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ECEIM > Neurology > Flashcards

Neurology Flashcards

1
Q

List the clinical signs for Cerebellar Abiotrophy and provide some differentials for this condition

A
  • 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 seizures as a cause for the tremors.

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2
Q

List the breeds commonly affected by cerebellar abiotrophy and the differences between them.

A

Arabian and Gotland foals (and their crosses: generally signs noted by 1 yr of age, most commonly 1-6mo); some Paso fino and TBs. 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).

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3
Q

is cerebellar abiotrophy genetically transmissible?

A

It is inherited as an autosomal recessive trait and is associated with a single-nucleotide polymorphism (SNP) on equine chromosome 2 (13074277G>A), located in the fourth exon of TOE1 and in proximity to MUTYH on the antisense strand.

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4
Q

List differentials for cerebellar disease and some defining points for each

A
  • Cerebellar abiotrophy: diagnosed based on signalment (Arabian, Gotland or Oldenburg breeds), typically foals.
  • Gomen Disease: geographically located to New Caledonia, progressive disease in horses allowed to roam free 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.
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5
Q

List the clinical signs of Shivers and the commonly affected breeds

A

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.

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6
Q

List the 4 gait patterns of shivering

A
  1. Hyperextension when backing and lifting the limb
  2. Hyperflexion and abduction during backward walking
  3. Shivering hyperflexion with abduction during backward walking
  4. Shivering-forward hyperflexion including intermittent hyperflexion and abduction with forward walking
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7
Q

List the breed, age and gender predilection for CVSM

A

Males, young horses (less than 7yo, commonly 1-2 yo, often well-fed rapidly growing), TBs, Tennessee Walking horses and WBs.

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8
Q

Define dynamic versus static compression with CVSM including effect of flexion versus extension of the neck.

A

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.

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9
Q

List the common clinical signs of CVSM

A
  • 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.
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10
Q

List medical and surgical treatment options for CVSM

A
  • 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.
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11
Q

Describe the clinical findings and pathogenesis of equine neuroaxonal dystrophy and equine degenerative myeloencephalopathy

A
  • Diffuse, symmetric degenerative neurologic disease
  • UMN and general proprioceptive deficits including symmetric ataxia, weakness, dysmetria (mostly hypometria), horses may pace. All 4 limbs are 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 Vit 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).
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12
Q

What is the epidemiology of equine neuroaxonal dystrophy and equine degenerative myeloencephalopathy

A

Affected breeds: Arabians, TBs, SBs, Paso fino, Morgans, APP, WBs & Lusitanian.

Horses genetically susceptible to α-tocopherol deficiency (inherited complex trail) and α-tocopherol deficiency in the first year produce the final Phenotype.

α tocopherol transfer protein gen mutation (in humans) was excluded in horses.

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13
Q

List the risk factors (incl geographical) for EPM

A

Main risk factors:

  • Exposure to opossums
  • 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
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14
Q

What are the common signalment and causative agents for EPM

A

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 are more commonly affected.

Causative agents:

  • S. neurona is most common,
  • N. hughesi is less common and seroprevalence is much lower to this parasite.
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15
Q

Describe the transmission of EPM

A
  • Contamination of feed/water sources with infected opossum 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.
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16
Q

List factors contributing to pathogenesis of EPM

A
  • 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
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17
Q

List clinical signs of EPM, including 3 A’s of EPM

A
  • 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.
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18
Q

List the diagnostic methods and pathological findings of EPM

A

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 perivascular infiltration of mononuclear cells (can affect grey or white matter)
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19
Q

List the differential diagnoses for EPM

A
  • CVCM
  • Viral encephalitis (WNV, EEEV, WEEV, EHV-1)
  • Meningitis
  • Trauma (TBI or SCI)
  • ENAD/EDM
  • Polyneuritis equi
  • Basically any neurologic disease depending on signs shown.
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20
Q

List treatment options for EPM and likelihood of success

A
  • Pyrimethamine and sulphonamides (caution with addition of folic acid - may increase 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.
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21
Q

List clinical signs of Equine Herpes Virus 1 Myeloencephalopathy (EHM)

A
  • Maybe 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 cases may become recumbent and may die in coma or convulsion.
  • Signs generally stabilise after 1-2 days and don’t progress.
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22
Q

List the 5 herpesviruses of horses and 3 of asinine and the disease associated with each (briefly)

A

Alpha-herpes:

  • EHV-1 (respiratory, 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
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23
Q

Describe infection and immune evasion of EHV-1

A
  • 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, infection to contiguous cell - extracellular phase not needed)
  • 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.
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24
Q

List epidemiologic factors of EHM

A
  • 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.
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25
Q

List the diagnostic methods and their challenges for EHM

A
  • 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 titre 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.
  • Immunofluorescence has high sensitivity but false positive.
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26
Q

List differential diagnoses for EHM

A
  • EPM
  • CVCM
  • Trauma/fracture
  • Polyneuritis equi
  • Fibrocartilagenous infarction
  • Aberrent parasite migration
  • ENAD/EDM
  • Viral encephalitis - flaviviruses and alphaviruses
  • Rabies
  • Botulism
  • CNS abscess
  • Plant & chemical toxicoses
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27
Q

List the ocular changes seen in some foals with EHV-1

A
  • Uveal vasculitis with perivascular mononuclear cuffing in the ciliary body and optic nerve
  • Retinal degeneration & hypopyon
  • Chorioretinopathy without anterior segment involvement
  • Occasionally you see ocular and neural damage in the absence of gross signs of neurologic or visual impairment.
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28
Q

What suggests involvement of the immune system in polyneuritis equi?

A

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.

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29
Q

What are the two forms of polyneuritis equi?

A

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.

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30
Q

List possible neurologic abnormalities with polyneuritis equi

A
  • 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

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31
Q

What is the primary finding in Acquired Equine Polyneuropathy in Scandinavia?

A

Acute onset bilateral pelvic limb digital extensor dysfunction and knuckling.

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32
Q

What is pathological finding in Acquired Equine Polyneuropathy in Scandinavia? and what is the seasonality?

A

Histo: inflammatory demyelinating polyneuropathy and intracisternal Schwann cell inclusion.

December to Avril, prevalence on 26% and fatality rate of 29%

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33
Q

List the most frequently isolated alphaviruses (encephalitis viruses), their distribution, vector, pathogenesis and clinical signs

A

EEEV, WEEV, VEEV: western hemisphere, mosquitoes, virus multiplies in muscle, enter the lymphatics, localises in lymph nodes. It replicates in macrophages and neutrophils 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, hyperesthesia, altered behaviour, compulsive walking, cranial nerve dysfunction; death is preceded by recumbency 1-7days

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34
Q

List diagnostic methods for togaviruses

A

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.

