Tina Neuro Papers

Question 1

3 manifestations of ataxia

Answer 1

: vestibular, cerebellar and general

Question 2

Ipsilateral facial neuropathy accompanies most cases of PVD due to

Answer 2

its close approximation to the vestibular nerve within the internal acoustic meatus and petrosal portion of the temporal bone.

Question 3

most common clinical presentations of unilateral PVD and facial neuropathy in the mature horse

Answer 3

Temporohyoid osteoarthropathy

Question 4

Important differentiating observations of central vestibular dysfunction compared to peripheral dysfunction are…

Answer 4

mentation changes,

presence of other cranial nerve deficits (facial nerve exception),

postural reaction deficits or UMN paresis.

Question 5

which horses tend to show Cerebellar ataxia

Answer 5

much more common in the neonate and foal.

may be developmental, as in cases of cerebellar abiotrophy and Dandy-Walker syndrome,

unusual in the mature horse: acquired from structural or inflammatory disturbances in the mature horse

Question 6

Clinical observations in cerebellar ataxia

Answer 6

• distinct hypermetria of the thoracic and occasionally pelvic limbs, which may worsen with gait speed.
• Postural reaction tests may be normal to exaggerated.
• Intention tremors of the head may be observed during voluntary movement or when stationary due to disturbances of cerebellar influence on fine motor control.
• Absent menace response may be observed with loss of cerebellar integration of the evoked blink reflex.
• Appropriate mentation is commonly observed in cases of congenital cerebellar disease but not aquired disease

Question 7

General proprioceptive ataxia can occur with any injury affecting

Answer 7

the sensory (afferent) components of the central nervous system; however, most spinal cord injuries disturb both sensory and motor (efferent) components given their anatomic proximity.

Question 8

where are the lumbosacral intumescences

Answer 8

(L4–S2)

Question 9

Extremely low head carriage, absent evidence of trauma, is suggestive of

Answer 9

a central nervous system or neuromuscular disorder.

Question 10

explain the cutaneous trunci reflex

Answer 10

can be triggered by tapping a blunt instrument along the dorsolateral dermis from the tuber coxae cranial to the shoulder.

Afferent stimulus is carried via spinal nerves to spinal cord motor neurons cranial to the

C7–T1 segments

and the efferent response is carried via the lateral thoracic nerve to the cutaneous trunci muscle

Question 11

Regional loss of the cutaneus trunci reflex is inidicative of

Answer 11

thoracic SCD or

brachial plexus/lateral thoracic nerve injury.

Question 12

What to do when the horse is severly lame during a neurologic exam ?

Answer 12

Re-examination is advised following regional or intra-articular anaesthesia.

Question 13

The appearance of a pacing gait in non-characteristic breeds suggest

Answer 13

ataxia

Question 14

Toe-dragging while backing is a compensatory sign of

Answer 14

weakness and decreased proprioception without the ability to visually compensate for limb placement

Question 15

Which benefits does the Raising of the head while walking have during neurologic examination?

Answer 15

removes visual compensation of thoracic limb placing and alters vestibular/proprioceptive influence on gait, increasing the dependence on proprioception and motor integration.

Mild thoracic limb hypermetria and delayed cranial phase of stride is expected in clinically normal horses while walking with the head raised, described as floating.

Question 16

Spinal cord dysfunction of the cervical spinal cord segments (C1–C5) results in

Answer 16

• UMN tetraparesis and general proprioceptive ataxia in all limbs. The severity of ataxia may appear more severe in the pelvic limbs and subtle in the thoracic limbs.
• +/- Horner

Question 17

Caudal cervical SCD (C5–T2 segments) can result in

Answer 17

• LMN dysfunction of the thoracic limbs and
• UMN dysfunction of the pelvic limbs.

Question 18

Thoracolumbar spinal cord segments T3–L3 SCD results in

Answer 18

• UMN paraparesis and pelvic limb general proprioceptive ataxia.

Compared with cervical SCD, thoracolumbar dysfunction is less common, or infrequently recognised in the horse.

Question 19

Defining features separating UMN from LMN paresis localisation in the ambulatory horse include:

Answer 19

• presence of ataxia (LMN dysfunction is not associated with ataxia),
• absence of the cutaneous trunci reflex (bilaterally suggests UMN pathology of C8–L3 spinal cord segments or associated spinal nerves) and
• intact extensor postural reactions (ability to support weight on the limb).
• Patellar hyperreflexia may be present in recumbent horses.

Question 20

The lumbosacral intumesence and terminal spinal cord (conus medullaris) are located within

Answer 20

Lumbosacral spinal cord segments L4–S2

• Thus SCDs cranial to the L4 vertebra cause general proprioceptive ataxia and UMN tetra/paraparesis.
• Injuries caudal to the L4 vertebra result in LMN deficits from dysfunction of the neuron cell bodies (spinal cord) or spinal nerves.

Question 21

Polyneuritis equi (cauda equina neuritis) affects

Answer 21

the spinal nerves of the lumbosacral and coccygeal segments causing LMN deficits recognised as

• loss of cutaneous sensation,
• loss of perineal reflex,
• weak tail/anal tone and
• urinary incontinence.

Question 22

most common deficits in horses with temporohyoid osteoarthropathy

Answer 22

The most common signs included

• auditory loss (100% of horses),
• vestibular and facial nerve dysfunction (83%), and
• exposure ulcerative keratitis (71%).
• Concurrent left laryngeal hemiparesis was observed in 61% of horses through endoscopy.

Question 23

unilateral or bilateral auditory dysfunction on THO?

Answer 23

Auditory dysfunction was bilateral in 50% of the cases (complete and partial), and unilateral affecting more commonly the right ear

Question 24

THO is

Answer 24

disorder of temporohyoid joint formed by the stylohyoid and petrous temporal bones.

