Neurology Flashcards
(83 cards)
1
Q
What abnormality is indicated with abnormal states of wakefulness (mentation)?
A
Abnormal cerebral function
2
Q
How to induce somnelence in a foal (without chemical sedation)
A
Madigan squeeze (usually only works once)
3
Q
Signs of cerebellar disease
A
Intention tremor (incompatible with life)
4
Q
Disease indicated with a head tilt
A
Vestibular
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)
6
Q
What is this horse suffering from?
A
Anisocoria
7
Q
What can ptosis be a clinical sign for?
A
Neurological (oculomotor control) or ocular pain
8
Q
Cranial nerve associated with horizontal nystagmus
A
III and VI
9
Q
Cranial nerve associated with vertical nystagmus
A
III and IV
10
Q
Cranial nerves responsible for facial sensation
A
Trigeminal
11
Q
Cranial nerve for palpebral/corneal sensation
A
Trigeminal/V
12
Q
Cranial nerve for facial expression
A
Facial nerve
13
Q
What cranial nerve dysfunction is this horse suffering from?
A
Left facial nerve dysfunction
14
Q
What cranial nerve dysfunction is this horse suffering from?
A
Vestibulocochlear/8
15
Q
Function of glossopharyngeal nerve
A
Sensory, taste (posterior 1/3)
Motor to tongue (extrinsic muscle)
Motor to pharynx
16
Q
How to test hypoglossal nerve function
A
Controls intrinsic muscles of tongue and pharynx so give animal food
17
Q
Testing spinal reflexes
A
Panniculus reflex
Anal tone
Tail tone
Foot placement (may just be obedient/sluggish horse)
18
Q
Scale for gait assessment in neurological cases
A
Mayhew ataxia scale
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
20
Q
Differentiating ataxia from lameness
A
Irregularly irregular vs regularly irregular
Ataxia evaluation on walk (more obvious) vs lameness on trot
21
Q
Spinal ataxia
A
Proprioceptive deficits
Crossing, abduction, circumduction, knuckling (ascending pathways)
Foot dragging, stumbling (descending pathways)
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
23
Q
Vestibular ataxia
A
Head tilt, leaning, falling to one side, wide base stance
24
Q
Cerebellar ataxia
A
Loss of modulatory effect of cerebellum
Wide base stance
Dysmetria (hyper/hypo)
No proprioceptive deficits
No weakness
25
Dysmetria
Inability to control the distance, speed, and range of motion necessary to perform smoothly coordinated movements
26
Vitamin E related ataxias
Equine degenerative myeloencephalopathy/axonal dystrophy (EDM)
Equine Motoneuron disease (weakness)
27
Why does compression of spinal cord lead to more proprioceptive deficits than motor deficits?
Sensory/ascending pathways are more superficial in spinal cord (deeper pressure required for motor deficits)
28
What disease does 'Wobbler's syndrome' refer to?
Cervical vertebral compressive myelopathy/CVCM
29
Most common non-infectious neurologic disease condition in horses
CVCM/wobbler's
30
Clinical presentation of Wobbler's
Moderate to severe ataxia (inability to perform, unsafe)
Typically diagnosed early in life (<4yo), but can manifest later in life (OA)
31
Factors in Wobblers (multifactorial disease)
Genetic predisposition
Dietary imbalances
Rapid growth rates
32
Clinical signs of wobblers
Ataxia, weakness and spasticity
Generally symmetrical deficits, sometimes asymmetric (OA)
Truncal sway, crossing and interferences when turning, hindlimb pivoting
33
Diagnosis of wobblers
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)
34
What does a walking tail pull assess?
Upper motor neurone
35
What does a standing tail pull assess?
Lower motor neurone
36
Medical treatment of wobblers in young horses
NSAIDs +/- steroids (acute phase)
Diet restrictions (limit overnutrition with protein/starch, maintain correct Ca:P, avoid excess copper)
37
Medical treatment of wobblers in adult horses
NSAIDs +/- steroids
Mesotherapy and exercises
Intra-articular facet joint injection (OA)
38
Surgical treatment of wobblers
Ventral interbody vertebral fusion
39
What level of improvement is seen with surgical treatment of wobblers?
