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Boards Review > Neurology Recap > Flashcards

Neurology Recap Flashcards

1
Q

What is the purpose of myelination?

A
  • Speeds up transmission of the electrical impulse.
  • Impulse will “jump” from node to node instead of going down the whole neuron (saltatory conduction)
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2
Q

What is the difference between white and grey matter?

A

White is mostly myelinated, grey is not

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3
Q

What are the spinal intumescences?
Where are they located?

A

“Swollen” areas of spinal cord where more cell bodies and nerve roots are located.

Cervical intumescence = C6-T2
Lumbar intumescence = L3-S3

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4
Q

Define Upper motor neuron

A

neuron that comes from brain down to spinal cord, DOES NOT LEAVE CNS.
Has to synapse onto an interneuron or lower motor neuron in the spinal cord.

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5
Q

Define Lower motor neuron

A

neuron that starts in spinal cord and ends in the motor unit (peripheral nerve)

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6
Q

Define Ganglia

A
  • Cluster of cell bodies located outside of the CNS, typically part of the autonomic or sensory nervous systems (not motor).
  • Located in the dorsal root of the spinal cord, associated with cranial nerves, and autonomic nervous system.
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7
Q

Define reflex

A

An involuntary arc that involves sensation (pain or stretch), ascends up to synapse in the spinal cord with the lower motor neuron, leading to a muscle response.
Does not require conscious thought, not learned.

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8
Q

What are the primary functions of the cerebellum?

A

Smooths and coordinates motor function for posture and movement by using subconscious proprioceptive information

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9
Q

What are the primary functions of the vestibular system?

A

Body equilibrium and balance, detects head position and movement.
Involves both inner ear and brainstem.

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10
Q

What are the primary functions of the brainstem?

A

location of cranial nerves- sensation and motor function to face/head primarily

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11
Q

What are the primary functions of the cerebral cortex?

A

thought, interpretation, voluntary motor functions, fine control of movement

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12
Q

What are the primary functions of the hypothalamus?

A

master control of the autonomic nervous system- hunger, thirst, sleep, body temp BP, hormones

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13
Q

What are the primary functions of the thalamus?

A

Pain sensation, alertness, memory

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14
Q

List the cranial nerves

A

I Olfactory nerve
II Optic nerve
III Oculomotor nerve
IV Trochlear nerve
V Trigeminal nerve
VI Abducent nerve
VII Facial nerve
VIII Vestibulocochlear nerve
IX Glossopharyngeal nerve
X Vagus nerve
XI Accessory nerve
XII Hypoglossal nerve

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15
Q

Function of Olfactory nerve (I)

A

A: Olfaction

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16
Q

Function of Optic nerve (II)

A

A: Vision

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17
Q

Function of Oculomotor nerve (III)

A

E: PLR (parasympathetic to pupil)
Extraocular muscles (ventral, medial, dorsal rectus, ventral oblique, levator palpebrae superiorismm)

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18
Q

Function of Trochlear nerve (IV)

A

E: Extraocular muscle (dorsal oblique m.)

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19
Q

Function of Trigeminal nerve (V)

A

A: facial sensation
Ophthalmic branch - cornea, superior eyelid
Maxillary branch - muzzle and inferior eyelid
Mandibular branch - mandibular skin

E: muscles of mastication (mandibular branch)
Tensor typani muscle of the middle ear

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20
Q

Function of the abducent nerve (VI)

A

E: extraocular muscles (lateral rectus and retractor bulbi mm)

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21
Q

Function of the facial nerve (VII)

A

A: taste and sensory to rostra 2/3 tongue
Sensory to inner pinnae

E: Motor to muscles of facial expression
Motor to strapedius muscle
Parasympathetic to palatine, lacrimal, and nasal glands
Parasympathetic to salivary glands (mandibular and sublingual)

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22
Q

Function of the Vestibulocochlear nerve (VIII)

A

A: vestibular function/balance
Hearing

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23
Q

Function of glossopharyngeal nerve (IX)

