Changes

====Signalment====

====Signalment====

Mostly Standardbreds and Thoroughbreds aged 1-6years.<ref name="Pasq">Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''' (Third edition), ''SUDZ Publishing'', 245-250.</ref>  Foal infection may be possible.<ref name="EPM8">Gray, L.C, Magdesian, K.G, Sturges, B.K, Madigan, J.E (2001) Suspected protozoal myeloencephalitis in a two-month-old colt.  ''Vet Rec'', 149:269-273.</ref>

Mostly Standardbreds and Thoroughbreds aged 1-6years.<ref name="Pasq">Pasquini, C, Pasquini, S, Woods, P (2005) '''Guide to Equine Clinics Volume 1: Equine Medicine''' (Third edition), ''SUDZ Publishing'', 245-250.</ref>  Foal infection may be possible.<ref name="EPM8">Gray, L.C, Magdesian, K.G, Sturges, B.K, Madigan, J.E (2001) Suspected protozoal myeloencephalitis in a two-month-old colt.  ''Vet Rec'', 149:269-273.</ref>

====Clinical Signs====

====Clinical Signs====

The disease onset may be acute, peracute of chronic.  The insidious onset is most typical and with such cases, the clinical examination may reveal a bright, alert horse bright perhaps with some focal muscle atrophy.(Furr)In all cases, the clinical signs are referable to diffuse focal and multifocal lesions of the white and grey matter of the spinal cord and brain (EPM3)

The disease onset may be acute, peracute or chronic.  An insidious onset ataxia is most typical and with such cases, the clinical examination may reveal a bright, alert horse, perhaps with some focal muscle atrophy.(Furr)In all cases, the clinical signs are referable to diffuse focal and multifocal lesions of the white and grey matter of the spinal cord and brain. (EPM3)The three characteristic 'As' (ataxia, asymmetry, atrophy) suggest multifocal or diffuse disease, but are not pathognomonic for EPM (Furr). 

Spinal cord:

*Ataxia, paresis or spastcity of one or more limbs, often asymmetrical, signs usually worse in hindlimbs, may see stumbling, falling, knuckling, toe dragging, circumduction, crossing over, tetraparesis - areflexia, hyporeflexia (LMN) or hyperreflexia (UMN) depending on site of lesion

|Spinal cord

|*Ataxia, paresis or spasticity of one or more limbs, often asymmetrical, signs usually worse in hindlimbs, may see stumbling, falling, knuckling, toe dragging, circumduction, crossing over, tetraparesis - areflexia, hyporeflexia (LMN) or hyperreflexia (UMN) depending on site of lesion

*Loss of reflexes or cutaneous anaesthesia

*Loss of reflexes or cutaneous anaesthesia

*Apparent lameness, particularly atypical or slight gait asymmetry of hindlimbs (not alleviated by local anesthesia)

*Apparent lameness, particularly atypical or slight gait asymmetry of hindlimbs (not alleviated by local anaesthesia)

*Abnormal placing reactions  

*Abnormal placing reactions  

*Focal muscle atrophy of individual muscle grps (Pasq), especially gluteal muscles, often asymmetrical  

*Focal muscle atrophy of individual muscle groups(Pasq), especially gluteal muscles, often asymmetrical  

*Generalized muscle atrophy or loss of condition

*Generalized muscle atrophy or loss of condition

*Localized sensory deficits and 'strip sweating' of dermatomes

*Localized sensory deficits and 'strip sweating' of dermatomes

*Sacrococcygeal involvement will produce signs that mimic ''polyneuritis equi''  

*Sacrococcygeal involvement will produce signs that mimic ''polyneuritis equi''  

Peripheral nerves: (may lead to injuries to muscle tendons or ligaments)  

*Upward fixation of the patella

|Peripheral nerves(may lead to injuries to muscle tendons or ligaments)  

|*Upward fixation of the patella

*Exertional rhabdomyolysis

*Exertional rhabdomyolysis

*Back pain

*Back pain

*Gait abnormality

*Gait abnormality

Brainstem (cranial nerve signs, <5% cases):

*Atrophy of temporalis and masseter muscles, loss of sensation to the face (V)

|Brainstem (cranial nerve signs, <5% cases)

*Abnormalities of facial (VII) and vestibulocochlear (VIII) nerves often observed together:  

|*Atrophy of ''temporalis'' and ''masseter'' muscles, loss of facial sensation (V)

**VIII - vestibular signs of nystagmus, head tilt, base-wide stance (peripheral or central vestibular disease)

*Facial (VII) and vestibulocochlear (VIII) nerve deficits often seen together:  

**VII - unilateral facial paralysis - muzzle deviation, ptosis, ear droop

**VIII - vestibular signs: nystagmus, head tilt, base-wide stance (peripheral or central vestibular disease)

**VII - unilateral facial paralysis: muzzle deviation, ptosis, ear droop

*Loss of tongue tone (XII)

*Loss of tongue tone (XII)

*Dysphagia(V, VII, IX, X, XII)  

*Dysphagia (V, VII, IX, X, XII)  

*Dorsal displacement of soft palate (IX, X)  

*Dorsal displacement of the soft palate (IX, X)  

*Laryngeal hemiplegia (X)

*Laryngeal hemiplegia (X)

*Abnormal menace response (II, VII)

*Abnormal menace response (II, VII)

*Headshaking(EPM 7)

*Headshaking(EPM 7)

*Blindness with or without abnormal pupillary reflexes (Pasq)

*Blindness with or without abnormal pupillary reflexes (Pasq)

Cerebrum, basal nuclei, cerebellum:

*Abnormal menace response

|Cerebrum, basal nuclei, cerebellum:

|*Abnormal menace response

*Circling

*Circling

*Seizures (may be the only clinical sign)(82 in Furr)

*Seizures (may be the only clinical sign)(82 in Furr)

*Abnormal EEG.

*Abnormal electroencephalogram (EEG)

*Asymmetrical central blindness

*Asymmetrical central blindness

*Facial hypoalgesia  

*Facial hypoalgesia  

*Narcolepsy-like syndrome  

*Narcolepsy-like syndrome  

Severe cases may:

Lesions of the brainstem, cerebrum or cerebellum are less frequently recognized than those of the spinal cord.  Horse with severe EPM may be unable to stand or swallow and, if left untreated, progress to recumbency within 14 days to 6 months. (Pasq) This deterioration may occur smoothly or spasmodically (Merck) but is likely to result in death. It has been suggested that rapidly progressive presentations reflect brainstem lesions.(Furr)

*Inability to stand  

*Inability to swallow

*Untreated progressive to recumbency in 14days to 6mths (Pasq)

Without treatment, progression to recumbency and death is likely.  This deterioration may occur smoothly or spasmodically over hours to years. (Merck)

 

Any gait abnormality in galloping/trotting race/dressage horses while in training which cannot be attributed to musculoskeletal abnormality may result from EPM and requires careful neurologic evaluation.(V)

 

Lesions of the brainstem, cerebrum or cerebellum are less frequently recognized.The three characteristic 'As' of EPM (ataxia, asymmetry, atrophy) suggest multifocal or diffuse disease, but are not pathognomonic.  It has been suggested that rapidly progressive presentations reflect brainstem lesions.

====Diagnosis====

====Diagnosis====