Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Equine (Poppy) > Neurology > Flashcards

Neurology Flashcards

1
Q

What abnormality is indicated with abnormal states of wakefulness (mentation)?

A

Abnormal cerebral function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How to induce somnelence in a foal (without chemical sedation)

A

Madigan squeeze (usually only works once)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Signs of cerebellar disease

A

Intention tremor (incompatible with life)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Disease indicated with a head tilt

A

Vestibular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Testing optic nerve function

A

Menace response (blink = facial nerve and withdrawal = central processing e.g. cerebral and cerebellar, learned and not present for first 14 days of life)
Pupillary light reflex (direct and consensual, oculomotor nerve/III)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is this horse suffering from?

A

Anisocoria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What can ptosis be a clinical sign for?

A

Neurological (oculomotor control) or ocular pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Cranial nerve associated with horizontal nystagmus

A

III and VI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Cranial nerve associated with vertical nystagmus

A

III and IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cranial nerves responsible for facial sensation

A

Trigeminal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Cranial nerve for palpebral/corneal sensation

A

Trigeminal/V

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Cranial nerve for facial expression

A

Facial nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What cranial nerve dysfunction is this horse suffering from?

A

Left facial nerve dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What cranial nerve dysfunction is this horse suffering from?

A

Vestibulocochlear/8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Function of glossopharyngeal nerve

A

Sensory, taste (posterior 1/3)
Motor to tongue (extrinsic muscle)
Motor to pharynx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How to test hypoglossal nerve function

A

Controls intrinsic muscles of tongue and pharynx so give animal food

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Testing spinal reflexes

A

Panniculus reflex
Anal tone
Tail tone
Foot placement (may just be obedient/sluggish horse)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Scale for gait assessment in neurological cases

A

Mayhew ataxia scale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Spinal ataxias with normal mentation

A

Cervical Vertebral Compressive Myelopathy (CVCM)
Equine Herpes Virus (EHV-1)
Equine protozoal myeloencephalopathy (EPM)
Vitamin E related ataxias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Differentiating ataxia from lameness

A

Irregularly irregular vs regularly irregular
Ataxia evaluation on walk (more obvious) vs lameness on trot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Spinal ataxia

A

Proprioceptive deficits
Crossing, abduction, circumduction, knuckling (ascending pathways)
Foot dragging, stumbling (descending pathways)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Is ataxia an abnormality of ascending or descending tracts?

A

Refers specifically to proprioceptive deficits (ascending tracts/sensory) but they run so close to UMN tracts (descending tracts/motor) that normally both occur simultaneously

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Vestibular ataxia

A

Head tilt, leaning, falling to one side, wide base stance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Cerebellar ataxia

A

Loss of modulatory effect of cerebellum
Wide base stance
Dysmetria (hyper/hypo)
No proprioceptive deficits
No weakness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Dysmetria

A

Inability to control the distance, speed, and range of motion necessary to perform smoothly coordinated movements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Vitamin E related ataxias

A

Equine degenerative myeloencephalopathy/axonal dystrophy (EDM)
Equine Motoneuron disease (weakness)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Why does compression of spinal cord lead to more proprioceptive deficits than motor deficits?

A

Sensory/ascending pathways are more superficial in spinal cord (deeper pressure required for motor deficits)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What disease does ‘Wobbler’s syndrome’ refer to?

A

Cervical vertebral compressive myelopathy/CVCM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Most common non-infectious neurologic disease condition in horses

A

CVCM/wobbler’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Clinical presentation of Wobbler’s

A

Moderate to severe ataxia (inability to perform, unsafe)
Typically diagnosed early in life (<4yo), but can manifest later in life (OA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Factors in Wobblers (multifactorial disease)

A

Genetic predisposition
Dietary imbalances
Rapid growth rates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Clinical signs of wobblers

A

Ataxia, weakness and spasticity
Generally symmetrical deficits, sometimes asymmetric (OA)
Truncal sway, crossing and interferences when turning, hindlimb pivoting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Diagnosis of wobblers

A

Radiograph (intervertebral ratios on good laterolateral)
Radiographic myelography (dorsal contrast column, total dural diameter, DCC reduction)
CT myelography and MRI (transverse plane images, better definition of tissues, anaesthesia risk)
(Strongest diagnostic test is post mortem, others have low sensitivity/specificity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What does a walking tail pull assess?

A

Upper motor neurone

35
Q

What does a standing tail pull assess?

A

Lower motor neurone

36
Q

Medical treatment of wobblers in young horses

A

NSAIDs +/- steroids (acute phase)
Diet restrictions (limit overnutrition with protein/starch, maintain correct Ca:P, avoid excess copper)

37
Q

Medical treatment of wobblers in adult horses

A

NSAIDs +/- steroids
Mesotherapy and exercises
Intra-articular facet joint injection (OA)

38
Q

Surgical treatment of wobblers

A

Ventral interbody vertebral fusion

39
Q

What level of improvement is seen with surgical treatment of wobblers?