The disorder is characterized by bony proliferation, fusion of the joint, and potential fracture of the involved or adjacent bones

Question 25

etiology THO

Answer 25

Proposed etiologies include

• inflammation,
• infection of the middle/ inner ear secondary to a hematogenous or ascending infection from the upper respiratory tract,
• extension of external ear infection, and
• primary degenerative process.

Question 26

Clinical signs of THO

Answer 26

Clinical signs vary

• head shaking,
• apparent resentment of manipulation of the head or ears,
• resistance to the bit,
• difficulty eating, and
• facial and vestibulocochlear nerve dysfunction. (Auditory loss appears to be a common neurologic abnormality in these horses)

Question 27

Prognosis of auditory loss in THO

Answer 27

Despite observed overall neurologic improvement (facial and vestibular function) in diseased horses, auditory dysfunction persisted (clinical evaluation: short-term n = 19/19, long-term n = 16/ 16; BAER evaluation: long-term n = 8/8). Further, auditory loss progressed in 3 of 5 horses with bilateral disease. However, this deficit did not appear to interfere with the horses’ daily activities

Question 28

The carrier status of lavender foal syndrome (LFS), cerebellar abiotrophy (CA), severe combined immunodeficiency (SCID), and occipitoatlantoaxial malformation (OAAM1) in foals with juvenile idiopathic epilepsy (JIE)?

Answer 28

Ten Egyptian Arabian horses (5 females and 5 males) were phenotyped as foals with JIE by electroencephalography (EEG).

All foals were negative for the genetic mutations that cause LFS, CA, SCID, and OAAM1 except for 1 foal that was a carrier of CA.

Question 29

Juvenile idiopathic epilepsy

Answer 29

(JIE) is a self-limiting epileptic syndrome described in Egyptian Arabian foals.1 This disorder is characterized by recurrent generalized tonic-clonic seizures with no apparent precipitating events or underlying disease with an early onset in life (median age, 2 months).1 Affected foals are clinically normal between seizures.1

Question 30

Neuroglycopenia refers to

Answer 30

a shortage of glucose in the brain resulting in neuronal dysfunction and death if left untreated.

Neuroglycopenia is presumed to occur in horses as the result of severe hypoglycemia. Subclinical seizures, and intermittent blindness and deafness of cortical origin can occur. Severe altered state of consciousness and seizures can be observed at a blood glucose cut-off value of < 42 mg/dL

Question 31

Sidewinder gait in horses

Answer 31

characterized by walking with the trunk and pelvic limbs drifting to 1 side.

Can be of neurological/orthopedic/muscular origin

The condition often has a poor prognosis for function and life

Case fatality was 79%.

Question 32

central nervous side affects of gentamicin in horses

Answer 32

Aleman 2021: Seven out of ten horses had auditory loss after 7 day course of Genta:

complete bilateral (N = 1),

complete unilateral (N = 2), and

partial unilateral ((N = 4)

long term???

Question 33

In vitro differntiation of different nerve fibers and findings in the recurrent laryngeal and phrenic nerves

Answer 33

Immunohistochemistry of FFPE-derived nerve samples with selected antibodies and specific antigen retrieval methods, enabled identification of myelinated and unmyelinated axons, cholinergic, sympathetic and peptidergic axons.

The recurrent laryngeal and phrenic nerves are composed of

• myelinated cholinergic (motor),
• myelinated sensory fibres and unmyelinated peptidergic (sensory) axons.
• unmyelinated adrenergic (sympathetic) axons

Question 34

Shivering is…

Answer 34

Equine shivering is a neuromuscular disease with characteristic signs of intermittent muscle fasciculations or ‘shivering’ of the hindlimb muscles that is elicited by specific locomotor movements [1,2].

Walking backward often results in either a hyperflexed abducted hindlimb or a rigidly extended hindlimb, whereas forward gaits often appear normal [3].

Hindlimb hyperflexion in horses with advanced shivering, however, can occur with initiation of forward walking or directional changes [3,4].

Question 35

new conclusions on 2018 shivering study

Answer 35

In summary, our data provide the first electrophysiological evidence that equine shivering is characterised by enhanced simultaneous recruitment of flexor and extensor muscles and a loss of the ability to modulate motor unit recruitment in the hindlimbs, particularly when walking backward.

Abnormal muscle activation in horses with shivering was consistent with the observed hyperflexion or hyperextension of hindlimbs and was associated with the presence of selective Purkinje cell axonal degeneration in deep cerebellar nuclei.

Question 36

Reported prevalance of CVM in Thoroughbred horses

Answer 36

1.3–2%

Question 37

Evidence based conservative treatment for adult horses in Cervical Vertebral Stenotic Myelopathy, indications and outcomes

Answer 37

Indication:

Horses with

• milder grades of ataxia (less than grade 3),
• normal vertebral canal Minimal Sagital Diameter ratios and
• moderate Articular Process Joint changes (grade 3a–4b)

are good candidates for medication (Hepburn 2012).

intra-articular medication

• corticosteroids: 32% of horses improved performance although in 50% of the improved cases the effect lasted only 1–6 months
• Older ataxic horses had a 60% improvement with an average 2 grades improvement of ataxia that was effective for 1–8 years (average 2 years) (Kristoffersen et al. 2014).

Question 38

Causes and sites of CVSM in the sceletally mature horse

Answer 38

In the skeletally mature horse, clinical signs of CVSM are due to degenerative pathology of the articular process joints and the surrounding soft tissues that result in static (most commonly) or dynamic cord compression most commonly in the caudal cervical articular process joints (C5 to T1)

Question 39

Ttrm of CVM in the young horse

What is the evidence?

Answer 39

Conservative treatment consists of combinations of

• strict stall confinement,
• anti-inflammatories and
• dietary modifications designed to reduce growth spurts in younger horses.

Resolution of neurological signs was observed in 75% of mildly affected (neurological) foals or yearlings with equivocal radiographic changes who were fed decreased protein and low nonstructural carbohydrates (total 1.5% bodyweight, which is 75% of the 2% bodyweight recommended feed for normal horses) with soaked hay, vitamin E and selenium and had prolonged total confinement (Donawick et al. 1993; Kronfeld 1993).

