Neuro 1 Flashcards

(98 cards)

1
Q

What are the words to use when describing level of consciousness?

A

Alert

Depressed

Stuporous/obtunded

Semicomatose

Comatose

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2
Q

Define amaurosis

A

partial or total loss of sight without pathology of the eye - caused by disase of hte optic nerve or brain (central blindness)

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3
Q

Central blindness, but intact PLR indicates ____ disease.

A

Cerebral

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4
Q

Seizures are a result of abnormal neuronal activity from the ______ cortex.

A

Cerebral

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5
Q

T/F: Generalized seizures result in a loss of consciousness

A

True

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6
Q

T/F: all focal seizures result in loss of consciousness.

A

False - consciousness may or may not be impaired

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7
Q

Head turning, grimace, urination/defecation are all signs of _______ seizure.

A

Generalized

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8
Q

_____ phase may precede seizures, and _____ phase may procede after seizures.

A

Prodromal; post-ictal

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9
Q

Neurologic exam: gate analysis - describe Grade 0 - Grade 5

A
  • Grade 0 = no deficits noted
  • Grade 1 = mild deficits only under special circumstances
  • Grade 2 = mild, difficult to recognize deficits under normal circumstances, and easily observable under special cericumstances
  • Grade 3 = readily recognizable, consistent, moderate deficits at straight walk
  • Grade 4 = severe deficits at the walk/almost falling down
  • Grade 5 = recumbent
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10
Q

T/F: Limbs crossed in a horse is normal.

A

False - abnormal

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11
Q

Lesions in the forbrain result in what CS?

A

Abnormal mentation, behavior changes, central blindness, aimless wandering, seizures, mild weakness, and proprioceptive deficits

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12
Q

Lesions of the brainstem result in what CS?

A

Altered consciousness, CN deficits, postural reaction deficits

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13
Q

Lesions of hte cerebellum cause what CS?

A

Hypermetra, ataxia, intention tremors

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14
Q

Lesions of hte spinal cord from C1-C5 CS?

A

UMN signs to forelimbs and pelvic limbs (horners syndrome if damage to vagosympathetic trunk)

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15
Q

Lesions of the spinal cord from C6-T2 - CS?

A

LMN to forelimbs, UMN to pelvic limbs

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16
Q

Lesions of the spinal cord from T3-L3 CS?

A

Normal forelimbs, UMN to pelvic limbs, UMN bladder

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17
Q

Lesions of the spinal cord from L4-S2 CS?

A

Normal forelimbs, LMN pelvic limbs, LMN bladder

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18
Q

Lesions in the S2-caudal region of spinal cord CS?

A

LMN bladder, lack of anal tone and tail tone

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19
Q

An “AO” CSF tap is a tap of the ________ cistern.

A

cerebello-medullary

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20
Q

T/F: “AO” tap requires general anesthesia.

A

True

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21
Q

“AO” tap is more reflected of ____ disease.

A

Intracranial

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22
Q

“AO” tap is contraindicated in ______

A

Head trauma

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23
Q

T/F: AO tap is easy to collect post mortem.

A

True

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24
Q

“LS” CSF tap is a tap from the ______ cistern.

