Neurology Flashcards
1
Q
Where are UMN located?
A
Travels within the CNS from the brain to synapse with circuits involving the LMN/peripheral nerves
2
Q
Where are LMN located?
A
- Projects outside the CNS to synapse with muscle
- In most instances, this equates to the motor nerves in the PNS
3
Q
What happens if an UMN is damaged?
A
- The distal portion (separated from the cell body) degenerates
- UMN input is mainly inhibitory, so reflex arcs
- Existing reflexes are stronger and easier to elicit
- Some normally inhibited reflexes become apparent
- Muscle tone increases
4
Q
What is the result of UMN dysfunction?
A
- Reduced movement (paresis) or no movement (plegia)
- Increased tone
- Present or increased reflexes
- Disuse atrophy occurs with time
5
Q
What happens if a LMN is damaged?
A
- The distal portion (separated from the cell body) degenerates
- The innervated muscles cannot be stimulated to contract
- The innervated muscle fibres die
- Existing reflexes are weaker or absent
- Muscle tone reduces
- Muscle mass decreased rapidly and severely
6
Q
What is the result of LMN dysfunction?
A
PRAT:
- Paresis or plegia
- Reflexes are reduced
- Atrophy is severe and rapid
- Tone reduced
7
Q
Distinguish the speed of neurogenic atrophy from LMN disease and disuse atrophy from orthopaedic disease.
A
Neurogenic - occurs over days
Disuse - occurs over weeks
8
Q
Distinguish the severity of neurogenic atrophy from LMN disease and disuse atrophy from orthopaedic disease.
A
Neurogenic - can be severe, may cause loss of entire muscle mas
Disuse - usually mild to moderate, never causes loss of all the muscle mass
9
Q
Distinguish the distribution of neurogenic atrophy from LMN disease and disuse atrophy from orthopaedic disease.
A
Neurogenic - localised to the innervated muscles of the affected nerve or nerves (so usually focal, but may be generalised with generalised nerve disease)
Disuse - not localised to the distribution of a specific nerve
10
Q
What are the cardinal neurological presentations that prompt neurological examination?
A
- Abnormal gait, stumbling or falling
- Abnormalities of the head and face
- Apparent blindness or deafness
- Abnormal behaviour – particularly episodic
- Exercise intolerance
- Incontinence abnormal behaviour
11
Q
Why can responses be used as a screening test?
A
Responses involve the forebrain, nerves, brains and spinal cord so act as a screening test - they cannot localise alone
12
Q
What structures of the nervous system do responses use?
A
Sensory nerve
Ascending tracts through spinal cord
Ascending tracts in brainstem
Forebrain
Descending tracts in brainstem
Cerebellum
Descending tracts in spinal cord
Motor nerve
Muscle
13
Q
What is the hopping response most useful for?
A
Forelimbs
14
Q
How is the hopping response tested?
A
- Look at foot
- Push body over to obscure it
- Foot should come back just into view
- Abnormal is limb knuckling over or having late or heavy movements
15
Q
What is the paw placement response the most useful for?
A
Pelvic limbs
16
Q
How is paw placement responses tested?
A
- Keep body still and stabilise with hand under caudal abdomen (pelvic limbs) or under thorax (thoracic limbs)
- Turn over paw, trying not to touch pads
- Foot should immediately be replaced
- Sometimes let you do this so need to move this weight off and off this. some dogs do not like feet being touched so don’t touch pads as to not obscure results
17
Q
How are reflexes used in localisation?
A
- Reflexes do not involve the forebrain
- Reflexes test well-defined sections of the PNS and CNS so they are used to pinpoint lesion localisation
18
Q
What does the perineal reflex test?
A
Pudendal nerve and S1-3 spinal cord
19
Q
How is perineal reflex tested?
A
Pinch perineum or tap ischium
Anus constricts, tail moves ventrally
This habituates sometimes so the first reflex is the most reliable
20
Q
What does the pelvic limb withdrawal reflex test?
A
Sciatic nerve and L6-S2 spinal cord
21
Q
How is pelvic limb withdrawal reflex tested?
A
- Pinch toe or interdigital web. Test first standing up and then test on their side if movement is not perfect
- All joints flex if normal – flex hip, flex hock, flex digits
- Hip and stifle flexors have large mass and lots of innervation so are only lost with severe LMN disease – focus attention on hock and digits
22
Q
What does the cutaneous trunci reflex test?
A
Segmental nerve, spinal cord cranial to this up to T1, lateral thoracic nerve
23
Q
How is the cutaneous trunci reflex tested?
A
- Pinch skin starting at ilial wing, going cranially
- See bilateral contraction of cutaneous trunci muscle if normal or cranial to lesion
- Not a straightforward reflex arc. Multiple inputs along both sides of spine have only 1 common output
24
Q
What does the thoracic limb withdrawal reflex test?
A
Sensory = median and ulnar nerves
Motor = musculocutaneous, median and ulnar nerves
25
How is the thoracic limb withdrawal reflex tested?
- Pinch toes or interdigital web on thoracic limbs
- All joints flex if normal
- Abnormal reaction is to flex shoulder and then kick backwards with the hindlimbs
26
How are C1-5 differentiated from C6-T2?
Thoracic Limb neurogenic muscle atrophy – this will only be seen in C6-T2 lesions
Gait – C1-C5 lesions have very different gait abnormalities from C6-T2 lesions
27
What are the C1-C5 typical gait abnormalities?
- Thoracic limbs are protracted and extended fully before making contact with the ground
- Goose/high-stepping or floating gait
28
What are the C6-T2 typical gait abnormalities?
- Short strides in thoracic limbs
- Longer, ataxic strides in pelvic limbs
- Two-engine gait
29
What is spinal shock?
Spinal shock is the temporary reduction in spinal reflexes caudal to an acute (severe) spinal cord injury occurring cranial usually to the affected reflex arcs. Resolves after a few days in dogs, patella very soon and then cervical region last
30
Explain the mechanisms of spinal shock.
- A severe, acute spinal cord injury occurs can temporarily lose reflexes caudal to an acute lesion
- This causes UMN dysfunction – loss or reduction in limb movement
- Loss of UMN facilitation temporarily also reduces LMN function
- Decreased tone, decreased reflexes and no reduced mass (functional lesion)
31
What are the typical T3-L3 gait disturbances?
- Dogs with little or no pelvic limb movement have some T3-L3 involvement, regardless of pelvic limb reflexes
- T3/L3 and spinal shock will look the same as a disease affecting T3/L3 AND L4/S2
32
How is each area of neurolocalisation characterised?
Forebrain - sensory, motor
Brainstem - reticular activating system, cranial nerve arcs, vestibular nuclei, motor and sensory pathways
Cerebellum - regulates movement, vestibular connections
Cranial nerves - specific sensory and motor
33
What are the 3 important tests for assessing forebrain function?
Behavioural responses (mentation)
Proprioceptive responses – hopping and paw placement
The menace response
34
What is always a sign of forebrain disease?
Seizures are always a sign of forebrain disease – abrupt changes in behaviour that then return to normal
35
How are proprioceptive responses used to assess for forebrain function?
- Proprioceptive responses on one side of the body are regulated by the contralateral forebrain
- Some forebrain diseases can only have mild gait disturbances, but dramatic proprioceptive deficits
36
What does the menace response screen function in?
Eye
Optic tract
Forebrain
Cerebellum
Brainstem
Facial nerve
37
Which cranial nerves have no reliable tests?
I/olfactory
IV/trochlear
XI/accessory spinal
38
What does head tilt test in neuro cases?
Vestibular nuclei in brainstem, CNVII and cerebellum
39
How are head tilts assessed for function?
- Always look for head tilt when dog walks towards you
- Look at horizontal axis of eyes when distracted (e.g. when walking)
- Interpretation – persistent tilt indicates cerebellar, brainstem (or possibly thalamic) dysfunction
40
What does masticatory muscle mass and tone test?
Mandibular branch of the trigeminal
41
How is masticatory muscle mass and tone assessed?
hould not be able to palpate inner edge of zygomatic arch = LMN lesion of V (mandibular) if unilateral, LMN lesion or myopathy if bilateral
Animals should be able to hold mouth closed and open them fully:
- Dropped jaw (inability to close) = bilateral trigeminal paresis
- Trismus (inability to open) almost always as masticatory muscle disease
42
How is the facial nerve/VII tested?
Watch, eyebrows, earls lips, nares and muzzle for movement
If there is no spontaneous movement at appropriate times, there is likely to be a facial nerve lesion
43
What can palpebral fissure narrowing be due to?
Can be III (oculomotor) or VII (facial) but almost always sympathetic denervation (Horner’s syndrome)
44
What can 3rd eyelid protrusion be due to?