Question 40

evidence on surgical correction of CVM

Answer 40

favourable long-term outcome in yearlings and skeletally mature horses for resolution of ataxia.

Although success rates of surgical correction in horses up to 18 months of age in which the dynamic form of CVSM are more commonly seen are greater (improvement 1-2 ataxia grades over 2 years), good outcome for mature horses with static degenerative myelopathy are also reported.

Question 41

APJ OC in foals and its link to CVM

Answer 41

Articular process joint OC in Warmblood foals is common and is not more prevalent at CVM predilection sites, suggesting that abnormalities of enchondral ossification may not be major contributors to CVM.

Question 42

most common cause of facial nerve paralysis

Answer 42

Sixty-four equids

• trauma (n = 20)
• central nervous system (CNS) disease (n = 16),
• idiopathic (n = 12): 4 “true” idiopathic, 8 “not investigated”),
• temporohyoid osteoarthropathy (n = 10),
• otitis media-interna (n = 3),
• lymphoma (n = 1),
• iatrogenic as a consequence of infiltration of local anesthetic (n = 1), and clostridial myositis

Facial nerve paralysis was unilateral in 92% (59/64) of cases and bilateral in 8% (5/64) of cases.

Question 43

long term follow up of facial nerve paralysis

Answer 43

Twenty-nine (53%) equids had full resolution of FNP,

14 (25%) were euthanized,

6 (11%) partially improved, and

6 (11%) were unchanged or worse.

Question 44

probably most common type of postanesthetic facial nerve paralysis

Answer 44

when the head of the anesthetized horse is positioned in such a way that the halter or other firm object compresses the buccal branches of the nerve as they cross the masseter muscle.

causing lip droop or muzzle deviation alone.

Question 45

Most common cause of FNP in humans and evidence based ttrm

Answer 45

In human medicine, idiopathic FNP (Bell’s palsy) accounts for approximately 70% of cases of FNP.

In 2007, a double-blinded, placebocontrolled, randomized study with 551 participants reported significant improvement in patients treated with prednisolone within 72 hours of onset. In small animals, the benefit of corticosteroid administration is not known.

Question 46

signs of facial nerve paralysis and how often do they occur

Answer 46

• 69% deviation of the muzzle
• 63% drooping of the lip.
• 55% ear droop or bilateral ear droop
• 53% Inability to blink the eye on the affected side
• 52 % ptosis of the eye
• • 53% of cases had ≥3 signs of FNP, and
• 16% of cases had all 5 signs (ptosis, ear droop, muzzle deviation, absent blink, and lip droop).
• Additional signs attributed to FNP included nares collapse (3 cases, in 1 case bilateral, causing respiratory distress).

Question 47

Kennedy et al. (2016) assessed the oral microbiome of horses with and without periodontal disease and found that

Answer 47

affected horses had a different, more diverse microbiome, with Prevotella species being the most prevalent.

Question 48

Congenital occipitoatlantoaxial malformation in Warmbloods

Answer 48

1 case report in 3 yr old WB mare including not only bony but muscular malformation

mostly arabian foals affected

Most horses affected by OAAM develop ataxia due to compressive damage to the spinal cord secondary to the bony malformations early in life.

Imostly in foals (Mayhew et al. 1978a; Gonda et al. 2001).

In some cases, ataxia develops progressively to the age of 2–3 years (Wilson et al. 1985).

no trtm, mostly euthanasia

Question 49

comparison between

percutaneous, ultrasound-guided CSF collection from the C1-C2 space in standing horses

Lumbosacral (LS) centesis in standing horses

Answer 49

CSF from C1-C2 space: decreased likelihood of clinically important blood contamination of samples. (significantly lower mean protein concentration and red blood cell count)

• Collection time,
• total nucleated cell count,
• EPM titers, and
• serum:CSF EPM titer ratios

were not significantly different between collection sites

Question 50

Does repeated CSF collection alter CSF analytes?

Answer 50

Repeat thecal puncture from the LS or C1-C2 space 2 weeks apart does not appear to impact CSF analytes.

Question 51

Are dysphagic foals less likely to race as adults and have altered athleticism (age of first race, Speed Index, Earnings Per Start Index) compared to healthy foals that raced as adults.

Answer 51

No. The athleticism of formerly dysphagic foals does not appear to be negatively impacted compared to normal foals as measured by age of first race, Earnings Per Start Index and Speed Index.

Question 52

Electroacupuncture in headshaking

Answer 52

report with 6 horses with grade 3 headshaking:

all responded ACCORDING to the OWNERS

electroacupuncture of the infraorbital nerve under light sedation. The nerve was stimulated with alternating 2 and 80 Hz frequencies for a period of 25 min with the current adjusted so that there was v_isible twitching of the nostrils and/or lips_.

Follow-up treatments were given when the signs recurred or 4–7 days later if there was no initial response. Once a response was achieved, the period of remission often increased with subsequent treatments.

Question 53

Osteochondroma of the cervical spine

imaging

Answer 53

Osteochondroma of the cervical spine is an uncommon benign neoplasia of the cervical spine with clinical symptoms related to its location with respect to adjacent structures.

CT guided biopsies.

Question 54

Spondylosis deformans in horses

clinical signs, diagnosis, ttrm, prognosis

Answer 54

low head carriage or difficulty lowering head or flexing

diagnosed w/ lateral radiographs

Spondylosis deformans (VENTRAL)is rare, typically identified from T10–T14 and, rarely, the lumbar spine in horses. largest lateral motion and axial rotation of the equine spine -> spondylosis?

Prognosis guarded, conservative ttrm with NSAIDs possible

Question 55

cervical and cranial thoracic Discospondylitis

Answer 55

= inflammatory condition involving the vertebral bodies adjacent to the intervertebral symphysis and their associated intervertebral disc.

unusual in horses and the majority of documented cases have been associated with infection.