1-2 grades
40
Clinical signs of equine herpes virus causing spinal ataxia
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
Usual progression of equine herpes virus
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
Diagnosis of equine herpes virus causing spinal ataxia
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
Treatment for equine herpes virus
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
Infectious agent in equine protozoal myeloencephalopathy
Sarcocystis neurona (and Neospora hughesi)
45
Key features of equine protozoal myeloencephalopathy
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
Clinical signs of equine protozoal myeloencephalitis
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
Diagnosis of equine protozoal myeloencephalitis
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
Treatment of equine protozoal myeloencephalitis
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
Prevention of EPM
Avoid exposure to opossum faeces
Daily administration of low dose Ponazuril/diclazuril/Nitazoxanide
50
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)
Equine degenerative myeloencephalopathy/axonal dystrophy
51
Clinical signs of equine degenerative myeloencephalopathy/axonal dystrophy
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
Cause of equine degenerative myeloencephalopathy
Low Vit E<2ug/ml but non responsive to treatment
53
Prevention of equine degenerative myeloencephalopathy
Supplementation in following circumstances:
Some breed lines might be predisposed (QH?)
Areas with Low VitE
Last month pregnancy and nursing period
54
Fast phase of nystagmus away or towards lesion side?
Away
55
Acquired progressive neurodegenerative disease that affects neurons in brain and spinal cord (LMD)
Equine motor neuron disease
56
Trigger for equine motor neurone disease
Vitamin E deficiency for longer than 18 months
57
Risk factors for equine motor neuron disease
Excess copper and no access to green forage
58
Equine motor neuron disease clinical signs
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
Diagnostics for equine motor neuron disease
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
Treatment of equine motor neuron disease
Vitamin E (water dispersible better): 5000-7000 IU/day for 3 months
61
Involuntary sudden violent repetitive movements of the head dorso-ventrally, horizontally or rotatory
Head shaking
62
Presentations of headshaking
Nose rubbing on stationary objects /floor/scratching
Lower head carriage
Snorting, sneezing, snoring
Excessive nasal discharge
63
Most common cause of head shaking
Idiopathic
64
Symptomatic head shaking
Cause can be found and withdrawal permanently removes the problem
65
Top cause of persistent head shaking
Trigeminal nerve/V mediated: facial/head noxious sensations
66
Signalment for head shaking
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
Triggers for head shaking
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
Diagnostic plan for head shaking
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
Medical treatment of head shaking
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
Surgical management of head shaking
All have poor response
(Infraorbital neurectomy with cryotherapy, chemical sclerosis, caudal compression of infraorbital nerve)
71
Other therapies for head shaking
EquiPENNS (percutaneous nerve stimulation)
Electro-acupuncture
72
Spectrum of CND disorders characterized by episodes of excessive sleepiness, muscular weakness and REM onset sleep
Narcolepsy
73
Episodes of collapse due to lack of regular resting/sleep
Sleep deprivation
74
Reasons for sleep deprivation
Chronic arthritis
Chronic pain
Fear to environment
75
Narcolepsy cause
Dysfunctional orexin system: hypocretins 1-2 and hypothalamic GABA neurons
Familiar in several breeds
76
Clinical signs of sleep deprivation and narcolepsy
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
Diagnosis of sleep deprivation or narcolepsy
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
Treatment of sleep deprivation and narcolepsy
Bute-trial
Thick bedding
Large stable
Inside barn
Remove rugs
79
Progressive, chronic neuromuscular disease in horses characterized by gait 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
Shivers
80
Cause of shivers
Damage of the deep cerebellar nuclei (function is fine-tune of planned movements, flexion and extension activated at the same time)
81
Clinical signs of shivers
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
Key features of shivers
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
Prognosis of shivers
Guarded, no treatment