A

A: pharynx sensation
Middle ear sensation
Taste of caudal 1/3 of tongue

E: Pharynx and larynx
Parasympathetic to salivary glands (zygomatic, parotid)

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24
Q

Function of Vagus nerve (X)

A

A: sensory to pharynx, larynx, external ear canal
Taste on root of tongue and epiglottis
Sensory of viscera

E: Pharynx, larynx, esophageal mm
Parasympathetic to viscera

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25
Q

Function of accessory nerve (XI)

A

E: larynx
parts of the trapezius, brachiocephalicus, and sternocephalicus mm

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26
Q

Function of hypoglossal nerve (XII)

A

E: tongue muscles (extrinsic and intrinsic)

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27
Q

What are the differences between the Parasympathetic and Sympathetic Nervous Systems in regard to origination in the CNS, location of ganglia, and neurotransmitters?— NEED TO FIND CHART

A
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28
Q

What is the difference between conscious and subconscious proprioception?

A

CP’s involve the cerebrum, SP’s involve the cerebellum. If you have both CP and SP deficits- usually spinal disease. Hopping assesses both, paw position is CP’s, reflex stepping (paper slide) is more SP’s. Wide based stance is usually SP deficit.

29
Q

Explain the differences between an upper motor neuron lesion and a lower motor neuron lesion on a neurologic exam.

A

“Upper motor neuron” = weakness/ataxia/paralysis WITHOUT reflex deficit (typically reflexes mildly increased”.

“Lower motor neuron” = weakness/ataxia/paralysis WITH reflex deficit (LMN goes from spinal cord down to muscle)

30
Q

List the functional spinal cord segments (ie the ones you use to localize spinal cord lesions).

A

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

31
Q

What would you expect to find on physical exam in a patient with a C1-C5 lesion?

A

All 4 limbs upper motor neuron signs
NO reflex deficits

32
Q

What would you expect to find on physical exam in a patient with a C6-T2 lesion?

A

LMN signs to forelimbs with reflex deficits
UMN signs to hind limbs

33
Q

What would you expect to find on physical exam in a patient with a T3-L3 lesion?

A

Forelimbs normal
UMN signs to hind limbs

Sometimes “Schiff Scherrington” posture (usually only if severe injury): Forelimbs very stiff/extended but technically neurologically normal. Due to loss of input from ascending inhibitory neurons

34
Q

What would you expect to find on physical exam in a patient with a L4-S3 lesion?

A

Forelimbs normal
LMN signs to hind limbs with reflex deficits

35
Q

List the classic signs of a lesion in the forebrain (cerebrum, thalamus).

A

Seizures
altered mentation
wide circles TOWARD lesion
CP deficits
CONTRALATERL sensory deficits
menace deficits
normal gait

36
Q

List the classic signs of a lesion in the Brainstem.

A

Depression/stupor
neck pain
abnormal gait/posture
CN deficits

37
Q

List the classic signs of a lesion in the Cerebellum.

A

Wide based stance
intention tremors
high stepping gait
NO Paresis
normal mentation

38
Q

List the classic signs of a lesion in the vestibular.

A

Head tilt (TOWARD)
falling/leaning/rolling (TOWARD)
tight circles (TOWARD)
nystagmus (AWAY)
+/- central signs if central vestibular

39
Q

DRAW the neuro-ophtho localization nerves (ie PLR, vision, etc).

A
40
Q

Localize the following lesion:

Menace absent in left eye, mydriasis left eye. Shining light into left eye- left eye absent PLR, right eye absent PLR. Shining light into right eye- right eye normal PLR, left eye reduced PLR.

A

LEFT OPTIC NERVE or LEFT RETINA

41
Q

Localize the following lesion:

Menace absent in both eyes with bilateral mydriasis. PLR absent in both eyes.