This study 2020: 8 cases presumably non infectious

clinic:

• neck stiffness,
• neck pain,
• a stiff or shortstepping forelimb gait and forelimb lameness.
• Ataxia is also reported as a clinical sign, associated with protrusion of disc material into the vertebral canal

dx: intervertebral disc space obliteration in lateral radiographs
ttrm: surgical fusion of the affected joints

Question 56

Phosphorylated neurofilament heavy protein (pNfH) as a serum biomarker

Answer 56

for detection of axonal degeneration

Serum pNfH concentrations are specifically increased (>1 ng/mL) in some horses with

• equine neuroaxonal dystrophy and the more severe pathological variant,
• equine degenerative myeloencephalopathy.
• 99% specificity and 12% sensitivity

Increased CSF pNfH concentrations (>3 ng/mL) can be observed with eNAD/EDM or CVCM.

in other studies Serum pNfH concentrations were significantly higher in EPM-affected horses compared to control horses and CVCM-affected horses, whereas

CSF pNfH concentrations of EPM-affected horses were reported to be four times higher than CVCM horses in this study and far higher in another one

therefore, it is unlikely that the magnitude of increase can be associated with a particular disease entity

Question 57

pastureassociated stringhalt (PSH)

what is it

causes

clinical signs

risk factors

diagnosis

treatment

prognosis

Answer 57

= peripheral neuropathy affecting the larger myelinated axons

cause: thought to be the result of exposure to a plant-derived neurotoxin, precise aetiology unknown
clinic: exaggerated, prolonged hindlimb flexion - exacerbated when affected horses appear agitated or disturbed.

risk factors:

• Drought-affected, poor-quality pasture
• presence of Hypochoeris radicata (löwenzahn)
• mature and taller animals

Dx of stringhalt has to be based on the clinical signs and absence of other neurologic and orthopaedic abnormalities.

ttrm: experimental
prognosis: Most horses recover spontaneously if removed from the presumptive source of toxin; recovery can be prolonged (years) and incomplete in occasional cases.

Question 58

Peripheral neuropathy of a forelimb in horses: 27 cases

predominant lesions

prognosis

Answer 58

Predominant lesions:

• radial nerve 14 horses
• suprascapular nerve: 11,
• axillary nerve 2

Most horses with peripheral neuropathy of a forelimb returned to athletic soundness following an adequate period of rest.

Horses with lesions of a radial nerve alone or in association with other nerves typically required longer recovery times than did those with predominant injuries of a suprascapular nerve.

Question 59

Concurrent Equine Degenerative Myeloencephalopathy and Equine Motor Neuron Disease in Three Young Horses

2016

Conclusion

Answer 59

EDM and EMND can occur concurrently in young related horses in association with an underlying a-TP deficiency.

Both NAD/EDM and EMND in horses are associated with a temporal deficiency in a-TP but

• EDM considered to be genetic (currently proposed mode of inheritance in the Quarter Horse as autosomal dominant with incomplete penetrance)
• EMND acquired

Question 60

eNAD/EDM:

definition

experimental antemortem tests

Answer 60

Equine neuroaxonal dystrophy/equine degenerative myeloencephalopathy () is a neurodegenerative disorder affecting genetically predisposed foals maintained on an α-tocopherol (α-TOH) deficient diet.

Currently no antemortem diagnostic test for eNAD/EDM is available.

Study: in Spinal Cord tissue samples (Post mortem), targeted markers of cholesterol oxidation, including 7-ketocholesterol, 7-hydroxycholesterol, and 7-keto-27-hydroxycholesterol were significantly increased with eNAD/EDM

NOT in CSF or serum

NO

Question 61

cervical vertebral osteosarcoma

Answer 61

One report describes a 2-year-old colt presented with sudden-onset ataxia in which a cervical vertebral osteosarcoma causing severe compression of the spinal cord was diagnosed.

Normally very rare

Dx: radiography and CT: Osteolytic and osteoscleroticc lesions. Laboratory analyses of the blood and the CSF tap showed only mild and unspecific changes.

some case reports of surgical extraction in other locations but most horses are subjected to euthanasia due to the locally invasive and destructive nature of the tumour

Question 62

Factors associated with outcome in 94 hospitalised foals diagnosed with neonatal encephalopathy

frequent clinical signs

survival

variables associated with nonsurvival

Answer 62

most frequently identified clinical signs included:

• abnormal udder seeking (59%),
• abnormal suckle (55%),
• inability to stand (42%),
• abnormal gastrointestinal motility (37%),
• abnormal consciousness (34%) and seizure activity (22%).

Survival: 75 (79.8%) foals survived to be discharged from the hospital and 19 foals died or were subjected to euthanasia.

Variables significantly associated with nonsurvival

• high serum total calcium concentration at admission
• low serum activity of ALP at admission
• recumbency,
• number of concurrent diseases, and
• use of vasopressors/inotropes. suggesting that persistent hypotension is associated with nonsurvival in the current population
• concurrent disease

Question 63

Sensitivity of radiography and radiographic myelography for vertebral canal stenosis

alternative?

Answer 63

Survey radiography : 42 and 63% for vertebral canal stenosis identified with intravertebral ratio (IVR) and DJD when compared with necropsy.

Misdiagnosis of compressive lesions with survey radiography alone occurs in

• 30%-60% of cases compared with radiographic myelography, and
• 61% of cases compared with necropsy

radiographic myelography in a multicenter study, radiographic myelography had a 68% correlation with necropsy findings

ALTERNATIVE: Computed tomography myelography

Question 64

leading causes of spinal ataxia reported for horses in the eastern United States.

