Neurological exam of the horse and neuro diseases Flashcards
(94 cards)
1
Q
What does hypermetria, intetion tremors and weakness point towards
A
Cerebellar lesion
2
Q
What is the first question to ask during neurological exam
A
Are there are cranial nerve signs present
3
Q
What virus can have neurological and respiratory presentations
A
Equine herpes virus
4
Q
What localisation would blindness, dementia, seizure, mild ataxia point towards
A
forebrain
5
Q
What location would gait CN signs, gait deficits, tetraparesis and altered consciousness point towards
A
Brainstem
6
Q
If we see tail/bladder paralysis, perineal hyperalgesia what localistion of lesion does this point towards
A
Sacral
7
Q
What behavioural abnormalities might we see with forebrain disease
A
Yawning
Wandering
Psychosis
Circling
Head pressing
Seizures
8
Q
What are some possible causes of forebrain dysfunction
A
Trauma to head
Hyponatraemia, hypoglycaemia
Hepatic encephalopathy hyperammoniaemia
Toxicity
Space occupying lesions
Intracarotd drug administration
9
Q
How quickly will a horse react to an intra carotid drug injection
A
Immediately off the needle
10
Q
How can we classify seizures
A
Either generalised or focal
Then focal split into simple focal or complex focal +/- secondary generalisation
11
Q
Difference between simple focal and complex focal seizures
A
Complex focal has impaired consciousness
12
Q
Signs of a generalised seizure
A
Loss of consciousness
Tonic clonic contraction
Limb paddling
Loss of continenance
Jaw clamping
13
Q
WHen might strabismus be normal
A
NEwborn foals
14
Q
What CN dysfunction causes a ventrolateral strabismus
A
CN III oculomotor nerve
15
Q
What CN dysfunction causes a medial strabismus
A
CN VI
16
Q
What CN dysfunction causes a dorsal strabismus
A
CN IV
17
Q
Pathway for pupillary light response
A
Photoreceptors –> optic enrve –> optic chiasm with 90% decussation –> contralateral optic tract –> visual cortex + some to pretectal nuclei to prasymp CN III nuclei for pupil constriction (some crossing back here hence consensual response)
18
Q
Which nerve is responsible for pupil constriction in PLR
A
CN III
19
Q
Difference between dazzle response and PLR
A
Dazzle response uses a higher level of response with rostral colliculi but sitll subcortical
ONly gone in very bad disease
20
Q
What do we expect to see with the swinging light test
A
Both pupils constrict with more constriction when light moved to contralateral eye
21
Q
PAlpebral reflex
A
Touch medial canthus; stimulates CNV trigeminal sensory branch
Get blink response via Facial nerve motor
22
Q
What is important to remember about the menace response
A
IT is learned; absent for a few days
23
Q
What might a slow, abnormal menace indicate
A
cerebellar disease since cerebellum has a role in coordination and smoothing the menace response
24
Q
What nerve controls head position and if there is a lesion which way does it go
A
VEstibulocochlear
Fall towards side of lesion
25
What are classic signs of facial nerve paralysis
Ear droop on that side
Eyelid droop
Muzzle twisted towards normal side
26
What is the cervicofacial reflex
Tap neck at C1-C2 and look for grimace from the corner of the mouth; tests C1/C2 nd CNVII
27
What would an animal with proprioceptive defects look like when walked; esp with head raised to move line of sight
Excessively floaty forelimbs
28
What disease would be shown up when horse blindfolded and asked to move
Proprioceptive defects with vestibular disease
29
What does it mean about deficits if proprioception is abnormal at rest vs when moving
If abnormal at rest = conscious deficits
If when moving = unconscious proprioceptiv deficits
30
Grades 0-5 ataxia
0 = normal
1 = mild neuro deficits only under special circumstances e.g walking in circles
2 = mild neuro deficits at all times/giats
3 = moderate deficits at all times
4 = severe deficits with tendency to buckle, stumble, trip, fall
5 = recumbent
31
Basic signs with UMN lesion
Paresis
Hyperreflexia
32
Basic signs with LMN lesion
Paralysis/paresis
Neurogenic muscle atrophy
Loss of reflexes
33
What would we see with gait at C-C5 lesion
UMN signs in fore and hindlimbs with hindlimbs looking worse
34
Wha would we see with C6-T2 lesion
LMN signs in forelimbs
UMN signs in hindlimbs
So forelimbs look 'worse'
35
What would we see with T3-L3 lesion
Normal forelimbs, UMN signs to hind lims
36
What would we see with L4-S1 lesoni
Normal forelimbs
LMN signs to hindlimbs
37
What would we see with sacral/caudal lesions
Normal forelimbs
Normal or LMN signs in hing limbs
Cauda eqiune sign e.g bladder issues
38
What is coup and contrecoup