- Sympathetic denervation (Horner’s – has other signs too)
- Retro bulbar mass (pushes eye and third eyelid forward - cannot retro pulse)
- Masticatory muscle atrophy (enophthalmus)
45
How are the pupils examined?
Examine in light and also use reflective tapetum to highlight pupil in dark
Mydriasis (inappropriate dilation) – large pupil will not constrict in light
Miosis (inappropriate constriction) – small pupil will not dilate in the dark
46
Explain how Horner's syndrome develops.
Lose sympathetic innervation to 1 of the eyes – can’t dilate, vasoconstrict, globe goes back as sympathetic tone keeps it forward. Often cannot get enophthalmos, but has scleral/conjunctival vasodilation, 3rd eyelid protrusion and small pupil.
47
What are the differential diagnoses for miosis?
Horner’s
Uveitis
Reflex constriction with corneal pain
48
What does the palpebral reflex assess?
Trigeminal V, brainstem and facial VII
49
How is the palpebral reflex assessed?
- Tap skin beside eye or stimulate cornea with clean material - medial canthus more reliable than lateral
- No blink = facial, brainstem or trigeminal lesion
- Medial canthus = maxillary trigeminal
- Cornea = ophthalmic trigeminal
50
What is the result and what is observed from a trigeminal lesion?
Sensory absent, motor intact
- No response to touching face
- Will move spontaneously
- May have masticatory atrophy or paresis
51
What is the result and what is observed from a facial lesion?
Sensory intact, motor to palpebral muscles absent
- Reduced spontaneous movement
- Other motor reflexes (head movement, globe retraction) intact and unaffected
52
Could a lesion give both facial and trigeminal dysfunction?
Yes but would need to affect other brainstem function too
53
How is the menace conducted?
- Make sure they are looking at you
- Hold head to cover contralateral eye
- Make sure they can blink by tapping face
- Make sure they are looking at you (again by tapping face)
- Then make small movement from far away
54
What may an absent menace response indicate?
Lesions in retina, optic tract, contralateral forebrain, ipsilateral cerebellum, brainstem or facial nerve – so very good screening test as it tests a lot of components
55
How does visual fixation test sight?
- Ask an animal to watch an object
- Should see eye or head movement
- Retinal, optic tract or forebrain lesions cause loss of visual fixation
- Requires attention so false negatives often seen in difficult to restrain patients
56
What does PLR assess?
Optic/II and oculomotor/III
57
What does absent PLR be due to?
Absent PLR can be due to a lesion in the retina, optic tract, brainstem, oculomotor nerve or iris
Consensual PLR = contralateral eye’s response to light
58
What are the differential diagnoses for the loss of PLR?
- Fear and anxiety (visual animal) – sympathetic tone overwhelms response
- Iris atrophy (visual animal) – constrict just not very much
- Retinal disease (blind animal)
- Optic tract disease (blind animal)
- Oculomotor disease (visual animal)
59
What is lack of eye movement due to?
- Vestibular input on side being moved towards is deficient (test for other vestibular signs)
- Extra-ocular muscles or nerves innervating them are affected
60
What is abnormal/pathological nystagmus a dysfunction of?
Vestibulocochlear/VIII and cerebellum
61
How is abnormal/pathological nystagmus assessed for?
Observe eyes for rhythmic movement with slow (pathological) and fast (corrective) phase when head is not moving
Nystagmus when the head is still (spontaneous nystagmus) indicates cerebellar or vestibular system disease
62
How is abnormal/positional nystagmus assessed for?
Some nystagmus is only visible when animals are in an abnormal position
Must test positional nystagmus but lying of back and looking in eye
63
When is assessment of strabismus helpful?
Not useful in isolation except to raise suspicion of hydrocephalus is bilateral
64
Why might there be strabismus?
- Abnormal skin/lid position (most common)
- Vestibular dysfunction
- Orbital disease (e.g. hydrocephalus)
65
What does ability to swallow test for?
The gag reflex, glossopharyngeal/IX, vagus/X and hypoglossal/XII
IX and X are both motor and sensory in this reflex
66
How is ability to swallow assessed?
- Open mouth and try to touch larynx
- Failure to push fingers out of way with tongue and pharynx movement is abnormal
67
How can owner assessment be useful for assessment of barking and swallowing?
- The owner’s assessment of swallowing and barking is more reliable than the gag reflex
- Gag reflex is only one part of the caudal brainstem function
- IX and X and XII also control swallowing and vocalisation
68
What is hypoglossal nerve dysfunction indicative of?
Mono-neuropathy
69
How are forebrain and cerebellar problems distinguished?
If no menace but can see with visual fixation = cerebellar
But because no menace and no visual tracking = forebrain
70
Why might there be loss of neurological function from degeneration?
Cell death in diseases of the nervous system. Examples: cognitive dysfunction
Hyperplasia and subsequent compression in diseases of tissues around the brain and spinal cord. Examples: disc protrusion
71
What is the 5 finger rule for localisation for a differential diagnosis?
Signalment
Onset
Progression
Symmetry
Pain
72
What is the onset for neurological aetiologies?
- Peracute – seconds to minutes
- Acute – minutes to hours (usually <24 hours)
- Subacute – 24-48 hours
- Insidious – over 48 hours, where you don’t know if they have reached their worse yet or not
73
What is progression a measure of?
Whether the most severe signs have already been reached
74
Describe the symmetry of vascular neurological aetiologies.
Very strongly asymmetrical
But blood borne or genetic diseases will affect all of brain or spinal cord equally
75
What are some strongly asymmetrical neurological aetiologies?
Occur when the cells affected are randomly selected – neoplasia, granulomas
76
What are some mildly asymmetrical neurological aetiologies?
Occur when there are multiple foci of disease (inflammatory diseases) or extensive secondary effects of the disease (most compressive diseases)
77
What are some symmetrical neurological aetiologies?
Occur when cells on both sides have an equal chance of being affected (blood borne diseases such as toxins or nutritional deficiencies or genetic diseases)
78
Where are nociceptors located?
- The spinal cord (and brain) does not contain any nociceptors
- But the spinal cord is surrounding by structure like the meninges, periosteum (and disc), which contain a lot of nociceptors
- Muscles, connective tissue etc contain some nociceptors
- Nerve roots have no nociceptors where they exit the vertebral canal but discharge if compressed or inflamed, sending input to the pain-sensing areas of the brain even though the receptors are not stimulated
79
What are the top 3 disease by localisation of the brain?
Meningioma/Glioma
Autoimmune encephalitis
Idipoathic epilepsy
80
What are the top 3 disease by localisation of the cranial nerves?
Idiopathic neuropathy
Nerve tumour
Inflammation of adjacent structures – otitis media/interna
81
What are the top 3 disease by localisation of the spinal cord?
Disc disease
Compression from vertebral structures
Infarction – fibrocartilaginous embolism
82
What are the top 2 disease by localisation of the spinal nerves?
- Nerve tumour
- Trauma (e.g. brachial plexus avulsion)
83
When is central disease likely?
- Obtunded – reticular activating system is affected
- Paretic – ascending and descending motor tracts are affected
Suspect peripheral disease if all signs can be explained by only one nerve not working
84
What are the steps taken once a vascular aetiology has been determined?
- Check for coagulopathy (e.g. lungworm)
- Check for hypercoagulability (e.g. Cushing's)
- Look for causes of spontaneous bleeding – lungworm, thrombocytopaenia
- Monitor for recovery if we cannot find an underlying cause with vascular
85
How is the size of peripheral fibres affected by compression?
- Larger, peripheral fibres more vulnerable than smaller, central ones
- Equally vulnerable to compression
- First fibres affected are the larger ones controlling proprioception
- Then smaller ones causing ataxia and paresis/plegia (recoverable)
- The smallest fibres causing plegia and lack of pain perception (unlikely to recover)
86
How is pain perceived by the nervous system?
- A behavioural response indicates pain perception; withdrawing the leg is a reflex only and can occur even if the spinal cord is severed
- Withdrawing is not a sign of sensation
- Deep pain negative = those with no reaction
87
What do the signs of brain injury reflect?
Signs often reflect localisation not severity
88
How is brain injury severity measured?
Use modified Glasgow coma score to monitor brain injury severity, which evaluated movement/motor activity, reflexes and consciousness
15-18 = good, 9-14 = guarded, 3-8 = grave
89
What is the Cushing's reflex?
Increased blood pressure with decreased heart rate in a comatose dog is likely to indicate raised intracranial pressure. Only see this in unconscious animals
90
Outline the stages of the Cushing's reflex to explain how this case be used to measure brain injury severity.
1. ICP increases - local brain perfusion reduced, sympathetic response to increase blood flow (increase HR and BP)
2. Hypertension - increased blood pressure sensed by peripheral baroreceptors, reflex slowing of heart rate
3. Bradycardia – pathognomonic hypertension and bradycardia
91
Describe a normal segment of the vertebral discs.