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35
Q

List the vaccination protocol for EEEV/WEEV recommended by AAEP

A

Adults: 2 doses 4-6 weeks apart. Annually or biannually depending on climate/mosquito prevalence, and timed to be before mosquito season starts

Foals: 3 doses with a 4-week interval (start at 2-3mo if high risk and unvaccinated mare); 4th dose at 10-12mo or before mosquito season starts

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36
Q

List important flaviviruses

A
  • Japanese encephalitis virus (mosquito)
  • St. Louis encephalitis (mosquito)
  • West Nile virus (mosquito)
  • Murray Valley encephalitis (mosquito)
  • Kunjin virus (mosquito)
  • Powassan (tick)
  • Louping Ill virus (tick).
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37
Q

List clinical signs of WNV

A
  • ~90% of horses seroconvert without clinical signs.
  • Weakness (LMN in SC)
  • Ataxia (LMN in SC)
  • Altered mentation (grey matter of midbrain and hindbrain)
  • Fever in early phase
  • Muscle fasciculations (commonly of the face, neck and muzzle)
  • Cranial nerve deficits (due to effects on grey matter of midbrain and hindbrain)
  • Recumbency
  • Anorexia & Bruxism
  • Hyperexcitability, apprehension or aggression may be seen (if thalamic involvement)
  • Sleep like states resembling narcolepsy may occur in rare cases.
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38
Q

What is the prognosis for recovery with WNV?

A

In horses that improve, 90% recover completely within 1-6mo.

Residual weakness and ataxia are common complications in those that don’t recover completely. Mild-moderate persistent fatigue on exercise is reported in some horses.

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39
Q

List the transmission of Bornavirus

A

Virus shed in body secretions gains access to a host via exposed nerve endings in nasal and pharyngeal mucosa. GP43 protein facilitates internalisation to cells via endocytosis; virus migrates to olfactory bulbs and has tropism for the limbic system.

The virus causes progressive severe immune-mediated nonsuppurative meningoencephalitis

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40
Q

List the clinical signs of Bornavirus

A
  • Slow-motion chewing or chewing motions of the mouth
  • Head pressing
  • Somnolence and stupor
  • Hyperexcitability, fearfulness or aggressiveness
  • Hypokinesia & Hyporeflexia
  • Abnormal posture
  • Head til & Neurogenic torticollis
  • Inability to swallow
  • Death in 1-4 weeks.
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41
Q

List the transmission routes for rabies

A
  • Saliva through bites
  • Droplet/aerosolisation inhalation
  • Oral transmission
  • Transplacentally
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42
Q

Where does rabies virus replicate?

A

Spinal and dorsal root ganglia of the peripheral nerve it has travelled up.

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43
Q

What is the incubation period for rabies virus

A

14-90 days and up to 1 year.

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44
Q

List the three forms of rabies and the clinical signs of each

A
  1. Cerebral/Furious form: aggressive behaviour, photophobia, hydrophobia, hyperaesthesia, self-mutilation, straining, muscle tremors, convulsions and blindness.
  2. Brainstem/Dumb form: obtundation, anorexia, head tilt, circling, excess salivation, facial and pharyngeal paralysis.
  3. Paralytic/Spinal form: progressive ascending paralysis, ataxia, shifting lameness with hyperaesthesia, self-mutilation of an extremity, flaccid tail and anus and urinary incontinence.

More than one form can occur concurrently. Anti-inflammatories delay virus progression but death occurs within 5-10 days of clinical signs.

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45
Q

List diagnostic tests for rabies

A
  • Direct fluorescent antibody test
  • Lymphocytic pleocytosis in CSF is supportive
  • Histology of the brain
  • Mouse inoculation test (inoculate intracerebrally with salivary or brain tissue and observe for development of disease)
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46
Q

Which muscle groups are primarily affected by wasting with EMND?

A

Quadriceps, triceps and gluteals

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47
Q

What ocular changes are seen with EMND?

A

Yellow-brown-black pigment with a reticulated appearance above the optic disc on fundic exam (at the tapetal-non-tapetal junction. Seen in 30% of cases

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48
Q

Where are degenerative changes primarily localised to with EMND?

A

Ventral horn cells (LMN) of the grey matter, nucleus ambiguous, and all brainstem cranial nerve somatic motor nuclei (except III, IV and VI).

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49
Q

Which muscle fibres are affected with denervation atrophy?

A

Type I and Type II. EMND primarily affects type I.

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50
Q

What is the prognosis for treatment with EMND?

A
  • 20% continue to deteriorate and are euthanased
  • 40% have stabilisation of clinical signs but the muscle mass does not return and they may develop severe gait abnormalities.
  • 40% show dramatic improvement with treatment and may regain normal muscle mass. They may then remain stable for 1-6 yrs+ however many relapse on return to exercise.
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51
Q

List the three tetanus exotoxins and which one is most clinically relevant.

A

Tetanolysin - binds almost irreversible to DT/GD1b & Receptor protein, inhibition of release GABA/Glycine. Most clinical importance.

Tetanospasmin - facilitated spread of infection by increasing local tissue necrosis.

Nonspasmogenic toxin - blocking transmission in peripheral neuromuscular junction.

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52
Q

Where does tetanospasmin localise? And what is the effect?

A
  • Ventral horn of the grey matter of the spinal cord binding to inhibitory interneurons called Renshaw cells.
  • Tetanospasmin blocks the postsynaptic inhibitory signal of the spinal cord motor neurons by preventing release of the inhibitory neurotransmitters glycine and GABA.
  • Hence you get continued stimulation of motor and reflex arcs causing muscle spasms and contractions, convulsions and respiratory arrest leading to death.
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53
Q

List the function of tetanolysin and nonspasmogenic toxin

A

Tetanolysin facilitates spread of infection by increasing local tissue necrosis.

The role of non-spasmogenic toxin is not well understood but may involve blocking transmission in peripheral neuromuscular junctions.

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54
Q

Does tetanospasmin affect the sympathetic NS, parasympathetic NS or both?

A

Both. Adrenergic stimulation can cause tachycardia, cardiac arrhythmias and peripheral vasoconstriction. Parasympathetic hyperactivity increases vagal tone that may cause bradyarrhythmias, AV block and sinus arrest.

