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Year 3 > CNS MOD > Flashcards

CNS MOD Flashcards

1
Q

What are the 4 main zones of a neuron?

A

Dendritic zone: receptor portion that converts stimulus into impulse
Axon: connects dendritic zone to telodendron
Cell body: contains nucleus and major organelles essential for neuron to function
Telodendron (synapse): termination of neuron, where impulse leaves to effector organ or another neuron

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2
Q

What is a nerve impulse?

A

The movement of an action potential along a nerve fibre in response to a stimulus

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3
Q

What does grey matter contain?

A

Cell bodies

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4
Q

What does white matter contain?

A

Mostly myelinated axon tracts

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5
Q

What is the difference between white and grey matter?

A

White: contains mostly myelinated axon tracts. Present in deep parts of brain and superficial spinal cord. Acts as a relay between different brain regions

Grey: contains cell bodies. Present in central spinal cord and surface of brain. Processes information

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6
Q

The forebrain is subdivivded into what?

A

Cerebral cortex

Diencephalon

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7
Q

The brainstem is subdivided into what?

A

Rostral to caudal:
Midbrain
Pons
Medulla oblongata

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8
Q

What are the 4 main divisions of the spine?

A

C1-C5
C6-T2
T3-L3
L4-S3

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9
Q

How many pairs of spinal nerves are there in the PNS?

A

36 plus 12 pairs of cranial nerves

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10
Q

Where are motor neuron cell bodies?

A

Ventral horn of spinal cord, or grey matter of brainstem

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11
Q

Where are sensory axon cell bodies?

A

Dorsal root ganglion

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12
Q

How does the ANS affect bladder filling?

A

Detrusor muscle relaxes and sphincter tone increases (via sympathetic and somatic)

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13
Q

How does the ANS affect bladder emptying?

A 
Detrusor muscle contracts (via parasympathetic)
Sphincters relax (via somatic to external sphincter and sympathetic to internal sphincter)
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14
Q

Which drug will increase detrusor muscle contraction in the bladder?

A

Bethanecol

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15
Q

If the bladder is distended and difficult to express, which drugs can you give and why?

A

Diazepam to decrease urethral tone (help it relax)

Bethanecol to increase detrusor contraction

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16
Q

If the bladder is continually overflowing and dribbling (incontinent), which drugs can you give and why?

A

Propantheline bromide to decrease detrusor hyperreflexia (frequent detrusor contractions)
Phenylpropanolamine to increase urethral tone

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17
Q

Describe how sympathetic supply reaches the eye from the brain

A

1st order neuron: starts in brainstem and courses caudally in cervical spinal cord
2nd order neuron: leaves spinal cord at T1-T3 using brachial plexus, courses rostrally through neck in vagosympathetic trunk, synapses at cranial cervical ganglion, ventromedial to tympanic bulla
3rd order neuron: courses rostrally towards eye

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18
Q

What does sympathetic supply to the eye innervate?

A

Smooth dilator of pupil
Orbitalis muscle
Smooth ciliaris muscle
Smooth muscle of blood vessels and sweat glands of head

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19
Q

What is miosis?

A

Constricted pupil

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20
Q

What is Horner’s syndrome?

A

Lesions in sympathetic supply to eye
Causes:
Miosis (constricted pupil; lesions prevent normal dilation)
Ptosis of upper eyelid (drooping)
Protruded 3rd eyelid
Enophtalmos (posterior displacement of eyeball due to loss of function of orbitalis muscle)

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21
Q

How can you test for Horner’s syndrome?

A

Give 1% phenylephrine or atropine to dilate pupil

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22
Q

Is the chemoreceptor trigger zone that stimulates vomitting inside or outside the BBB?

A

Outside, so is exposed to circulating drugs and toxins

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23
Q

Where is the BBB?

What is it?

A

Between plasma and extracellular fluid in interstitial space at capillaries
Non-fenestrated, tightly joined layer of endothelial cells surrounded by a thick basement membrane and layer of foot processes of astrocytes

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24
Q

Give the different layers of the meninges

A

Dura mater: thick outer layer
Arachnoids: thin layer
Subarachnoid space: CSF, blood vessels, nerve roots
Pia mater: thin, inner layer

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25
Q

How does CSF flow?

A

By pulsations of blood in the choroid plexus

Courses caudally

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26
Q

Where is CSF produced?

A

Choroid plexuses of the ventricles of the brain

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27
Q

Give the functions of CSF

A

Protect CNS
Parenchyma suspended in fluid
Modulate pressure changes
Helps regulate ICP (intra0cranial pressure)
Helps maintain ionic balance
Transport of metabolites and nutrients between blood and CNS
Transport of neuroendocrines and neurotransmitters

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28
Q

When sampling CSF, how much should you take from a dog and cat?

A

Dog: 1ml
Cat: 0.5ml
Don’t suck -> herniation/suck brain out

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29
Q

How much CSF does a dog, cat and horse have?

A

Dog: 7.8 - 24ml
Cat: 4 - 4.9ml
Horse: 170 - 300ml

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30
Q

How would you sample CSF?

A

Spinal tap

Don’t suck -> herniation/suck brain out

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31
Q

What abnormal findings may you see in a CSF analysis?

A

WBC (inflammation
RBC (haemorrhage)
Protein (BBB disruption- proteins aren’t usually able to cross BBB due to their large size)

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32
Q

Where do most cranial nerves arise?

A

Brainstem (midbrain, pons, medulla)

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33
Q

What are the 12 pairs of cranial nerves?

A 
Olfactory
Optic
Occulomotor
Trochlear
Trigeminal
Abducens
Facial
Vestibulocochlear
Glossopharyngeal
Vagus
Accessory
Hypoglossal
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34
Q

How do you remember which cranial nerves are sensory, motor or both?