A

Lumbo-sacral

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25
T/F: LS tap needs to be done under general anesthesia.
False - is obtained standing
26
LS tap is more reflective of _____ disease.
Spinal cord
27
LS tap is taken at the level of the \_\_\_\_\_\_\_
cauda equina
28
CSF is an ultrafiltrate of \_\_\_\_\_\_, that bathes the CNS, ventricles and subarachnoid spcaes.
plasma
29
In a routine CSF analysis - a normal CSF should be ____ in color, the protein concnetration should be between ___ and ____ mg/dL, and the nucleated cell count should be \< ___ cells/microliter, and the red cell count should be \_\_\_\_\_. The nucleated cell count should also be compromised of mostly \_\_\_\_\_\_\_.
Clear; 50-100; \<6; zero small mononuclear cells (NOT neutrophils)
30
A yellowish discoloration in a CSF tap is defined as _____ and represents what?
Xanthochromia - indicates we have a break down of RBCs within the CSF- can be due to trauma or EHV-1
31
Define pleocytosis on routine CSF analysis
Elevated nucleated cell count
32
T/F: Cerebellar abiotrophy is a progressive cerebellar degeneration that is present at birth.
False - it is NOT present at birth
33
Signs of cerebellar abiotrophy are evident between ___ to ____ months of age.
1-6
34
Clinical signs of cerebellar abiotrophy:
Diffuse, symmetrical cerebellar signs: Base-wide stance with hypermetric ataxia, head bob/intention tremor, absent menace response
35
T/F: In occipito-atlantoaxial malformations, ataxia is noted at birth, and is progressive.
True
36
Juvenile epilepsy is a ____ epilipsy of ____ foals.
benign; Arabian
37
Horses will outgrow juvenile epilepsy by ____ months of age.
12
38
How do you treat juvenile epilepsy?
Phenobarbital for several months
39
Lavender foal syndrome is known as the "\_\_\_\_ syndrome of egyption Arabian foals"
Tetany
40
\_\_% of egyptian arabians are carriers of lavender foal syndrome.
10%
41
Clinical signs of lavendar foal syndrome
Coat color dilution - striking iridescent silver/ale lavender coat color - LETHAL Recumbent from birth (tetanic episodes of muscle contractions, opisthotonus, paddling limb movements, spontaneous and tactile provoked seizures)
42
Lavendar foal syndrome is an autosomal ____ genetic disorder.
recessive
43
Perinatal asphyxia syndrome is also known as:
dummy foal syndrome hypoxic ischemic enphalopathy
44
How does a foal get perinatal asphyxia syndrome (aka dummy foal syndrome)?
Compromise of oxygen supply in utero or during delivery coupled with reperfusion injury.
45
Symptoms of perinatal asphyxia (aka dummy foal syndrome)
Range from inability to sucke to recumbency and seizures
46
T/F: In perinatal asphyxia syndrome, most foals improve over time with supprotive care.
True (however, seizures will worsen prognosis)
47
Flipping injuryes consist of \_\_\_% of traumatic brain injuries in horses.
44
48
Basisphenoid fractures occur secondarily to flipping over backwards, as a result of avulsion fractures of the rectus capitus muscle, casuing fractures at the insertion of ____ and _____ bones.
Basisphenoid and basioccipital
49
In flipping injuries, basilar bone fractures occur due to traction forces from the _____ muscle.
rectus capitus ventralis
50
Flipping injuries can lead to unresponsive mydriasis how?
Attenuation of the optic vasculature --\> peri-papillary degeneration after 2-4 weeks Prognosis for return of vision is unfavorable
51
Temporohyoid osteoarthropathy is an idiopathic chronic inflammation of hte ____ joint.
Temporohyoid (TH)
52
Temporohyoid osteoarthropathy can be secondary to _______ idiopathically, via hematogenous spread, or ascending menigitis.
Otitis media/interna
53
Temporohyoid osteoarthropathy can lead to progressive ankylosis and fractures of the ____ and ____ bones, leading to CN ___ and ____ deficits.
petrous temporal and stylohyoid bones CN VII and CN VIII deficits
54
What procedure is recommended in horses with temporohyoid osteoarthropathy to prevent additional fractures and recurrence of clinical signs?
Ceratohyoidectomy
55
Temporohyoid osteoarthropathy clinical signs can be asymptomatic, mild, to severe. What CS are associated with CN VII and VIII deficits?
Proximal facial nerve deficits - mild head tilt, CN 7 also controls lacrimal gland secretion - so we might see corneal ulcers
56
What is the best diagnostic test for temprohyoid osteoarthropathy?
CT scan
57
Tx of temporohyoid osteoarthropathy:
Antibiotics and anti-inflammatories Surgery - ceratohyoidectomy
58
Llist three arboviral ecephalitises from the family Togaviridae:
Easterin equine encephalitis Western equine ecephalitis Venezuelan Equine encephalomyelitis
59
