Horse

Temporohyoid osteoarthropathy

• disorder of articulation between temporal & stylohyoid bones in adult horses

• otitis externa/media → chronic temporal tympanic bulla inflammation → temporohyoid joint fusion → impaired hyoid flexibility + fracture of temporal bone → CN VII + VIII damaged

• clinical signs: facial deviation away from affected side, drooping ear, eyelid dysfunction & reduced lacrimal secretion, head tilt toward affected side, nystagmus, ataxia, ± Horner’s

Equine protozoal myeloencephalitis

• Dz affecting spinal cord, brainstem, & cerebrum caused by S. neurona or N. hughesi (definitive host opossum, shed in feces, horse is aberrant host)

• causes focal-multifocal asymmetric lesions, typically chronic-progressive

• clinical signs: asymmetric mm. atrophy, ataxia, weakness, proprioceptive deficits

• highest risk in horses 1-4yrs, predisposed by stressful conditions

• ~50% exposed, ~1% develop clinical Dz

• Dx: serology of serum + CSF

Cerebellar abiotrophy

• mutation of MUTYH gene (encodes DNA repair enzyme), expression increased w/age & signs appear after 6wks

• causes degeneration of Purkinje cells + granular cells & disorganization of molecular + granular layers

• clinical signs: head/intentional tremors, ataxia, hypermetria, abnormal fine motor activity, recumbency

• progressive Dz, poor to grave prognosis

Idiopathic epilepsy

• primarily affects Egyptian Arabian foals, suspect genetic recessive inheritance

• signs appear days to weeks after birth, normalize by ~1yr

• pre-ictal phase rarely observed in foals, blindness most common post-ictal sign

• seizures may be focal head-twitching to generalized tonic-clonic w/paddling, last seconds-minutes

Neonatal maladjustment syndrome

• brain ischemia/hypoxia + increased progesterone concentration → altered neuronal cell function

• signs may start at birth or develop in the first 1-2 days

• clinical signs: disorientation, lack of mare affinity, wall-licking, ± seizures & nystagmus, ± sepsis

• prognosis good w/timely treatment

Nigropallidal necrosis/encephalomalacia

• caused by ingestion of yellow star thistle or Russian knapweed (repin toxicity)

• causes necrosis of substantia nigra, globus pallidus, basal nuclei

• clinical signs: excessive jaw tone, inability to chew, ± other neuro signs

Leukoencephalomalacia

• caused by ingestion of corn w/F. verticillioides mold

• produces fumonisins that interfere with/spingolipid metabolism

• causes liquefactive necrosis/softening of white matter (pathognomonic) ± liver injury

Horner’s sydrome

• acquired secondary to local Dz/iatrogenic causes that interrupt sympathetic innervation to the head

• typically associated w/head & neck lesions

Hepatic encephalopathy

• failure of liver to clear intestinal byproducts → increased concentrations reaching brain → altered neuronal function

• clinical signs: lethargy, encephalopathy, convulsions

Laryngeal hemiplegia

• affects upper airway (decreased airflow)

• caused by vagus nerve/recurrent laryngeal n. lesion → paralysis of arytenoids (most commonly L)

• causes “roaring” when exercised

• most common in Thoroughbreds

• Dx: standing endoscopy

Cervicovertebral malformation (Wobblers)

• developmental Dz, stenosis of spinal canal → cervical spinal cord compression → ataxia, weakness, spasticity

• cervicovertebral instability = dynamic intermittent compression during flexion (C3-5, younger animals)

• cervicovertebral static stenosis = static continuous compression (C5-7, older animals)

• most common in growing males

• generally guarded prognosis

Clinical signs of Wobblers

• symmetric ataxia, paresis, spasticity

  • ataxia may be progressive → stabilized

• toe dragging, circumduction, trunk lateralization, hypermetria, pacing

• ± resting proprioceptive deficits

• worse in pelvic limbs, tracts to/from rear are more superficial in cervical spinal cord

• infrequent: pain, hypoalgesia, neurogenic muscle

• young animals may show developmental orthopedic Dz & flexural deformities

Pathogenesis of Wobblers

• assoc. w/other ortho problems, OCD lesions may be present at articular facets

• environmental + genetic + nutritional contributions

  • copper/zinc deficiency, excess carbs

• compresses spinal cord tracts, dorsal (conscious) & dorsolateral (unconscious) ascending tracts first

• wallerian degeneration & fibrosis at compression site

Dx of Wobblers

• rads: narrowing of spinal canal (minimal sagittal diameter aka ratio of vertebral canal:vertebral body <50%)

• definitive: myelogram (avoided if clinical signs severe)

Spinal cord trauma

• often guarded-poor prognosis

• clinical signs from mild ataxia to recumbency depending on location, duration, & severity, caused by hemorrhage, edema, & thrombosis

• fractures may be present

Equine herpesvirus type I myeloencephalopathy

• causes respiratory Dz, abortion, & neonatal Dz, neuro form uncommon

  • neuro form has increased replicative efficiency

• viral inhalation → adheres to resp epi → replicates in lymphoid tissue → migrates in phagocytes to CNS endo → vasculitis & thrombosis of spinal cord → hypoxia, degeneration, necrosis, hemorrhage → spinal ataxia + LMN signs

• clinical signs: ascending symmetric ataxia (worse in rear), proprioceptive deficits, circumduction, weakness, paresis/paralysis, poor tail tone, incontinence

• Dx: PCR on nasal swab or whole blood

• mgmt: animal isolation + facility quarantine, disinfect w/bleach

Equine degenerative myeloencephalopathy

• diffuse (brainstem-spinal cord), non-compressive, symmetric neurodegenerative Dz

• causes ataxia, weakness, & spasticity in young horses

  • all limbs involved, worse in rear

• clinical signs: proprioceptive deficits, hyporeflexia, hypometria but no CN deficits, neurogenic mm. atrophy, or skin sensation loss

• pathology: neuroaxonal dystrophy w/lipofucsin accumulation, severe lesions in spinocerebellar tract at thoracic region

• more common in horses <2yrs

• definitive Dx postmortem

Equine motor neuron Dz

• neurodegenerative Dz caused by vitamin E deficiency or excessive antioxidant demand → oxidative damage of motor neurons in spinal cord (ventra + CN nuclei)

• clinical signs: mm. tremors + wasting, no ataxia

West Nile Virus encephalomyelitis

• ataxia-recumbency w/muscle fasciculations, mostly febrile

  • infection often asymptomatic

• Culex mosquito vector, bird amplifier host

• neurotropic in horses

• Dx: IgM-capture ELISA

• supportive/palliative treatment

• prevention via vaccine + environmental mgmt of standing water

• zoonotic

Eastern Equine Encephalitis virus

• ssRNA virus w/wide distribution, lineage I endemic in North America (most common in SE, recent outbreaks in OH + MI)

  • common near freshwater hardwood swamps in late summer/early fall

• mosquito vector, bird amplifying host

• clinical signs: fever, obtunded, ataxia, paralysis, anorexia

  • signs progressive, 90% case fatality

• pathology: profound inflammation in basal ganglia + brainstem

• Dx: IgM titer in peripheral blood or CSF, virus isolation from neural tissue, neutrophilic pleocytosis of CSF

• prevent via vector control + vaccination

• not directly zoonotic but horses used as sentinel for human Dz