Specific Neurologic Disorders Flashcards
List the clinical signs for Cerebellar Abiotrophy and provide some differentials for this condition
- Intention tremor
- Base wide stance
- Lack of menace & failure to blink in bright light
- Ataxia
- Dysmetria and spasticity
DDX: cranial malformation, congenital spinal malformation (incl atlantoaxial malformation), stenotic myelopathy, cerebellar inflammation/infection and trauma. EEG may help to rule out seizure as a cause for the tremors.
List the breeds commonly affected by cerebellar abiotrophy and the differences between them.
Arabian and Gotland foals (and their crosses: generally signs noted by 1 yr of age, most commonly 1-6mo. Signs are generally progressive for several months but once the animal reaches maturity they become static or may improve slightly.
Oldenburgs: generally progressive and fatal with atypical histological findings compared with those of Arabian foals (Arabian foals typically have apoptosis of purkinje cells).
List differentials for cerebellar disease and some defining points for each
- Cerebellar abiotrophy: diagnosed based on signalment (Arabian, Gotland or Oldenburg breeds), typically foals.
- Gomen Disease: geographically located to New Caledonia, progressive disease in horses at pasture over 3-4 yrs until they die or are euthanised.
- Dandy-Walker syndrome: defect in the midline of the cerebellum and cystic dilation of the 4th Ventricle. May be abnormal from birth: reported in Arabs and TBs.
- Cerebellar hypoplasia or dysplasia: reported rarely in TBs with variable clinical signs and ranging from foals to adults.
- Strep equi equi abscess: history of previous strangles.
- Aberrant parasitic migration: often accompanied by other neurological deficits
- Chronic methylmercurial poisoning: signs include cerebellar ataxia, lethargy, anorexia, exudative dermatitis, and laminitis.
List the clinical signs of Shivers and the commonly affected breeds
Chronic progressive movement disorder
- Difficulty walking backwards and may have tremors, hyperflexed pelvic limb posture, may progress to involve thoracic limb movement.
- Muscle atrophy and reduced muscle strength
- Exercise intolerance
- Facial twitching and or elevated tail head
Breeds: Draft breeds, TBs, WBs and less commonly Connemara, Welsh, QH, SB, saddlebred, Tennessee Walking horse, Missouri Fox Trotters, Paint and Morgans.
List the 4 gait patterns of shivering
- Hyperextension when backing and lifting the limb
- Hyperflexion and abduction during backward walking
- Shivering hyperflexion with abduction during backward walking
- Shivering-forward hyperflexion including intermittent hyperflexion and abduction with forward walking
List the breed, age and gender predilection for CVSM
Males, young horses (less than 7yrs, often well-fed rapidly growing), TBs, Tennessee Walking horses and WBs.
Define dynamic versus static compression with CVSM including effect of flexion versus extension of the neck.
Dynamic: compression is intermittent and occurs when the cervical vertebrae are flexed (cranial vertebral lesions) or extended (caudal vertebral lesions).
Static: compression is continuous regardless of cervical position.
List the common clinical signs of CVSM
- Symmetric ataxia
- UMN extensor paresis (weak on dynamic tail pull) & dysmetria (usually worse in pelvic than thoracic limbs due to superficial location of pelvic limb spinocerebellar proprioceptive tracts)
- Circumduction of pelvic limbs on circling
- Flexor paresis (toe dragging)
- Forelimb hypometria, particularly up and down a hill/with head elevation
- May have concurrent OCD/DOD of the appendicular skeleton.
List medical and surgical treatment options for CVSM
- Dietary protein and energy restriction (likely only effective in horses 1-2yrs age) and close monitoring of trace elements such as zinc and copper
- Stall rest/exercise restriction (more effective in young horses)
- Supplementation with vitamin E and Se (EDM is a differential in young horses)
- Anti-inflammatories/corticosteroids (realistically one of the few options in adult horses with acute neuro dz)
- Medication of DAPJ if evidence of OA
- Intervertebral fusion (fenestrated basket or threaded cylinder) - most effective if only one site and if only mild neurological disease.
Describe/List the clinical findings, signalment and pathogenesis of equine neuroaxonal dystrophy and equine degenerative myeloencephalopathy
- Diffuse, symmetric degenerative neurologic disease
- UMN and general proprioceptive deficits including symmetric ataxia, weakness, dysmetria (mostly hypometria), horses may pace. All 4 limbs affected, usually worse in pelvic limbs.
- May pivot on the inside and circumduct the outside hindlimb when circled
- Some LMN signs such as hyporeflexia of the trunk and neck with absent or reduced cervical, cervicofacial, cutaneous trunci and laryngea adductor reflexes.
- No gender or sex predilection; affects young horses, usually in the first yr of life but can be as young as 1 month up to several years.
- May be inherited as a complex trait that predisposes horses then subject to vit E deficiency
- Exposure of susceptible horses to diets deficient in vitamin E is thought to be involved in the pathogenesis due to oxidative damage and lipid peroxidation of cell membranes.
- Vit E deficiency is not consistent among all affected horses, but supplementation during the first year of life may reduce incidence and severity of disease
- Definitive diagnosis required histo, although low serum vit E in a horse with compatible clinical signs is supportive.
- Not, or very slowly progressive, but horses don’t recover (usually stabilise by 3yrs but remain neurologically abnormal/unfit to perform).
List the risk factors (incl geographical), common signalment and causative agents for EPM
Main risk factors:
- Exposure to opposums
- Housing indoors on straw or corn stalks, and lack of rodent proof feed storage
- Use for racing increased the risk.
- Presence of a stressor such as transport, heavy exercise, injury, parturition etc may increase the risk.
Other risk factors:
- High seroprevalence in the USA, which increases with increasing temperature as well as increasing patient age
- Racing and showing animals are at higher risk than breeding or pleasure horses
Signalment:
- Average age of affected horses is 4yrs, higher risk animals are thought to be 1-5yrs or greater than 13yrs.
- No gender predilection but TB, SB, WB and QH more commonly affected.
Causative agents:
S. neurona is most common, N. hughesi is less common and seroprevalence is much lower to this parasite.
Describe the transmission of EPM
- Contamination of feed/water sources with infected opposum faeces.
- No horizontal transmission in horses of S. neurona
- Transplacental transfer is very uncommon or absent
- Some reports of trans-placental transmission of N. hughesi.
List factors contributing to pathogenesis of EPM
- *- Parasite dose is likely a factor - the immune clearance of the parasite is likely very effective given the high rate of exposure relative to disease incidence.
- Physiologic stress may influence susceptibility to clinical disease
- Entry into the CNS thought to be either via endothelial cells or leucocytes
List clinical signs of EPM, including 3 A’s of EPM
- Acute-chronic insidious onset neurological signs that may be focal or multifocal
- Can include brain, brainstem or spinal cord
- Signs are variable due to random distribution o lesions within the CNS.
- Grey matter involvement leads to focal muscle atrophy and severe muscle weakness
- White matter involvement results in ataxia and weakness in limbs caudal to the lesion.
- Horses are usually bright and alert with no alterations in physical exam findings.
- Neuro exam typically shows asymmetric ataxia, weakness, spasticity (quadrilateral).
- If brain or brainstem involvement may see obtundation, head tilt, cranial nerve dysfunction (often facial) and dysphagia.
- 3 A’s: ataxia, asymmetry and atrophy.
List the diagnostic methods and pathologic findings
Diagnosis:
- Presumptive diagnosis based on clinical signs and absence of other causes of neurological dysfunction
- Immunodiagnostic testing of serum and CSF to show intrathecal antibody production.
- Positive serum titre does not confirm disease due to high seroprevalence; likewise detection in CSF alone does not confirm due to passive transfer across the BBB.
Pathology:
- Haemorrhage and foci of malacia mostly in the spinal cord.
- Brainstem more commonly involved than other areas of the brain.
- Lesions characterised by focal to diffuse areas of nonsuppurative inflammation and necrosis with pervascular infiltration of mononuclear cells (can affect grey or white matter)
List the differential diagnoses for EPM
- CVSM
- Viral encephalitis (WNV, EEEV, WEEV, EHV-1)
- Meningitis
- Trauma (TBI or SCI)
- ENAD/EDM
- Polyneuritis equi
Basically any neurologic disease depending on signs shown.
List treatment options for EPM and likelihood of success
- Pyrimethamine and sulphonamides (caution with addition of folic acid - may increased toxicity - used to reduce risk of anaemia)
- Ponazuril (benzeneacetonitrile compound) broad spectrum anticoccidial
- Anti-inflammatories symptomatically to treat acute neurological disease
- Regardless of treatment method, approximately 60-75% improvement rate is generally seen with standard therapies.
List clinical signs of EHV-1 Myeloencephalopathy
- May be preceded or accompanied by URT disease, fever, inappetence or hindlimb oedema.
- Acute onset neuro signs, predominantly of spinal white matter (hence flexor reflexes are normal and perineal reflexes are preserved).
- Ataxia and paresis
- Hypotonia of tail and anus or tail elevation
- Urinary incontinence
- Conscious proprioceptive deficits
- Limb weakness (can become recumbent)
- Severe case may become recumbent, and may die in coma or convulsion.
- signs generally stabilise after 1-2 days and don’t progress.
List the 5 herpesviruses of horses and 3 of asinines and the disease associated with each (briefly)
Alpha-herpes: - EHV-1 (abortion and myelopathy) - EHV-4 (equine rhinopneumonitis; rarely abortion & myeloencephalopathy) - EHV-3 (equine coital exanthema) Gamma-herpes: - EVH-2 (rhinitis) - EHV-5 (EMNPF) Asinine alpha-herpes: - AHV-1 - AHV-2 - AHV-3
Describe infection and immune evasion of EHV-1
- Inhalation or ingestion of virus in respiratory, abortion, salivary, ocular and faecal products.