A 
S= sensory, M= motor B= both
Some
Say 
Marry 
Money
But
My
Brother
Says
Big
Breasts
Matter
More
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35
Q

Where are the cell bodies of the olfactory cranial nerve?

A

Olfactory epithelium

Axons pass through cribriform plate and synapse in olfactory bulb (then to piriform lobe)

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36
Q

Occulomotor nerve axons exit the skull where?

A

Through orbital fissure

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37
Q

Which muscles does the occulomotor nerve supply?

A

Dorsal, ventral, medial rectus muscles of eye
Ventral oblique muscle of eye
Parasympathetic component controls pupillary constriction

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38
Q

The trochlear nerve innervates which muscle?

What happens to the eye if this nerve’s function is impaired?

A

Dorsal oblique of eye

Dorsomedial strabismum

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39
Q

The abducens nerve innervates which muscles?

What happens to the eye if this nerve’s function is impaired?

A

Lateral rectus and retractor bulbi

Medial strabismus

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40
Q

What are the 3 primary branches of the trigeminal nerve?

A

Ophthalmic
Maxillary
Mandibular

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41
Q

What does the facial nerve supply?

A

Motor innervation to muscles of facial expression
Sensory innervation to rostral 2/3 of tongue and palate
Parasympathetic innervation to lacrimal, mandibular and sublingual glands

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42
Q

Where do facial nerve axons exit the skull>

A

Stylomastoid foramen (then middle ear)

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43
Q

What does the glossopharyngeal nerve supply?

A

Motor innervation of pharynx and palate
Sensory innervation of caudal 1/3 of tongue and pharynx
Parasympathetic innervation of parotid and zygomatic glands

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44
Q

What does the vagus nerve supply?

A

Motor innervation of larynx, pharynx and oesophagus
Sensory innervation of larynx, pharynx and thoracic and abdominal viscera
Parasympathetic innervation to all thoracic and abdominal viscera (except pelvic region)

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45
Q

What does the hypoglossal nerve supply?

A

Motor innervation to tongue

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46
Q

What is the lower motor neuron system?

A

Efferent neurons of PNS that connect the CNS with the muscle to be innervated
Neuronal cell bodies are in ventral grey matter of spinal cord
Axons leave the spinal cord through ventral root

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47
Q

What is the function of glial cells?

Give some examples

A

Surround neurons and provide support and insulation between them
Oligodendrocytes, astrocytes, microglia

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48
Q

Describe the pathway of a LMN reflex

A
  1. Stimulus -> dendritic zone of sensory nerve in skin/muscle
  2. Sensory peripheral nerve -> dorsal root of spinal cord -> passes to dendritic zone of relay neuron in grey matter
  3. Can be direct (monosynaptic-patellar) or through an interneuron (polysynaptic-withdrawal)
  4. Exits spinal cord though ventral root -> motor neuron -> telodendron in muscle
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49
Q

Which spinal nerves supply thoracic limbs?

Which supply pelvic limbs?

A

C6-T2 (brachial plexus)

L4-S3

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50
Q

The UMN (upper motor neuron) system is confined to where?

A

CNS

Axons are in tracts in white matter and synapse in grey matter of spinal cord

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51
Q

What is the function of the upper motor neuron system?

A

Initiates voluntary movement
Maintains muscle tone
Controls muscular activity associated with visceral functions

Can be pyramidal and extra-pyramidal

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52
Q

Describe the pryamidal part of the UMN system

A

Skilled movement
Starts in cerebral cortex and passes through pyramids of medulla
Poorly developed in small animals

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53
Q

Describe the extrapyramidal part of the UMN system

A

Mainly starts in brainstem, doesn’t pass through pyramids of medulla
Provides tonic mechanisms for support of body against gravity, and spinal reflexes for initiation of voluntary movement
Most important nuclei are in the midbrain, pons and medulla, some also in cerebral cortex and thalamus

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54
Q

What is proprioception?

A

Part of sensory system that detects position and movement of muscles and joints

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55
Q

What is the difference between conscious and unconscious proprioception?

A

Unconscious: reflex activity. Involves transmission of proprioceptive information to cerebellum

Conscious: Involves transmission of proprioceptive information to sensory cerebral cortex

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56
Q

Where are cell bodies of afferent neurons?

A

Dorsal root ganglion

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57
Q

Describe the conscious pathway of proprioception

A

Spinal tracts cross to contralateral side in medulla -> thalamus -> motor cerebral cortex

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58
Q

What does the vestibular system do?

A

Maintains balance
Maintains normal orientation relative to the gravitational field
Maintains position of eyes, neck, trunk and limbs relative to position and movement of head

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59
Q

How many vestibular nuclei are there?

What do they do?

A

4 in either side of the pons and medulla
Receive info from CN8 (vestibulocochlear) and project to spinal cord, brainstem (eye movement, vomiting centre, conscious perception of balance) and cerebellum

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60
Q

What are the functions of the cerebellum?

A

Control of motor activity
Coordinates and smooths out movement induced by UMN system
Maintains equilibrium
Regulation of muscle tone to preserve normal body position

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61
Q

How do animals walk? (ie UMNs, LMNs etc)

A

UMNs initiate voluntary movement and modulate activity of LMNs
LMNs connect the CNS with the muscles
Need general proprioception to know where body parts are
Need cerebellum to coordinate the movement
Need vestibular system to maintain balance

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62
Q

How many neuronal layers does the retina have?

A

10, comprised of 3 types of neurons

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63
Q

Give the 10 neuronal layers of the retina, ending with the optic nerve

A 
Pigment epithelium
Photoreceptors
Horizontal cells
Outer synaptic layer
Bipolar cells
Amacrine cells
Inner synaptic layer
Ganglion cells 
Optic nerve fibres
Optic nerve
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64
Q

What are the names of the 3 ossicles in the ear?

