27.6.4: Neurological horse - normal mentation Flashcards
Causative agents of spinal ataxis
- Cervical vertebral compression myelopathy (CVCM)
- Equine Herpes Virus (EHV-1)
- Equine protozoal myelencephalopathy (EPM)
- Vitamin E-related ataxia
Clinical signs of spinal ataxia
Relating to the ascending pathways:
* Crossing legs
* Abduction
* Circumduction
* Knuckling
Relating to the descending pathways:
* Foot dragging
* Stumbling
Which tracts does ataxia affect?
Ataxia: specifically this is proprioceptive deficits (i.e. ascending tracts) but these run so close to UMN tracts / descending tracts that normally both occur simultaneously.
Clinical signs of vestibular ataxia
- Head tilt
- Leaning
- Falling to one side
- Wide based stance
Clinical signs of cerebellar ataxia
- Wide-based stance
- Dysmetria (hyper or hypo)
- No proprioceptive deficits
- No weakness
1
2
3
4
Clinical signs of CVCM
- Ataxia
- Weakness
- Spasticity
- Generally symmetrical deficits, can sometimes be assymetric (e.g. if OA)
- Truncal sway
- Crossing and interferences when turning
- Hindlimb pivoting
Diagnosis of CVCM
- Radiographic sagittal ratios - laterolateral view with no obliquity - shows likelihood of compression but doesn’t prove it!
- Radiographic myelography- can prove compression.
- CT myelography - best, but cannot do flexed views on CT
- Post-mortem = gold standard
Treatment of CVCM
- Young horses <12 months: NSAIDS ± steroids, diet restrictions to limit overnutrition (protein ± starch), maintain correct Ca:P in feeds, avoid excess copper in diet
- Adult horses: NSAIDs ± steroids, mesotherapy and exercise
- Surgery: ventral interbody vertebral fusion - stops movement up and down - can improve 1-2 grades
When are horses typically diagnosed with CVCM and what effect does it have?
- Typically diagnosed early in life <4 y.o.
- Can manifest later in life (OA)
- If moderate to severe ataxia, will be unable to perform and will be unsafe
Clinical signs of Equine Herpes Virus 1
- Previous resp disease: intermitten cough, serous nasal discharge, conjunctivitis (6-10 days prior to presentation)
- Symmetric ataxia ± weakness
- Bladder distension/ urinary incontinence
- Poor anal tone
- Recumbency
- Inconsistent fever
- Chorioretinitis
- Stabilisation over 48hrs, improvement starts at 5 days
- Most horses fully recover
Diagnosis of EHV-1
- Signalment: recent competition/ movement/ horses on yard with resp disease
- Nasopharyngeal swab PCR
- Serology and complement fixation test if unvaccinated
- CSF tap often unrewarding but may see xanthochromia and increased protein
Xanthochromia
Xanthochromia : yellow discoloration indicating the presence of bilirubin in CSF which appears as oxyhaemoglobin released from the breakdown of red blood cells following haemorrhage into the CSF is converted in vivo into bilirubin in a time-dependent manner
Treatment of EHV-1
- Quarantine to prevent spread: isolate affected horses, monitor temperatures, 21 day movement restriction, foot baths, gloves, overalls
- Valacyclovir 30mg/kg q 8hr then 20mg/kg q 12hrs
- Low molecular heparin SC
- NSAIDs/ steroids -> if treat the resp disease early enough -> less fever -> less viraemia -> lower likelihood of neuro disease
- Give time for recovery
Causative agent of equine protozoal myeloencephalopathy (EPM)
Sarcocystis neurona and Neospora hughesi
Horse is an aberrant host
How do horses become infected with EPM?
- Ingestion of contaminated feed: concentrate/ hay/ grass
- Seropositive does not prove this is the aetiology
- Can be reactivation from trigeminal carrier
Clinical signs of EPM
- Any possible neuro signs (insidious or acute onset)
- Asymmetric ± cranial nerve deficits (CN VIII, VII, X)
- Weakness and muscle atrophy (gluteus, biceps femoris, epaxial musculature)
- Poor anal tone, cauda equina syndrome
Diagnosis of EPM
- Clinical signs occurring in an area with opposums
- Response to treatment
- PM histology
- Can assess intrathecal production of antibody; can assess serum : CSF, positive if <1
- Do not treat seropositive results in areas of high prevalence
Treatment of EPM
NSAIDs/steroids in acute severe stages
Long term Vitamin E supplementation
Options
* Pyrimethamine and sulfadiazine - 90 days treatment, rapid absorption into CNS
* Diclazuril/ ponazuril - 60 days treatment, takes 7 days tp reach adequate CNS concentrations
Which animals should you not give Pyrimethamine and sulfadiazine to?
- Don’t se in pregnant mares or stallions
- Don’t feed with hay
Prevention of EPM
- Avoid exposure to opossum faeces -> sealed feed containers, anti-opossum fences
- Daily administration of low dose ponazuril/ diclazuril/ nitazoxanide - only in areas of high prevalence
What forms of Vitamin E related ataxias and weakness are there?