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55
Q

What is the treatment for tetanus?

A
  • Binding is almost irreversible
  • Local & parenteral antibiotics to stop further production of toxin (penicillin at high doses is drug of choice, others are tetracyclines, macrolides in foals and metronidazole)
  • Tetanus antitoxin to neutralise unbound toxin (500o-2.5x10^6 IU/animal) can be intrathecal although questionable advantages?
  • Muscle relaxants such as phenothiazines, benzodiazepines, α2-agonists all may be helpful. Magnesium sulphate. Methocarbamol.
  • Quiet environment and general nursing (catheterisation, rectal evacuation etc if required)
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56
Q

What is the vaccination protocol for tetanus?

A

Adults: 2 vaccines 4-6 weeks apart then annually.
Foals: 2 vaccines 4-6 weeks apart starting at 4-6mo age then a third vaccine at 10-12 mo then annual if mare was vaccinated; if unvaccinated mare start at 1-4mo age, boost 4 weeks later then 3rd dose 4 weeks later.

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57
Q

What are the 3 routes of infection with botulism toxin?

A
  1. food borne - ingestion of pre-formed toxin in feed.
  2. toxicoinfectious - release of toxin from the GIT, typically in foals 2wk-8mo age (Shaker foal syndrome); toxins are then absorbed into the bloodstream.
  3. wound botulism - infection of a wound with C. botulinum that then germinate and release toxin under anaerobic conditions
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58
Q

Where do botulism toxins (BoNT) exert their effects?

A

Peripheral nerve terminals, primarily of skeletal and autonomic cholinergic nerves (can’t cross the BBB).

59
Q

Describe the effects of BoNT at their site.

A

Act presynaptically at the peripheral cholinergic neuromuscular junction resulting in inhibition of neurotransmitter (acetylcholine) release and hence neuroparalysis. This is reversible.

60
Q

What are the characteristic clinical signs of botulism?

A
  • Mydriasis and ptosis,
  • sluggish PLR,
  • reduced tongue tone and slow tongue retraction delayed prehension of feed (grain test - 8ounces of sweet feed should be eaten in under 2 mins, but may take much longer +/- be dropped out of the mouth with botulism),
  • generalised weakness and low head carriage,
  • muscle fasciculations that start at the shoulder and progress to severe generalised trembling.
  • Usually dysphagic and reduced tail tone.
61
Q

Where are the neuronal lesions found in horses with EGS?

A

Most severe in the autonomic ganglia (cranial cervical, stellate and celiacomesenteric) and enteric nerves. Also seen in the brainstem nuclei and the somatic efferent LMN of the spinal cord.

62
Q

What specific findings will you see on biopsy with EGS?

A

Neuronal loss in both the submucosal and myenteric plexuses throughout the GIT and reduction of interstitial cells of Cajal in the myenteric plexus regions of the GIT

63
Q

What does the phenylephrine test show in cases of EGS?

A

Application of 0.5% phenylephrine topically to the cornea should abolish the ptosis thereby confirming the presence of smooth muscle paralysis.

64
Q

What are the common seasons for Lymes disease?

A

Spring, summer and fall; peak incidence in June and July.

65
Q

List the clinical signs of Lymes (Borrelia burgdorferi).

A

Chronic weight loss, sporadic lameness, laminitis, mild fever, swollen joints (may develop chronic arthritis), muscle tenderness, anterior uveitis, encephalitis and abortion.

66
Q

List differential diagnosis for equine borreliosis (lymes)

A
  • Anaplasma phagocytophilia,
  • chronic disease,
  • vasculitis,
  • immune mediated-arthritis.
67
Q

Which nerves are commonly blocked for diagnosis of headshaking in horses

A

Infraorbital nerve (part of the maxillary branch) & caudal nasal nerve/posterior ethmoidal nerve (branch of the ophthalmic nerve).

68
Q

What is the proposed mechanism of photic headshaking?

A

Optic-trigeminal summation: stimulation of the optic nerve results in referred sensation to parts of the nose innervated by the trigeminal nerve.

69
Q

What are the therapeutic/medical treatments for headshaking?

A
  • Transcunatela Electrical neurostimulation.
  • Cyproheptadine: antihistamine and serotonin antagonist with anticholinergic effects. Also blocks calcium channels.
  • Carbamazepine: sodium channel blocker and antiepileptic - drug of choice for trigeminal neuralgia in people.
  • Steroids, antihistamines NSAIDs have also been used.
70
Q

What are the common sites affected by Halicephalobus gingivalis?

And what are the typical lesions?

A

Brain, spinal cord, nasal and oral cavities, pituitary gland and kidneys.
Malacia, granulomatous and lymphohistiocytic inflammatory infiltration, meningitis and vasculitis.

71
Q

What stage of strongyles cause strongyle encephalomyelitis and how do they enter the CNS?

A

Fourth and fifth stage larvae.

They are present in the intima of the aorta or left ventricle, causing endothelial damage, stimulating the clotting cascade and formation of a thrombus that contains the parasitic larvae. Hence they are transferred to the CNS in the thrombus.

72
Q

List suitable antiparasitics for treatment of verminous encephalomyelitis.

A

Benimidazole compounds (oxfenbendazole, thiabendazole, fenbendazole, mebendazole), diethylcarbamazine and ivermectin for nematodes (ivermectin has delayed killing so may not be ideal); organophosphates have been advocated for warble fly but should be used with caution. 3-day course of fenbendazole might be appropriate.

73
Q

What is the common site for cholesterol granuloma?

A

Choroid plexus of the fourth ventricle.

Less commonly in the lateral ventricles, but these may be more likely to result in clinical signs.

74
Q

What specific clinical signs would make cholesterol granuloma a more likely diagnosis?

A

Waxing and waning forebrain signs.

75
Q

What is the most common secondary neoplasm of the CNS?

List other common secondary neoplasms.

A

Lymphoma.

Melanoma of the SC, meninges and brain; adenocarcinoma and carcinoma.

76
Q

List the two syndromes associated with equine leukoencephalomalacia and their associated signs.

A

Neurologic syndrome (most common): incoordination, aimless wandering, intermittent anorexia, lethargy, obtundation, blindness and head pressing; followed by hyperexcitability, belligerance, extreme agitation, profuse sweating, delirium, recumbency with seizure and death.

Hepatotoxic syndrome with swelling of the lips and muzzle, somnolence, icterus, petechial haemorrhage, abdominal breathing and cyanosis - resembles hepatic or intestinal encephalopathy.