A

BILATERAL RETINA or BILATERAL OPTIC NERVE or OPTIC CHIASM

42
Q

Localize the following lesion:

Menace absent in left eye, pupil size normal OU, PLR normal OU

A

RIGHT SIDED CORTICAL BLINDNESS
Also: right optic tract, lateral geniculate nucleus

43
Q

Localize the following lesion:

Menace present OU, Mydriasis of left eye, right eye normal pupil size. Shining light into left eye- left eye absent PLR, right eye normal PLR. Shining light into right eye- right eye normal PLR, left eye absent PLR.

A

LEFT CRANIAL NERVE III

44
Q

Define cluster seizures

A

2 or more seizure occur in 24 hours separated by normal interictal periods

45
Q

Define Status epilepticus

A

when a seizure state is continual for longer than 5 minutes or when a series of seizures occur without full recovery of consciousness between the seizures for 30 minutes

46
Q

List the main pros/cons of phenobarbital

A
  • Most evidence for effectiveness
  • Moderate half life- works fairly quickly if loaded
  • Cheap
  • BID dosing
  • Need to monitor it due to altered hepatic clearance over time and possible adverse effects
  • Side effects: sedation/ataxia, polyphagia, PU/PD, possible hepatic damage at high doses, expected changes in ALP and T4, rare acute/idiosyncratic hepatic damage, rare blood dyscrasias
  • Unreliable blood levels in cats
47
Q

List the main pros/cons of KBr.

A
  • Fair evidence for effectiveness
  • VERY LONG half life- takes a while to work and a while to get rid of it. Typically have to load it.
  • Cheap
  • Ideally monitor levels, but not absolutely necessary
  • Side effects: sedation/ataxia, polyphagia, PU/PD, possible pancreatitis/GI signs
  • Can be “Flushed out” with high chloride diets or IVF
  • NO in cats
48
Q

List the main pros/cons of Levetiracetam.

A
  • Least evidence for effectiveness
  • Reasonably cheap
  • TID dosing- extremely short half life, but should be effective quickly (if it works), so no real need to load it
  • Minimal to no side effects, minimal monitoring needed
49
Q

List the main pros/cons of zonisamide

A
  • Fairly expensive
  • Need higher doses if using with pheno
  • BID
  • Fair evidence for effectiveness
  • Side effects: sedation/ataxia, GI signs, rare idiosyncratic hepatotoxicity or blood dyscrasias
50
Q

List the main pros/cons of gabapentin

A

DOESN’T WORK
Need very high dose- severe sedation, but otherwise no side effects

51
Q

List the main pros/cons of pregabalin

A
  • Some recent evidence in dogs refractory to other therapies
  • TID
  • Extremely expensive
  • Minimal side effects (sedation, ataxia)
52
Q

Discuss FCE:
Onset of signs
Symmetry
Painful?
Location
Breed

A

Onset of signs: Sudden, non progressive
Symmetry: typically asymmetrical
Painful?: NO (may yelp once at first)
Location: Anywhere
Breed: young large breed dogs most common

53
Q

Discuss IVDD:
Onset of signs
Symmetry
Painful?
Location
Breed

A

Onset of signs: Sometimes progressive, sometimes sudden
Symmetry: usually more symmetrical
Painful?: YES
Location: Cervical or TL junction most likely
Breed: middle aged small breed dogs most common

54
Q

Argue for steroid use in IVDD

A
  • can reduce inflammation/free radicals, pain relief.
  • High doses have more anti-free radical effects, low doses are just anti-inflammatory.
  • A few trials in humans have shown minor improvements in outcomes in some groups.
55
Q

Argue against steroid use in IVDD

A
  • Most studies have not shown any improvement in outcome with steroids vs no steroids.
  • Some have shown harm.
  • Significant risk of side effects with steroids (GI, hyperglycemia, wound infections, impaired healing, pneumonia, sepsis).
56
Q

List the 4 most common lower motor neuron diseases.

A

Tick paralysis
Coonhound paralysis (acute idiopathic poylradiculoneuritis)
Botulism
Myasthenia gravis

57
Q

List the key clinical features of Tick paralysis

A
  • Flaccid paralysis (absent reflexes)
  • 7-9 days after tick exposure, RAPIDLY improves once tick is removed
  • Ataxia rapidly progressing to flaccid paralysis
  • Usually whole body at once (not hind end first)
  • Cranial nerve involvement uncommon (if so, mild)
58
Q

List the key clinical features of Coonhound paralysis (acute idiopathic polyradiculoneuritis)

A
  • Flaccid paralysis (absent reflexes)
  • Pelvic limb paresis which ascends, usually quickly over 24-48 hrs
  • Cranial nerve involvement uncommon
  • Usually 7-14 days after raccoon exposure (not always), can last 3-6 weeks
  • Characteristic EMG findings
59
Q

List the key clinical features of Botulism

A
  • Flaccid paralysis (absent reflexes)
  • Progressive symmetric LMN signs, usually ASCENDING
  • DOES affect cranial nerves
  • May affect multiple animals if all exposed
  • Lasts < 14 days
60
Q

List the key clinical features of Myasthenia gravis

A
  • Flaccid paralysis (absent reflexes)
  • Typically less “dramatic” than the others, but acute fulminant MG can cause acute generalized LMN weakness
  • DOES affect cranial nerves, typically also have megaesophagus
61
Q

What 3 parameters does the MGCS evaluate? How is it scored?

A

Level of consciousness
Brain stem reflexes (pupils + physiologic nystag)
Motor reflexes
Each 0-6 higher number is better (max 18)

62
Q

What are the 2 main types of cerebral autoregulation?

A

Pressure autoregulation: maintenance of CBF over a wide range of MAP (50-150)

Chemical autoregulation: increased CO2 or low O2 🡪 vasodilation

63
Q

List some mechanisms of secondary brain injury with trauma

A
  • Increased excitatory neurotransmitter release (glutamate) 🡪ATP depletion
  • Calcium and sodium enter cells (cell swelling 🡪 cytotoxic edema)
  • Release of ROS 🡪 peroxidation injury
  • Bleeding 🡪 iron 🡪 worsening of ROS
  • Disruption of BBB due to inflammation = vasogenic edema (extracellular water)
  • NO induction 🡪 vasodilation (increased ICP) + loss of pressure autoregulation
  • Increased ICP 🡪 decreased CBF 🡪 ischemia 🡪 worsened injury
  • Systemic hypotension/hypoxia contributes to ischemia
64
Q

What is the Monroe Kelley Doctrine?

A

The volume inside the skull is constant, so if one component increases, another must decrease to compensate.
If the volume increase is too large, the pressure increases dramatically because the ability to compensate is lost.

65
Q

What is cerebral perfusion pressure? What is the goal for this parameter in humans with TBI?

A

CPP = MAP –ICP
goal is 60-70

66
Q

Explain the pros/cons of hyperventilation as a treatment for increased intracranial pressure?

A

Short-term hyperventilation will drop the pCO2 in blood, leading to cereberal vasoconstriction, which will reduce ICP.

HOWEVER, this also markedly reduces cerebral blood flow, which in the end will cause more ischemic damage/edema.

Goal is to maintain near normocapnia (> 25-30 mmHg)

67
Q

What are the main drugs used to reduce ICP?

A

Mannitol
Hypertonic

68
Q

What is the mechanism of mannitol to reduce ICP?

A
  • Immediate effect: decreased blood viscosity and improved cerebral blood flow 

  • Delayed effect: osmotic effect to move water out of the brain tissue into the vessels for excretion 

  • Free radical scavenging 

  • Can worsen hypovolemia (diuretic)- avoid if hypotensive
69
Q

What is the mechanism of hypertonic to reduce ICP?

A
  • Dehydrates endothelial cells -> improved cerebral blood flow 

  • Osmotic effect to move water out of the brain tissue into the vessels for excretion 

  • Decreases excitotoxicity 

  • Reduces the inflammatory response 

  • Brain effects last longer than volume-expanding effects 

  • Avoid if dehydrated or significant sodium imbalance 


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