Answer 64

CVCM and eNAD-EDM

Question 65

Postmortem diagnoses of spinal ataxia in 316 horses in California

“horses with eNAD-EDM were 2.95 times as likely to have been…”

Answer 65

AQHs,

a breed known to have breed-specific diseases such as hyperkalemic periodic paralysis, hereditary regional dermal asthenia, glycogen branching enzyme deficiency, type 1 polysaccharide storage myopathy, and malignant hyperthermia

a breed predisposition to eNAD-EDM had not been reported before the present study

Question 66

α-tocopherol metabolism in horses with equine neuroaxonal dystrophy

Answer 66

• aberrant vitE metabolism in QHs with eNAD/EDM, defined primarily by increased α-TOH metabolism in serum and urine, after a PO dose of RRR-α-TOH.
• higher urinary α-CEHC concentrations at similar serum α-TOH concentrations. (Similar to results obtained in human patients with AVED Ataxia with Vitamin E deficiency)
• increased hepatic expression of CYP4F2, the major metabolizer of vitE, was observed in eNAD/EDM-affected horses across breeds. -> Enhanced metabolism of α-TOH would lead to a higher α-TOH requirement in eNAD/EDM-affected horses.

Question 67

Treatment of temporohyoid osteoarthropathy in horses

Answer 67

• medical: reducing inflammation and providing analgesia through administration of NSAIDs, corticosteroids, gabapentin, and antimicrobials

medical management doesn’t work or risk for acute fracture of the petrous temporal bone:

• surgical:
  
  • partial stylohyoidectomy: complications such as laceration of the lingual artery, hypoglossal neuropathy, transient dysphagia, stylohyoid bone regrowth, and permanent problems with prehension when performed bilaterally, partial stylohyoidectomy has been replaced with
  • ceratohyoidectomy: complications: iatrogenic trauma to the ipsilateral hypoglossal nerve, linguofacial vein, and branches of the lingual nerve owing to their close association with the proximal aspect of the ceratohyoid bone
  • experimental: successful basihyoid-ceratohyoid disarticulation of 6 horses in standing and sedated horses
• Prognosis for survival:
  
  • good to excellent after surgical intervention
  • fair for those treated with medical management alone

Question 68

Toxoplasma gondii seroprevalence and association with equine protozoal myeloencephalitis: A case–control study of Californian horses

Answer 68

association between high T. gondii titres and clinical signs compatible with EPM is potentially reflective of toxoplasmosis in equines. Serologic testing of cerebrospinal fluid and isolation of T. gondii in EPM suspect cases should be considered. Future studies investigating the relationship between T. gondii and EPM are warranted.

Question 69

Cerebrospinal fluid Lyme multiplex assay

Answer 69

Positive Lyme multiplex results were common in horses with neurologic diseases and did not adequately differentiate horses with neuroborreliosis from horses with other disorders.

Cerebrospinal fluid Lyme multiplex assay results are not diagnostic in horses with neuroborreliosis

Question 70

If a tapetal reflex can be visualised through retroillumination (shining a light at arm’s length into the eye and looking for the tapetal reflection), the cause of blindness can be localised

Answer 70

either to the retina or the visual pathway. If the fundus appears normal, a neurogenic cause of blindness should be strongly suspected.

Question 71

In the absence of facial nerve dysfunction or cerebellar disease, loss of menace response indicates

Answer 71

severe visual loss.

Question 72

The pupillary light reflex test…

Answer 72

= brainstem reflex that tests

• the visual components of the eyeball and the central visual pathway to the level of the midbrain (mesencephalic pretectal nuclei).
• motor response requires oculomotor nerve integrity from the oculomotor nuclei in the midbrain through the orbital fissure into the periorbita and ciliary ganglion, as well as short ciliary nerves from the ganglion to the eye.
• Due to decussation of neurons at the optic chiasm and again at the caudal commissure, light directed into one eye stimulates both oculomotor nerves such that pupillary constriction should occur in both eyes.

Question 73

Lesions that destroy the retina or optic nerve in one eye cause

Answer 73

blindness with a normal to slightly dilated pupil (due to light entering the normal eye and stimulating both oculomotor nuclei). If light is directed into the blind eye, neither pupil constricts;

Question 74

Retrobulbar lesions often affect

Answer 74

both the optic nerve and oculomotor nerve of one eye; the affected eye will be blind with a dilated pupil, and light directed into the affected eye does not cause constriction in either eye, whereas light directed into the unaffected eye causes constriction only in that eye

Question 75

Unilateral forebrain lesions in the optic tract, lateral geniculate nucleus, optic radiation or visual cortex cause

Answer 75

blindness in the CONTRALATERAL eye

because of the degree of decussation in the optic chiasm. Pupillary light reflexes generally remain normal in both eyes. Bilateral forebrain lesions cause bilateral blindness with preservation of pupillary light reflexes.

Question 76

Causes of neurogenic blindness in the horse

Answer 76

• Traumatic optic neuropathy most commonly occurs after head trauma sustained during falls or collisions (Martin et al. 1986). One common scenario is the horse that rears and flips over backwards (due to tying, fear or another reason), causing shearing or severing of the optic nerves as the brain moves away from the fixed, intracanalicular optic nerves
• One important anatomical feature to remember is that the optic nerves are located immediately dorsal to the sphenopalatine sinuses, which are relatively thin-walled. Infections, inflammatory processes, granulomas or neoplasia in the sphenopalatine sinuses can cause blindness that is slowly progressive or acute in onset (Barnett et al. 2008; Radcliffe et al. 2016) but also other cranial nerves affected: III, IV, V and VI
• ischaemic optic neuropathy is associated with sudden hypoxia as might occur during severe hypovolaemia or hypotension (as can occur with acute severe blood loss) or surgical occlusion of the external and internal carotid arteries (Freeman et al. 1990; Hardy et al. 1990)
• Optic neuritis can occur due to extension of local inflammatory disease or primary central nervous system diseases
• meningitis can affect the optic nerves, as can CNS neoplasia. Finally, toxic insults have been implicated in optic nerve degeneration
• Metabolic encephalopathies are probably the most common cause of bilateral central blindness and can occur due to hepatic disease, renal disease, intestinal disease (hyperammonemia), electrolyte derangements or other metabolic abnormalities.
• Rarely, horses show transient (<5 days) central blindness following routine myelography
• Any disease that causes seizure activity can cause post-ictal central blindness that might persist for several days
• Unintentional intracarotid injections can cause acute cerebral toxicity or infarction of the ipsilateral forebrain resulting in contralateral blindness.