77
Q

What is the causative agent of equine leukoencephalomalacia?

A

Fumonisin B1 intoxication (metabolite of mycotoxin fusarium moniliforme, usually from corn).

78
Q

What are the prominent signs of nigropallidal encephalomalacia associated with Yellow Star Thistle and Russian Knapweed?

A
  • Impairment of eating and drinking
  • lack of coordination of movements of prehension, mastication and deglutition.
  • Can swallow if food/water is positioned at the back of the pharynx - may immerse their muzzle deeply in water to force it to the back of the pharynx.
  • Often the mouth is held partially open with the lips retracted and the tongue protruding.
79
Q

What differences on histology would you expect between acute and chronic hepatic encephalopathy?

A

Acute: astrocyte swelling, acute cytotoxic cerebral oedema and intracranial hypertension.

Chronic: evidence of Alzheimer type II changes in addition to the above findings.

80
Q

List the clinical signs of Horner’s syndrome and the possible causes

A

Symptoms: Ptosis, miosis, protrusion of the 3rd eyelid, unilateral facial sweating, increased facial temperature and hyperaemia of the nasal and conjunctival membranes

Causes: Perivascular injection, guttural pouch disease, trauma/infarction/haematoma/neoplasia (incl to cranial thoracic spinal cord or caudal cervical spinal cord), avulsion of the brachial plexus, damage to the sympathetic nerves in the vagosympathetic trunk (due to above causes), orbital/retrobulbar disease/injury.

81
Q

What is the pathogenesis of Horner’s syndrome?

A

Loss of sympathetic innervation to the head (axons from UMN in the caudal hypothalamus, midbrain, pons, medulla oblongata descend in the cervical spinal cord to preganglionic neurons in the cranial thoracic spinal cord; from here they leave the cord and join the paravertebral sympathetic trunk, ascend the neck and synapse in the cranial cervical ganglion in the guttural pouch

82
Q

List possible cranial nerves responsible for deviation in eye position

A
  • CN III - lateral strabismus
  • CN IV - dorsomedial strabismus
  • CN VI - medial estrabidmus
  • CN VIII ventrolateral strabismus (loss/damage to connection with the nuclei in the brainstem)
  • Can occur with head trauma or mid-brain lesions (can be normal in foals)
83
Q

List the clinical signs of damage to CN VIII

A
  • Head tilt (poll towards the lesion/affected side)
  • Disorientation (often)
  • Proprioceptive deficits, asymmetric (may compensate visually with time) but preservation of strength*
  • Falling &/or circling
  • Horizontal nystagmus (initially; often only for 48-72hrs)
  • Fast phase of nystagmus is away from the lesion if peripheral disease; if central, the nystagmus may be vertical, rotary or horizontal and may change with changing head position.
84
Q

Describe the grades of ataxia (1-5 scale)

A
  1. Normal
  2. Requires careful examination to identify an abnormality. needs provocation to see (eg circle).
  3. Deficits are mild-moderate but obvious to most observers as soon as the horse begins to move. present all times, visible to experienced observer only.
  4. Deficits are obvious and exaggerated by negotiation of a slope or head elevation. obvious to anyone with eyes
  5. May cause a horse to fall or nearly fall, often abnormal positioning while standing still. falls spontaneously (ie when walking or standing, not when tightly circled or hopped etc)
  6. Recumbent
85
Q

List the signs of LMN vs UMN dysfunction

A

LMN: Muscle atrophy, sensory loss, weakness, flaccid paralysis with hyporeflexia or areflexia, muscular hypotony.

UMN: Weakness, loss of voluntary motor function, however muscle tone may be increased and spinal reflexes may be normal to hyperactive - you can see spastic movement (due to reduced inhibition of extensor motor neurons)

86
Q

List signs of cerebellar dysfunction

A
  • Intention tremors, particularly of the head
  • Failure to blink in bright light
  • Lack of menace
  • Ataxia/loss of coordination
  • Dysmetria/hypermetria/jerky or stiff gait
  • Truncal sway
  • Vestibular signs or paradoxic vestibular syndrome (head tilt is away from lesion and nystagmus fast phase is towards the lesion - opposite to true vestibular disease)
87
Q

Localise spinal cord disease based on affected region (thoracic limb, pelvic limb, both, tail tone, perineum etc)

A

Pelvic limb only: Caudal to T2 (T2/3-L3)

Thoracic limb primarily: C6-T2

Both: Typically pelvic limbs are one grade worse than thoracic limbs due to superficial location of pelvic limb spinocerebellar tracts in the SC; lesion is in the cervical spinal cord, cranial to C6

Reduced sensation and paresis of the tail & perineum +/- urinary and faecal incontinence/retention: (S3-S5) can produce hypalgesia, hypotonia and hyporeflexia of the tail, perineum and anus or total analgesia and paralysis.

88
Q

List causes of increased CSF pressure

A
  • Changes in systemic blood pressure
  • Space occupying mass (tumour, abscess)
  • Secondary to trauma/hypoxic injury (haemorrhage, oedema)
  • Hypercapnoea (increases cerebral blood flow, therefore, CSF pressure; may exacerbate cerebral oedema)
  • Inflammation, especially of the arachnoid villi (reduced absorption of CSF)
  • Venous compression increases blood volume in the cranial cavity and compression of the CSF space thus increasing CSF pressure (iatrogenic or post jugular thrombosis)
89
Q

List causes of xanthochromia

A
  • Haemorrhage (usually previous)
  • Inflammation
  • Increased protein
  • Direct bilirubin leakage
  • Leakage of indirect bilirubin across a damaged BBB
90
Q

List common changes to CSF cytology and possible causes (broad categories rather than specific diseases)

A
  • Increased large mononuclear cells: diseases of axonal degeneration, some encephalitis viruses (EEEV [also some neutropils], WEEV, WNV [primarily lymphocytes], Kunjin [also some neutrophils])
  • Increased neutrophils: Encephalomyelitis, bacterial meningitis, parasitism, any disease with extensive inflammation
  • Increased eosinophils: Severe parasitic disease.
  • Increased lactate: EEEV, trauma, brain abscess (may be the only abnormality of CSF with a brain abscess)
91
Q

What is the normal configuration of a motor unit action potential (MUAP)?

A

Triphasic (can also get monophasic, biphasic and polyphasic - a few polyphasic potentials occur in normal muscle but shouldn’t exceed 5-15% of the MUAP observed).

Duration 15ms, amplitude 500-3000µV

92
Q

What is the normal effect of probe insertion in the muscle?