A

Malleus, incus, stapes

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65
Q

How does an animal hear?

A

Sound wave -> external ear canal and typanum -> 3 ossicles (malleus -> incus -> stapes) -> vestibular window -> perilymph in scala vestibuli -> wave flow is reflected to basilar membrane -> movement of hair cells -> bending of stereocillia -> impulse in cochlear neurons

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66
Q

Where does the vestibulocochlear nerve terminate?

A

Dorsal and ventral cochlear nerve in medulla

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67
Q

What is the function of the limbic system?

A

Involved in emotional and behavioural patterns
Receives info from sensory systems
Projects mainly to hypothalamus and brainstem, influencing visceral motor neurons

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68
Q

What is the function of the hypothalamus?

A

Regulation of visceral activity
UMN for the autonomic nervous system (rostral= parasympathetic, caudal= sympathetic)
Regulates sleep
Regulates activity of major part of endocrine system

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69
Q

What is the function of the thalamus?

A

Conscious perception pathway for all sensory systems except olfaction
Relay for motor systems
Most rostral portion of ARAS (ascending reticular activating system)

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70
Q

Describe the ARAS

A

Ascending reticular activating system
Receives info from all conscious projection pathways of sensory systems
Information: brainstem -> thalamus -> cerebral cortex
Functions: arouse cortex, awaken brain to a conscious level, prepare brain to receive sensory information

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71
Q

Why should you observe before doing a neuro exam?

A

Mentation
Behaviour
Gait
Posture

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72
Q

What should you ask an owner when taking a history before a neuro exam?

A 
How did it happen and how long ago? History of trauma?
Acute or slow onset?
Painful?
Progressive/static/improving?
Episodic?
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73
Q

What does stuporous mean?

A

Unconscious but can be roused by painful stimuli

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74
Q

What does comatose mean?

A

Unconscious and unresponsive to any environmental stimuli

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75
Q

A problem with mentation will arise where?

A

Forebain or brainstem

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76
Q

A neurological problem affecting behaviour will arise where?

A

Forebrain

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77
Q

Give some examples of changes in behaviour in animals with forebrain lesions

A 
Aggression
Compulsive walking/circling
Vocalisation
Loss of learnt behaviour
Hemineglact syndrome: will ignore half of their environment (contralateral side to lesion)
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78
Q

A head tilt is indicative of a lesion where in the brain?

A

Vestibules

Loss of tone to the antigravity muscles of the neck

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79
Q

A head and/or body turn is indicative of a lesion where in the brain?

A

Forebrain (aversion syndrome)

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80
Q

What is Schiff-Sherrington?

A

Hyperextension of forelimbs, paralysis of hindlimbs

Lesion in thoracic or cranial lumbar spine

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81
Q

What is ataxia?

A

Uncoordinated gait:

  • Spinal or less commonly peripheral nerve disease
  • Vestibular disease (‘off balance’)
  • Cerebellar lesions (‘drunken gait’)
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82
Q

What is paresis?

A

Weakness, reduced voluntary movement, either ambulatory (can walk) or non-ambulatory (can only walk if weight is supported)

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83
Q

What is paralysis/plegia?

A

Complete loss of voluntary movement

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84
Q

What is spinal ataxia?

A

Uncoordintaed gait due to decreased sensory information from the limbs to tell CNS where they are in space at any given time
‘Legs don’t know where they are or what they should be doing’

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85
Q

What is vestibular ataxia?

A

Loss of orientation of the head with the eyes, neck, trunk and limbs
Results in loss of balance
Leaning, falling, rolling towards side of lesion

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86
Q

What is cerebellar ataxia?

A

Inability to regulate rate, range or force of movement
Dysmetria: hypometria (reduced lifting of feet off floor)
hypermetria (excessive lifting of feet off floor; puts paws high up when walking)

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87
Q

Give the system for grading spinal lesions

A

1) No deficits, just pain
2) Paresis, ambulatory
3) Paresis, non-ambulatory
4) Paralysis
5) No pain sensation

88
Q

What are the 4 primary things you should test in a neurological exam?

A
  1. Postural reactions
  2. Spinal reflexes and muscle tone
  3. Spinal pain
  4. Cranial nerve examination
89
Q

Which tests can you perform to test postural reactions in a neuro exam?

A

Paw position (turn paw so dorsal surface bears weight and see how quickly it is replaced), hopping (support 3 limbs and hop patient laterally), hip sway, wheelbarrow, placing responses (pick up patient and bring limbs to edge of table so that dorsal surface toucher surface, see how quickly it is replaced)

90
Q

How can you test spinal reflexes and muscle tone during a neuro exam?

A

FL withdrawals: extensor carpi radialis, biceps, triceps
HL withdrawals: patellar, cranial tibial, gastrocnemius, perineal
Cutaneous trunci

91
Q

Information regarding proprioception is sent where?

A

From proprioceptors in joints/tendons/muscles -> forebrain (for conscious perception) or cerebellum (for unconscious)

92
Q

How can you test cranial nerves in a neuro exam?

A

Palpebral reflex, corneal, PLR, gag, physiological nystagmus, menace response, nasal mucosa stimulation

93
Q

What is the difference between UMNs and LMNs?

A

UMNs= efferent or motor neurons in the cerebrum and brainstem which synapse with a LMN, regulating its activity.

LMNs= efferent neuron connecting CNS with effector organ (muscle or gland). Cell body in spinal cord grey matter or within nucleus of a central nerve and its axon becomes the peripheral nerve.

94
Q

Is Horner’s syndrome associated with UMN or LMN lesions?

A

LMN (loss of sympathetic innervation to eye)

95
Q

What 3 things are necessary for a reflex to be present?

A

A sensory neuron in PNS, a connector (internuncial) neuron in the CNS, and a LMN

96
Q

How do you carry out a withdrawal test in a neuro exam?

A

Pinch digit -> reflex contraction of flexor muscles and withdrawal of limb

97
Q

Explain the cutaneous trunci reflex (panniculus)

A

Pinching of skin -> sensory information enters spinal cord approx 2 vertebral spaces cranially -> ascends to C8-T1 -> bilateral synapse with motor neurons of lateral thoracic nerve -> brachial plexus -> cutaneous trunci muscle -> bilateral contraction of these muscles

98
Q

Cutaneous trunci reflex is useful for identifying lesions where?

A

T3-L3

Brachial plexus

99
Q

What behavioural responses would you see when doing a pain perception test?

A

Turning head
Vocalising
Trying to bite

WITHDRAWAL IS NOT A SIGN OF PAIN

100
Q

How do you look for spinal pain in a neuro exam?

A

Palpate all spine, starting gently and progressively increasing degree of pressure
Move neck in all directions; look for pain and resistance/reluctance to move
Move tail and palpate lumbosacral region

101
Q

How do you asses trigeminal nerve dysfunction?

A

Size and symmetry of masticatory muscles, sensory function (corneal, palpebral, nasal)

102
Q

How do you test the palpebral reflex?

State the nerves involved

A

Touch medial and/or lateral canthus of eye -> blink
Input=trigeminal nerve
-> Brainstem
Output=facial

103
Q

How do you test for physiological nystagmus?

State the nerves involved

A 
(=nystagmus induced by moving head)
Lift head or put dog upside down 
Input=vestibulocochlear nerve
-> Brainstem
Output=occulomotor, trochlear, abducens
104
Q

How do you test the corneal reflex?

State the nerves involved

A

Lightly touch cornea -> blink and eye globe retraction
Input=trigeminal (ophthalmic branch)
-> Brainstem
Output=abducens (globe retraction), facial (blink)

105
Q

How do you do the nasal mucosal stimulation test?

State the nerves involved

A

Touch nasal mucosa -> head withdrawal
Input=trigeminal (ophthalmic)
Forebrain, brainstem
No output

106
Q

How do you test the menace response?

State the nerves involved

A

Cover opposite eye, do menace gesture -> blink
Input=optic
Forebrain, cerebellum, brainstem
Output=facial

Not a reflex-learnt response
Present from 10-12 weeks

107
Q

How do you test the pupillary light response?

State the nerves involved

A

Shine light into eye -> constriction of same pupil (direct PLR) and opposite pupil (consensual PLR)
Input=optic
-> Brainstem
Output=occulomotor

108
Q

How do you test the gag reflex?

State the nerves involved

A

Open mouth or touch pharynx -> contraction of pharynx
Input=glossopharyngeal and vagus
-> Brainstem
Output=glossopharyngeal and vagus

109
Q

What are the key functions of the forebrain?

A 
Thinking
Behaviour
Vision, hearing
Conscious perception of touch, pain, temperature, body position
Fine motor activity
110
Q

What would you see with forebrain lesions?

A

Disorientation, depression
Contralateral blindness (abnormal menace with normal PLR); facial hypoasthesia
Normal gait
Circling (usually ipsilateral), head turn, head pressing, pacing
Decreased postural responses in contralateral limbs
Seizures, behavioural changes, hemineglect syndrome

111
Q

What are the key functions of the brainstem?

A

Ascending reticular activating system (ARAS)
Regulatory centres for CV system and breathing
Cranial nerves originate here (III-XII)
All tracts (sensory and motor) pass through here
Vestibular nuclei

112
Q

What would you see with brainstem lesions?

A

Depression, stupor, coma
Cranial nerve deficits (III-XII)
Vestibular signs
Paresis of all or ipsilateral limbs
Decerebrate rigidity (hyperextension of back, head back)
Decreased postural responses in all limbs or just in ipsilateral limbs
Respiratory or cardiac abnormalities

113
Q

What are the key functions of the cerebellum?

A

Controls motor activity (regulator not initiator)
Coordinates and smooths out movement induced by UMN system, eg spinal cord function and postural tonus
Inhibits vestibular system

114
Q

What would you see with cerebellar lesions?

A

Normal mentation
Ipsilateral abnormal menace with normal vision and PLR
Vestibular signs
Ataxia, broad-based stance, hypermetria (lifting paws up when walk)
Intention tremors
Decerebellate rigidity (hyperextension of back, head back)
Delayed initiation and then often hypermetric postural responses
Rarely increased frequency of urination

115
Q

What are the key functions of the vestibular system?

A

Maintains balance
Maintains position of the eyes, neck, trunk and limbs relative to position and movement of the head at all times
Components:
-Receptors in inner ear transmit info to vestibulocochlear nerve
-Vestibular nuclei in brainstem under some control from cerebellum

116
Q

What would you see with vestibular system lesions?

A

Ipsilateral head tilt
Nystagmus
Ataxia with leaning and falling, less commonly tight circling
Positional strabismus

117
Q

Are paresis and proprioception deficits caused by peripheral or central lesions?

A

Central

118
Q

Which legs are affected by lesions located:
C1-T2
T3-S3

A

C1-T2: all legs

T3-S3: pelvic limbs

119
Q

Regarding spinal reflexes, where should you test to see if LMNs are working in the thoracic and pelvic limbs?

A

C6-T2: spinal reflexes in thoracic limbs

L4-S3: spinal reflexes in pelvic limbs

120
Q

What would you see with spinal lesions located at C1-C5?

A

Tetra or hemiparesis/plegia
Normal spinal reflexes
Normal muscle tone, no muscle atrophy
Possible Horner’s syndrome, resp difficulties, urinary retention

121
Q

What would you see with spinal lesions located at C6-T2?

A

Tetra or hemiparesis/plegia
Reduced muscle tone and atrophy
Reduced spinal reflexes in thoracic limbs
Possible reduced cutaneous trunci reflex

122
Q

What would you see with spinal lesions located at T3-L3?

A

Paraparesis/plegia (normal thoracic limbs)
Reduced cutaneous trunci reflex caudal to spinal lesion
Normal spinal reflexes

123
Q

What would you see with spinal lesions located at L4-S3?

A

Paraparesis/plegia of pelvic limbs
Reduced muscle tone, and atrophy in pelvic limbs
Reduced spinal reflexes in pelvic limbs, reduced anal tone and perineal reflex in more caudal lesions

124
Q

What do the following affect:
Neuropathies
Junctionopathies
Myopathies

A

Neuropathies: peripheral nerve
Junctionopathies: neuromuscular junction
Myopathies: muscle

125
Q

How would you tell if a neuropathy is motor or sensory in origin?

A 
Motor= flaccid paresis and reduced tone and muscle atrophy
Sensory= proprioceptive deficits, decreased sensation or paraesthesia (self-mutilation)

Can affect one, a group or most/all nerves
Cause reduced spinal or cranial nerve reflexes

126
Q

What clinical signs are associated with myopathies?

A

Generalised weakness and/or exercise intolerance-stiff stilted gait; neck ventroflexion
No proprioceptive deficits
Variable muscle tone and bulk

127
Q

What do you look out for regarding posture when doing a neuro exam of a horse?

A

Head tilt
Wide stance
Head and/or body turn
Walk horse, stop suddenly but leave head collar loose, does horse correct its stance?

128
Q

How can you test a horse’s sight ? (optic nerve)

A

Walk horse loosely over obstacles-can horse see them and step over them?

129
Q

How can you check facial sensation in a horse?

A

Touch horse in various places on face and see if it reacts

130
Q

How would you tell if a horse has facial nerve paralysis?

A

Drooping eye, ear, lip, lack of facial symmetry

131
Q

How can you tell if a horse has vestibular problems?

A

Head posture, induced eyeball movement, normal vestibular nystagmus
Horses can compensate for vestibular problems through sight, eg correcting a head tilt, so if you blindfold a horse and there is still a head tilt/ataxia etc you know there’s vestibular disease

132
Q

How would you perform the slap test on a horse?

A

Put hands on larynx, slap horse over scapula on one side, opposite arytenoid should flick open

133
Q

How can you asses hypoglosal nerve function in a horse?

A

Try to grab tongue, should be lot of resistance. Do on both sides.

134
Q

Give the cause of each:
Generalised weakness, no ataxia and spasticity
Localised weakness
Weakness and ataxia

A

Generalised weakness, no ataxia and spasticity: neuromuscular disease
Localised weakness: LMN or peripheral nerve disease
Weakness and ataxia: UMN descending motor pathway, ipsilateral and caudal to the site of the lesion
“Weakness” associated with vestibular disease: tend to lean and fall towards the side of the lesion

135
Q

Compare clinical signs of UMN and LMN lesions

A 
UMN: 
–Spinal cord and brainstem 
–↑ muscle tone 
–↑ reflexes 
–No atrophy 
–Variable weakness and sensory loss depending on depth of lesion 
LMN: 
–Spinal cord grey matter and peripheral nerves 
–↓ muscle tone 
–↓ reflexes 
–Muscle atrophy 
–Weakness and sensory loss
136
Q

How can you test for paresis in a horse?

A

Look for hoof wear: dragging toes, low arc of flight of hoof
Tail pull (see if horse corrects itself): at rest (LMN) and during walk (UMN)
Hopping, circling, slope: trembling, buckling of weak limb, knuckling over
Generalised weakness: horses walk better than they stand

137
Q

How do you test for proprioceptive deficits in a horse?

A

Look for poor coordination, swaying, limb moving excessively during swing phase (weaving, abduction, adduction, crossing of limbs, stepping on themselves)
Exaggerated by tight circles: pivoting, circumduction, serpentine, sudden stopping, backing, hills, raising the head

138
Q

Cell bodies of LMNs are located where?

A

Grey matter (ventral horn) of spinal cord

139
Q

Cell bodies of UMNs are located where?

A

Motor centre of brain

140
Q

Abnormalities in the brainstem or spinal cord white matter result in what?

A

Ataxia, paresis, hypermetria, hypometria

141
Q

Abnormalities in the vestibular system result in what?

A

Ataxia, hypometria

142
Q

Abnormalities in the cerebellum result in what?

A

Ataxia, hypermetria

143
Q

Abnormalities in the ventral grey matter or motor nerves (LMN) result in what?

A

Paresis

144
Q

Give some signs of spinal cord disease in a horse

A

Ataxia, paresis, weakness, hypermetria, hypometria, postural deficits, recumbency
As compression increases: loss of proprioception, motor weakness, loss of sensory perception, loss of pain

145
Q

What is the cauda equina?

A

Bundle of spinal nerves and spinal nerve roots consisting of the second through fifth lumbar nerve pairs, first through fifth sacral nerve pairs, and the coccygeal nerve, all of which arise from the lumbar enlargment and conus medullaris of spinal cord

146
Q

How do you class the deficits associated with spinal cord disease in a horse?

A

Subtle: deficits barely detected at normal gait, occur during backing, stopping, turning, swaying, neck extension
Mild: detected at normal gait, exaggerated by above manoeuvres
Moderate: prominent at normal gait, tend to buckle and fall with above manoeuvres
Severe: tripping and falling spontaneously at normal gait to complete paralysis

147
Q

If a recumbent horse has good use of its thoracic limbs, where is the spinal lesion located?
What about if it has weak use of its thoracic limbs?

