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ACVIM General copy > Neuro > Flashcards

Neuro Flashcards

1
Q

What are the steps of neurotransmission?

A
  1. Action potential reaches terminal
  2. Voltage gated Ca channels open
  3. Synaptic vesicles fuse with terminal membrane
  4. ACh released into synaptic cleft
  5. ACh binds to receptors
  6. Ligand gated Na/K channels open → end plate potential
  7. ACE degrades ACh
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2
Q

Which cranial nerves have general somatic efferent components?

A

3, 4, 5, 6, 7, 9, 10, 11, 12

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3
Q

Where are the cell bodies for spinal nerve GSE LMN for the thoracic limbs located?

A

C6-T2

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4
Q

Where are the cell bodies for spinal nerve GSE LMN for the pelvic limbs located?

A

L4-S3

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5
Q

Where is the cell body located for cranial nerve 3?

A

Oculomotor N

Midbrain

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6
Q

Where is the cell body located for cranial nerve 4?

A

Trochlear N

Midbrain

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7
Q

Where is the cell body located for cranial nerve 5?

A

Trigeminal N

Pons

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8
Q

Where is the cell body located for cranial nerve 7?

A

Facial N

Rostral medulla

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9
Q

Where is the cell body located for cranial nerve 9?

A

Glossopharyngeal N

Medulla

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10
Q

Where is the cell body located for cranial nerve 10?

A

Vagus N

Medulla

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11
Q

Where is the cell body located for cranial nerve 11?

A

Accessory N

Medulla

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12
Q

Where is the cell body located for cranial nerve 12?

A

Hypoglossal N

Medulla

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13
Q

What is the function of general somatic efferent fibers?

A
  1. Final motor innervation of muscles

2. Motor component of reflexes

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14
Q

What is the function of general somatic afferent fibers?

A
  1. Detect temperature, touch, and nociception
    - For conscious awareness
    - For reflex arcs
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15
Q

General somatic afferent fiber ascending tracts will reach the (ipsalateral/contralateral) cerebral cortex

A

CONTRALATERAL

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16
Q

What is the function of general proprioception pathways?

A
  1. Detects position and movement in muscles and joints
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17
Q

What are the components of all reflex arcs?

A
  1. Peripheral sensory component (GSA)
  2. Central Component
    - In spinal cord for spinal reflexes
    - In brain region for cranial nerve reflexes
  3. Peripheral motor component (GSE)
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18
Q

A lesion anywhere in a reflex arc will lead to (increased/decreased) reflexes

A

Decreased

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19
Q

A spinal cord lesion cranial to a reflex arc can lead to (increased/decreased) reflexes

A

Increased

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20
Q

Withdrawal Reflex (Thoracic Limb)

  1. Spinal Cord Segment
  2. Nerves
  3. Muscles
A
  1. C6-T2
  2. All thoracic limb nerves
  3. All flexors
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21
Q

Patellar Reflex

  1. Spinal Cord Segment
  2. Nerves
  3. Muscles
A
  1. L4-L6
  2. Femoral n.
  3. Extensors
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22
Q

Withdrawal Reflex (Pelvic Limb)

  1. Spinal Cord Segment
  2. Nerves
  3. Muscles
A
  1. L6-S1
  2. Sciatic n.
  3. Flexors
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23
Q

Cutaneous Trunci Reflex

  1. Spinal Cord Segment
  2. Nerves
  3. Muscles
A
  1. C8-T1
  2. Sensory: Segmental spinal nerves.
    Motor: Lateral thoracic nerve
  3. Cutaneous trunci muscle
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24
Q

Perineal Reflex

  1. Spinal Cord Segment
  2. Nerves
A
  1. S1-S3

2. Pudendal

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25
Q

Anal Sphincter Tone

  1. Spinal Cord Segment
  2. Nerves
  3. Muscles
A
  1. S1-S3
  2. Caudal rectal n.
  3. External anal sphincter
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26
Q

Which cranial nerves are associated with the prosencephalon?

A

1 and 2

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27
Q

Which cranial nerves are associated with the midbrain?

A

3 and 4

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28
Q

Which cranial nerves are associated with the pons?

A

5

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29
Q

Which cranial nerves are associated with the medulla?

A

6-12

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30
Q

All cranial nerves enter/exit their respective brain region (ipsilaterally/contralaterally)

A

Ipsilaterally

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31
Q

The prosencephalon processes sensory information from (ipsilateral/contralateral) cranial nerves

A

Contralateral

- ex. visual information from the right eye is processed by the left cerebrum

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32
Q

Pupillary light reflex

  1. Sensory nerve
  2. Motor nerve
  3. Normal result
A
  1. CN 2
  2. CN 3
  3. Pupil constriction
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33
Q

Menace response

  1. Sensory nerve
  2. Motor nerve
  3. Normal result
A
  1. CN 2, contralateral cerebral cortex
  2. CN 7
  3. Blink
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34
Q

Palpebral reflex

  1. Sensory nerve
  2. Motor nerve
  3. Normal result
A
  1. CN 5
  2. CN 7
  3. Blink
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35
Q

Temporal muscle symmetry

  1. Sensory nerve
  2. Motor nerve
  3. Normal result
A
  1. -
  2. CN 5
  3. Should be symmetrical, no atrophy
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36
Q

Lip tone/symmetry

  1. Sensory nerve
  2. Motor nerve
  3. Normal result
A
  1. -
  2. CN 7
  3. Should be symmetrical
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37
Q

Physiological nystagmus

  1. Sensory nerve
  2. Motor nerve
  3. Normal result
A
  1. CN 8
  2. CN 3 and 6
  3. Fast phase in direction of movement
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38
Q

Fixed strabismus

  1. Sensory nerve
  2. Motor nerve
  3. Normal result
A
  1. -
  2. CN 3, 4, or 6
  3. Normal pupil vector
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39
Q

Positional strabismus

  1. Sensory nerve
  2. Motor nerve
  3. Normal result
A
  1. CN 8
  2. -
  3. Eyes track with head position
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40
Q

Nasal sensation

  1. Sensory nerve
  2. Motor nerve
  3. Normal result
A
  1. CN 5, contralateral cerebral cortex
  2. -
  3. Respond to noxious stimulus
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41
Q

Gag reflex

  1. Sensory nerve
  2. Motor nerve
  3. Normal result
A
  1. CN 9 and 10
  2. CN 9 and 10
  3. Cough/Repel finger
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42
Q

What are the functions of general visceral efferent fibers?

A
  1. LMNs of the autonomic nervous system

2. Innervate smooth muscle of blood vessels, visceral structures, glands, and cardiac muscle

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43
Q

Where are the preganglionic neurons located for the parasympathetic nervous system GVE?

A
  1. Brainstem nuclei of CN 3, 7, 9, and 10

2. Spinal cord segments S1-S3

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44
Q

Where are the preganglionic neurons located for the sympathetic nervous system GVE?

A
  1. Spinal cord segments T1-L4/5
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45
Q

What is the primary integrating center for the autonomic nervous system?

A
  1. Hypothalamus
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46
Q

Parasympathetic

The preganglionic axon is (long/short) and the postganglionic axon is (long/short)

A
  1. Long

2. Short

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47
Q

Sympathetic

The preganglionic axon is (long/short) and the postganglionic axon is (long/short)

A
  1. Short

2. Long

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48
Q

Postganglionic Neurotransmitter

  1. Parasympathetic
  2. Sympathetic
A
  1. ACh

2. Norepinephrine

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49
Q

Where are the preganglionic cell bodies located for the GVE parasympathetic

A
  1. Nuclei in midbrain and medulla

2. Nuclei in lateral horn of sacral spinal cord segments

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50
Q

What receptor is used for GVE parasympathetic neurotransmitters?

A
  1. Muscarinic ACh receptors
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51
Q

Where are the preganglionic cell bodies for the GVE sympathetic fibers located?

A
  1. Lateral/ventral horn of spinal cord segments T1-L4
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52
Q

The general visceral afferents travel to the CNS mainly through which cranial nerves?

A
  1. Facial n → from salivary and lacrimal glands
  2. Glossopharyngeal n → pharyngeal mucosa, caudal 1/3 of tongue, and carotid sinus
  3. Vagus n → larynx, trachea, esophagus, thoracic and abdominal viscera
    - Vagus is 80% GVA fibers
    - Cell body location: distal vagal ganglion
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53
Q

Which nucleus is shared by the general visceral afferents? Where is it located?

A
  1. Solitary nucleus

2. Medulla

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54
Q

What are the important GVE LMN components?

A
  1. Control of the pupils
  2. Control of micturition and defecation
  3. Control of the enteric system
  4. Control of the cardiorespiratory system
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55
Q

Describe the parasympathetic innervation to the eye

  1. Preganglionic cell body location
  2. Cranial nerve carrying preganglionic fibers
  3. Ganglion
  4. Effector organ
  5. Effect
A
  1. Parasympathetic nucleus of cranial nerve 3, rostral midbrain
  2. Cranial nerve 3
  3. Ciliary ganglion
  4. Postganglionic axons to the ciliary body
  5. Pupillary constriction
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56
Q

What would you expect with dysfunction of the parasympathetic portion of CN 3?

A
  1. Mydriasis
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57
Q

Describe the sympathetic innervation to the eye

  1. Preganglionic cell body location
  2. Cranial nerve carrying preganglionic fibers
  3. Ganglion
  4. Effector organ
  5. Effect
A
  • UMNs from hypothalamus via lateral tectotegmentospinal tract
    1. Lateral horn T1-T4
    2. Ventral root → ramps communicans → sympathetic trunk → vagosympathetic trunk
    3. Cranial cervical ganglion, pass through tympanic bulla, travel with CN V to orbit
    4. Orbitalis muscle, ciliary body, pupillary dilator
    5. Pupillary dilation
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58
Q

What is the only sensory system that lacks a thalamic nucleus for projection to the cerebral cortex?

A

Olfaction

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59
Q

An abnormal mentation indicates a general localization to which area?

A

Intracranial

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60
Q

If an animal is showing abnormal mentation there is a problem in either the ______ or ______.

A
  1. Prosencephalon (Telencephalon + Diencephalon)
    * Rarely causes stupor or coma but can cause obtundation or dementia
  2. Caudal Fossa (Midbrain, pons, medulla)
    * Can lead to obtundation, stupor, or coma
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61
Q

Define

  1. Paresis

2. Plegia

A
  1. Decreased voluntary motor function

2. NO voluntary motor function (paralysis)

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62
Q

What would be indicated by short, choppy steps, crouched stance, look weak?

A
  1. LMN paresis/plagia
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63
Q

How would the gait of an animal with a LMN paresis/plageia appear?

A

Short, choppy steps, crouched stance, look weak

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64
Q

What would be indicated by long, lopey steps, exaggerated, look stiff?

A
  1. UMN paresis/plagia
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65
Q

How would the gait of an animal with an UMN paresis/plagia appear?

A

Long, lopey steps, exaggerated, look stiff

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66
Q

Where does a head tilt (eyes are not parallel to the floor) localize?

A

Vestibular

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67
Q

Where does a head turn (entire head facing one direction) localize?

A

Prosencephalon

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68
Q

When does decerebrate rigidity occur?

A
  1. Severe brainstem lesions
  2. Cerebrum is disconnected from brainstem
    * UNCONSCIOUS
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69
Q

When does decerebellate rigidity occur?

A
  1. Cerebellum significantly affected

* NORMAL mentation

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70
Q

When does Schiff Sherrington posturing occur?

A
  1. Severe thoracolumbar spinal cord injury

2. ASCENDING UMNs from pelvic limbs to thoracic limbs are lost → loss of UMNs to pelvic limbs

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71
Q

White matter is (axons/cell bodies) and gray matter is (axons/cell bodies)

A
  1. Axons

2. Cell Bodies

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72
Q

The dorsal white matter is (ascending/descending) (sensory/motor) projections and are involved in _____.

A
  1. Ascending
  2. Sensory
  3. Postural reactions
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73
Q

The ventral white matter is (ascending/descending) (sensory/motor)

A
  1. Descending
  2. Motor
    * These are upper motor neurons
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74
Q

The ventral horn cells bodies are what?

A

Lower motor neurons

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75
Q

UMNs are generally (excitatory/inhibitory) to the LMNs they synapse with

A

Inhibitory

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76
Q

Loss of LMNs to the pelvic limbs will affect which region of the spinal cord and will affect which muscular groups?

A
  • L4-Caudal*
    1. Pelvic limbs
  • Flaccid paraparesis/paraplegia
  • Decreased/absent PL reflexes
  • Decreased PL tone
    2. External urethral sphincter
  • LMN urinary incontinence
  • Constant dribbling
    3. Anal sphincter
  • Dilated anus
  • LMN fecal incontinence
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77
Q

What happens to the pelvic limbs with a T3-L3 lesion?

A
  • Loss of UMNs*
    1. Pelvic limbs
  • Spastic paraparesis/paraplegia
  • Normal to increased PL reflexes
  • Increased muscle tone
    2. External urethral sphincter
  • UMN urinary incontinence
    3. Loss of ascending sensory projections from pelvic limbs
  • General proprioceptive ataxia → crossing midline when walking
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78
Q

What happens in C6-T2 lesions?

A
  1. Loss of LMNs to thoracic limbs
    - Flaccid paresis/plegia
    - Decreased/absent TL reflexes
    - Decreased/absent TL muscle tone
  2. Loss of UMNs to pelvic limbs
    - Spastic paresis/plegia
    - Normal to increased PL reflexes
    - Increased muscle tone
    - GP ataxia
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79
Q

What happens in C1-C5 lesions?

A
  1. Loss of UMNs to both thoracic and pelvic limbs
    - Spastic tetraparesis/tetraplegia
    - Normal to increased TL and PL reflexes
    - Increased muscle tone
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80
Q

What happens in diffuse neuromuscular lesions?

A
  1. Loss of LMNs to thoracic and pelvic limbs
    - Flaccid tetraparesis/tetraplegia
    - Decreased to absent TL and PL reflexes
    - Decreased muscle tone x4
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81
Q

Neuromuscular disease (does/does not) affect ascending sensory projections. What does this mean?

A
  1. Does not

2. Postural reactions are intact → if there is enough motor function and the examiner is supporting

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82
Q

Lesions in the caudal fossa will have deficits (ipsilateral/contralateral) to the lesion

A

Ipsilateral

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83
Q

What deficits would you anticipate with a caudal fossa lesion?

A
  1. Abnormal mentation (obtundation, stupor, coma)
  2. Proprioceptive ataxia
  3. Upper motor neuron tetraparesis
  4. Cranial nerve deficits
    - Reduced eye movements
    - Increased pupil size
    - Inability to close eyelids
    - Abnormal gag reflex
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84
Q

Lesions in the prosencephalon will have deficits (ipsilateral/contralateral) to the lesion

A

Contralateral

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85
Q

The prosencephalon (is/is not) involved in gait generation

A

Is not

- NO GAIT DEFICITS with prosencephalic lesion

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86
Q

What are anticipated deficits with prosencephalic lesions?

A
  1. Abnormal mentation (obtundation/demented)
  2. Normal gait BUT circling TOWARD lesion, head turned TOWARD lesion
  3. Contralateral deficits
    - Postural reaction deficits
    - Cranial nerve deficits
  4. Seizures = prosencephalon
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87
Q

What are the three anatomical components of the vestibular system?

A
  1. Peripheral vestibular system (CN 8 in inner ear)
  2. Central vestibular system (vestibular nuclei in rostral medulla)
  3. Flocculonodular lobe of cerebellum and caudal cerebellar peduncle
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88
Q

What are the four hallmarks of vestibular disease?

A
  1. Head tilt
  2. Vestibular ataxia
  3. Spontaneous nystagmus
  4. Positional strabismus
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89
Q

The cerebellum is inhibitory to the (ipsilateral/contralateral) vestibular nuclei

A

Ipsilateral

*The cerebellum tones down the ipsilateral vestibular system

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90
Q

The fast phase of nystagmus will be (toward/away from) the lesion with vestibular dysfunction

A

Away from
* The lesion will remove the vestibular input from the affected side, therefore the brain interprets this as an increase in input from the unaffected side → the brain thinks you are turning toward the unaffected side → nystagmus is generated away from the lesion

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91
Q

A patient with ipsilateral CN 7 deficits or ipsilateral Horner’s syndrome indicates (peripheral/central) vestibular disease

A

Peripheral

92
Q

A patient with ipsilateral CN 5-12 deficits indicates (peripheral/central) vestibular disease

A

Central

93
Q

What are the clinical signs associated with classic vestibular disease?

A
  1. Ipsilateral head tilt
  2. Nystagmus fast phase away from the lesion
  3. Circling toward the lesion
  4. +/- ipsilateral postural reactions if central
94
Q

What are the clinical signs associated with paradoxical vestibular disease?

A
  1. Contralateral head tilt
  2. Nystagmus fast phase toward the lesion
  3. +/- ipsilateral postural reactions
95
Q

What is the key difference between paradoxical vestibular disease and classic central vestibular disease?

A

Posture reaction deficits on the opposite side of their head tilt
* The lesion will always be on the side of the posture deficit

96
Q

The cerebellar pathways are always (ipsilateral/contralateral)

A

Ipsilateral

97
Q

What are the common clinical signs associated with cerebellar lesions?

A
  1. Cerebella ataxia - hypermetria
  2. Intention tremors
  3. Truncal sway
  4. Postural reaction deficits
  5. +/- paraxodixical vestibular signs if flocculonodular lobe is involved
  6. MENTATION IS NORMAL
98
Q

Horner’s syndrome occurs due to loss of (sympathetic/parasympathetic) innervation of the eye

A

Sympathetic

99
Q

What are the components of Horner’s Syndrome?

A
  1. Miosis
  2. Enophthalmos
  3. Ptosis
  4. Protrusion of the 3rd eyelid
100
Q

What are the standing/extensor tracts? The walking/flexor tracts?

A
  1. Reticulospinal (midbrain, pons, medulla) & vestibulospinal (vestibular nuclei of medulla)
  2. Corticospinal & rubrospinal (midbrain)
101
Q

CSF is produced mainly by what structure? Where

A
  1. Choroid plexus

2. Lateral and 3rd/4th Ventricles

102
Q

The blood brain barrier is due to what characteristic of endothelial cells?

A
  1. Tight junctions
103
Q

The muscles of mastication have innervation from which cranial nerve?

A

CN 5

104
Q

Describe decerebellate posture

A
  1. Extension of neck and thoracic limbs

2. Flexion of the pelvic limbs

105
Q

Describe Schiff Scherington posture

A
  1. Flaccid paralysis of pelvic limbs

2. Extensor rigidity of thoracic limbs and opisthotonus

106
Q

Where does the sympathetic innervation of the eye originate? Where does it travel through?

A
  1. T1-T3

2. Vagosympathetic trunk

107
Q

What controls the movement of the eye?

A
  • LR6 SO4*
    1. Lateral rectus and retractor bulbs - CN 6
    2. Superior oblique - CN4
    3. Everything else (dorsal, medial, and ventral rectus and ventral oblique) - CN3
108
Q

What drug could cause central vestibular signs in dogs and cats?

A

Metronidazole

109
Q

Which infectious disease commonly causes central vestibular disease?

A

Rocky Mountain spotted fever

110
Q

What are differentials for peripheral vestibular disease?

A
  1. Idiopathic → old dogs and middle aged cats
  2. Otitis media/interna → 50% have CN 7 signs too
  3. Congenital vestibular disease
  4. Aminoglycosides
  5. Chlorhexidine ear flush
111
Q

Describe the production of epinephrine

A
  • Tyrosine → hydroxylated to dopa → decarboxylated to dopamine → transport of dopamine into vesicles → dopamine hydroxylated to norepinephrine
  • In adrenal gland → 80% of norepinephrine is methylated to epinephrine
112
Q

Which cranial nerves have parasympathetic components?

A

CN 3, 7, 9, 10

113
Q

A patient presents with Horner’s syndrome. 2.5% phenylephrine is placed in the eye and the eye does not dilate. Where is the lesion?

A
  1. PRE-ganglionic
114
Q

A patient presents with Horner’s syndrome. 2.5% phenylephrine is placed in the eye and the eye dilates. Where is the lesion?

A
  1. POST-ganglionic
115
Q

What are differentials for pre-ganglionic lesions causing Horner’s syndrome?

A
  1. Intracranial disease
  2. C1-T3 myelopathy
  3. Thoracic disease
  4. Jugular furrow
116
Q

What are differentials for post-ganglionic lesions causing Horner’s syndrome?

A
  1. Cats - retrovirus
  2. Evidence of otitis media/interna?
    - No: assume idiopathic - monitor
    - Yes: fluoroquinolone for 3 months or MRI
  3. Mass
117
Q

What are metabolic causes of polyneuropathy?

A
  1. Diabetes mellitus
  2. HYPOthyroidism
  3. HYPERthyroidism (in cats)
  4. Uremic encephalopathy
  5. Hepatic encephalopathy
  6. HYPOadrenocorticism
  7. HYPERadrenocorticism
  8. Pheochromocytomas
118
Q

What is the pathophysiology for diabetes mellitus causing polyneuropathy?

A
  1. Increased aldose reductase activity → accumulation of sorbitol and fructose
  2. Increased production/decreased scavenging of oxygen free radicals and impaired mitochondrial function
  3. Activation of protein kinase C → promotion of vasoconstriction and ischemia
119
Q

When does uremic encephalopathy occur?

A
  1. GFR <10-20% of normal
120
Q

True/False

The clinical signs of hepatic encephalopathy are correlated to the ammonia levels

A

False

121
Q

Where does absorption of the CSF occur?

A

Arachnoid villi

122
Q

Discospondylitis occurring due to migrating grass awns is most likely going to occur in what location?

A
  1. L2-L4
123
Q

What is the most common cause of discospondylitis?

A
  1. Hematogenous spread
    - Bacterial endocarditis, dental disease, UTI
    - Brucella spreads from a genital infection
124
Q

Which organisms are most commonly associated with discospondylitis?

A
  1. Coagulase + staphylococcus (S. aureus and S. pseudintermedius)
  2. Brucella
125
Q

What clinical signs are often associated with discospondylitis?

A
  1. FUO
  2. Osteomyelitis of other sties
  3. Paravertebral draining tracts
126
Q

What are radiographic findings associated with discospondylitis?

A
  1. Destruction of endplates adjacent to the affected disk
  2. Collapse of disc space
  3. Bone proliferation
127
Q

How is discospondylitis treated?

A
  1. Cephalosporins
  2. Beta lactase restant antibiotics
  3. TMS
  4. Chloramphenicol
128
Q

Masticatory Muscle Myositis

  1. Serum CK
  2. 2M Antibodies
  3. Other diagnostics
A
  1. Normal
  2. Positive (can be negative in chronic cases)
  3. Biopsy temporalis muscle
129
Q

Treatment for masticatory muscle myositis?

A

Steroids

130
Q

Polymyositis

  1. Serum CK
  2. 2M Antibodies
  3. Other diagnostics
A
  1. Normal
  2. Negative
  3. Biopsy large proximal limp muscles
131
Q

What are clinical signs associated with polymyositis?

A
  1. Stiff stilted gait
  2. Muscle atrophy
  3. Hyperesthesia
132
Q

Extraocular muscle myositis

  1. Serum CK
  2. 2M Antibodies
  3. Other diagnostics
A
  1. Normal
  2. Negative
  3. Demonstrate extra ocular muscle swelling by orbital ultrasound or MRI
133
Q

What clinical signs are associated with extra ocular muscle myositis?

A
  1. Restrictive strabismus

2. Can have bilateral exophthalmus

134
Q

How is extra ocular muscle myositis treated?

A
  1. Steroids
135
Q

What is the origin of dermatomyositis?

A

Familial immune mediated disease of striated muscle, skin, and MICROVASCULATURE

136
Q

What breed is predisposed to dermatomyositis?

A

Collies

137
Q

Which muscles are preferentially affected in dermatomyositis?

A
  1. Distal limb muscles and temporals

* Dermatitis due to microvasculature problems occur first then myositis

138
Q

What are causes of infectious inflammatory myopathies?

A
  1. Neosporum caninum

2. Toxoplasma gondii

139
Q

How is neospora treated?.

A

Clindamycin + TMS

140
Q

How is toxoplasma gondii treated?

A

Clindamycin

141
Q

Hypothyroid Myopathy

1. Serum CK

A
  1. Normal
142
Q

Hyperthyroid Myopathy

1. Serum CK

A
  1. Markedly elevated
143
Q

What breed is predisposed to Cushing’s myopathy/myotonia?

A

Apricot poodles

144
Q

What is seen on biopsies of Cushing’s myopathy/myotonia?

A
  1. Type 2 fiber atrophy and excessive lipid accumulation
145
Q

Which muscles are preferentially affected in steroid myopathies?

A
  1. Masticatory muscles → whole body can be affected as well
146
Q

What is seen on histopathology with steroid myopathies?

A
  1. Type 2 fiber atrophy and excessive lipid accumulation
147
Q

What clinical signs are associated with Coonhound Paralysis?

A
  1. Ascending tetraparesis or tetraplegia
    - Usually retain the ability to wag their tail
  2. Axonal loss predominates
148
Q

What is seen on biopsy in patients with coonhound paralysis?

A
  1. Lymphocytic radiculitis

2. Demyelination of the ventral (more common) and dorsal nerve roots

149
Q

What is the treatment for coonhound paralysis? Prognosis?

A
  1. Supportive care

2. Usually recover over months

150
Q

Bacterial encephalitis/meningitis

  1. Signalment/Clinical Signs
  2. CSF findings
  3. Treatment
A
  1. High fever
  2. NEUTROPHILIC pleocytosis
  3. Steroids once at the begninning
    - Gram + (ampicillin, cephalosporins, TMS, minocycline)
    - Gram - (metronidazole, chloramphenicol, gentamicin)
    - Usually pick one from gram + and one from gram -
151
Q

Viral Encephalitis/Meningitis

  1. CSF findings
  2. Treatment
A
  1. Lymphocytic/plasmacytic pleocytosis

2. Supportive care

152
Q

Protozoal Encephalitis/Meningitis

  1. Signalment/Clinical Signs
  2. CSF findings
  3. Treatment
A
  1. Severe muscle involvement → HIGH CK, spastic hindlimbs, eosinophilia
  2. Eosinophilic pleocytosis
  3. Toxo: Muscular involvement - clindamycin, CNS involvement - TMS
    Neospora: TMS + pyrimethamine
153
Q

Mycotic Encephalitis/Meningitis

  1. Causative Agent
  2. CSF findings
  3. Treatmetn
A
  1. Cryptococcus
  2. Eosinophilic pleocytosis
  3. Ampho + fluconazole; then itraconazole as long term maintenance
154
Q

Granulomatous Meningoecephalitis

  1. Signalment/Clinical Signs
  2. CSF findings
  3. Treatment
A
  1. Yorkies
  2. Eosinophilic pleocytosis
  3. Steroids temporary improvement
155
Q

Steroid response menvngoarteritis (SRMA)

  1. Signalment/Clinical Signs
  2. CSF findings
  3. Treatment
A
  1. High fever, neutrophilic, cervical hyperesthesia
  2. High IgA in serum and CSF (90%)
  3. Prednisone
156
Q

Distemper encephalitis

  1. Signalment/Clinical Signs
  2. CSF findings
A
  1. Lymphopenia, 20% have hyperkeratosis of footpads and nose
    * Can occur post-vaccinial
  2. Lymphocytic/plasmacytic pleocytosis
157
Q

What is associated with the osseous lesions in canine cervical spondylomyelopathy (wobblers)

A
  1. Young Danes with malformation of the CERVICAL VERTEBRAE leading to stenosis
158
Q

What is associated with soft tissue lesions in young dogs with cervical spondylomyelopathy (wobblers)

A
  1. Dorsal or Lateral due to
    - Ligamentum flavus hypertrophy
    - Joint capsule proliferation
    - Synovial cyst formation
159
Q

What is associated with soft tissue lesions in old dogs with cervical spondylomyelopathy (wobblers)

A
  1. Ventral

- Intervertebral disk degeneration

160
Q

What is type 1 IVDD

A
  • Chondrodystrophic breeds

- NUCLEUS PULPOSIS ruptures into spinal cord ACUTELY

161
Q

What is type 2 IVDD

A
  • Larger breeds

- ANNULUS FIBROSIS bulges into spinal cord CHRONICALLY

162
Q

Hypogastric Nerve

  1. Spinal Cord Segments
  2. Sensory Actions
  3. Motor Actions
A
  1. Sympathetic L1-L4
  2. Detects bladder distension/pain
  3. a. Relaxation of the detrusor (storage)
    b. Contraction of the internal urethral sphincter
163
Q