A

Short bursts (shouldn’t last more than 1-2 seconds) of high amplitude moderate-high frequency electrical activity (<200Hz)

Prolonged insertional activity can be caused by hyperirritability and instability of the muscle fibre membrane; might be suggestive of early denervation atrophy, myotonic disorders or myositis

93
Q

What are the main differentials for an absence of insertional activity?

A
  • Muscle fibre fibrosis (complete)
  • Functional inexciteability such as with HYPP or familial periodic paralysis
  • Faulty electrode
94
Q

Describe the pathogenesis for polyphasic MUAP (myopathic potentials) and list the differentials for this finding

A

Pathogenesis: increased frequency but decreased amplitude and duration resulting from an increased number of action potentials for a given strength of contraction. They are due to diffuse loss of muscle fibres hence more motor units are required to perform the work normally done by fewer motor units. Most common in primary myopathies:

  • Myotonia-like syndromes
  • Periodic paralysis
  • Myositis
  • Botulism
  • Myasthenia gravis-like syndromes
95
Q

List the differentials for fibrillation potentials (initial positive deflection) and the use of these for monitoring

A
  • Spontaneous discharge from acetylcholine-hypersensitive denervated muscle fibres,
  • Inflammation and focal muscle degeneration
  • Muscle atrophy
  • Denervation (may also have positive sharp waves) before clinical atrophy
  • Reinervation (decrease in fibrillation potentials followed by recording of MUAP over time)
96
Q

List the differentials for positive sharp waves (primary deflection is downward followed by a lower amplitude longer duration negative deflection)

A
  • Myositis, exertional rhabdomyolysis, spinal shock
  • Denervated muscle post RER, myotonia, EPM, laryngeal hemiplegia, suprascapular nerve injury, compressive myelopathy
97
Q

List the differentials for fasciculation potentials and myotonic/high-frequency potentials

A
  • Disease of anterior horn cells
  • Irritative-type lesions of spinal root or peripheral nerve
  • Myotonic: associated with hyperexcitability of the muscle cell membrane
  • LMN diseases, steroid-induced myopathy, polymyositis, chronic denervation, HYPP, myotonia congenita and dystrophica.
98
Q

List the findings on needle EMG for radial and suprascapular nerve injuries.

A

Radial: Positive sharp waves and fibrillation potentials in the triceps brachii and extensor carpi radialis muscles

Suprascapular: Positive sharp waves and fibrillation potentials in the supraspinatus and infraspinatus (or could be damage to these muscles). If there is post-insertional activity in these muscle groups and the lateral head of the triceps it suggests brachial plexus damage.

99
Q

List the correlation between the waves of BAER and their anatomic generator sites

A
  • Wave I = cochlear nerve;
  • Wave II = cochlear nucleus;
  • Wave III = olivary nucleus;
  • Wave IV = lateral lemniscus;
  • Wave V = caudal colliculus
100
Q

List the most common pathological causes of an abnormal BAER

A
  • THO
  • Congenital sensorineural deafness (Paint Horses, particularly lots of white marking on the face and blue iris)
  • Multifocal brain disease
  • Otitis media/interna
  • Sepsis/neonatal encephalopathy/NIE/prematurity in foals - this is usually permanent
101
Q

What represent an EEG recording?

A

Spontaneous electrical activity primarily synaptic, excitatory postsynaptic potentials, and inhibitory postsynaptic potentials from cortical neurons. Pyramidal cells are the most important neuronal source for the EEG.

It is estimated that a minimum of 108 neurons or an area of 6 cm2 is required to produce a detectable change in voltage. Thalamic oscillations are transmitted to the cortex via projection neurons and are thought to be responsible for the slow waves and spindles associated with slow-wave sleep (SWS-not visible in GA). This electrical activity might be modified by deeper structures such as the brainstem, reticular activating system, and thalamus.

102
Q

What is transcranial magnetic motor evoked potentials:

A

Technique is based on the induction of electrical currents by a strong magnetic pulse, created by a coil, which is placed on the forehead of the horse with subsequent activation of axons in the motor cortex taking place.

The generated action potentials are relayed by upper motor neurons (UMNs) before further conduction takes place along the motor pathway of the corticospinal tract, the lower motor neurons (LMN) and finally the motor nerves to the skeletal muscles. The descending tracts, which carry motor information from the brain to spinal cord neurons are more used.

103
Q

What are the MRI principles?

A

T1: time for magnetic moment of tissue to return to the direction of the main magnetic field; Fat hyperintense(bright) & Fluid hypointense)

T2: time for the phase coherence to degrade; Fat hypointense & Fluid hyperintense.

FLAIR: fluid alteration inversion recovery, signal for CSF specially nulled using an inversion pulse, abnormal fluid is more apparent in tissue (brain)

104
Q

What is the Transcranial Electrical Stimulation?

A

TES technique entails direct application of an electrical current to a pair of needle electrodes, which are subcutaneously inserted on the forehead of the horse. this technique bypasses predominantly the route via the motor cortex of the brain to the pyramidal tract.

105
Q

Define the following: Epilepsy, epileptic seizure, status epilepticus, convulsions

A

Epilepsy: A disorder of the brain characterised by an enduring predisposition to generate epileptic seizures (recurrent seizures).

Epileptic seizure: A transient occurrence of signs and/or symptoms due to abnormal excessive or synchronous neuronal activity in the brain.

Status epilepticus: A condition resulting either from the failure of the mechanisms responsible for seizure termination or from the initiation of mechanisms which lead to abnormally prolonged seizures after time point 1 (5min), and can have long-term consequences after time point 2 (30min).

Convulsions are seizures accompanied by tonic-clonic muscle activity and loss of consciousness.

106
Q

Differentiate partial from generalised seizures

A

Partial seizures involve a discrete area of cerebral cortex and cause localised clinical signs (facial twitch, limb twitching etc).

Generalised seizures affect the whole body with loss of consciousness. They can be primary (generalised from the onset) or secondary (progression from partial seizures).

107
Q

Describe the pathogenesis of a seizure

A

Abnormal hypersynchronous electrical activity of neurons caused by imbalance between excitation and inhibition in the brain. If the balance shifts towards excitation a seizure might occur.