- Well hydrated nucleus pulposis
- Normal disc space width
Degenerating disc – normal for discs to get whiter and degenerate with age
92
Describe an abnormal segment of a degenerating vertebral disc.
- Dehydration
- Proliferative replacement of nucleus with collagen
- Loss of fluid signal on MRI - asymptomatic
93
Describe a segment of a late degenerative disc.
- Further collagen deposits within disc
- Some tearing and healing of anulus
- Proliferative changes of bone around segment
- Enthesiophyte formation (spondylosis)
- Spondylosis is a normal ageing feature of the spine and only, very rarely, causes nerve entrapment. It is not an indicator of spinal disease
94
Name the 3 types of disc disease.
- Non-compressive nucleus pulposis extrusion (traumatic)
- Disc extrusion
- Disc protrusion
95
What are non-compression nucleus pulposis extrusion disc diseases?
- Normal segment subjected to supramaximal force
- Small fragment of hydrated nucleus herniates and contuses cord with no compression (as its is only a small amount of contusion material)
96
Where are non-compression nucleus pulposis extrusion dis diseases localised?
T3-L3 > C1-T2 > L4-S2
97
What are disc extrusion diseases?
- Nucleus pulposis undergoes chondroid degeneration (chondrodystrophic breeds)
- Calcified nucleus extrudes under every-day pressure and causes compression and contusion
98
Where are disc extrusion diseases localised?
T3-L3 > C1-T2 > L4-S2
99
What are disc protrusion diseases?
- Continued, progressive fibroid degeneration occurs
- Anulus degenerates, tears and hypertrophies causing progressive compression
100
Where are disc protrusion diseases localised?
C1-T2 > T3-L3 = L4-S2
101
How is thoracolumbar disc disease conservatively managed?
Rest:
- Aim to prevent further material extruding
- At-risk period seems up to 5 weeks
- Prevent provocative movements that extend back
NSAIDs if spinal pain
102
How long does thoracolumbar disc disease take to heal from conservative management?
Contusion, oedema resolves over 3-6 weeks
Compression, revascularisation takes place over weeks to months
103
Which disc diseases do not benefit from decompressive surgery?
Acute non compressive hydrate nucleus pulposis extrusions
104
What surgery is used for ventrolateral material compression?
Mini-hemilaminectomy
105
What surgery is used for lateral or dorsolateral material compression?
Hemilaminectomy
106
What surgery is used for ventral material compression?
Corpectomy - take away a bit of ventral body to pull compression down
107
Do we operate on dogs with disc disease that can walk?
No, little benefit
108
What surgery can reduce risk of recurrence of disc disease?
Fenestration of adjacent discs during surgery of discs reduces recurrence – window in edge of the disc to allow nucleus to come out laterally rather than dorsally where the spinal cord is
109
How are thoracolumbar disc protrusions treated?
- Non-surgical management suitable for mildly affected cases as may start to resolve in time if the main injury is traumatic (from ruptured annulus)
- Surgery indicated for progressive cases
110
How is cervical disc extrusion treated?
- Rest may cause resolution of signs
- Surgical treatment is usually ventral slot
111
What are the degenerative changes in disc protrusions/wobbler?
- Flaval ligament hypertrophy
- Dorsal ligament hypertrophy
- Disc prolapse
112
What are the changes in degenerative hyperplasia/wobbler?
- Vertebral malformation (less common)
- Articular facet hypertrophy (more common)
113
How is wobblers treated?
- Decompression – ventral slot
- Distraction fusion – implants
114
What is myelomalacia?
- Progressive spinal cord death
- Fatal, untreatable and irreversible
- Occurs 1-5 days after any spinal cord injury in 20% of pain negative dogs
115
What are the clinical signs of myelomalacia?
- Agitation/lethargy
- Hyperthermia/hypothermia
- Ascending cutaneous trunci reflex cut-off
116
What is the pathogenesis of ischaemic myelopathy?
- Usually fibrocartilaginous/neoplastic/septic/parasitic embolism
- Embolus usually lodges in ventral artery
- Near degenerate disc, but how the material gets into the arteries is unclear
- Fibrocartilaginous emboli behave almost identically to acute non compressive nucleus pulposis extrusions
117
What is the presentation of haemorrhagic myelopathy?
- Acute onset, not painful and non progressive
- Often multifocal
- Usually also see scleral, mucosal or subdermal haemorrhages
- Most commonly caused by angiostrongylus
118
What is done with animals with laceration of the spinal cord?
We recommend PTS for most pain negative fractures
Animals with intact sensation have a similar outcome to type 1 disc extrusions
119
What is degenerative myelopathy?
- Non-painful, progressive neuronal death in spinal cord
- Possibly an analogue of ALS (motor neuron disease) in humans
120
How is degenerative myelopathy diagnosed?
- Genetic testing (SOD1 mutation is the most common risk factor) – but some dogs can have this without the mutation
- Normal spinal cord with T3/L3 localisation on imaging
121
What is arachnoid fibrosis/arachnoid diverticulum?
- Non-painful, progressive obstruction to CSF flow around spinal cord
- Adhesions in the arachnoid space
- Due to a meningeal injury or developmental anomaly
- Walking but faecally and/or urinary incontinence
122
How is arachnoid fibrosis/diverticulum treated?
- May not need treatment if static
- Usually progressive so surgical treatment involving removing adhesions, stabilising spine or diverting CSF flow is necessary
123
What are vertebral malformations caused by?
- Wide array of defects in bone formation can cause deformity of the spine
- Cause damage by instability, direct compression or adjacent disc protrusion
124
How are vertebral malformations treated?
- May not need treatment if static
- Usually progressive so surgical treatment involving stabilisaton (with decompression) is necessary for those
125
Which spinal tumours have fair and guarded prognoses?
- Meningioma (surgery)
- Myeloma (chemo)
- Guarded prognosis – nephroblastoma (surgery and radiation) and lymphoma (chemo)
- Hopeless prognosis – all others
126
What are the causes of myelitis and meningiomyelitis in dogs and cats?
Dogs have immune mediated > neospora > toxoplasma
Cats have FIP > immune mediated > toxoplasma
127
What is steroid responsive meningitis/arteritis SRMA?
- Immune mediated inflammation of the meninges and small arteries
- Systemic disease with pyrexia and lethargy
- Classic neck pain
128
How is steroid responsive meningitis/arteritis SRMA diagnosed?
- Elevated body temperature, circulated neutrophils and c-reactive protein
- Cisternal spinal fluid analysis (usually) shows huge neutrophilic pleocytosis
129
How is steroid responsive meningitis/arteritis SRMA treated?
Immune suppression
130
What is the pathogenesis of atlantoaxial subluxation?
- Failure of dens (that geos into the vertebral canal, stops bones moving too far apart) to form properly or traumatic fracture
- Can cause neurological deficits too
- Subluxation of C1/2 is very painful
131
What are the differentials for neck pain?
<2yo = SRMA or AA luxation
>2yo = disc, disco or tumour
132
What is discospondylitis?
- Haematogenous spread of bacteria or fungus to vertebrae allows local invasion into discs
- Poor blood supply and immune surveillance allows slow development of abscess in disc
- Spreads back to end plates and vertebrae
133
How is discospondylitis diagnosed?
- Systemic disease so weight loss, pyrexia, poor condition all strongly supportive
- Radiographs good for diagnosis after around 3 weeks of signs
- MRI and CT may be better
- Disc aspirate diagnostic, blood and urine culture supportive
- Brucella testing in dogs that have travelled or been imported is essential
134
How is discospondylitis treated?
Appropriate antibiotics with debridement surgical stabilisation if very painful
135
How do lumbosacral compressions compare with thoracolumbar compressions.
- Compression of spinal cord causes paresis and ataxia
- Compression of nerve roots causes severe pain as well as LMN paresis
136
What does degenerative hypertrophy in the lumbosacral region cause?
Degenerative hypertrophy of any structure or extrusion of disc material causes compression of the L7 and/or sacral and caudal nerve roots
137
What does compression of the sacral roots cause?
Tail flaccidity and incontinence
138
How is the cauda equine compressed?
By a combination of degenerative changes in the vertebrae and/or traumatic damage from a disc extrusion giving a varied onset and progression
139
How is lumbosacral disease treated?
- Rest
- Epidural steroids
- Surgical stabilsation and/or decompression
140
How do cerebrovascular accidents cause strokes?
Thrombus or thromboembolism > vessel occlusion > ischaemic stroke
Vessel rupture > haemorrhagic stroke
141
How are cerebrovascular accidents diagnosed?
- MRI – sharply defined intra-axial lesion
- CSF often unremarkable
- Rule out underlying causes (endocrine, neoplastic, cardiac, lungworm)
142
How are cerebrovascular accidents treated?
