 7 days, and >1wk respectively for the first 3 forms
 Clinical signs common to all subsets include: depression, anorexia, colic (moderate with AGS/SAGS and
mild with CGS), excess salivation, constipation, nasogastric fluid secretion, patchy sweating, muscle
tremors and eyelid drooping.
 Diagnosis
->in the live animal- requires a thorough clinical examination including a rectal examination.
 Definitive diagnosis can only be made at surgery (where biopsies of the gut are taken) or at post-mortem
(where biopsies from the nerves are taken).
 Differential diagnoses for grass sickness are varied and include: any other cause of colic and weight loss,
tying-up, laminitis, botulism, choke and dental problems.
 There is no treatment for grass sickness.
LESIONS:
 In acute cases, stomach and small intestine are distended with fluid and large intestine is impacted
 In chronic cases, GI tract is usually empty
 All forms show splenomegaly, linear ulcerations of the esophagus and hard tarry fecal balls
 Neuronal degeneration of pre- and post- ganglionic sympathetic and parasympathetic neurons is common
 A specific distribution of chromatolytic autonomic and somatic lower motor neurons is found in the brain
stem and spinal cord

2. EQUINE DEGENERATIVE ENCEPHALOMYELOPATHY(DEGENERATIVE)
 progressive neurologic disorder of horses and zebras characterized by diffuse degeneration of axons,
myelin and neurons in the spinal cord and to a lesser degree, the brain stem.
ETIOLOGY:
 unknown but Vitamin E deficiency and genetic factors are suspected
 Vitamin E also plays a role in neurological functions.
 Clinical signs usually become apparent during the first year of life.
CLINICAL SIGNS:
 ataxia and weakness in all 4 limbs ; hindlimbs may be more severely affected.
 There is no definitive diagnostic test
PREVENTION:
 Supplementation of pregnant mares and newborn foals with vitamin E is preventive in predisposed
families, and affected horses may improve with vitamin E supplementation.
CERVICAL SPONDYLOMYELOPATHY/ CERVICAL VERTEBRAL MALFORMATION-MALARTICULATION/
WOBBLER SYNDROME (DEGENERATIVE)
 compression of the spinal cord
ETIOLOGY:
 abnormal development of the cervical vertebrae
 most common noninfectious disease of the spinal cord and occurs in many breeds of horses ; mid cervical
region is most commonly affected
DIAGNOSIS:
• based on imaging
• plain radiographs may show abnormal articular facets and stenosis of the vertebral canal
• Myelography for definitive diagnosis and surgical planning
 TREATMENT:
-NSAID and Dimethyl sulfoxide to reduce inflammation
-In yearlings, diet modification can help
-Surgery
EQUINE MOTOR NEURON DISEASE (DEGENERATIVE)

3.  progressive, non inflammatory degeneration of motor neurons in the spinal cord and brainstem of horses
ETIOLOGY:
 uncertain but Vitamin E deficiency is a strong risk factor
CLINICAL SIGNS:
• generalized symmetric weakness, trembling, and muscle atrophy
• affected horses have retinal abnormalities
DIAGNOSIS:
 electromyography and biopsy of the spinal accessory nerve or the sacrodorsalis caudalis muscle
TREATMENT:
 no specific treatment
PREVENTION:
 Vitamin E supplementation
POLYNEURITIS EQUI
 Polyneuritis equi is uncommon and caused by a progressive immune-mediated lymphocytic infiltration
and demyelination of the sacrococcygeal and lumbosacral nerve roots of the cauda equina. Nerves
outside the cauda equina, such as the cranial nerves, may also be affected.
ETIOLOGY:
 The aetiology of the disease is unknown, but evidence suggests that it is an allergic-mediated
polyneuropathy similar to Guillain-Barré syndrome in humans and experimental allergic neuritis (EAN) of
laboratory rodents. Infection with Equine Herpesvirus-1 and Campylobacter have been proposed, but
there has been no confirmation.
CLINICAL SIGN:
 Typically, there is a slow progressive paralysis of the tail, rectum, anus and bladder and hindlimb
weakness and ataxia.
 There will be urine scalding of the hindlimbs, hyperaesthesia and muscle fasciculations over the
hindquarters.
 Muscle atrophy is variably present.
 Cranial nerve involvement, particularly CN V, VII and VIII, may also be present and is usually asymmetric.
This will present as paralysis of the facial muscles, head tilt, nystagmus, tongue paralysis and difficulty
swallowing.
DIAGNOSIS:
 Currently there are no specific antemortem tests to detect the disease in horses.
 The diagnosis is one of exclusion, supported by the clinical signs and history.