Where the brain is shaken inside the skull causing acceleration decelleration injuries which cause bruising and swelling to cranial and caudal aspects of the brain
39
What effect can be seen over 1-2 weeks after coup contrecoup with head trauma
Loss of vision due to optic nerve twang during swinging and slow degeneration
40
What happens in a rectus capitus muscle avulsion
caused by hyperextension of neck
Muscle can rip off temporal bone causing huge haemorrhage, nose bleed
41
Why might we choose to take CSF from the lumbosacral space after a head injury
Because there is a risk of cerebellar herniation if the ICP is raised and atlanto-occipital puncture is done
42
Things to consider in approach to head trauma (treatment)
CT best
Manage seizures
Reduce intracranial pressure if needed; hypertonic saline
NSAIDs
Vit E
Steroids
O2 if needed
43
How to manage seizures in a horse
Diazepam, phenobarbital, KBr
44
Signs of hyperammonaemia causing cerebral oedema
Yawning
Dullness
Wandering
Head pressing
Aggression
45
What two things can cause hyperammonaemia
Liver disease
Intestinal disease
46
Approach to dealing with hyperammonaemia
Deal with underlying disease
Add lactulose to convert ammonia to ammonium salt so less is absorbed
Antimicrobials to change gut slora
47
Why do horses with equine motor neuron disease look worse when standing than walking
Because the postural type 1 muscles are most affected since these have higher oxidative requirement
48
Aetiology of equine motor neuron disease
Vitamin E deficiency causing oxidative neuronal damage and neurogenic muscle atrophy
= neurodegenerative disease causing LMN signs
49
What things can lead to vitamin E deficiency in equine motor neuron disease
Dietary: lack of access to fresh pasture
INability to absorb vit E due to GI tract disease
Excess dietary copper
50
Treatment and prognosis of equine motor neuron disease
Treat with non-synthetic vitamin E suppleentation
40% improve a lot, 40% stabilise and 20% deteriorate
= guarded prognossi
51
Diagnosis of equine motor neuron disease
Muscle biopsy for neurogenic atrophy
Can measure vitamine E serum concentration but this is not specicifc
52
Clinical signs of equine motor neuron disease
Weakness and muscle atrophy
Narrow base stance
WEight shifting
Pigment retinopathy
53
What is polyneuritis equi
Granulomatous infiltration of extradural cauda equina
Signs = tail/anus/perineum/bladder/rectum paralysis as with caudal equine syndrome
+ cranila nerve signs
Poor prognosis
54
What cranial nerve signs are esp common with polyneuritis equi
facial nerve, trigeminal, vestibular signs
55
What is temporohyoid osteoarthropathy
Degenerative change at the temporohyoid articulartion; due to osseous proliferation at the joint and then pathological fractures of petrous temporal bone
--> Causes damage to vestibulo-cochlear (+/- facial nerve)
56
What are some possible aetiologies of temporohyoid osteoarthropathy
Spread of infection from middle/inner ear
Non-septic degenerative joint disease
Trauma
57
Clinical signs of temporohyoid osteoarthropathy + diagnosis
Vestibulocochlear nerve dysfunction: head tilt, nystagmus, dizziness, ataxia, dysphagia
Facial nerve dysfunction: asymmetry, corneal ulcers from exposure keratopathy
Diagnosis = seeing endoscopic thickening of articulation of sytohyoid bone in dorsal guttural pouch
[+ could do CT; or DV plain X-ray and compare the two sides]
58
Treatment of temporohyoid osteoarthropathy
Anti-inflammatories
+/- antibiotics
Surgical ceratohyoidectomy
59
What is Horner's syndrome and what are the signs
Interruption of the sympathetic innervation to face
Lesion can be anywhere on pathway e.g neck, guttural pouch, cranial thorax
Signs = sweating, miosis, ptosis
60
What is shivers
Muscular condition of unknown origin where limbs with shivering flexed hindlimb posture
Progressive with no treatment; can progress to forelimbs
61
3 post-anaesthetic neuro complications and their signs
Facial neve paralysis: muzzle deviated away from lesion, may see corneal ulcers due to exposure keratitis (reduced saliva and tear production)
Radial nerve paralysis: dropped elbow and unable to bear weight
Spinal cord malacia; dog sitting with flaccid paralysis caudal to lesion after GA
62
Whta is the cause of cervical vertebral stenotic myelopathy in young vs old horses and which areas are affected
Young horses: malformation of vertebral canal/ligaments/cervical vertebrae
--> Affects mid cervical spine
Old horses: osteoarthritic change of articular process joints
-> Affects caudal cervical spin
63
What is static vs dynamic cervical vertebral stenotic myelopathy
Static = where there is compression in a neutral position
Dynamic = compression when the head is flexed/extended
64
Why are hindlimbs affected first in cervical vertebral stenotic myelopathy