Question 77

presenting complaints of Lyme borreliosis

Answer 77

• Cranial or peripheral neuropathies were common. Facial nerve palsy, as observed in 4/16 of the horses in this study and in 3/7 previously reported cases of equine NB,6,7 occurs in 8% of human NB cases.24 Dysphagia was frequently observed and has been described in the human literature in association with Borrelia brainstem encephalitis.25 Histologic findings from this report indicate that the cause of dysphagia might be multifocal including cranial neuritis, guttural diverticulitis, and tongue and esophageal myositis. Recurrent laryngeal nerve paralysis has also been reported as a rare complication of human NB that can result in dysphonia and respiratory failure requiring tracheostomy.26–28 Fever and neck stiffness (noted in 2 and 6 horses, respectively) were present in 15% of the 118 patients with acute NB.29
• Uveitis was the most frequent extraneural manifestation of Borrelia infection. Five cases of equine uveitis associated with Borrelia have been reported

Question 78

Newborn foal with atypical myopathy

story

theories

Answer 78

• foal’s dam was diagnosed with AM in the 6th month of gestation based on clinical signs of a myopathy, elevated serum activity of creatine kinase, metabolomic analysis and the presence of methylenecyclopropyl acetyl carnitine (MCPA-carnitine) in the blood. At the time of delivery, the mare was grazing on a pasture near sycamore trees but was free of clinical signs of AM.
• Two theories could explain this observation (a) hypoglycin A or its metabolites accumulated in the mare’s placenta with consequent transfer to fetus or (b) these compounds were secreted into mare’s milk.

Question 79

The lack of clinical disc disease in the horse is attributed to

Answer 79

the absence or poorly developed nucleus pulposus, and relatively thin width of the intervertebral discs. Equine intervertebral discs have a central fibrocartilaginous area that becomes more fibrous peripherally and is relatively thin, making horses less susceptible to disc prolapse

Question 80

Somatic innervation of the bladder originates from

Answer 80

m the sacral cord (S1–S2) by way of the pelvic nerve and branches of the pudendal nerve, which also innervate the perineum and external anal sphincter

Question 81

Articular processes joint enlargement has been associated with

Answer 81

vertebral canal stenosis and spinal cord compression in ataxic horses diagnosed with cervical vertebral stenotic myelopathy (CVSM) (cervical vertebral malformation, wobbler syndrome) and with nerve root compression at the intervertebral foramen, leading to local cervical pain, muscle atrophy and thoracic limb lameness

Question 82

Computed tomography and myelography of the equine cervical spine: 180 cases (2013–2018)

the most common pathology reported was…

Answer 82

OA of the APJs at the articulations of C5–C6, C6–C7, C4–C5 and C3–C4.

Question 83

Which imaging modality can be considered the gold standard for studying the central nervous system, including the brain and cranial nerves, as well as the extracranial soft tissues, including the orbit, lymph nodes, blood vessels, muscles and salivary glands.

Answer 83

MRI

Question 84

Which imaging modality can be considered the gold standard for studying the skull bones, the temporomandibular joint, the temporohyoid articulation and teeth. also adequate for studying the nasal passages and paranasal sinuses, being particularly useful for identifying subtle nasal and sinusal osseous wall lesions

Answer 84

CT

Question 85

In 2 retrospective studies involving 34 and 47 horses with traumatic head injury, neurological deficits were most commonly associated with

Answer 85

basisphenoid/basioccipital bone fractures.

Question 86

Who provides sensory innervation to the pharynx

Answer 86

CNIX and CNX

Question 87

dysphagia, right laryngeal paralysis, dysphonia, and lack of a gag reflex 5 days after poll injury

Answer 87

possibly Delayed onset vagus nerve paralysis after occipital condyle fracture

IX and X near the condyle

XI could be damaged too due to proximity

*In the present case, CNXI function appeared to be intact as evidenced by the lack of electromyographic changes over the right trapezoid muscle and the absence of muscle atrophy both clinically and on postmortem examination. The CNs IX, X, and XI share the same outlet from the skull, however once they exit, CNIX and CNX follow a cranio-ventral route. In contrast, CNXI travels caudally soon after leaving the skull.

Question 88

Apart from cranial nerve signs, unilateral CNX damage can also cause

Answer 88

stomach acid secretion disorders and transient delayed gastric emptying

Question 89

MRI and CSF findings in Transient bilateral blindness associated with idiopathic hypertrophic pachymeningitis

which other test is indicated for definitive diagnosis?

Answer 89

CSF: Basophilic inflammation

MRI diffuse, marked thickening and moderate contrast enhancement of the pachymeninges overlying the cerebrum + apparent increase in cerebrospinal fluid (CSF) volume

biopsy of the meninges

Question 90

Accurate antemortem EPM diagnosis requires

Answer 90

evidence of intrathecal antibody production against S. neurona or N. hughesi.

Question 91

How can SAA and CRP aid in the diagnosis of EPM?

Answer 91

Neither SAA nor CRP in serum or CSF aid diagnosis of EPM

Question 92

The most likely differential diagnoses for enlargement of the pituitary gland in the horse, seen on CT images, are

Answer 92

age-related changes or melanotrope hyperplasia and macroadenoma formation in the pituitary pars intermedia

…..

abscess formation possible

Question 93

On impact, the compressive forces are transmitted through the brain causing

Answer 93

compression of the brain against the lagging or opposite surface of the skull, resulting in a larger contrecoup lesion at that location.

Question 94

how can ataxia grading be objectified?

Answer 94

Motion capture can objectively aid the assessment of horses with ataxia. Furthermore, blindfolding increases variation in distal pelvic limb kinematics making it a useful clinical tool.

For horses with a median ataxia grade ≥2, coefficient of variation for the location of maximum vertical displacement of pelvic and thoracic distal limbs generated good diagnostic yield. The hoofs of the thoracic limbs yielded an Area Under the Curve of 0.81 with 64% sensitivity and 90% specificity. Blindfolding exacerbated the variation for ataxic horses compared to non-ataxic horses with the hoof marker having an AUC of 0.89 with 82% sensitivity and 90% specificity.

Question 95

surgical TTRM of cervical vertebral compressive myelopathy and new techniques

Answer 95

different ventral interbody fusions

new: placement of an interbody fusion device and polyaxial pedicle screw and rod construct for cervical vertebral fusion (19) but only 10 horses

Question 96

EquiPENS :

success rates in idiopathic headshaking and where is it placed?

Answer 96

The recently developed, equine specific, neurostimulation device EquiPENS1 has now been used in over 130 TMHS horses with approximately 50% successfully returning to the previous level of activity

. Ultrasonographic guidance is used to direct the probe percutaneously such that it lies approximately 1 mm superficial to the infraorbital nerve prior to stimulation (Roberts et al. 2016)

Question 97

What is the theory behind Therapeutic application of electricity for pain

Answer 97

gate control theory of pain by Melzack and Wall (1965)

substantia gelatinosa in the dorsal horn of the spinal cord: = gate control system, which modulates the synaptic transmission of nerve impulses from peripheral fibres to the central nervous system.

• Small nociceptive A-d and C fibres hold the ‘gate’ in an open position,
• stimulation of large mechanoreceptive A-b fibres by touch, pressure or vibration close the ‘gate’ and inhibit pain transmission to the brain.

Small nociceptive fibres: higher activation threshold than larger mechanoreceptive fibres => selective low level stimulation of mechanoreceptors can prevent or reduce pain transmission. Activation of these large A-b fibres recruits inhibitory interneurons within the substantia gelatinosa of the spinal cord which exert their inhibitory action on both large and small diameter fibres synapsing higher up the spinal cord.

additional activation of the descending inhibitory pathway => release of endogenous opioids and alterations of many other neuro-excitatory or inhibitory compounds

Question 98

When the poll strikes a hard surface such as pavement during rearing and flip-over injury

Answer 98

the nuchal crest acts as a pivot causing the head to flip into extension resulting in sudden and dramatic stretch of the rectus capitis ventralis muscles. This often leads to a fracture of the basioccipital and basisphenoid bones and tearing of the adjacent blood vessels which may include the occipital artery causing haemorrhage into the guttural pouch and ear canals.

Question 99

MMEP cutoff values for detection of spinal cord dysfunction in horses

Answer 99

Transcranial magnetic stimulation (TMS) and recording of magnetic motor evoked potentials (MMEP) can detect neurological dysfunction in horses

To detect spinal cord dysfunction caused by compression, the optimal cutoff for thoracic limbs remained 22 milliseconds, while it increased to 43 milliseconds in pelvic limbs (sensitivity, 100% [100%-100%]; specificity, 100% [100%-100%] for thoracic and pelvic limbs).

Question 100

compare diagnostic accuracy of TMS, cervical radiography, and neurological examination for spinal cord dysfunction/compression and ataxia

Answer 100

Sensitivity and specificity

• of neurological examination: 97.6 and 74.7%
• of radiography 43.0 and 77.3
• of transcranial magnetic stimulation 87.5 and 97.4 For TMS, the highest accuracy was obtained using the minimum latency time for the pelvic limbs (Youden’s index = 0.85).

=> combination of neuro exam and TMS best

Question 101

sensitivity

Answer 101

= ability to correctly identify diseased

Question 102

specificity

what if its low?

Answer 102

ability to detect non diseased

if it is low you have many false positives

Question 103

reported atypical form of EMND

Answer 103

additionally to usual clin signs: Reduced tongue tone associated with degeneration of the hypoglossal nerve nucleus

normally the disease affects many cranial nerve nuclei (histologically) but it is suspected that cranial nerve signs do not appear bc only a certain percentage of neurons are damaged

achtung geht normalerweise auf type I muskeln und zunge ist typ 2!!!

Question 104

3 main post mortem findings to diagnose EMND

Answer 104

• denervation atrophy of muscles with a higher prevalence of type I myofibres,
• lipopigment accumulation in endothelial cells
• degeneration of neuronal somata and axons

Question 105

Prevalence of headshaking within the equine population in the UK(owner questionaire)

Answer 105

The estimated prevalence of owner-reported headshaking in the sample population of horses (n = 1014), within the last year, was 4.6% whereas 6.2% of horses were reported by their owners to have shown signs of headshaking at any time-point since ownership.

There was no association of sex or breed. Nineteen percent of headshaking horses were reported to show headshaking at rest.

Fewer than one-third (30.2%, n = 19) of headshaking horses had been examined by a veterinarian for headshaking. Of horses seen by a veterinarian, the cause for headshaking remained unknown in the majority of cases (57.9% responses) and trigeminal-mediated headshaking was reported as a diagnosis in just one case

Question 106

A pilot study of optical neuronavigation-guided brain biopsy in the horse using anatomic landmarks and fiducial arrays for patient registration

Answer 106

Optical neuronavigation using the Brainsight Vet 2 system is feasible in horses and, based on our preliminary data, the use of anatomic landmarks appears to be a feasible option for registration. Optical neuronavigation should be considered when performing brain biopsies or surgical procedures in horses that may require a high degree of accuracy, such as surgical treatment of Cushing’s disease and biopsy or resection of inflammatory lesions, granulomas, or other masses, and may allow such procedures to become more feasible

Question 107

The diagnosis of EPM relies heavily on the clinical examination. The sensitivity and specificity of the Western blot analysis for antibodies to S. neurona in cerebrospinal fluid (CSF) have been reported to be

Answer 107

89 and 89%, respectively, based on comparison to postmortem evaluation in severely affected horses.

Question 108

Interobserver Variation in the Diagnosis of Neurologic Abnormalities in the Horse

Answer 108

The agreement among observers was either good or excellent for 80% of horses when evaluating for the presence or absence of neurologic abnormalities.