- Treat underlying cause
- Supportive care
143
How does haemorrhage from cerebrovascular accidents cause death?
Haemorrhage in the CNS > clot > gets bigger > increased intracranial pressure > death
144
What should you be suspicious of if there is sudden onset haemorrhage?
Lungworm
145
What are cerebrovascular accidents treated?
Treat underlying cause
Supportive care
146
What are the sudden onset cerebellar signs?
- Ataxia, hypermetria
- Progressive symmetrical
- Toxic, inflammatory
147
What are the changes in the brain due to metronidazole toxicity?
Acute, progressive. In the brain, particular change – 2 areas of necrosis at the level of the vestibular nuclei, severe lesions. Stop this treatment and the lesions disappear.
148
What is a characteristics of idiopathic cerebellitis?
CSF is increased in WBC count but not dramatically – so may not be inflammatory but some respond to anti-inflammatory treatment
149
What are the causes of meningoencephalitis?
- Inflammatory non infectious – MUO (meningoencephalitis of unknown origin)
- FIP, distemper
- Fungal e.g. cryptococcus
- Protozoal – toxoplasma (cat), Neospora (dogs)
- Typically insidious onset-some infectious encephalitis – Neospora in dogs and FIP in cats) can be more chronic
150
How is non-infectious meningioencephalitis diagnosed?
- Rule out metabolic causes first
- MRI – multifocal lesions
- CSF – mononuclear pleocytosis
- Rule out common infections
151
How is non-infectious meningioencephalitis treated?
Immunosuppression
152
What is pathophysiology of FIP?
Immune mediated reaction to virus
153
What are the clinical signs of FIP?
With/without systemic signs, central nervous system only infection
154
How is FIP diagnosed?
- A negative blood coronavirus serology helps you rule out FIP, while a positive serology is only evidence of exposure to the coronavirus
- Bloods – anaemia, hyperglobulinemia
- MRI – secondary hydrocephalus
- CSF – neutrophilic pleocytosis
- PCR on CSF
155
How is FIP treated?
Palliative with steroids, promising anti-viral treatment
156
How are brain tumours treated?
- Palliative – prednisolone
- Surgery – decompression
- And/or radiation
- And/or chemotherapy (lymphoma)
157
What is the prognosis of brain tumour treatment?
Poor for lymphoma, guarded for most gliomas, good for most meningiomas (solid and grows slowly, grows in meninges outside the brain so can remove)
158
What is the features of physical examination for congenital hydrocephalus?
Domed shaped head
Downcast eyes
Fontanelles still open
159
How is congenital hydrocephalus treated?
Palliative – prednisolone
Surgery – ventriculoperitoneal shunt to defer fluid from the brain to outside of the brain into a tube that will come outside of the body and re-enter into the abdomen
160
How is degenerative brain disease diagnosed?
- Bloods – often normal
- MRI – can be normal
- CSF – often normal
- Metabolic urine or blood screening
- Genetic testing
161
What is the treatment and prognosis of degenerative brain disease?
Supportive, poor long term
162
How and why do seizures occur?
- GABA is part of the inhibitory system
- Glutamine is part of the excitatory system
- Normal brain activity is a balance between inhibitory and excitatory potentials
- Seizures are excessive/synchronous firing of multiple groups of neurones
163
Define seizure.
Transient occurrence of signs due to abnormal excessive or synchronous neuronal activity in the brain
164
Define epilepsy.
Recurrence of seizures
165
Define interictal phase.
Seizure >5 min or 2 seizures without complete recovery in between. Emergency treatment
166
Define cluster seizure.
2 or more seizures in a 24h period with complete recovery in-between. Emergency treatment
167
What are the consequences of seizures?
Loses of nutrients and oxygen In the brain causing cerebral oedema and necrosis of the brain
168
What aspects of the nervous system do seizures affect?
- Sensory – blindness secondary to seizure that will return in a few hours
- Motor – ataxia
- Autonomic
- Consciousness
- Emotional state
- Memory
- Cognition
- Behaviour
169
What are the phases of seizures?
Prodromal phase
Aura
Ictus (proper seizure)
Post ictal phase
170
What are the types of generalised seizures?
Involves several parts of the brain:
Tonic-clonic
Tonic
Clonic
Myoclonic
Atonic
Absence
171
What are partial/focal seizures?
Involving only 1 part of the brain:
- Simple (unimpaired consciousness) – can call to animal and responds
- Complex (impaired consciousness) – can call to animal can they do not respond
172
What can 14% of seizures by triggered by?
Stress
Excitement
Flashing lights
Noises
173
What are the characteristic of seizures?
- Abrupt onset
- Rarely triggers
- Last less than 2 minutes
- Consciousness is impaired stereotypic
- Autonomic signs
- Post ictal signs
174
What are the episodes mimicking seizures?
Pain
Syncope
Movement disorders
Behavioural – compulsive disorders
175
What are the possible aetiologies of seizures of patients less than 1 year old?
- Viral, bacterial, protozoal, rickettsial
- Hydrocephalus, lissencephaly
- Hypoglycaemia, portosystemic shunt
- Storage disorders, inborn metabolic errors
176
What are the possible aetiologies of seizures of patients 1-6 years old?
- MUO
- Idiopathic epilepsy
177
What are the possible aetiologies of seizures of patients 6-8 years old?
- Infarction, haemorrhage
- Hypoglycaemia (insulinoma)
- Idiopathic epilepsy
- Neoplasia
178
How are toxic extracranial causes of seizures treated?
Treatment – specific antidotes, often supportive
179
How are metabolic extracranial causes of seizures treated?
Hypoglycaemia – young dog, toy breed, Addison’s, liver dysfunction
Hepatic encephalopathy – young dog = congenital portosystemic shunt, old dog = liver failure
Electrolytes – lactating bitch = hypocalcaemia
180
What is the presentation of structural intracranial causes of seizures?
- Abnormal neurological exam for structural causes
- Brain tumours, cerebrovascular, MUO, infectious encephalitis, hydrocephalus
- Changes in mental status/behaviour, walking in circles/head pressing
- Deficits in postural reactions contralateral to the lesion
- Visual deficits (contralateral to the lesion)
- Decreased/absent facial sensation (contralateral to the lesion)
- Decreased/absent menace response (contralateral to the lesion)
181
What is idiopathic epilepsy?
Idiopathic epilepsy = no cause found, suspected
Less than 5% risk of finding a structural brain lesion in an animal between 6m and 6y with normal inter-ictal neuro exam and normal metabolic investigation
182
What is tier 1 evidence for idiopathic epilepsy?
- Recurrent seizures
- Animal between 6 months and 6 years
- Normal inter-ictal neurological examination
- Normal metabolic investigation
183
What is tier 2 evidence for idiopathic epilepsy?
- Normal MRI scan of the brain
- Normal CSF
184
What is tier 3 evidence for idiopathic epilepsy?
Abnormal electroencephalography (EEG) during seizure
185
Classifying the causes of a seizuring patient based on neurological examination?
Normal exam = idiopathic epilepsy (interictal period), silent forebrain lesion, reactive epilepsy
Abnormal exam = structural epilepsy, idiopathic epilepsy (post-ictal period), reactive epilepsy
186
What blood work is done for the seizuring patient?
- Haematology – infection, anaemia, polycythaemia
- Blood chemistry – glucose, electrolytes, liver/kidney profile CK and AST
- Liver function – NH3, bile acids
- Coagulation – fibrinogen
187
What is looked for on serology for a seizuring patient?
FIP, FIV, FeLV, distemper
Sepsis
Toxoplasma, neospora
Cryptosporidium
188
What is looked for on imaging for a seizuring patient?
Metastasis check
Cardiac disease
Lung disease (verminosis)
Liver disease
189
What is the minimum database for a seizuring patient?
Haematology, biochemistry, GLU, BAST
190
What are the goals for managing recurrent seizures?
- Reduce seizure frequency
- Reduce severity
- With acceptable side effects
- With acceptable costs
191
What is assessed in distant examination for neurological disorders in cattle?
- Demeanour
- Musculoskeletal signs – standing/recumbent, ability to walk
- Central deficits
192
How are the cranial nerves in cattle assessed?
- Facial nerve – facial asymmetry. Any dropping of the ear, drooping of the eye, lop sided muzzle, lolling tongue, any head asymmetry
- Head tilt from nerve 8/vestibulocochlear nerve
- Lingual paralysis from nerve 12/hypoglossal
- Drooling and inability to swallow from nerve 9/glossopharyngeal nerve
- Test facial sensation – nerve 5/trigeminal. Poking them in the nose, face or ear to test for response
193
How are the eyes and vision assessed in cattle?