A

1-2 grades

40
Q

Clinical signs of equine herpes virus causing spinal ataxia

A

Previous respiratory disease 6-10d prior (intermittent cough, serous nasal discharge, conjunctivitis)
Symmetric ataxia ± weakness (bladder distension/urinary incontinence, poor anal tone, recumbency)
Inconsistent fever
Chorioretinitis

41
Q

Usual progression of equine herpes virus

A

Respiratory disease 6-10 days prior (primary replication, replicates in LNs, establishes in trigeminal ganglia/respiratory lymphoid organs, secondary replication in secondary organs e.g. pregnant uterus, CNS, eye)
Stabilisation over 24 hours
Majority of horses fully recover

42
Q

Diagnosis of equine herpes virus causing spinal ataxia

A

Signalment (high risk e.g. movement, resp. disease)
Nasopharyngeal swab PCR
Whole blood PCR
Serology (complement fixation test if unvaccinated)
CSF tap (often unrewarding, xanthochromia and increased protein)

43
Q

Treatment for equine herpes virus

A

Prevent spread (isolate, monitor temperatures, 21 days movement restriction, biosecurity)
Valacyclovir 30mg/kg q 8h for 48h, then 20mg/kg q12h
Low-molecular heparin SC
NSAIDs/Steroids? (Treat respiratory disease early enough = less fever = less viraemia = lower likelihood of neurological disease)

44
Q

Infectious agent in equine protozoal myeloencephalopathy

A

Sarcocystis neurona (and Neospora hughesi)

45
Q

Key features of equine protozoal myeloencephalopathy

A

Definitive host opossum
Horse only aberrant host
Migration of schizonts and merozoites to CNS
N. hughensi transplacental too?
USA and South America most common (S. neurona prevalence 10-90%, N. hughesi prevalence 10%)
Ingestion of contaminated feed (concentrate/hay/grass)
Seropositive ≠ aetiology

46
Q

Clinical signs of equine protozoal myeloencephalitis

A

Any possible neurological sign/insidious or acute
Asymmetric ataxia with/without cranial nerve deficits (VIII, VII, X)
Weakness and muscle atrophy (gluteus, biceps femoris, epaxial musculature)
Poor anal tone, “cauda equina syndrome”

47
Q

Diagnosis of equine protozoal myeloencephalitis

A

Challenging but intrathecal production of antibody (S.neurona): SAG
Serum: CSF ratio< 1
Do not trust serum + results in areas of high prevalence
Routine CSF analysis often unrewarding: high protein and high WBC rare
Clinical signs + area with opossums
Response to treatment?
Post-mortem: histopathology confirmation

48
Q

Treatment of equine protozoal myeloencephalitis

A

Pyrimethamine and sulfadiazine (90 days treatment)
Diclazuril/ponazuril (60 day treatment)
NSAIDs/Steroids acute severe stages
Long term Vitamin E supplementation
Relapse in 10% of cases

49
Q

Prevention of EPM

A

Avoid exposure to opossum faeces
Daily administration of low dose Ponazuril/diclazuril/Nitazoxanide

50
Q

Diffuse degenerative disease of the equine spinal cords and caudal portion of the brainstem and primarily affects young horses (<1yo), but can take longer to diagnose (<5yo)

A

Equine degenerative myeloencephalopathy/axonal dystrophy

51
Q

Clinical signs of equine degenerative myeloencephalopathy/axonal dystrophy

A

Insidious onset of symmetric spasticity, ataxia, and paresis
Pelvic limbs are usually more severely affected than the thoracic limbs
Some horses will have decease menace response , lethargy or behavioural changes
Long-term poor performance

52
Q

Cause of equine degenerative myeloencephalopathy

A

Low Vit E<2ug/ml but non responsive to treatment

53
Q

Prevention of equine degenerative myeloencephalopathy

A

Supplementation in following circumstances:
Some breed lines might be predisposed (QH?)
Areas with Low VitE
Last month pregnancy and nursing period

54
Q

Fast phase of nystagmus away or towards lesion side?