Because the spincerebellar tracts are more peripherally located so they are compressed first
65
What is the classic history/signalment for young horses with cervical vertebral stenotic myelopathy
= after a period of recent rapid growth
First sign is reduced proprioception which progresses to paresis or spasticity
66
Diagnosis of cervical vertebral stenotic myelopathy
CT best
Myelography/plain radiographs
Take flaexed and neutral positions because dynamic lesions may only be noticed when neck is flexed
Compression normally visible from dorsoventrally
67
Conservative management of CVSM
Anti-inflammatories
Restrict diet in younf horses
Restrict exercise
68
Clinical signs of tetanus
Third eyelid protrusion
Saw horse rigid stance
Raised tailhead
Lockjaw
Dysphagia
Miosis
Hyperaesthesa
69
How does tetanus work
Clostridim tetani contaminated wounds and produces tetanospasmin and tetanolysin toxins
Tetanospasmin undergoes haematogenous spread then retrograde transport up peripheral nerves to inhibtiory interneuros and prevents synaptic release of GABA
Get spastic paralysi s
70
Treatment of tetanus
Give antitoxin
Clean and debride wound, make it aerobic to eliminate C tetani
Antibiotics; use metrnodazole
Tetanus toxoid vaccine (at distal site to anti-toxin)
Control muscle spasm: methocarbamol, diazepam, alpha 2 agonist sedation
Nursing care
71
Vaccine protocol for tetanus
Vaccinate at 6 months with 2 vaccines 4 weeks apart
Boost in last trimester to protect foal
72
When might we give tetanus antitoxin as tetanus prevention
For risk periods e.g any unvaccinated horse where wound/castration/abscess noticed
73
What are the possible ways to get botulism
Ingesting spores so toxin produced in GI tract
Infection of wound with C botulinum
Ingestion of pre-formed toxin in forage (spoiled food)
74
Pathogenesis of botulism
Haematogenous spread of toxin, binds to NMJ terminal and blocks ACh release causing flaccid paralysis
75
Pathogenesis of equine herpes myeloencephalitis
Ubiquitous EHV1 enters resp epithelial cells --> lymphocytes/monocytes --> lymphatics/blood --> dissemination
Have. background of respiraotry disease then sudden onset of neurosigns
76
Signs with equine herpes myeloencephalitis
Ataxia esp in hindlimbs
Bladder distension/incontinence, penile protrusion, flaccid tail and anus
77
Treatment for equine herpes myeloencephalitis
Supportive care with NSAIDs, nrusing
Antivirals; valacyclovir, gangiclovir 1
78
Why do we not use acyclovir in horses
Low bioavailability and poor effect
79
Prognosis for equine herpesvirus myeloencephalitis
50-70% survival
May have neuro deficits for life
80
How does vaccination help with equine herpesvirus myeloencephalitis
Decreases overal environmental load of EHV1
BUT does not protect against EHV myeloecenpahtiis
81
What is west nile virus
Flavivirus not currently in UK but with potential to come here as we have mosquito vector
82
Which species are amplifier hosts for west nile virus and which are dead end
Birds are amplifiers
Horses are dead end
83
Clinical signs of west nile virus
Most show no signs
Dullness, facial paralysis, dsphagia, muscle fasciculations, hyperexcitabiltiy. ataxia, recumbency
84
What is neuroborreliosis and what are the clinical signs
Disease due to borrelia burgdorferis which is transmitted by ixodes ticks
Causes muscle atropgy/weight loss, CN dysfunction ataxia, shifting lameness, pyrexia, joint effusio
85
Why must we take care with diagnosing Lyme disease from serology
ARound 1/3 of healthy horses are seropositive so may not be relevant to signs
86
As well as antibody titre what can we do to help diagnose neuroborreliosis
Use silver stain on joint effusion fluid and look for spirochaetes
87
Treatment of neuroborreliosis
MOnths long tetracyclines; starting with IV oxytet and moving to oral doxy
88
What type of virus is rabies
lyssavirus
89
Incubation time and clinical signs of rabies
INcubation = 2 weeks to several months
Signs: ataxia, pyrexia, colic, lethargy, self-mutilation, aggression
= fatal
90
What is equine protozoal myeloencephalitis
Protozoal disease from sarcocystis neurona and Neospora nughesia
affects white and grey matter at any CNS site
See atypical lameness, can get seizures, ataxia, dyphaia
NOT in UK
91
Why is monitoring horses important to assess western/eastern/venezualean equine encephalitis rsisk to human health
Horses are sentinel hosts so can be used to predict risk to humansS
92
Signs of western/eastern/venezualean equine encephaliti
Pyrexia, dullness, cirlcing/head pressing, dysphagia, paralysis, death
93
What causes western/eastern/venezualean equine encephaliti
Togavirus
Primary reservoir in birds/rodents
94