- Equine degenerative myeloencephalopathy/axonal dystrophy
- Equine motorneurone disease
Clinical signs of Equine degenerative myeloencephalopathy/ axonal dystrophy
This is a diffuse degenerative disease of the spinal cord and caudal portion of the brainstem.
Primarily affects young horses <1 y.o. but can take up to 5 yrs to diagnose.
- Insidious onset of symmetric spasticity, ataxia, and paresis
- Pelvic limbs are usually more severely affected than the thoracic limbs
- Some horses will have decreased menace response, lethargy or behavioural changes
- Long-term poor performance
- Clinical signs may progress slowly or stabilise
- Low Vitamin E but not responsive to treatment antemortem diagnosis
Prevention of Equine degenerative myeloencephalopathy / axonal dystrophy
- Some breed lines may be predisposed (QH)
- Areas with low Vitamin E
- Supplementation in the last month of pregnancy and during the nursing period
Cause and risk factors of Equine motorneuron disease
- Acquired progressive neurodegenerative disease that affects neurones in the brain and spinal cord
- Triggered by Vitamin E deficiency for periods >18 months
- Risk factors include excess copper and no access to green forage
Clinical signs of Equine motorneuron disease
- Generalised weakness: slow gait, dragging toe, narrow-based stance
- Shifting weight between limbs
- Muscle fasciculations of the anti-gravitatory muscles (T>P)
- Generalised sweating
- Neurogenic muscle atrophy: Type I fibres
- Pigmentary retinopathy
This life cycle shows the transmission of which disease?
Equine protozoal myeloencephalopathy (EPM)
What clinical sign is shown here and which disease is it characteristic of?
Pigmentary retinopathy
* Sign of Equine motorneuron disease
Diagnosis of Equine motorneuron disease
- Low Vitamin E in serum
- Confirmation of diagnosis: myelinated axon degeneration in Sacrocaudalis dorsalis medialis muscle in the tail
- At PM: loss of motor neurons from the ventral horn of the spinal cord
Treatment and prognosis for Equine motorneuron disease
- Vitamin E (ideally water-dispersible) 5000-7000 IU/ day for 3 months
- 40% horses showed improvemenet in 6 weeks and were normal in 3 months, 40% stabilised clinical signs with some chronic deficits, 20% progressed despite treatment
Triggers for head shaking
- Photic: bright light, photoperiod, cystic ccorpora nigra, floaters in posterior / anterior chamber
- Allergic rhinitis
- Sinusitis, otisi (Trombicula autumnalis), GP mycosis
- Structural: skull fractures, dental disease, THO, TMJ -> facial / head hyperaesthesia
- Bit or bridle issues
Diagnostic plan for horse with head shaking
- History including environment and management
- Physical exam
- Ocular exam
- Dental exam
- Upper airway endoscopy including guttural pouch
- Nerve blocks (infraorbital, maxillary)
- Skull radiographs, CT
- Otoscopy
Mecical treatment options for head shaking
- Cyproheptadine
- Carbamazepine
- Nose nets
- Ocular sunglasses
- Other options include gabapentin, inhaled steroids, magnesium sulphate, antihistamines, melatonin, change in bridle or bit
Surgical treatment options for head shaking
- Infraorbital neurectomy with cryotherapy
- Chemical sclerosis of infraorbital nerve
- Caudal compression of the infraorbital nerve
Clinical signs of sleep deprivation / narcolepsy
- Staggering
- Lowering the head and neck
- Buckling of the thoracic limbs
- Kneeling posture
- Flaccidity of the hips
- Unexplained abrasions on knees, lips
- Kneeling when tightening the girth
Diagnosis of sleep deprivation / narcolepsy
- Age, recent changes in environment, stable, barn, premises, wildlife
- Consider quality of bedding, tight rugs in winter etc.
- Concurrent disease: arthritis - back, hocks, carpus, PPID
- True narcolepsy is a diagnosis of exclusion
Treatment for sleep deprivation / narcolepsy
- Trial oral phenylbutazone
- Thick straw bedding
- Large stable
- Inside barn
- Remove rugs
Pathogenesis of shivers
- Progressive, chronic neuromuscular disease in horses characterised by gait abnormalities when backing up, trembling of tail while held erect, trembling of thigh muscles, and a flexed and trembling hindlimb when held
- Damage of the deep cerebellar nuclei (responsible for fine-tune of planned movement) - as a result flex and extension are activated at the same time
Clinical signs of shivers
- Difficulty backing up: hyperextension of the hindlimbs, inability to pick up hindlimbs, offering contralateral limb, hyperextension
- Normal ambulation otherwise: fine to walk forward, trot, canter, and for performing
Typical signalment of shivers
- Normally starts ~5 y.o.
- Normally progressive and performance-limiting
What is the treatment and prognosis for shivers and what other conditions should you rule out when investigating it?
Ddx to rule out:
* Upper fixation of the patella
* Stifle osteoarthritis
* Sacroiliac pain
No treatment and guarded prognosis.