A

Away

55
Q

Acquired progressive neurodegenerative disease that affects neurons in brain and spinal cord (LMD)

A

Equine motor neuron disease

56
Q

Trigger for equine motor neurone disease

A

Vitamin E deficiency for longer than 18 months

57
Q

Risk factors for equine motor neuron disease

A

Excess copper and no access to green forage

58
Q

Equine motor neuron disease clinical signs

A

Generalized weakness (slow gait, dragging toe, base-narrow stance)
Shifting weight between limbs
Muscle fasciculations of anti-gravitatory muscles (T>P)
Generalized sweating
Neurogenic muscle atrophy (Type I fibres)
Pigmentary retinopathy

59
Q

Diagnostics for equine motor neuron disease

A

Low Vit E in serum <2ug/,l
Confirmatory: sacrocaudalis dorsalis medialis muscle (tail) shows myelinated axons degeneration
Post mortem: loss of motor neurons from ventral horn spinal cord

60
Q

Treatment of equine motor neuron disease

A

Vitamin E (water dispersible better): 5000-7000 IU/day for 3 months

61
Q

Involuntary sudden violent repetitive movements of the head dorso-ventrally, horizontally or rotatory

A

Head shaking

62
Q

Presentations of headshaking

A

Nose rubbing on stationary objects /floor/scratching
Lower head carriage
Snorting, sneezing, snoring
Excessive nasal discharge

63
Q

Most common cause of head shaking

A

Idiopathic

64
Q

Symptomatic head shaking

A

Cause can be found and withdrawal permanently removes the problem

65
Q

Top cause of persistent head shaking

A

Trigeminal nerve/V mediated: facial/head noxious sensations

66
Q

Signalment for head shaking

A

Young geldings 5-12yo
Pleasure horses and sport horses
April-summer
95% during ridden exercise, 53% during lunging, 26% when turnout in pasture and 12% stabled

67
Q

Triggers for head shaking

A

Photic (bright light, photoperiod, cystic corpora nigra, floaters in posterior/anterior chamber)
Allergic (rhinitis)
Sinusitis, otitis (Trombicula autumnalis), GP mycosis
Structural: skull fractures, dental disease, THO, TMJ (hyperesthesia)
Bit bridle

68
Q

Diagnostic plan for head shaking

A

Aim is to identify potential triggers:
Physical exam/environment/ management
Ocular exam
Dental exam
Upper airway endoscopy including GP
Nerve blocks (infraorbital and maxillary)
Skull x-rays/CT
Otoscopy

69
Q

Medical treatment of head shaking

A

Cyproheptadine 0.3mg/kg PO BID
Carbamazepine (4mg/kg)
Gabapentin (25mg/kg q 8h)
Steroids (inhaled)
Magnesium sulphate 40mg/kg)
Antihistamine drugs
Melatonin 4 mg/kg BW, q6h
Nose nets
Ocular sunglasses
Bridles bit

70
Q

Surgical management of head shaking

A

All have poor response
(Infraorbital neurectomy with cryotherapy, chemical sclerosis, caudal compression of infraorbital nerve)

71
Q

Other therapies for head shaking

A

EquiPENNS (percutaneous nerve stimulation)
Electro-acupuncture

72
Q

Spectrum of CND disorders characterized by episodes of excessive sleepiness, muscular weakness and REM onset sleep

A

Narcolepsy

73
Q

Episodes of collapse due to lack of regular resting/sleep

A

Sleep deprivation

74
Q

Reasons for sleep deprivation

A

Chronic arthritis
Chronic pain
Fear to environment

75
Q

Narcolepsy cause

A

Dysfunctional orexin system: hypocretins 1-2 and hypothalamic GABA neurons
Familiar in several breeds

76
Q

Clinical signs of sleep deprivation and narcolepsy

A

Staggering, lowering the head and neck, buckling of the thoracic limbs, kneeling posture, flaccidity of lips
Unexplained abrasions wounds (knees, lips)
Kneeling when tightening the girth

77
Q

Diagnosis of sleep deprivation or narcolepsy

A

Age, recent changes in environment, stable, barn, premises, wild life
Concurrent disease: arthritis: back, hocks, carpus, PPID
Quality of bedding, tight rungs in winter
True narcolepsy: rule out differentials

78
Q

Treatment of sleep deprivation and narcolepsy

A

Bute-trial
Thick bedding
Large stable
Inside barn
Remove rugs

79
Q

Progressive, chronic neuromuscular disease in horses characterized bygait abnormalities when backing up, trembling of the tail while held erect, trembling of the thigh muscles and a flexed and trembling hind limb when held

A

Shivers

80
Q

Cause of shivers

A

Damage of the deep cerebellar nuclei (function is fine-tune of planned movements, flexion and extension activated at the same time)

81
Q

Clinical signs of shivers

A

Backing manoeuvre: hyperextension of hindlimbs
Inability of picking up the hind limbs: offers contralateral limb, hyperextension
Normal ambulation otherwise: walk forward, trot, cantering, performing

82
Q

Key features of shivers

A

Normally starts around 5 years of age
Normally progressive and performance limiting
Rule out other conditions: upper fixation of patella, stifle OA, sacro-iliac pain

83
Q

Prognosis of shivers

A

Guarded, no treatment

Equine (Poppy) (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions