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Boards: Neurology + Ophthalmology > Neuro Emerg 6-16 > Flashcards

Neuro Emerg 6-16 Flashcards

1
Q

If a lesions is restricted to one cerebral hemisphere, what are the expected clinical signs?

A
  • obtundation
  • contralateral visual and menace deficits
  • contralateral hemiparesis
  • contralateral loss of placing reactions
  • circling towards the affected side

e.g., Left lesion
> r-sided loss of vision and menace
> r-sided hemiparesis and loss of placing reaction
> l-sided circling

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2
Q

What is the site of lesion causing decerebrate rigidity and how is the rigidity caused and what are the clinical signs

A

lesion of the midbrain or cerebrum - causing functional separation of the cerebrum from the brainstem

loss of inhibition of the vestibulospinal and reticulospinal tracts

signs:
* altered mentation (usually comatose)
* rigid extension of all limbs
* opisthotonus

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3
Q

What does 1-3 days old hemorrhage look like on T1, T2 or T2 with flare MRIs?

A

T1 isointensity
T2 hypointensity
T2 marked hypointensity

due to deoxyhemoglobin

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4
Q

List advanced diagnostics you could apply in an animal presenting in a coma

A
  • MRI
  • CT
  • CSF analysis - caution!
  • Brainstem auditory evoked response
  • Electroencephlaography
  • Somatosensory evoked potential

preserved BAER indicated preserved brainstem function

preserved EEG indicated preserved cerebral function

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5
Q

What are the most common signs of hydrocephalus?

A
  • altered mentation
  • inappropriate behavior
  • cortical blindness
  • seizures
  • ventrolateral strabismus
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6
Q

How does brain hypoxia cuase cell death?

A
  • loss of energy metabolism
  • secondary effects of excitatory neurotransmitters (buildup of glutamate and aspartate)
  • intracellular Ca increase
  • free radical formation
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7
Q

What are the most vulnerable brain structures to hypoxia?

A
  • cerebral cortex
  • hippocampus
  • certain basal nuclei
  • thalamus
  • cerebellar purkinje cell layers
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8
Q

What are typical MRI findings of hypertensive encephalopathy?

A

FLAIR MRI
hyperintensity within the white-matter tract of the forebrain

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9
Q

What is the prodrome or aura?

A

prodrome - behavioral change hours to days before seizure

auro - subjective sensation marking the onset of a seizure

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10
Q

What are the typical resting and threshold potentials of neurons?

A

resting -70 mV
threshold -55 mV

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11
Q

What are the main excitatory and inhibitory neurotransmitters of the brain?

A

Glutamate

GABA

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12
Q

How is glutamate produced an recycled?

A

produced via glutaminase from glutamine (in the mitochondria)

synaptic glutamate&raquo_space; taken up by astrocytes&raquo_space; metabolize it back to glutamine

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13
Q

What are typical signs of forebrain lesions?

A
  • altered behavior
  • altered consciousness
  • contralateral facial sensory awareness impaired
  • contralateral proprioceptive deficits
  • hemi-neglect
  • central blindness/cortical blindness
  • ipsilateral head turn (not tilt!) or circling
  • seizures
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14
Q

Do disorders of the LMN cause ataxia?

A

no

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15
Q

What are typical signs of thiamine deficiency?

A
  • vestibular and proprioceptive ataxia
  • blindness
  • mydriasis
  • cervical ventroflexion
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16
Q

Which tract of the UMN system does not inhibit the lower motor neurons?

A

vestibulospinal tract

17
Q

Describe exam findings with UMN versus LMN urinary bladders

A

UMN: large, firm, difficult to express - over-flow incontinence if ver large
LMN: large, flaccid, easily expressed (but incomplete) - frequent urine dribbling

18
Q

What parts of the spine can be evaluated with the cutaneous trunci reflex?

A

C8 - L3

19
Q

What are the neurolocalizations for an UMN versus LMN urinary bladder?

A

UMN - cranial to S1

LMN - caudal to S1

20
Q

Fill in the blanks

A
21
Q

How common is megaesophagus in polyradiculoneuritis?

A

not a feature of coonhound paralysis

22
Q

What leads to paralysis in polyradiculoneuritis?

A

destruction of myelin sheets of the ventral roots and peripheral nerves

mononuclear interstitial infiltrate

23
Q

What are the clinical characteristics of Polyradiculoneuritis?

A
  • acute onset flaccid paraparesis - then progressing to the forelimbs (progression typically takes 4-5 days)
  • CN typically normal (dysphonia and facial weakness possible though)
  • no megaesophagus
  • normal perineal reflex and urination
  • early: hyperaesthesia
  • mental status stays normal, may wag tail
  • EMG only altered 5-7 days after onset of signs (not helpful early on)
  • CSF: protein elevation but normal cell coutn and cytology
  • course of disease 4-6 weeks
24
Q

What is the most common causative agent for discospondylitis?

A

Stpahyloccocus aureus

25
Q

What are the most common spinal neoplasias in dogs versus cats?

A

dogs: fibrosarcoma, osteosarcoma

cats: lymphoma, osteosarcoma

26
Q

List the parts of the visual system

A
  • retina
  • optic nerves
  • optic chiasm
  • optic tracts
  • lateral geniculate nucleus
  • optic radiations
  • visual cortices (occipital cortices)
27
Q

What are the parts of the vestibular system?

A
  • receptor organ - i.e., inner ear
  • vestibular nerve
  • brainstem nuclei in the medulla oblongate
28
Q

What causes leaning towards the side in vestibular disease?

A

leaning/falling towards the affected side

vestibular system affects limb tone via the vestibulospinal tract - affects the extensor muscles on the same side

affected side&raquo_space; decreased extensor tone&raquo_space; falling to that side

29
Q

What are signs typically seen with both peripheral and central vestibular disease?

A
  • vestibular ataxia
  • nystagmus
  • positional strabismus
  • head tilt
30
Q

What signs are indicative of central vestibular disease over peripheral?

A
  • altered mentation
  • proprioceptive deficits + proprioceptive ataxia
  • UMN signs
31
Q

How can the character of the nystagmus help differentiate peripheral versus central vestibular disease?

A

both: horiztonal or rotary
central only: vertical or variable nystagmus

central: slower nystagmus pace than peripheral

32
Q

What is paradoxical vestibular disease?

A

cerebellar lesions can occasionally cause vestibular disease on the contralateral side

Boards: Neurology + Ophthalmology (14 decks)

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