A

Good use of thoracic limbs: caudal to T2

Weak use of thoracic limbs: caudal to cervical vertebrae

148
Q

What should you ask when taking a history of a cow as part of a neuro exam?

A 
Age 
When calved?
Acute onset?
Continuous or episodic?
Number of animals affected?
Did problems start when housed or at pasture?
Possibility of access to poisons 
Diet, recent dietary changes?
Time of year
149
Q

When investigating a neurological problem in a cow, what should you look for in the surroundings?

A 
Lead (old batteries/paint)
Cadavers
Poisonous plants
Ration:
-Proportion of concentrates in ration
-Rough assessment of VitD supply
-Quality of silage
150
Q

Is circling usually in the same or opposite direction to the cortex lesion that causes it?

A

Opposite

151
Q

Falling over is associated with lesions where?

A

Cerebellum

152
Q

Headpressing normally indicates what?

A

Increased cranial pressure/encephalitis

153
Q

What should you observe before doing a neuro exam on a cow?

A

Behaviour: circling, headpressing, blindness
Consciousness: over-excited, response to stimuli, depressed, coma etc
Stance: tremors, spams
Locomotion: ataxia, weakness

154
Q

How can you test coordination reflexes in a cow?

A

Eye movement: when head is turned, eye should move in opposite direction
‘Crossover’: cross one leg in front of the other, does animal correct instantly?
Conscious proprioceptive: walk towards small obstacle, animal will lift leg when it arrives at it
Unconscious proprioceptive coordination: same but blindfolded-will animal correct when it feels the obstacle?

155
Q

How would you identify an animal with Hypoglossal nerve dysfunction?

A

Tongue cannot be retracted and hangs out of mouth

156
Q

How can you test spinal reflexes in a cow?

A

Pinch withers
Tail reflex (touch perineum or perineal side of tail)
Anus reflex (thermometer -> contract sphincter)
Scrotal reflex (wrinkling of scrotal skin when touched)
Patella reflex (calves)
Pinch skin between claws-> bend leg

157
Q

What 3 things should you not see in CSF?

A

Protein, WBC, bacterial growth

158
Q

Give some conditions which cause cortical signs in cows

A 
Rabies 
Pseudorabies 
Meningitis 
Lead poisoning 
BSE
Brain abscess/ tumour
159
Q

Describe meningitis in cows

A

Affects calves 1 weeks of age which have not had enough colostrum
Extension of local infection (sinusitis) or haematogenous- look for another lesion
Diarrhoea, fever, anorexia, stiff neck, hyperaesthesia (abnormal increase in sensitivity to touch, pain or other sensory stimuli), head pressing, weakness, lack of suck reflex, depression
May present like hypomagnesaemia (‘staggers’)
Early treatment essential, prognosis poor

160
Q

Why is penicillin not a good drug choice when treating meningitis?

A

No activity against gram negatives

161
Q

Give some antibiotics you would use to treat meningitis

A

Doxycycline
Trimethoprim
Fluoroquinalones

162
Q

What is CCN?

A

Cerebro-cortical necrosis
Necrosis of the grey matter, caused by thiamine (vit B1) deficiency
More common in cattle 6-18 months old (pre-ruminant age, Vit B1 is formed by microorganisms in rumen)
Can be an absolute deficiency (pre-ruminant calves) or relative deficiency (large amount of bacterial thiaminases produced when overindulging on concentrates)
Early signs: head up in the air, appears blind, diarrhoea, hyperaesthesia, muscle tremors
Late signs: opisthotonos (hyperextension of back, head back), headpressing, strabismus, miosis (pupil constriction), repetitive chewing, facial twitching, convulsions
Good response to treatment if diagnosed early

163
Q

How do you diagnose CCN? (Cerebro-cortical necrosis)

A 
History
Clinical signs 
Response to treatment 
Blood thiamine assay
Postmortem: brain pale and swollen, patchy yellow discolouration (accumulation of lipofusion pigments in lipophages- cells that ingest fat), fluoresce under UV light
164
Q

How do you treat CCN (cerebro-cortical necrosis)?

A

10-15mg/kg thiamine (Vit B1) every 4 hours for 24 hours
Responds in 3-6 hours
Corticosteroids and mannitol (osmotic diuretic)
Identify and rectify underlying cause
Thiamine-supplemented ration; introduce concentrates slowly

165
Q

Describe lead poisoning in cows

A

Primarily young cattle (due to curious nature)
Acces to old car batteries, engine oil, old lead paint, asphalt roofing, environmental pollution
Acute encephalopathy
Cerebral and GI signs
Poor prognosis
Consider whether meat or milk is suitable for human consumption; estimated 6-7 months for blood and milk levels to return to normal
Alert APHA

166
Q

What are the clinical signs of lead poisoning in cows?

A

First stages: stand alone, depressed, hyperaesthesia, muscular fasciculations
Progresses to ataxia, blindness (but PLR present), head pressing, episodic manic behaviour, convulsions, coma, bloat, abdominal pain, frothy mouth
Severe cases: die in 12-24 hours

167
Q

How do you treat lead poisoning in cows?