- Attaches to and replicates on nasopharyngeal epithelium where it infiltrates phagocytic cells
- Incubation is 2-10 days
- Migration of infected phagocytes into circulation results in viraemia (predominantly T lymphocytes of the buffy coat)
- Transfers to the vascular endothelium of the CNS
- Results in vasculitis and thrombosis of arterioles of the brain and spinal cord, hence development of neuro Dz.
- Evades host immune system in part by downregulating major histocompatibility complex class I expression at the cell surface.
List epidemiologic factors of EHV-1 myeloencephalopathy
- Virus shed by clinically affected, subclinically affected and carrier animals for 3+ weeks
- Survives in the environment for 14 days
- Survives on horses hair for 35-42 days
- Can occur any time of the year but highest incidence in late winter, spring and early summer
- Restrict movement for at least 3 weeks after resolution of clinical signs in the last clinical case
- Demonstration of stable or declining titres in affected or exposed horses helps determine when clinical spread has ceased.
List the diagnostic methods and their challenges for EHV-1 Myeloencephalopathy
- Virus isolation from nasopharyngeal swabs or buffy coat (PCR)
- Virus isolation from CSF (rare)
- Presence of antibodies to EHV-1 in CSF (but, need to take into account the albumin and serum IgG concentrations as it can simply reflect leakage of antibodies across a damaged BBB with vasculitis)
- Rising tire on paired samples (but, many horses don’t show the prescribed rise because of rapid antibody production within 6-10 days of infection hence they may have peaked by the time of developing clinical signs).
- Testing paired serum samples from in-contact horses is a good means as many seroconvert despite not showing clinical signs, or may go on to develop clinical signs.
- Many tests don’t differentiate between EHV-4 and EHV-1.
List differential diagnoses for EHV-1 Myeloencephalopathy
- EPM
- CVSM
- Trauma/fracture
- Polyneuritis equi
- Fibrocartilagenous infarction
- Aberrent parasite migration
- ENAD/EDM
- Viral encephalitis (flaviviruses and alphaviruses
- Rabies
- Botulism
- CNS abscess
- Plant & chemical intoxicoses
List the ocular changes seen in some foals with EHV-1
- Uveal vasculitis with perivascular mononuclear cuffing in the ciliary body and optic nerve
- Retinal degeneration & hypopyon
- Chorioretinopathy without anterior segment involvement
- Occassionally you see ocular and neural damage in the absence of gross signs of neurologic or visual impairment.
What suggests involvement of the immune system in polyneuritis equi?
Circulation of antibodies to P2 myelin protein.
Inflammatory lesions contain both T and B lymphocytes, suggesting the possibility of an immune-mediated reaction to myelin.
What are the two forms of polyneuritis equi?
Acute/early signs include hyperaesthesia of the perineal or head regions (or both)
The chronic form involves paralysis of the tail, anus, rectum and bladder, often accompanied by urinary or faecal retention.
List possible neurologic abnormalities with polyneuritis equi
- Tail, anus, bladder paralysis (may have faecal/urinary retention)
- Ataxia (pelvic limbs usually worse and symmetric)
- Muscle atrophy (gluteals and head - head often asymmetrically)
- Cranial nerve dysfunction (often asymmetric) primarily of CNV, CNVII and CNVIII; note these are peripheral; no alteration in mentation
- Head tilt, ear droop, lip droop and ptosis are common signs.
- Typically lesions involve extradural nerve roots but can also involve intradural nerve roots
What is the primary finding in Acquired Equine Polyneuropathy in Scandinavia?
Acute onset bilateral pelvic limb digital extensor dysfunction and knuckling.
List the most frequently isolated alphaviruses (encephalitis viruses), their distribution, vector, pathogenesis and clinical signs
EEEV, WEEV, VEEV: western hemisphere, mosquitoes, virus multiplies in muscle, enters the lymphatics, localises in lymph nodes. It replicates in macrophages and neutophils and is shed in small numbers at which time many viral particles are cleared. If clearance is incomplete remaining virus infects endothelial cells and concentrates in vascular organs (liver and spleen) where it replicates further, causing viraemia and early clinical signs. Infection of the CNS occurs within 3-5 days.
Clinical signs include fever, anorexia, stiffness, obtundation, hyperesthaesia, altered behaviour, compulsive walking, cranial nerve dysfunction; death is preceded by recumbency 1-7days
List diagnostic methods for togaviruses
Clinical signs, IgM antibody capture enzyme-linked immunosorbent assay (not produced by vaccination), paired samples are not always reliable as titres increase within 24 hours of viraemia, PCR, FAT and ELISA for necropsy specimens.