108
Q

List the differentials for seizure in a horse under 1 year old

A
  • Congenital: hydrocephalus, hydranencephaly, idiopathic epilepsy.
  • Metabolic: hypoxia, hyponatremia, hypoglycemia, hyperkalemia.
  • Toxic: Organophosphates, strychnine, metaldehyde, moldy corn, locoweed.
  • Traumatic: brain trauma, lightning.
  • Vascular: NMS
  • Infectious: Septicemia, hyperthermia, bacterial meningitis, cerebral abscesses, rabies, viral encephalitis.
  • Most common in foals under 2 weeks: NMS, HIE, trauma and bacterial meningitis.
109
Q

List the differentials for seizure in a horse older than 1 year

A
  • Metabolic: HE, hypocalcemia, uremia, hyperlipidaemia
  • Toxic: organophosphates, strychnine, metaldehyde, moldy corn, locoweed, bracken fern, lead, arsenic, mercury, ryegrass
  • Traumatic: brain trauma.
  • Vascular: Strongylus vulgaris, cerebral thromboembolism, intracarotid injection, neoplasia, haemarthroma, cholesterol granuloma
  • Infectious: cerebral abscess, rabies, arbovirus encephalitis, mycotic cryptococcosis, EPM.
  • Most common in adults: brain trauma, HE and toxicity. Tumours such as melanoma, pituitary adenoma, cholesteatoma and rarely glioma can cause seizures.
110
Q

Describe the roles of NMDA receptors and GABA in the pathogenesis of seizure development

A

NMDA: binding of glutamate to NMDA receptors opens Na and Ca channels causing post-synaptic depolarizations. If exacerbated, intracellular Ca overload causes neuronal necrosis by activation of lytic enzyme systems and nitric oxide synthase with generation of free radicals.

GABA: in response to the above depolarisation shift GABA-ergic inhibitory zones are established to prevent spread of epileptic activity. This can be pre or postsynaptic. If this system fails, the abnormal depolarization shift will continue and once a critical mass is reached uncontrolled spread over the cerebral cortex may occur and can result in a seizure.

111
Q

What are the electrolyte derangements noted during the inter-ictal period?

A

Increased K concentration, decreased intracellular Ca, Mg and Cl. Alterations in Na conductance, particularly rapid influx into the neuron, may also be involved.

112
Q

What changes on EEG do you expect to see with seizures

A

Spikes, sharp waves, spike-and-wave discharges and other transient events.

113
Q

List the treatments (short term) for seizure, including the benefits and contraindications for each

A
  • Benzodiazepines (diazepam, midazolam) - bind to GABA receptors, hyperpolarising neuronal cells, therefore, decreasing electrical activity of the seizure focus and increasing the seizure threshold. They have a short half-life (10-15 min for diazepam), prolonged use can result in respiratory depression/arrest and drug accumulation in foals;
  • Barbituric: phenobarbital - rapidly provides high serum concentrations; reduces cerebral metabolic rate, facilitates inhibitory neurotransmission by GABA receptors, inhibits postsynaptic potentials produced by glutamate and inhibits the voltage-gated Ca channels at excitatory nerve terminals. Lower doses should be used in foals, including the loading dose. Sodium pentobarbital - more useful in foals due to anaesthetic effects but may be helpful in adults with status epilepticus (as well as propofol and ketamine);
  • Primidone (metabolised to phenobarbital and to a lesser extent phenylethylmalonamide which might potentiate effects of phenobarbital) has been advocated for foals.
  • Phenytoin inactivates voltage-dependent neuronal sodium channels, preventing depolarisation hence reducing release of glutamate. Adverse effects are prolonged depression in foals, AV block and decreased blood pressure in adults.
  • ACP may reduce seizure threshold.
  • Ketamine may exacerbate seizures due to increased cerebral blood flow, O2 consumption and intracranial pressure, but also antagonises NMDA receptors hence may be useful.
114
Q

List the treatments (long term) for seizure, including the benefits and contraindications for each

A
  • Phenobarbital (drug of choice): remember it induces cytochrome P450 enzyme complex therefore increased its own metabolism so therapeutic monitoring is required (every 60 days once stable). Adverse effects include excessive sedation, respiratory depression, bradycardia, hypotension and hypothermia in neonates. Avoid drugs with interactions such as ivermectin. Tetracyclines and chloramphenicol inhibit microsomal enzymes, therefore, prolonging effects of phenobarbital.
  • Potassium bromide: competes with Cl to hyperpolarise neuronal membranes and enhances GABA-activated Cl conductance. Takes a few weeks to reach steady-state so shouldn’t be used alone. Can reduce dose of phenobarbital by 20% and add Potassium bromide.
  • Phenytoin: inactivates voltage-dependent neuronal Na channels, preventing depolarisation hence reducing release of glutamate. Adverse effects are prolonged depression in foals, AV block and decreased blood pressure in adults.
  • Primidone: metabolised to phenobarbital and to a lesser extent phenylethylmalonamide which might potentiate effects of phenobarbital; has been advocated for foals.
  • Other drugs used in other species: felbamate, gabapentin, clorozepate, toparimate, levetiracetam and zonisamide. These potentially have improved therapeutic indices.
115
Q

List the breeds associated with familial narcolepsy

A

Shetland, Suffolk, American miniatures and Lippizaners.

116
Q

List the described triggers for an episode of narcolepsy and cataplexy

A

Initiation of eating or drinking, petting/stroking the head or neck, hosing with cold water after exercise and leading out of a stable.

117
Q

Differentiate narcolepsy from other causes of collapse

A
  • Narcolepsy: gradual lowering of the head precipitates a collapse episode. Neurologically and cardiovascularly normal between episodes.
  • Sleep deprivation: may also include a gradual lowering of the head and buckling; no cataplexy.
  • Syncope: Not preceded by lowering of the head or drowsiness.
  • Seizure: loss of consciousness and tonic-clonic activity in generalised seizures.
  • Botulism: Additional neurological signs (progressive weakness, dysphagia, weak tongue tone etc).
  • HYPP: remain alert, often anxious and may have prolapse of the third eyelid.
118
Q

List treatments for narcolepsy

A

Drugs that stimulate monoamine systems (dopamine, noradrenaline, serotonin) should be effective narcolepsy suppressors; those that stimulate cholinergic activity exacerbate narcolepsy.

Atropine sulphate reduces the severity of cataplectic attacks and can prevent reoccurrence for 12-30 hours.

Imiprimine (tricyclic antidepressant) blocks the uptake of serotonin and noradrenaline and decreases REM sleep. Oral Tx produces inconsistent results, although no adverse results. Adverse effects of IV tx exceeding 2mg/kg include muscle fasciculations, tachycardia, hyperresponsiveness to sound and haemolysis.

Tyrosine - increase Dopamine concentration, improve CSx in some horses.

119
Q

List differentials for a collapsing horse

A
  • Seizure
  • Sleep deprivation
  • Narcolepsy
  • Syncope
  • Hypersomnia
  • REM disorders
120
Q

List the common pathologies secondary to flipping over backwards

A

Fracture (petrous temporal bone, squamous temporal and parietal bones, basilar bones)

Haemorrhage into retropharyngeal space and guttural pouch (laceration of vessels and/or rupture of rectus capitus ventralis muscle)

Cerebral contusion secondary to acceleration-deceleration forces

121
Q

List the common pathologies secondary to impact on the dorsal surface of the head

A
  • Fracture (frontal or parietal bones)
  • Cerebral cortical injury
  • Spinal cord injury/cervical vertebral damage
  • Damage to CN XII where it exits the hypoglossal foramen
  • Stretching of the optic nerves and subsequent blindness.
122
Q

Define primary versus secondary traumatic brain injury

A

Primary: immediate mechanical disruption of brain tissue characterised by damage to neuronal cell bodies, dendritic arborization, axons, glial cells and brain vasculature (often irreversibly). Can be focal, multifocal or diffuse.

Secondary: A cascade of molecular, cellular and biochemical events that can occur for days-months after injury, causing delayed tissue damage. Hypoxia, ischaemia, brain swelling, altered intracranial pressure (disruption to cerebral autoregulation results in increased intracranial pressure, therefore, reduced cerebral perfusion/blood flow), breakdown of the BBB and impaired energy metabolism.

123
Q

Define the Cushing’s Reflex

A

Hypothalamic response to brain ischaemia that results from acute increased intracranial pressure. You get hypertension and secondary baroreceptor-mediated bradycardia.

Continued elevation of intracranial pressure and reduction of cerebral blood flow results in increased sympathetic discharge with subsequent myocardial ischaemia and development of cardiac arrhythmias - “brain-heart syndrome”.

124
Q

List the signs of brainstem injury

A
  • Coma, depression (damage to the RAS)
  • Strabismus, anisocoria, loss of PLR (due to damage to CNIII)
  • Apneustic or erratic breathing (poor prognosis)
  • Bilaterally dilated pupils/unresponsive to light (indicates an irreversible brainstem lesion)
  • Decorticate posture (rigid extension of the neck, back and limbs)
  • To differentiate caudal brainstem from rostral cervical spine assess mentation and function of CNX and CNXII (mentation abnormal and tongue weakness and/or lack of vagal input with brainstem only)
125
Q

List the signs of cerebral injury

A
  • Seizures (usually generalised)
  • Impaired vision and menace (contralateral to the lesion; PLR should be intact)
  • Decreased facial sensation contralateral to the lesion (parietal cortex)
  • Altered behaviour (circling, head pressing, hyperexcitability, aggression)
126
Q

List the signs of cerebellar injury/disease

A
  • Ataxia
  • Inability to regulate rate, range and force of movement
  • Jerky/awkward initiation of movement
  • Intention tremors
  • Truncal sway
  • Hypertonia causing a spastic gait
  • Signs can be bilateral or unilateral depending on focal or diffuse disease.
  • Vestibular signs if flocculonodular lobe or vastigial nucleus involved (dysequilibrium, nystagmus with fast phase way from the lesion, head and body tilt toward the lesion).
  • Paradoxic vestibular disease (head tilt away from the lesion and nystagmus with fast phase toward the lesion) if cerebellar peduncle is involved.
127
Q

List the treatment for TBI

A
  • Optimise cerebral blood flow (optimise MAP and ensure intracranial pressure is not increased)
  • If increased intracranial pressure: hyperventilation (risk is reduction of cerebral blood flow may cause ischaemia), hyperosmolar agents (hypertonic saline, mannitol), barbiturates, head elevation, CSF drainage? - only if obstruction to outflow, decompressive surgery?
  • Crystalloid fluid therapy (slightly less than maintenance)
  • Keep blood glucose concentration between 7.5-8mmol/L.
  • Hypothermia
  • Anti-inflammatories (NSAIDs, steroids? controversial; DMSO? controversial; vitamin E and C? possibly don’t reach therapeutic concentrations in time for acute disease)
  • Control seizures to reduce secondary injury
  • Avoid ketamine due to increases in cerebral blood flow and intracranial pressure.
  • Barbiturates if intracranial pressure elevation is refractory to other treatments (decreases cerebral metabolism so protects against ischaemia but also cause hypotension)
128
Q

List the mechanisms of action of hypertonic saline

A

Hypertonic saline: produces an osmotic gradient b/w the intravascular and interstitial-intracellular compartments leading to shrinkage of brain tissue, therefore decreasing intracranial pressure. It also augments volume resuscitation and increases circulating volume, MAP and cerebral perfusion pressure. In addition in restores neuronal membrane potential maintains BBB integrity and modulates the inflammatory response by reducing adhesion of leukocytes to the endothelium. Contraindicated with dehydration, intracerebral haemorrhage, hypernatraemia, renal failure, HYPP and hypothermia. Need to monitor CVP and Na/K concentrations.

Mannitol: induces changes in blood rheology and increases cardiac output, leading to improved cerebral perfusion pressure and cerebral oxygenation. The effects of this are cerebral artery vasoconstriction and subsequent reduction in cerebral blood volume and intracranial pressure. Multiple doses may be associated with renal and CNS effects including intravascular dehydration, hypotension and reduction of cerebral blood flow. Concurrent use with furosemide may prolong the effects and diminish the potential for rebound intracranial pressure elevation.

129
Q

List the mechanisms of action of mannitol

A

Induces changes in blood rheology and increases cardiac output, leading to improved cerebral perfusion pressure and cerebral oxygenation. The effects of this are cerebral artery vasoconstriction and subsequent reduction in cerebral blood volume and intracranial pressure. Multiple doses may be associated with renal and CNS effects including intravascular dehydration, hypotension and reduction of cerebral blood flow. Concurrent use with furosemide may prolong the effects and diminish the potential for rebound intracranial pressure elevation.

130
Q

List common vertebral fracture sites in adults and foals

A

Foals: C1-C3 and T15-T18; axial dens fracture with atlantoaxial subluxation (usually disruption of the physis of the dens and separation of the odontoid process)

Occipital-atlantoaxial region, C5-T1 and caudal thoracic. It may be more common in young horses due to late closure of cervical vertebral growth plates (4-5yrs)

131
Q

Are ataxia and loss of proprioception and motor function or loss of deep pain associated with more severe injury and why?