A

Control fits with IV pentobarbitone (dose to effect)
CaEDTA (binds lead) slow drip, 110mg/kg IV every 2nd day for 3 treatments
Thiamine 20-100mg/kg SC daily (mobilised intracellular lead into blood)
Oral magnesium sulphate 500-1000g to precipitate lead from GI tract

168
Q

Describe nervous ketosis in cows

A

Aetiology same as ketosis (acetonaemia, too many ketones in blood)
Acute onset of obsessive licking, circling, staggering, head pressing, pica, aggression
Signs last 1-2 hours; recur at ~ 10-hourly intervals
Diagnosis – ketones in blood or Rotheroes test
Treatment 40% dextrose i.v, propylene glycol BID, corticosteroids

169
Q

Describe hypomagnesaemia in cows

A

Especially in pastured lactating beef cows in first months after calving, as Mg is expressed in milk (but also non-lactating animals); Occasionally in 3-6 month old ruminants (on poor diet; little Mg in milk, less able to resorb from bones > 3 m)
Classically in spring but also autumn/winter
Mg stored in body not readily available
If uptake disturbed (Na:K ratio in rumen, stressors, not enough in diet) -> levels rapidly dangerously low

170
Q

What are the clinical signs of hypomagnesaemia in cows?

A

Hyperexcitable, may charge
Erect ears, ear twitching, hyperaethesia
Muscle fasciculations / tremors
Frenzied running turning into staggering
Lateral recumbency with violent episodes of ophistotonus (hyperextension of back, head back) and convulsions (can be triggered by any stimulus)
Dead within an hour of the seizure episodes

171
Q

What causes salt poisoning in cows?

A

Either water containing too much salt or water deprivation
Sodium deposition in the brain blocks anaerobic glycolytic pathways; increased intracranial pressure may also occur (attracts water)

172
Q

When does salt poisoning occur in cows?

What are the clinical signs?

A

Mostly during summer; normally a clear clue in the history Dehydrated, depression, diarrhoea and colic, star-gazing, blindness, aggressiveness, hyperexcitability, vocalisation, head pressing, teeth grinding

173
Q

How do you treat salt poisoning in cows?

A

Poor prognosis; rehydrate first then hypertonic saline (otherwise intracranial pressure increased)

174
Q

Describe pseudo rabies in cows

A

(Aujesky’s disease, Mad Itch)
Depression, ataxia, conscious prioprioceptive deficit, circling, nystagmus, strabismus, aggression, pruritus (of the head), dead within 2 days.
Contact with pigs.

175
Q

What would you see in a cow with rabies?

A

Hyperexcitability, fear, rage, depression, flaccid paralysis

176
Q

Describe ‘occasional acute cortical disease’ (Hydrocephalus) in cows

A

Holstein, Jersey, Friesan, Guernsey
Failure of drainage of CSF -> increased intracranial pressure
Domed cranium
Diffuse cerebral signs: mania, head pressing, muscle tremor, convulsions, blindness, weakness

177
Q

Brain abscesses in cows are usually caused by what?

A

Arcanobacterium pyogenes

Often extension of sinus infection (so initially in front cortex)

178
Q

Give the clinical signs of brain abscesses in cows

A

slower onset and more asymmetric signs than meningitis.
Initially vision loss/mydriasis (dilation) in contralateral eye, may progress to compulsive walking, head pressing, circling, head tilt (towards lesion), depression or mania, coma.
When extending to base of the brain may give ‘cranial nerve signs’. Later stages: hypertonicity, hyperflexia, opisthotonusm (hyperextension of back, head back), coma, convulsions.

179
Q

How do you treat a brain abscess in cows?

A

Antibiotics (same as meningitis):
Doxycycline
Trimethoprim
Fluoroquinalones

180
Q

What would you see on a histological slide of the brain of a cow infected with BSE?

A

Vacuolisation of brainstem; spongy brain tissue

181
Q

What causes BSE?

A

Aetiology unknown
Prion hypothesis: infectivity caused by a struturally modified form of the host protein PrP (normal membrane-associated protein found in CNS) Modified PrP promotes the conversion of other PrP molecules which accumulate within the affected neurones
No evidence of cattle to cattle transmission

182
Q

What are the clinical signs of BSE?

A

3-6 years
Initial signs often subtle but always progressive, rate of progression variable from 2-3 weeks to several months
Weight loss
Hyperaesthesia, fine fasiculations of head and neck shoulder flank, teeth grinding
Apprehensive when approached, reluctant to be milked or moved through gate ways
Ataxia
Aggression

183
Q

What action must be carried out if a cow is suspected of having BSE?

A

Notifiable Disease -> Inform DEFRA
Veterinary officer will inspect animal and decide whether to PTS
Farmer will be compensated and trace put out on the offspring of animal
If disease is confirmed, offspring will also be culled (10% more likely to develop BSE)

184
Q

How do you diagnose BSE in the lab?

A

Long incubation period of BSE makes diagnostic and screening tests difficult
Current tests for PM only; no test for live animals
Histopathology
Western Blotting
Immunocytochemistry

185
Q

Describe hypovitaminosis A in cattle

A

Deficiency in Vit A or carotene (precursor)
Vitamin A is plentiful in green feeds and forages
Deficiency is usually seen in housed animals with straw/cereal based diets
Signs caused by thickening of dura mater/ abnormal bony growth in the brain cavity, increased CSF pressure
Congenital or acquired
Can also cause retinal degeneration- absent PLR

186
Q

How would you describe the fundus of a cow with hypovitaminosis A?

A

Pale and enlarged optic disc with indistinct edges

187
Q

Give the clinic signs of hypovitaminosis A for:
Calves born to deficient dams
Deficienct calves
Older cattle

A

Calves born to deficient dams: blindness, weakness, domed forehead, thickened carpal joints
Deficient calves: blindness, anorexia, diarrhoea, pneumonia (‘ill thrift’) Older cattle: blindness, star gazing, nystagmus, ataxia (hind limbs first), convulsions; also diarrhoea and occasionally thickening and whitening of cornea

188
Q

What is the treatment for hypovitaminosis A in cattle?