- Menace – ability to see and move the eyelids
- PLR – difficult to do in farm animals as we need to get environmental dark enough
- Ocular abnormalities – nystagmus, strabismus
194
How are the peripheral nerves of cattle assessed?
Sensation, motor control. Artery forceps between digits for sensation. Someway of lifting the animal to test motor control
195
What is the pathogenesis of listeriosis in cattle?
- Listeria monocytogenes in spoiled feed – poorly preserved silage, soil content
- Exposure to soil
- Entry via oral mucosa > trigeminal nerve > brain stem > meningoencephalitis
- 2 week delay between ingestion and signs
- Also abortion/uveitis
196
What are the clinical signs of listeriosis in cattle?
- Depression with/without pyrexia
- With/without weight loss
- With/without dehydration
197
What do the neurological signs of listeriosis in cattle depend on?
Depend on cranial nerves affected by microabscesses
198
How might listeriosis in cattle affect the cranial nerves
Trigeminal - weakness in masticatory muscles
Facial - drooping ear, eyelid, muzzle, asymmetry
Vestibulocochlear - head tilt, ataxia, circling
Glossopharyngeal and vagus - dysphagia
Hypoglossal - protrusion or weakness of tongue
199
How is listeriosis in cattle treated?
- Nursing care – dehydration/ability to eat
- NSAIDs
- Systemic antibiotics – gram positive, can cross BBB, high dose penicillin
200
What is the prognosis of listeriosis in cattle?
May have some permanent neurological deficits
Zoonosis – milk from infected cows should be discarded
201
What are the behavioural changes of bovine spongiform encephalopathy?
Apprehension
Change in temperament - aggression
202
What are the nervous signs of bovine spongiform encephalopathy?
- Hyperaesthesia – kicking at milking
- Compulsive licking
- Nibbling response when scratched
- Bruxism
- Ear tremors/twitching
203
What are the hindlimb motor deficits from bovine spongiform encephalopathy?
Ataxia
Hypermetria
Paresis
Knuckling
Stumbling
Recumbency
204
What are the systemic changes associated with bovine spongiform encephalopathy?
Loss of body condition in the face of a usually normal appetite
205
What is the pathogenesis of brain abscesses in cattle?
Either originates from
- Dehorning sinusitis
- Haematogenous spread from another site of infection
Abscess development is usually slower in onset than acute meningioencephalitis
206
What are the clinical signs of brain abscesses in cattle?
- Location determines signs
- Cranial nerve deficits
- Head-pressing
- Depression
- Central blindness
207
How are brain abscesses in cattle treated?
Antibiotics – long duration often required
NSAIDs
May be left with permanent neurological deficits
208
What is the pathogenesis of spinal abscesses in cattle?
- T. Pyogenes, F. necrophorum
- Haematogenous spread
209
What are the clinical signs of spinal abscesses in cattle?
- Progressive ataxia
- Incontinence
- Poor anal and tail tone
- Perineal hypoalgesia
- Rectal exam useful
210
What are the clinical signs of vertebral trauma in cattle?
- Acute onset stiffness
- Ataxia
- Paralysis of the hindlimbs
211
How is vertebral trauma in cattle treated?
- Nursing – lifting, deep straw bed
- NSAIDS
212
Why is BVD a herd level disease?
Affects fertility and calf health
213
Name the 2 congenital abnormalities caused by BVD in young cattle.
Internal hydrocephalus
Cerebellar hypoplasia
No treatment for either
214
What is the aetiology of internal hydrocephalus in calves?
BVD most common cause, can be inherited (bulldog calves have a combination of inherited abnormalities including internal hydrocephalus)
215
What are the clinical signs of internal hydrocephalus in calves?
- Neurological deficits (depression/ataxia)
- With/without abnormal skull shape
- Born weak and die in a few days or still born
216
What is the aetiology of cerebellar hypoplasia in calves?
BVD most common cause, can be inherited
217
What are the clinical signs of cerebellar hypoplasia in calves?
- Neurological deficits (largely proprioceptive)
- Ataxia with/without wide based stance
- Intention tremor with/without hypermetria
- Inability to stand
218
What is the pathogenesis of schmallenberg disease in calves?
Vector born (midge)
Before pregnancy leads to dam immunity
During pregnancy leads to
- Congenital malformations with/without abortion/still birth
- Neurological signs in the foetus
219
What are the clinical signs of schmallenberg disease in calves?
- Neurological signs
- ‘Dummy’ presentation
- Bilateral blindness
- Ataxia
- Recumbency
- Inability to suck
220
What is cerebral anoxia in calves?
With/without prolonged birth/dystocia with/without assistance
Usually unable to stand and CNS signs
221
How is cerebral anoxia in calves treated?
- IV fluids spiked with bicarbonate to correct metabolic acidosis
- Colostrum by stomach tube
- Nursing
222
What is the aetiology of cerebrocortical necrosis/CCN in calves?
- Thiamine is normally formed by rumen flora in sufficient quantities
- Thiamine is essential for glucose metabolism
- Glucose is most important energy source for brain
- Thiaminases produced by certain rumenal bacteria and in some plants
- Lack of uptake in SI following enteritis
- Thiamine deficiency (lack of energy source for cerebrum) leads to cerebral oedema, pressure necrosis due to oedema, and necrosis of cerebral cortex
223
Why are young cattle more at risk of cerebrocortical necrosis/CCN?
Young cattle are most at risk due to rapid growth and lower natural thiamine levels
224
What are the clinical signs of cerebrocortical necrosis/CCN?
Initially – depressed, bilateral central blindness, aimless wandering
Progressing to – ataxia, muscle tremors
Ending with – collapse, convulsions, opisthotonus, mortality 25-50%,normal temperature and normal rumen activity
225
How is cerebrocortical necrosis/CCN diagnosed in calves?
- Clinical signs
- Response to treatment with Thiamine (Vit B1)
- PME
226
What are the post mortem findings of cerebrocortical necrosis/CCN?
- Generally good body condition
- Swelling and coning of brain into foramen magnum (due to cerebral oedema)
- Gyri yellow and soft (due to necrosis)
- Fluorescence under UV light
227
What are the differential diagnoses of cerebrocortical necrosis/CCN in calves?
- Lead poisoning
- Hypovitaminosis A
- Bilateral central blindness
- Papilloedema
- Meningitis – usually pyrexic, nystagmus
- Listeriosis – asymmetrical cranial nerve deficits, unilateral, central blindness, may be pyrexic
228
How is cerebrocortical necrosis/CCN treated in calves?
- High doses of Thiamine (vit B1) IV (every 3 hours for 5 occasions)
- Frusemide to reduce cerebral oedema
229
How is cerebrocortical necrosis/CCN in calves treated?
- Thiamine IM in the face of an outbreak
- Correct nutrition >60% forage in diet
230
What is the aetiology of meningitis in calves?
- Most commonly E coli
- Low level of protection – failure of passive transfer
- Sequel to neonatal septicaemia with/without navel/joint ill
231
What are the systemic signs of meningitis in calves?
Lethargy
Loss of suck reflex
Collapse
Signs of shock
With/without pyrexia
232
What are the neurological signs of meningitis in calves?
Bilateral nystagmus
Star gazing
Head pressing
Tremors
Opisthotonus
Convulsions
233
How is meningitis in calves treated?
Systemic antibiotics - must be able to cross the BBB. First line – Amoxycillin, TMPS or Florfenicol
NSAIDs
Supportive therapy and nursing – IVFT, with/without IV glucose, heat lamp
234
What is the aetiology of middle ear disease in calves?
- Ascending infection from respiratory tract, often with a recent history of pneumonia
- Occasionally progression from otitis externa
- Mycoplasma bovis
235
What are the clinical signs of middle ear disease in calves?
- Head tilt towards affected side
- No cranial nerve deficits
- Calf remains BAR and feeding
- Usually no vestibular disease
236
How is middle ear disease in calves treated?
Systemic antibiotics
237
What are the risk factors of hypocalcaemia in calves?
- Neonates
- Inadequate colostrum intake
- Inadequate feeding
- Hypothermia
- Other systemic disease (especially scour and septicaemia)
238
What are the clinical signs of hypocalcaemia in calves?
- Depression
- Weakness
- Ataxia
- Seizures, coma, death
239
How is hypocalcaemia in claves treated?
IV glucose, address risk factors
240
When do neurological and gastrointestinal signs of lead poisoning occur in calves?
Neuro – acute, high exposure and small body mass
Gastro – chronic, low exposure and large body mass
241
What are the neurological clinical signs of lead poisoning in calves?
- Bilateral central blindness
- Muscle fasciculations
- Bruxism, jaw champing and bellowing
- Head pressing
- Hyperaesthesia and excitability
- Seizures
242
How is lead poisoning in calves diagnosed?