4.  An ELISA can be performed to detect antibodies against P2-myelin protein, but the test is not available
commercially and is not specific for the disease.
 On routine haematology: evidence of chronic inflammation is usually detected.
 Analysis of the CSF reveals: xanthochromia and a mildly increased protein and cell count.
 Differential diagnosis that should be ruled out before a diagnosis of PNE is considered include:
-Equine herpesvirus-1 myeloencephalopathy
-Sacral/coccygeal trauma
-Equine motor neuron disease
-Abberant parasite migration (e.g. Strongylus spp.)
-In endemic areas, such as the USA
-Sarcocystis neurona myelitis (equine protozoal myelitis)
-Rabies
-Rhodococcus equi myeloencephalitis should also be considered.
TREATMENT:
 Treatment is palliative, including management of urinary and faecal incontinence, managing cystitis and
minimizing urine scalding.
 Horses with dysphagia may need tube feeding.
 Treatment with corticosteroids has provided some palliative benefits but the effect is short-lived.
 The condition is slowly progressive, but the prognosis is generally poor.
CEREBRAL HYPOXIA
 occurs when there is insufficient of O2 supply to the brain
CLINICAL SIGNS:
 tetraparalysis
 unconsciousness
 lethargy
 dullness
 ataxia
 blindness
 convulsion
TREATMENT:
 respiratory stimulant(such as doxaprom)

5.  oxygenation
INCREASED INTRACRANIAL
PRESSURE/CEREBRAL EDEMA/
BRAIN SWELLING
-commonly a transient phenomenon and fatal
ETIOLOGY:
 vasogenic edema
 limited ability for accommodation of increasing volume within the confines of the dura and the cranium
CLINICAL SIGN:
 central blindness and periodic attacks of abnormality occur in which opisthotonos, nystagmus, muscle
tremor and convulsion
TREATMENT:
 Cerebral decompression
HYDROCEPHALUS
 Congenital: hopeless - euthanasia is usually indicated.
 Acquired: animals which recover are often mentally deficient ('dummy foals') and unthrifty.
OTITIS MEDIA/ INTERNA
 is an inflammation of the inner ear and is usually considered synonymous with labyrinthitis
 occurs in young animals of all species
 horses usually present with the sudden onset of severe whirling vertigo, nausea, and vomiting. The
symptoms can be so severe and disabling that patients require vestibular suppressants such as diazepam
or meclozine in order horses to lessen vertigo.
 Symptoms typically subside over a few days, but may leave the patient with vague imbalance which
slowly improves over weeks to months. Occasionally a bacterial infection of the middle ear can spread to
the inner ear and cause this disease. In this situation antibiotic treatment may be helpful.
CLINICAL SIGN:
 violent, uncontrollable behavior including throwing themselves on the ground, rolling, and trashing
TREATMENT:
 dependent on either a positive tympanocentesis
ENCEPHALOMALACIA
 abnormal softening of the brain
 leukoencephalomalacia-white matter of the brain

6. ETIOLOGY:
 ischemic encephalopathy
 metabolic and circulatory disorders
 intoxications and toxic-infectious diseases
 nutritional diseases
 Hereditary
CLINICAL SIGN:
 weakness of all four limbs: dullness, blindness,ataxia,head pressing,circling,terminal coma
 gross lesions include areas of softening,cavitation and laminar necrosIs of the cortex
TREATMENT:
 Depends on the nature of the lesion