• best agreement: presence or absence of neurologic signs, lameness, ataxia, and truncal sway,
• worst agreement: assessing muscle atrophy, spasticity, and severity of neurologic deficits

Question 109

intracranial infections in the literature: causing agents?

Answer 109

Previous reports have attributed intracranial infections in 20 horses to abscesses caused by Streptococcus equi spp. equi and spp. zooepidemicus (50%) or mixed bacterial and fungal infections of the calverium extending from trauma, paranasal sinusitis, pituitary gland abscesses and/or pneumonia (50%).

Curiously, infection with Streptococcus equi spp. equi and spp. zooepidemicus was more likely to result in metastatic cerebral abscessation , while infection with other organisms was more likely associated with extension of sinus infections or trauma or possibly associated with chronic pneumonia.

Question 110

prognosis of brain abscess/intracranial infection

Answer 110

reports demonstrate that the prognosis is guarded (4/20 survived) and poor with medical treatment alone (0 survived).

Question 111

oral supplementation of XXX decreases headshaking

Answer 111

6 headshakers and 6 controls:

Combined magnesium-boron supplementation induced the highest IRR reduction (64%) in headshaking behavior when compared to hay diet only. Similarly, magnesium-boron supplementation had the greatest IRR reduction (36%) in headshaking behavior when compared to a diet containing pelleted feed. The most severely affected horses had the most benefit to supplementation providing magnesium

Question 112

Magnesium requirements of the horse

Answer 112

The requirement for magnesium in horses is 13 mg/kg BW and for an average 500 kg horse, the requirement would be 6.5 g of magnesium a day

Question 113

presumed mechanisms of action for mg in headshaking

Answer 113

1500-2000 mg/kg of PO MgSO IV led to a 29% reduction in head-shaking rate

• acts as a blocking agent to N-methyl-D-aspartate (NMDA) receptors, which have been shown to have an effect on trigeminal neurons
• inhibit Ca2+-dependent presynaptic excitation-secretion coupling
• magnesium has been utilized in anesthesia as an analgesic agent (effect unknown)

Question 114

Headshaking and LH

Answer 114

: Horses affected with headshaking did not have significant differences in circulating LH during the late summer as compared to control horses.

Question 115

Main findings of the study: Management of equine ataxia caused by cervical vertebral stenotic myelopathy: A European perspective 2010–2015

Answer 115

Among treated horses, 69% of conservatively managed and 43% of surgical cases returned to use. Surgical cervical vertebral interbody fusion using threaded kerf-cut cylinders resulted in sufficient stabilisation and thus, remains a reliable technique particularly in more severely affected horses.

Question 116

intrathecal pain management for laminitis cases

Answer 116

Caudal epidural administration of a mixture of opioids and ɑ2-agonists is now routinely used to provide analgesia to the pelvic limbs. More recently, the use of larger volumes to extend the analgesic effect to the thoracic limbs has also been advocated (

Question 117

caudal epidural administration of morphine and detomidine in a pony - case report side effects

Answer 117

Presumed generalised seizure

theory is the sudden increase in epidural and intracranial pressures (injection over 90s) precipitated the seizure. Take home message:

injection of large volumes over several minutes. to facilitate this, use a prolongation to minimise needle movement

Question 118

prevalence of morphologic variation at C6 and C7 and what does that mean clinically

Answer 118

28.6% in one study concerning warmbloods

Homologous morphologic variation is common in the caudal cervical spine of Warmbloods. This variation does not appear to be associated with clinical signs and in fact is less frequent in clinical cases than in control animals

Question 119

Use of threshold testing for tactile sensory, mechanical and thermal nociceptive stimulations in the face of horses

Answer 119

The combined application of all three modalities enables comprehensive evaluation of the equine trigeminal sensory function with good reliability

Question 120

What is myokymia

Answer 120

muscle twitching

continuous undulating movements

Myokymia is a clinical sign of neuromyotonia.

Question 121

Neuromyotonia is clinically characterized by

Answer 121

a combination of muscle twitching or myokymia, persistent muscle contraction, muscle stiffness, impaired muscle relaxation, and continuous electromyographic activity.27–29 Clinical and electromyographic examinations are important to differentiate neuromyotonia and myokymia, although these clinical entities can occur simultaneously.

Question 122

differentiate neuromyotonia and myokymia

Answer 122

Electromyographic recordings in cases of neuromyotonia disclose spontaneous, continuous, irregularly occurring doublet, triplet, or multiplet single or partial motor unit discharges, firing at a high intraburst frequency (30-300 Hz). Spontaneous discharges at the highest frequencies (150-300 Hz) that occur in prolonged bursts, and which begin and end abruptly and often wane in amplitude, have been called neuromyotonic discharges. Each burst of electrical activity usually occurs irregularly, with variable interburst frequencies (from 100 milliseconds to >10 seconds). Myokymic discharges tend to occur at lower frequencies (often <60 Hz), often as doublets, triplets, or multiplets, in short semi-rhythmic bursts, followed by a few seconds of silence.6,28 The horse described here showed clinical and electromyographic signs of myokymia and neuromyotonia, and a mixed neurogenic-myopathic histological pattern also was observed.

Question 123

clinical signs of myotonia

Answer 123

Affected animals have gait impairment, muscle hypertrophy, stiffness, and hypertonicity. Myotonia can occur concurrently or without muscular dystrophy.

Question 124

How does myotonia look like during EMG?

Answer 124

Myotonic potentials are a common finding in these animals and represent spontaneous repetitive discharges with waxing and waning amplitudes and frequencies

Question 125

What is Dystrophic myotonia

Answer 125

a progressive disorder initially characterized by generalized myotonia with hypertrophy and hypertonicity of the larger hind limb and forelimb proximal muscles. It is associated with a dystrophic histological pattern (ie, sarcoplasmic masses, ringed fibers, moth-eaten fibers, adipose and connective tissue inflammation). A few cases have been described in horses.