- Clinical signs
- Blood lead levels
- Kidney lead levels at PME
243
How is lead poisoning in calves treated?
- Supportive and symptomatic – xylazine and fluids
- Oral salts to precipitate soluble lead – MgSO4
- Lead chelating agents – IV Calcium disodium EDTA
244
When animals have a head tilt or are circling, will this be towards or away from the side of the lesion?
Towards
245
You are called to Wyndhurst to look at a recently calved dairy cow behaving strangely…. On distant examination she is in low body condition, shows hypermetria, on closer examination she is hyperaesthetic, non-pyrexic and with no cranial nerve deficits identified. What is the most likely diagnosis?
BSE – narrow differentials with further diagnostics (biochemistry for Mg). If suspect BSE, contact APHA.
246
You are called to a small dairy herd; this cow got stuck in the cubicles; she was wedged in the metalwork between 2 cubicles and had to be pulled out with a tractor; she can stand but is extremely wobbly, she has a very stiff gait taking tiny steps with her hind legs; what is your diagnosis and action plan?
Vertebral trauma – give NSAIDs and supportive care
247
You diagnose Listeriosis: What antibiotic would you choose for treatment?
Penicillin
248
An out of hours call; urgent request to examine a two day old collapsed, dairy heifer calf, born to a maiden heifer. On examination the calf is dull and unresponsive she has sunken eyes, bilateral central blindness with nystagmus, MM congested and CRT >3secs. HR 160, RR 50, T36.5C, she has mild diarrhoea. What is the most likely diagnosis?
E.coli meningitis
249
You visit a calf rearing unit. They buy in weaned cross bred calves from eight weeks of age and rear them on an ad lib home mix of barley and oats, with hay. Three calves have developed acute onset neurological signs, one calf is recumbent. At a distance this calf shows ataxia and aimless wandering, with occasional head pressing. On clinical exam you find; this calf is dull and depressed, there is bilateral central blindness, there are no other cranial nerve deficits. T 38.3-39C. Rumen turnover: 3 in 2 minutes. What is the most likely diagnosis?
Cerebrocortical necrosis
250
What treatment is required for CCN in cattle?
IV vitamin B1 to 3 affected calves now
251
What is observed in sheep neurological cases from distant examination/observation?
- Social/grazing behaviour – will often isolate themselves
- Irritable – response to flies, other sheep, humans?
- Stance – wide-based stance to keep balance
- Locomotion – ataxia or collapse on running
- Head tilt/Circling/Head Pressing
- Recumbency
252
What is the signalment of CCN in sheep?
- Lambs older than 12 weeks, and adults
- Cereal diet or after dietary change
- Disease progresses over 3-5 days
253
What are the clinical signs of CCN in sheep?
- Dull
- Wander aimlessly
- Appear blind
- Ataxic and staggering gait
- Recumbent with opisthotonus
254
What are the differential diagnoses of CCN in sheep?
- Sulphur toxicity – very similar clinical signs but will not respond to thiamine treatment
- Brain abscess
- Meningitis
- Listeriosis
- Visna
- Louping ill
255
What is done post mortem to identify CCN in sheep?
- Histopathology of brain
- Fluoresce under UV light
256
How is CCN treated in sheep?
- Vitamin B1 IV (high dose)
- Then IM every 3 hours
- Treat for 3 days
- Response to treatment confirms diagnosis and if good if treated early
257
What is coernurosis/gid and when is it seen in sheep?
- Seen in areas where sheep carcases are not disposed of correctly
- Coenuris cerebralis is the larval stage of T multiceps
258
What are the clinical signs of gid in sheep?
- Chronic, progressive disease with weight loss
- CNS signs variable. Usually unilateral
- Animals appear ‘giddy’
- Skull over cyst may be soft
259
What are the differential diagnoses of god in sheep?
- Listeriosis
- CCN
- Visna
- Louping ill
- Brain abscess
260
What is the post mortem finding of gid in sheep?
Hydatid cysts in the brain
261
How is gid treated in sheep?
- Surgical Removal of Cyst
- Euthanasia
262
How is gid in sheep prevented?
- Education of farmers and dog owners
- Regular praziquantel for dogs to kill tapeworms
- Dispose of sheep carcasses
- Avoid grazing sheep on ground recently used by hounds or for sheep trials
- Do not feed uncooked sheep heads to dogs
263
Distinguish classical and atypical scrapie in sheep.
Classical scrapie – animals aged between 2 and 5 years old, highly contagious, spread via colostrum and milk, areas contaminated with birth fluids/placenta
Atypical scrapie – animals usually over 5 years old, usually seen in individual animals so probably not contagious
264
What are the clinical signs of classical scrapie?
Should be suspected if 2 or more of the following:
- Abnormal behaviour
- Absent menace response
- Positive scratch test or alopecia/skin damage
- Incoordination
- Tremor
265
What are the clinical signs of atypical scrapie in sheep?
Should be suspected if animal over 5 years old and 2 or more of the following:
- Abnormal behaviour
- Absent menace response
- Compulsive circling or circling when blindfolded
- Incoordination
- Tremor
- Loss of body condition
266
How is scrapie in sheep diagnosed?
Post mortem exam with brain histopathology, positive scratch test
267
What does listeriosis cause in sheep?
Meningoencephalitis
268
What are the clinical signs of listeriosis in sheep?
Dull
Pyrexic
Drool saliva
Facial paralysis
Circling
Head tilt
Collapse
Depression
Can also lead to abortion and septicaemia diarrhoea
Death within 10-14 days
269
How is listeriosis diagnosed in sheep?
CSF – lymphocytosis, monocytosis, organisms but may be normal CSF
Haematology – neutrophilia
270
How is listeriosis treated in sheep?
High dose Penicillin - twice a day for 5 days
Husbandry
271
What are the clinical signs of louping ill in sheep?
- Initial pyrexia
- Ataxia
- Seizures
- Stiff, jerky movements
- Sheep will have a prolonged recovery period or sudden death
272
How is louping ill controlled in sheep?
- Control of ticks (difficult)
- Avoid buying in sheep from a different area
- New vaccine currently in development
273
What is ryegrass staggers in sheep?
- Sheep on rye-grass infected with fungus
- Incoordination, especially when moved
- May collapse, then improve
- Improve when stop eating affected pasture
274
What happens to lambs exposed to border disease days 0-60 in gestation?
- Abortion or lamb persistently infected
- Hairy and brown pigmented fleece
- Ataxia, hypermetria, tremor
- Limb and head deformities
- Clinical signs may resolve with time but will continue to act as reservoir for disease in flock
275
What happens to lambs exposed to border disease days 60-85 in gestation?
- Abortion or CNS malformations – cerebellum and/or cerebrum
- Skeletal abnormalities
- Cerebellar signs and dull
276
What happens to lambs exposed to border disease days 85+ in gestation?
Abortion or lamb mounts an immune response born normal or weak
277
What are the differential diagnoses of border disease in sheep?
Other causes of abortion
White muscle disease
Swayback
278
How is border disease diagnosed?
- Post Mortem histopathology
- High antibody titres in dam
- BDV RNA in lambs
279
What is swayback in sheep a consequence of?
Copper deficiency in mid-late pregnancy
280
What are the different outcomes of swayback in sheep?
Still birth
Small weak lambs +/- fine tremor of head
Bright, but incoordinate lambs with weakness of pelvic limbs – often fine boned and dull coated
Delayed form – slow, progressive weakness and muscle atrophy of pelvic limbs in older lambs
281
How is swayback diagnosed in sheep?
Liver copper assay, histopathology of brain or spinal cord
282
How is swayback prevented?
Dietary management
283
What is daft lamb disease?
Degenerative inherited disease of cerebellum
284
What are the clinical signs of daft lamb disease?
Aimless wandering
Wide-based stance
Stargazing
Intention tremor
285
How is daft lamb disease treated?
No treatment, euthanasia
286
Which region are spinal abscesses found in most commonly in sheep?
Thoracolumbar
287
What are the clinical signs of spinal abscesses in sheep?
- Sudden onset hindlimb paresis or paralysis - proprioceptive deficits, may ‘dog sit’
- Lamb usually bright and alert
288
How are spinal abscesses diagnosed in sheep?
- Clinical signs and neuro exam
- CSF analysis
- Radiograph
289
How are spinal abscesses treated in sheep?
Euthanasia recommended, prolonged antibiotic treatment has a very poor prognosis
290
What is the pathogenesis of tetanus in sheep?
- Unvaccinated animals
- C.tetani invades wounds (after tail docking/castration)
- Releases neurotoxin leads to spasmodic, tonic contractions of muscle
291
What are the clinical signs of tetanus in sheep?
- Stiffness of masseter and neck muscles, hindlimbs and region of wound
- Followed by general stiffness
- Then tonic spasms and hyperesthesia
- Eventually death
292
How is tetanus in sheep treated and prevented?