A

Spinal cord damage is typically worse in large myelinated motor and proprioceptive fibres compared with smaller non-myelinated nociceptive fibres hence you see ataxia and loss of both proprioceptive and motor function before you see loss of deep pain.

132
Q

List the 3 phases of spinal cord injury and repair in a temporal manner

A
  1. Vascular and biochemical changes within the spinal cord (first 48 hours)
  2. Effects of inflammatory cells response (peaks approximately 4 hours after injury to 4 days)
  3. Axonal regeneration and lesion repair (from about 1 week after injury)
133
Q

Why do you sometimes see impaired ventilation, bradycardia and hypotension with spinal cord injury?

A

Lesions cranial to C5 can affect the respiratory centre or cranial to T2, the origin of the sympathetic outflow for the thoracolumbar spinal cord.

134
Q

Discuss the use of anti-inflammatories with SCI

A

Corticosteroids: thought to primarily help with free radical scavenging but may also decrease catecholamines and glutamate and decrease apoptosis-related cell death and spread of morphologic damage, preventing loss of axonal conduction and reflex activity. May also preserve vascular membrane integrity and stabilise white matter neural cell membranes. May help reduce fibrin and oedema and reduce Na/K imbalance secondary to oedema and necrosis. No longer used in humans. Evidence of positive effect is lacking.

DMSO: increases brain and SC blood flow, decreases brain and SC oedema, increases vasodilating PGE1, decreases platelet aggregation, decreases PGE2 and PGF2, protects cell membranes and traps hydroxyl radicals. Exact mechanisms is unknown. Evidence lacking and use is controversial.

Vit E and Se: beneficial for antioxidant effects although may not be of benefit in acute injury due to time taken to reach therapeutic concentrations.

Others: Peroxisome (proliferation activate receptors); GM6001 (broad-spectrum MMPPs inhibitor); and Rilazole (Na channel blocker).

135
Q

List management strategies for recumbent horses

A
  • Massage/therapeutic ultrasound and or hydrotherapy of affected limbs/muscle groups for 10-15min 2+ times daily to encourage blood flow
  • Flexion and extension of all limbs to maintain range of motion
  • Turning at least every 3-4 hours to reduce compartment syndromes/pressure necrosis.
136
Q

Define the direction of nystagmus and the control of the fast and slow phase

A

The direction of the fast phase defines the direction of nystagmus, so if the head is turned to the left the fast phase will also be to the left. The fast phase is under control of the brainstem and the slow phase is under vestibular control.

137
Q

Differentiate physiologic nystagmus from the oculocephalic reflex

A

Physiologic nystagmus is the normal movement of the eye (controlled by the motor nuclei of CNIII, CNIV and CNVI) when the head moves; also called vestibular-ocular nystagmus.

The oculocephalic reflex is independent of vision and associated with rapid manipulation of the head. If you cannot elicit this reflex disease is either bilateral or involves damage to the medial longitudinal fasciculus and hence extensive brainstem damage.

138
Q

Describe the anatomic association of the facial and vestibular nerves

A

The facial nerve emerges from the lateral medulla ventral to the vestibulocochlear nerve at the level of the trapezoid body. The two nerves are associated closely with the petrous temporal bone and enter the internal auditory meatus together. After this, the facial nerve separates and courses through the facial canal of the petrosal bone and exits through the stylomastoid foramen.

139
Q

List the clinical signs of peripheral vestibular system dysfunction

A
  • Head tilt (poll toward the lesion)
  • Horizontal nystagmus (fast phase directed away from the lesion)
  • Falling and or circling (lean or circle towards the lesion)
  • Reluctance to move (if forced may take short uncoordinated steps)
  • Asymmetric ataxia (with preservation of strength)
  • Loss of hearing

Note: if bilateral, ataxia is often symmetric and you may not see nystagmus, head tilt or circling and the oculocephalic reflex cannot be induced. Head may sway with wide excursions.

140
Q

Why do you see asymmetric ataxia with peripheral vestibular disease?

A

Asymmetric ataxia (with preservation of strength) occurs due to extensor hypotonia ipsilateral (due to loss of faciliatory neurons of the vestibulospinal tract to ipsilateral extensor muscles), and mild extensor hypertonia and hypereflexia contralateral (due to loss of inhibitory neurons and unopposed extensor tone of the contralateral vestibulospinal tract).

141
Q

List the clinical signs of central vestibular disease and how you would differentiate from peripheral disease

A
  • Head tilt
  • Nystagmus can be horizontal, vertical or rotatory (you only see vertical or rotatory with central Dz). Fast phase is away from the lesion - in rotatory the direction is defined by the movement of the limbus from the 12 o’clock position during the fast phase. Compensation is slower with central compared to peripheral Dz.
  • Falling and circling towards the lesion
  • Proprioceptive deficits (only see this with central Dz) due to damage within the brainstem of the descending UMN tracts of the limbs - if there is damage to the spinocerebellar tracts or caudal cerebellar peduncles you get abnormal unconscious proprioception and hypermetria.
  • Obtundation (differentiates central from peripheral Dz.)
  • Involvement of other cranial nerves (differentiates central from peripheral Dz)
  • Evidence of cerebellar disease

*Note: if bilateral, ataxia is often symmetric and you may not see nystagmus, head tilt or circling and the oculocephalic reflex cannot be induced. Head may sway with wide excursions.

142
Q

Define paradoxic vestibular disease or cerebellar-vestibular disease.

A

The eyes are maintained centrally because the vestibulo-ocular pathways are opposed in an equal and opposite manner. If disease is unilateral this upsets the balance resulting in slow deviation of both eyes towards the lesion.

143
Q

List differentials for vestibular signs

A
  • Inflammatory brain disease/inflammation of the CNS
  • Space occupying lesions
    • abscess - Strep equi equi,
    • fungal granuloma - eg Aspergillus or Cryptococcus neoformans,
    • cholesterol granuloma).
    • Neoplasms include lymphoma, ependymoma, meningeal melanoma and melanotic hamartoma.
  • EPM and rabies depending on geography
  • Polyneuritis equi (although caudal equina signs predominante)
  • EHV myelitis (primarily spinal ataxia but maybe a vestibular component)
  • Togaviruses (EEEV, WEEV, VEEV - primarily depression and seizures but cranial nerve deficits may include vestibular signs)
  • WNV (may have a component of vestibular disease among other CN dysfunctions)
  • Aberrant parasite migration (usually quite varied neurological signs)

ECEIM (16 decks)

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