Pelvic Nerve

  1. Spinal Cord Segments
  2. Sensory Actions
  3. Motor Actions
A
  1. Parasympathetic (S1-S3)
  2. Detects bladder filling, sensory to rectum and genitalia
  3. Detrusor contraction
164
Q

Pudendal Nerve

  1. Spinal Cord Segments
  2. Sensory Actions
  3. Motor Actions
A
  1. Somatic innervation (S1-S3)
  2. Anal sphincter, urethral sphincter, perineum, genitalia
  3. Contraction of external urethral sphincter
165
Q

Describe the process of micturition

A
  1. Bladder filling stimulates afferent pelvic nerve (senses filling)
  2. Pudendal nerve efferents inhibited, allowing relaxation of external urethral sphincter
  3. Hypogastric nerve allows relaxation of the internal urethral sphincter
  4. Pelvic nerve efferents stimulated, causing detrusor contraction
166
Q

How does rabies virus travel in peripheral nerves?

A

Retrograde axoplasmic flow

167
Q

Where does rabies virus replicate?

A

Spinal cord neurons

168
Q

What does salivary gland infection of rabies indicate?

A

That the brain is infected

169
Q

What are the phases of rabies infection?

A
  1. Prodromal phase (2-3 days) → dog acts anxious/nervous
  2. Furious phase (1-7 days) → FOREBRAIN involvement
  3. Paralytic/Dumb phase (2-4 days after clinical signs appear, lasts 2-4 days) → BRAINSTEM signs can predominate
170
Q

How is rabies definitively diagnosed?

A
  1. Detection of rabies virus ANTIGEN in brain tissue by DIRECT FA (VERY SENSITIVE)
171
Q

What are the clinical signs associated with botulism?

A
  1. Diffuse LMN disease, flaccid paralysis, hyporeflexia
  2. Ascending weakness starting in the hind limbs
  3. NO HYPERESTHESIA
  4. CAN have involvement of cranial nerves
172
Q

What are the clinical signs associated with tetanus?

A
  1. HYPERESTHETIC responses to stimuli
  2. Tonic contractions can lead to generalize convulsions
  3. Hyperthermia from continual muscle contractions
173
Q

Which species of tick is most commonly associated with tick paralysis in North America?

A

Dermacentor

174
Q

What are the clinical signs associated with tick paralysis?

A
  1. Weakness ascending from the hind limbs
  2. Hyporeflexia
  3. Dysphonia
  4. Facial nerve weakness - but no significant cranial nerve involvement
  5. Pain sensation is intact
175
Q

What is the most common polyneuropathy in dogs?

A

Polyradiculoneuritis (Coonhound paralysis)

176
Q

Histopathology of dogs affected by coonhound paralysis shows monocytic inflammation of what?

A
  1. Ventral nerve roots
177
Q

What is the most common form of mengititis?

A

Steroid responsive meningitis arteritis

178
Q

What are the clinical signs associated with steroid responsive meningitis arteritis?

A
  1. Neurologic deficits usually absent
  2. Neck pain
  3. Fever
179
Q

What is the MOA of atropine?

A
  1. Blocks muscarinic receptor - goes into CNS
180
Q

What is the MOA of edrophonium chloride?

A
  1. Acetylcholinesterase inhibitor → affects all cholinergic junctions
181
Q

What is the MOA of 2-PAM?

A

Reactivates acetylcholinesterase by promoting dephosphorylation

182
Q

What is the MOA of glycopyrrolate?

A

Blocks muscarinic receptor - does NOT go into CNS

183
Q

What is the MOA of bromide?

A
  1. Acts by migrating through neuronal chloride channels → hyperpolarization
184
Q

What spurious lab result can occur with bromide administration?

A
  1. Hyperchloremia
185
Q

What is a contraindication of bromide administration?

A

Renal disease → it is excreted through the kidneys

186
Q

What are possible toxicities with phenobarbital?

A
  1. Hepatotoxicity
  2. Bone marrow toxicity → thrombocytopenia and neutropenia
  3. Polyphagia, PU/PD
187
Q

What can phenobarbital interfere with?

A
  1. Thyroid hormones

2. Induces p450 enzymes

188
Q

What contributes to cerebral vasodilation and increased blood flow? (Increase/Decreased)

  1. PCO2
  2. PO2
A
  1. Increased PCO2 → has the most influence

2. Decreased PO2

189
Q

Hypoxemia can lead to cerebral (vasoconstriction/vasodilation) and (increased/decreased) intracranial pressure

A
  1. Vasodilation

2. Increased

190
Q

MRI: T1

A
  1. Bone and Fat are bright
  2. CSF is dark
  3. Good for anatomy
191
Q

MRI: T2

A
  1. Bone and Fluid are bright

2. Highlights edema, inflammation, and neoplasia

192
Q

MRI: T2 Flair

A
  1. CSF is not bright, otherwise like T2

2. Better visualization of periventricular inflammation

193
Q

MRI: T2 STAR

A
  1. Iron in blood is black

2. Shows acute and chronic hemorrhage

194
Q

MRI: STIR

A
  1. T1 with suppression of fat signal
  2. Fat is dark, enhances other signals
  3. Hemorrhage will be bright for the first few days
195
Q

Where are α1 receptors located?

A
  1. Vascular smooth muscle
  2. Bladder and GI sphincters
  3. Iris
196
Q

What is the MOA of α1 receptors?

A

Gq protein → stimulate phospholipase C and increase in IP3 and intracellular Ca

197
Q

What neurotransmitter are α1 receptors sensitive to?

A

Equally sensitive to Norepi and Epi

198
Q

What is the consequence of α1 receptor activation?

A
  1. Contract/Constrict
199
Q

Where are α2 receptors located?

A
  1. Sympathetic post-ganglionic nerves
  2. Platelets
  3. Adipocytes
  4. Walls of GI tract
200
Q

What is the MOA of α2 receptors?

A
  1. Gi protein → inhibit adenylate cyclase and decrease cAMP
201
Q

What is the consequence of α2 receptor activation?

A
  1. Relax/Dilate
202
Q

Where are β1 receptors located?

A
  1. SA and AV nodes

2. Ventricular muscle of the heart

203
Q

What is the MOA of β1 receptors?

A
  1. Gs protein → stimulate adenylate cyclase and increase cAMP
204
Q

What is the consequence of β1 receptor activation?

A
  1. Excite the heart
    - Increased HR
    - Increased conduction velocity
    - Increased contractility
205
Q

What neurotransmitter are β1 receptors sensitive to?

A
  1. Sensitive to Epi and Norepi

- More sensitive than α1 receptors

206
Q

Where are β2 receptors located?

A
  1. Vascular skeletal muscle
  2. Bronchial smooth muscle
  3. Walls of GI tract and bladder
207
Q

What is the MOA of β2 receptors?

A
  1. Gs protein → stimulated adenylate cyclase and increase cAMP
208
Q

What is the consequence of β2 receptor activation?

A
  1. Relax/Dilate
209
Q

What neurotransmitter are β2 receptors sensitive to?

A
  1. More sensitive to epinephrine than norepinephrine

- More sensitive to epinephrine than α1 receptors

210
Q

Where are nicotinic receptors located?

A
  1. Autonomic ganglia of the SNS and PNS → N(N) receptors
  2. Neuromuscular junctions → N(M) receptors
  3. Adrenal medulla → N(N) receptors
211
Q

What neurotransmitters are nicotinic receptors sensitive to?

A
  1. ACh

2. Nicotine

212
Q

How are nicotinic receptors blocked? Where?

A
  1. Ganglionic blockers (hexamethionium)

2. Only in the ganglia, NOT IN THE NMJ

213
Q

What is the MOA of nicotinic receptors

A
  1. ACh binds to the α subunit of the nicotinic ACh receptor → these are also Na and K ion channels
214
Q

Where are muscarinic receptors located?

A
  1. Heart → M2 receptor
  2. Smooth muscle → M3 receptor
  3. Glands → M3 receptor
215
Q

Which muscarinic receptors are inhibitory? Excitatory?

A
  1. M2

2. M3

216
Q

How are muscarinic receptors blocked?

A
  1. Atropine
217
Q

What is the mechanism of M2 muscarinic receptors?

A
  1. Gi protein → inhibit adenylate cyclase → open K channels → slows phase 4 depolarization → decrease HR
218
Q

What is the mechanism of M3 muscarinic receptors?

A
  1. Gq protein → stimulate phospholipase C → increase IP3 and intracellular Ca
219
Q

α1 receptor

  1. Agonist
  2. Antagonist
A
  1. Norepinephrine, Phenylephrine

2. Phenoxybenzamine, Phentolamine, Prazosin

220
Q

α2 receptor

  1. Agonist
  2. Antagonist
A
  1. Clonidine

2. Yohimbine

221
Q

β1 receptor

  1. Agonist
  2. Antagonist
A
  1. Norepinephrine, Isoproterenol, Dobutamine

2. Propranolol, Metoprolol

222
Q

β2 receptor

  1. Agonist
  2. Antagonist
A
  1. Isoproterenol, Albuterol

2. Propranolol, Butoxamine

223
Q

Nicotinic receptor

  1. Agonist
  2. Antagonist
A
  1. ACh, Nicotine, Carbachol

2. Curare, Hexamethonium

224
Q

Muscarinic receptor

  1. Agonist
  2. Antagonist
A
  1. ACh, Nicotine, Carbachol

2. Atropine

225
Q

The semicircular canals detect _____ and the utricle and saccule detect _____.

A
  1. Angular/Rotational acceleration

2. Linear acceleration

226
Q

What kind of cell is the output of the cerebellar cortex?

A
  1. Purkinje cells

ACVIM General copy (15 decks)

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