- High dose penicillin
- Anti-toxin
Prevent with routine vaccination
293
What does cerebracortical necrosis/CCN occur as a result of?
A change in diet
294
What is the best method of prevention for gid?
Regular treatment of sheep dogs with praziquantel
295
Match the neurological diseases of sheep with the neurolocalisation.
CCN = cerebrum
Scrapie = cerebellum
Louping ill = peripheral nerves
Listeriosis = brainstem
296
You are called to examine a sick lamb, the lamb had been born 1 week ago. On physical exam you note that the lamb is bright and alert, but its coat seems dull. You do not note any deficits of cranial nerves. The forelimbs appear normal. However, you note ataxia of the pelvic limbs. What is the most likely diagnosis?
Swayback
297
What is the pathogenesis of tetanus in horses?
1. Necrosis and pus > anaerobic > spore germination
2. Exotoxin
3. Bloodstream and nerve axons
4. CNS presynaptic inhibitory interneurones
5. Inhibits neurotransmitter release here
6. Inhibits inhibition
7. Spastic paralysis (7-10 days)
298
What are the clinical signs of tetanus in horses?
- Hypertonia of muscles with spasms – worse with stimulation
- ‘Sawhorse’ stance
- Extended, rigid tail
- Stiff gait, can progress to recumbent
- Trismus (lockjaw)
- Prolapse nictitating membrane
- Pyrexia – as all the muscles are spasming
299
What is the morbidity of tetanus in horses due to?
Respiratory failure
Aspiration pneumonia from dysphagia
300
What are the complications of tetanus in horses?
- Decubital ulcers
- Dysphagia
- Dysuria
- Impaction and gaseous distension
301
How long is recovery from tetanus in horses?
Slow recovery (about 1 month) as you have to mange then until new receptors form
302
What are the 5 goals of treatment of tetanus toxins?
1. Interruption of toxin production - penicillin
2. Neutralising unbound toxin - tetanus antitoxin (TAT) produced from sera of hyperimmunised horses, antibodies neutralise unbound toxin
3. Control of muscular spasms - Phenothiazines, Benzodiazepines
4. Supportive care - minimal stimulation, manage recumbency, dysuria, dysphagia, hyperthermia
5. Vaccination
303
What are the vaccination schedules for tetanus in pregnant mares and foals?
Pregnant mares – booster 4-6 weeks before foaling
Foal
- Unvaccinated mare, but good colostral uptake = vaccinate
- Failure of passive transfer of immunity = hyperimmune plasma
304
Where is a tetanus vaccine administered?
Give away from vaccination site – work against each other at the same site, okay at opposite ends of horse
305
What is the aetiopathogenesis of botulism in horses?
- Toxin acts pre-synaptically at the peripheral cholinergic neuromuscular junction
- Prevents synaptic vesicle from releasing acetylcholine
- Flaccid paralysis
- Once toxin is bound, recovery only by regeneration of new motor end plates (4-10 days)
306
What are the 3 mechanisms of clinical botulism?
1. Ingestion of pre-formed toxin in feed that has been contaminated by bacteria. Horses more susceptible than cattle
2. Wound botulism
3. Toxicoinfectious botulism (shaker foal syndrome
307
What are the clinical signs of botulism in horses?
- Onset usually within 24h of exposure
- Weakness – but not ataxic
- Dysphagia
- Poor muscle tone
- Recumbency
- Death from respiratory failure
308
How is botulism diagnosed in horses?
- Clinical signs
- Detect toxin in feed, serum, GI content, faeces, debris from wound
309
How is botulism in horses treated?
- Antitoxin (US)
- Nursing
- Tube feeding
- Laxatives
- Mechanical ventilation?
310
How is botulism prevented in horses?
- Type B vaccination (US)
- Cattle vaccine (C and D)
- Most important is good husbandry and proper processing and storage of feed material
311
What is the pathogenesis of equine grass sickness/dysautonomia?
- Acquired degenerative polyneuropathy
- Neurotoxin
- Neurons of autonomic and enteric nervous system
- Altered autonomic activity > decrease intestinal peristalsis > ileus, colonic impaction
312
What are the risk factors of equine grass sickness/dysautonomia?
- 3 –5 years old
- In contacts
- Outbreaks
- But if in contact and no disease, 10 x less likely to develop disease
- Recently moved premises
- Live out
- Soil disturbance
- Spring and Autumn
313
What are the acute clinical signs of equine grass sickness/dysautonomia?
- Acute onset GI ileus > gastric and SI distension > colic, hypovolaemia
- Tachycardia
- Sweating
- Muscle fasciculations
- Pyrexia
- Dysphagia
- Ptosis
- Secondary impaction
314
What are the subacute clinical signs of equine grass sickness/dysautonomia?
- 3-7 days
- Less severe, often no reflux
- Large colon impactions
- Rhinitis sicca
315
What are the chronic clinical signs of equine grass sickness/dysautonomia?
Cachexia
Empty GI tract
Rhinitis sicca
Muscle tremors
Base narrow stance
316
How is equine grass sickness/dysautonomia diagnosed?
- Phenylephrine eye drops?
- Ileal biopsy
- Post mortem
317
How is equine grass sickness/dysautonomia treated?
- No effective cure
- Acute cases respond initially to gastric decompression and fluid therapy
- Nursing
- Promising work on a vaccine
318
What is the reason behind trigeminal mediated headshaking?
- Neuropathic facial pain condition (varying intensities of pins and needles, burning, electric shock like pain)
- Due to the threshold potential for firing of the infra-orbital nerve being about 10x lower than normal
319
What are the clinical signs of trigeminal mediated headshaking?
- As if a bee is up their nose’
- Snorting, sneezing, twitching lips
- Vertical headshaking accompanied by sharp, vertical twitches and flicks
- Can strike at nose with forelimbs
- Worse at exercise than rest though can be affected at rest
- No longer shakes head when LA into ophthalmic branch of trigeminal nerve
320
How is trigeminal mediated headshaking managed?
- Nose net?
- Gate-control theory? – spinal cord is not multi-tasker and will send touch sensation before pain sensation (clutch arm hen bash elbow). Pharmaceuticals
- Mg – small effect
- EquiPENS Neuromodulation
321
What are the aspects of distant neurological examination in horses?
- Observe from a distance
- Mentation
- Just watching them eat tells you a lot about cranial nerve function
- Muscle (a)symmetry
322
How are the cranial nerves in horses tested?
- Must be bale to smell snack, be bale to move nose to try get at hand, open mouth and masticate and swallow
- If you move head side to side, should see nystagmus (not if head still), if lift head, eye should drop (doll’s eye)
- If these are normal, do not need to do more tests. If abnormal, do more
323
How are the neck flexion tests used in neurological examination in horses?
Carrot tests, if not used to doing this then may appear to have abnormal neck flexion so look for asymmetry. C6-7 arthritis very common when older
324
What are the stages of lead neurological exams in horses and what is looked for?
- Straight line – ataxic, dysmetria, irregularly irregular gait (could be multi-limb lame)?
- Serpentine – look for any ataxia – outside leg of curve will swing round if ataxic
- Tail pull (hindlimb lame horses will have weak tail pull) – spinal cord or NMJ lesions
- Backing – they have difficulty doing this so this is not abnormal behaviour but if ataxic they are quite stiff ad lose usual rhythm
325
What are the characteristics of neuromuscular diseases on clinical assessment of the motor unit?
- Decreased spinal reflexes
- Denervation atrophy of the muscles
- Decreased muscle tone
326
What are the tests for neuromuscular diseases?
- Electrodiagnostic studies
- Nerve and muscle biopsy
- CK and AST elevations
327
What are the differential diagnoses for generalised acute loss of reflexes and muscle atrophy?
Polyradiculoneuritis
Fulminant myasthenia gravis
Botulism
Tick paralysis (No UK)
328
What are the differential diagnoses for focal acute loss of reflexes and muscle atrophy?
Brachial plexus avulsion
Tail pull injury
329
What is polyradiculoneuritis?
An immune mediated disease that predominantly attacks the axons in dogs
330
What are the clinical signs of polyradiculoneuritis?
- Weakness, can’t even support the head
- Postural reactions are affected in - if the body weight is through the limbs they cannot correct postural changes but if you sustain them, they can correct them, loss of spinal reflexes (sensation is not gone but does not have the strength to repel)
- In a week may be flaccid, flaccid and unable to move – cutaneous effects, respiratory effects
331
How is polyradiculoneuritis diagnosed?
- Rule out metabolic differentials and myasthenia gravis (No megaoesophagus)
- Electrodiagnostics show diffuse axonal disease and nerve roots
- Elevated CSF protein with normal cell count
332
How is polyradiculoneuritis treated?