A

400iu/kg vitamin A daily (good response even in fitting animals; within 48hrs)
Older cattle with occular form often do not respond
Check diet contains 40iu/kg BW per day (green feed)

189
Q

Describe cerebellar hypoplasia in cattle

A 
Acquired (BVD) – dam is infected at 90-170 days gestation 
Severity varies: affects balance (ataxia, falling backward) or unable to stand, tremor, hypermetria, nystagmus 
Severe opisthotonus (hyperextension of back, head back)
190
Q

Describe listeriosis in cattle

A

Listeria monocytogena
Environmental pathogen, infections are sporadic and usually associated with feeding poor quality silage, fermentation and soil contamination
Infection travels up to brainstem from conjunctiva in the face/mouth via trigeminal nerve. Forms microabscesses in brain stem/cerebellum/spinal cord; may progress to meningoencephalitis

191
Q

Give the clinical signs of listeriosis in cattle

A

Fever
Dull; loss of lip and cheek muscle tone: difficulty in eating chewing, accumulation of cud in cheek, salivation, tongue protruding
Ptosis (drooping eyelid), drooping of ear on the deviant side, circling Headpressing, propulsive walking

192
Q

How do you treat listeriosis in cattle?

A

Aim is stop disease getting worse as neurological deficits may not resolve
High doses of penicillin: 44,000iu/kg BID for 7-14 days followed by 22,000iu/kg BID for 7-14 days
High doses of oxytetracyclines
Remove underlying cause ie silage

193
Q

Spinal fractures usually affect cows of what age?

Give some underlying causes

A

3-6 month old calves

Investigate underlying cause; VitD, calcium or copper deficiency?

194
Q

Spinal abscesses in cattle are usually secondary to what?

A 
Osteomyelitis of vertebrae
Haematogenous 
Injections 
Bacteria: A. pyogenes, Staph. aureus, Fusobacterium necrophorum, P. haemolitica
Often cervical
195
Q

Who do you treat spinal abscesses in cattle?

A

Antibiotics:
Fluoroquinalones
Doxycycline
Trimethoprim

196
Q

What clinics signs do you see in cows affected with spinal abscesses?

A

Pain, beta, swelling, animals are stiff and reluctant to eat from ground
If abscess is close to brain: hyperaesthesia, spastic muscle contractions, recurrent profuse sweating

197
Q

What is spastic paresis?

A

Asymmetric spasticity and hypertonia of the extensor muscles of the rear limbs
Continuous when the animal stands, but not when it lays down
Most breeds, from a few weeks to 6 months
Genetic predisposition?

198
Q

What are the clinical signs of spastic paresis in cattle?

A

Excessive tone of gastrocnemius muscle -> hyperextended hock
Unilateral or bilateral
If unilateral, the affected leg is thrust out behind during walking, and advanced with a swinging motion without touching the ground. Unable to flex hock.
Often spend longer lying down

199
Q

How do you treat spastic paresis in cattle?

A

Neurectomy of the tibial nerve rootless innervating the gastrocnemius muscle
High epidural or GA
If bilateral then leave 6-10 weeks inbetween
Success rate= 60%

200
Q

Describe tetanus

A

Exotoxins produced by Clostridium tetani, found in soil and GI tract
Spores enter wounds eg castration wound, or spread directly from GI tract
Multiplies at site of infection (anaerobic) producing neurotoxins

201
Q

What are the clinical signs of tetanus in cattle?

A

Incubation variable, normally 2-4 weeks
Progression of disease takes 4-5 days
Prolapsed 3rd eyelid, RUMEN TYMPANY, tail elevation
Progression to generalised muscular tetany and ‘rocking horse’ position
Wide leg stance
Extended head posture
Recumbency, convulsions, death

202
Q

How can you diagnose tetanus in cattle?

A

No test
No characteristic PM signs
Identify site of infection and attempt to culture

203
Q

How do you treat tetanus in cattle?

A

Full blown tetanus: poor prognosis -> PTS
Keep animal well-bedded, kept in dark, quiet
High doses of penicillin
Irrigate infection site with penicillin and antitoxin
Muscle relaxants like ACP until signs resolve
Vaccination

204
Q

What is botulism?

A

Clostridium botulinum in poultry waste given as food (illegal), poultry litter applied to pasture or used as bedding
Poor quality BBS

205
Q

Give the clinical signs of botulism in cattle

A

Muscle weakness -> ataxia -> paralysis
Anorexia, dilated pupils
Excessive drooling
Droopy expression, tongue hanging out of mouth
Decreased rumen motility, bloat, constipation
Resp failure -> death

206
Q

How do you diagnose botulism in cattle?

A 
History
Clinical signs 
No specific PM findings 
Toxin in serum ELISA 
Samples of feed or bedding may help consult with lab
207
Q

How do you treat botulism in cattle?

A

Treatment is suppurative
Fluids
Emetics to remove toxins
Poor prognosis, but may recover if caught early and infection removed

208
Q

Peripheral neuropathies in cattle involve which nerves?

A

Obturator
Peroneal
Sciatic

209
Q

Obturator neuropathy in cattle occurs when?

A

Following dystocia esp heifers

Obturator nerve damaged by foetal pressure

210
Q

What are the clinical signs of obturator neuropathy in cattle?

A

Unable to adduct limbs

211
Q

What is the treatment for obturator neuropathy in cattle?

A

Chain between hind limbs, soft bedding, corticosteroids

212
Q

Peroneal nerve is a branch of what nerve?

A

Sciatic

213
Q

Give the clinical signs of peroneal neuropathy in cattle

A

Hyperextension of hock, fetlock and digits flexed (knuckled over)
Loss of skin sensation below fetlock dorsal surface

214
Q

Describe sciatic neuropathy in cattle

A

Damage occurs when cow is recumbent and struggling to rise
Non weight bearing, no sensation distal to stifle
Guarded prognosis

215
Q

What is malacia?

A

Softening of an organ or tissue

Year 3 (28 decks)

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