Physiotherapy (to prevent muscle contractures)
333
What is the prognosis of polyradiculoneuritis?
Very good, most dogs recover to walk but may remain slightly atrophied, takes 1-3 months
334
How is brachial plexus avulsion diagnosed?
- History of trauma, scratches, wound
- X-rays, CT – rule out concurrent fractures
- Electrodiagnostics – abnormal after 4-5 days
335
How is brachial plexus avulsion treated?
- Physiotherapy
- Amputation if self trauma
336
What is the main differential diagnosis of brachial plexus avulsion in cats?
Thromboembolism – make sure you can feel a pulse
337
What are some possible clinical features of brachial plexus avulsion?
If trauma is severe enough trauma to cause denervation of the whole nerve root, limb is useless and they can self-mutilate or cause damage to it as they do not know what it is
Not infrequent presentation to have dysfunction/horner’s in ipsilateral eye
338
What are the clinical signs of tail pull injuries?
- Bladder denervation
- Flaccid tail
- With/without flaccid anus
- With/without urinary incontinence
- With/without sciatic nerve deficits – difficulty rising and using the leg
339
How is tail pull injury treated?
Bladder management
340
What is the prognosis of tail pull injury?
Fair to guarded, prognostic value of tail base sensation particularly in first 48h, if regain in this time, more likely to regain ability to urinate on their own
341
What are the differential diagnoses for loss of muscle mass?
Generalised:
- Polymyositis
- Congenital myopathy
Focal – nerve sheath tumour
342
What is the aetiology of polymyositis?
Infectious disease such as neospora, which can also cause myositis and polyradiculoneuritis in puppies
Toxoplasmosis
Masticatory muscle myositis
343
How are brachial plexus tumours treated?
Surgery – tumour removal with/without amputation
Palliative
344
What are the differential diagnoses for exercise induced weakness?
Myasthenia gravis
Cardiorespiratory diseases
Metabolic diseases
345
What is the differential diagnoses for progressive weakness?
Degenerative polyneuropathy
346
What are the clinical signs of myasthenia gravis?
Generalised neuromuscular neurolocalisation and megaoesophagus
They have regurgitation – burp, messy when eat, drooling and hypersalivation
347
How is myasthenia gravis diagnosed from imaging?
Radiography on awake dog:
See megaoesophagus, look at mediastinum as frequently associated with a mass that is triggering the antibodies against ACh
348
How is myasthenia gravis treated?
- Acetylcholinesterase inhibitors (pyridostigmine)
- With/without immune suppression
- Postural feeding
349
How is degenerative polyneuropathy diagnosed?
- Electrodiagnostics – supportive
- Nerve biopsy – often mild changes
- Genetic testing
350
What are the main 2 features of degenerative polyneuropathy and why?
- Laryngeal paralysis is an early sign of generalised neuromuscular pathology
- As you ask to keep walking, hock drops further and further down and is walking mostly with forelimbs
- These 2 changes due to sciatic and laryngeal nerves are some of the longest nerves in the body
351
Name 5 acute cranial neuropathies.
Idiopathic facial nerve paralysis
Idiopathic peripheral vestibular syndrome
Idiopathic trigeminal neuritis
Otitis media/interna
Idiopathic Horner syndrome
352
Name a chronic cranial neuropathy.
Nerve sheath tumour
353
What is important for treatment of idiopathic facial nerve paralysis?
In some cases, not all, can have lacrimal tear not enough to lubricate ethe eye so provide artificial tears
No steroids
354
What is important with idiopathic peripheral vestibular syndrome management?
- Supportive, no steroids
- This is the most common differential for peripheral vestibular disease – normally gets better so avoid euthanasia
- Dramatic disease – so hard to do neurological exam for neurolocalisation
355
What are the differential diagnoses for peripheral vestibular syndrome?
Idiopathic
Otitis media/interna
Neoplasia
Trauma
Dogs = idiopathic > otitis
Cats = otitis (polyps) > idiopathic
356
What in the nervous system do we want to balance?
Inhibitory system GABA – promoting inhibition
Excitation glutamate – reducing excitation
357
What are the characteristics of anti-convulsant medications?
- Very short half life:
- Rapid onset of action
- Short acting
- Emergency management
Diazepam, midazolam, propofol
358
What are the characteristics of anti-epilepsy medications?
- Longer half life
- Slow onset of action
- Long acting
- Long term management
Phenobarbitone, Imepitoin, Levetiracetam, KBr
359
When is monitoring appropriate for seizures?
- Known toxic trigger
- Long interictal period
- Single seizure
360
When is long term medication for seizures appropriate?
- Underlying structural or metabolic cause (until fixed)
- Cluster seizures or Status epilepticus
- If > 1 seizure per month Increasing frequency
361
What are the goals of epilepsy management?
- Reduce seizure frequency by 50% or more. Aim for less than one seizure per month or per 3 months
- Reduce severity
- Acceptable side effects
- Acceptable costs
- Practical
362
What is the 1st line choice of drug in dogs and cats for epilepsy management?
Phenobarbitone
363
What are the 2nd line choices of drugs in dogs for epilepsy management?
Imepitoin – dogs without cluster seizures and with long interictal period
Potassium bromide – dogs only, if liver dysfunction
364
What are the 2nd line choices of drugs in cats for epilepsy management?
Levetiracetam
Imipetoin
Do not used potassium bromide in cats – toxic
365
What are the dose related side effects of phenobarbitone?
PUPD
Sedation
Ataxia
Polyphagia
366
What are the idiosyncratic reactions of phenobarbitone?
Dermatitis
Liver failure
Cytopaenias
Pseudolymphoma
367
What are he dose related side effects of imepitoin?
PUPD
Sedation
Ataxia
368
What are he dose related side effects of potassium bromide?
PUPD
Sedation
Ataxia
Vomiting
369
What are the idiosyncratic reactions of potassium bromide?
Pancreatitis
Pneumonitis
370
What is the steady state and site of metabolism of phenobarbitone?
2-3 weeks, liver
371
What is the steady state and site of metabolism of imepitoin?
2-3 days
Liver
372
What is the steady state and site of metabolism of potassium bromide?
2-3 months
Kidneys
Can accumulate so need to monitor
373
What are the signs of phenobarbitone toxicity?
Laboratory changes related to PB administration in dogs are elevation in ATP, ALP, cholesterol and triglycerides
Changes suggestive of PB induced hepatotoxicity effects – albumin decreased, bilirubin, ASFT and GGT elevated, abnormal bile acid stimulations
374
When is drug monitoring done for anticonvulsants?
- At steady state
- If seizure control lost
- If signs of toxicity
- Every 6-12 months
375
When is another anticonvulsant drug added?
- Improper seizure control despite appropriate use of first line drug
- If increasing the first line drug leads to unacceptable side effects
- If increasing the first line drug means reaching a possible toxic blood level
376
What are some alternative antiepileptic options?
2nd line drug - Kbr in dogs, levetiracetam in cats
3rd line drugs – levetiracetam (dogs), zonisamide
4th line drugs – gabapentin? Pregabalin? Felbamate? Topiramate?
377
What are the steps in emergency seizure management?
1. Check vital parameters
2. Protect patient
3. Try to get IV access
4. Check blood glucose
5. Give anticonvulsant
378
What are the drug options for emergency seizure management?
- Diazepam – intravenously, rectally, not IM
- Midazolam – intravenously, intranasal
- Midazolam CRI
- Goal = to stop the seizure
- Can repeat diazepam and midazolam up to 3 times
379
What medications are considered for acute recurrent seizure management?
Use anti-epileptic – longer acting. To prevent further seizure
- Phenobarbitone loading dose IV
- Levetiracetam
Consider CRI – ketamine, propofol
380
What are the clinical signs of vestibular dysfunction?
- Pathological nystagmus
- Loss of balance - drifting, rolling
- With/without head tilt
- With/without head vomiting, motion sickness
- With/without head positional nystagmus
381
What are the 3 things that make up vestibular syndrome?
Head tilt
Nystagmus
Loss of balance
Independent of central or peripheral origin
382
Which neurological findings suggest a central origin?
Brainstem = proprioceptive deficits, cranial nerve deficits 3-12, abnormal mentation, ataxia, head tilt, nystagmus
Middle ear = CVIII deficits, with/without CNVII and Horner's, ataxia, head tilt, nystagmus
383
Can CSF being unremarkable rule out inflammatory cause?
No
384
What are the differential diagnoses for brain masses?
Haematoma
Granuloma
Neoplasia
385
What are the possible causes of an infectious granulomatous brain mass?
Fungal - cryptococcus is rare and has no CSF changes
Viral - FIP. Serology and PCRs negative
Parasitic - toxoplasma. Serology and PCRs negative
386
What are the possible causes of a non-infectious granulomatous brain mass?
Immune mediated