List an arboviral encephalitis from the family flavivridae?
West nile viral encephalomyelitis (WN)
60
Strangles can cause brain abscesses, from this pathogen.
*Streptococcus equi ss equi*
61
Bacterial meningitis/meningioencephalitis can be caused in neonatal ____ and ____ adults.
septicemia; immunocompromised
62
Fungal meningitis can be the result of an ascending infection from the ____ or can occur in _____ adults.
Sinuses; immunocompromised
63
Lyme diases is a neuroborreliosis caused by an infection with the spirochete \_\_\_\_\_\_.
*Borrelia burgdorferi*
64
Equine protozoal myeloecephalitis (EPM) is most commonly caused by which two organisms:
* Sarcocystis neurona* * Neospora hughesi*
65
What is the definitive host for *Sarcocystis neurona*? How does a horse acquire the infection?
Opposum - horse acquire EPM following ingestion of food contaminated with opossum feces
66
Asymmetrical and focal skeleton muscle atrophy (neurogenic atrophy) is a strong sign of ____ involvement in horses affected with EPM.
LMN
67
Moldy corn intoxication leads to \_\_\_\_\_.
Leukoencephalomalacia
68
Leukoencephalomalacia from moldy corn disease is the result of _____ toxin, which is a metabolit of the _____ species.
Fumonesin B1 toxin; metabolite of *Fusarium sp*
69
The fumonensin B1 toxin in modly corn disease causes disruption in \_\_\_\_\_, which is an important lipid for neuronal lipid membranes.
Sphingomyelin
70
"blind staggers" is a sign for _____ disease.
Moldy corn disease
71
CS of moldy corn disease
Lack of coordination, blindness, aimless walking, head pressing Hyperexcitability, extreme agitation, delerium
72
Yellowstar Thistle and Russian knapweed found in the western US causes ______ encephalomalacia.
Nigropallidal
73
Nigropallidal encephalomalacia from yellowstar thistle and russian knapweed cause necrosis of the _____ and \_\_\_\_.
Globus pallidus and substantia nigra
74
Nigropallidal encephalomalcia is often reffered to as the "\_\_\_\_\_ disease"
Chewing
75
C/S of nigropallidal encephalomalacia
Lack of coordinated prehention, mastication, and deglutination Able to swallow if food or water is placed in posterior pharynx
76
Locoweed intoxcation leeds to progressive ______ ataxia, causing staggering gait and trembling.
cerebellar
77
What is the toxin found in locoweed? And what does it do?
Swainsonine alkaloid - Produced by endophyte fungus, inhibits lysosomal alpha mannosidase enzymes, leading to the formation of lysosome vacuoles wihtin the CNS
78
Fluphenazine is a toxin that is a ______ receptor agonist.
domaine (D2)
79
Fluphenazine can be uused as a _____ neuroleptic, and is formulated as a long acting IM sedation in horses.
Phenothiazine
80
Phenothiazine neuroleptic - fluphenazine binds to D2 receptors with a very slow \_\_\_\_\_.
Dissociation
81
Using a phenothiazine neuroleptic cuases increased risk of adverse _____ signs.
Extrapyramidal
82
Symptoms of toxicity with fluphenazine:
Agiation, profuse sweating, hypermetria Aimless circling, intesne pawing, striking with forelimbs Rhythmic swinging of head and neck Alternating with periods of severe stupor
83
T/F: Horses intoxicated with fluphenazine are dangeraouse and are often euthanized as a result.
True
84
What are treatments for fluphenazine?
Treatment is based on management - can give diphenhydramine to improve symptoms, anti-cholinergic drugs, phenobarbital. But mainly you have to wait it out - can take up to several weeks to resolve.
85
What is the most common intracranial "tumor" in the equine?
Cholesterinic granuloma
86
T/F: Cholesterinic granuola is an infalmmatory lesion, that is a common incidental finding in older horses.
True
87
Although less common, Cholesterinic granulomas can enlarge and obstruct the CSF, leading to \_\_\_\_\_
acquired hydrocephalus
88
PPID can result in macro and microadenomas. Which one cuases neurologic deficits?
Macroadenomas
89
Narcolepsy is defined as excessive daytime sleepiness and pathologic episodes of ___ sleep.
REM
90
Narcolepsy is often triggered by \_\_\_\_\_\_.
excitement
91
During a narcoleptic event, there is an absence of _____ relfexes, and may last a few hours, but the horse can be aroused.
spinal
92
During narcoleptic event, cataplexy is common. What is catapelxy?
Loss of muscle tone
93
Narcolepsy can be herediatory or sporadic. In what horses is in familiar?
Miniature horse and shetland pony foals
94
It is thought that narcolepsy is linked to low _____ which is produced by the hypothalamus.
hypocretin-1
95
T/F: Sleep deprivation is a true narcolepsy.
False
96
During sleep deprivation, the horse will fall asleep without falling by ....
bucklint at the knees
97
What are reasons for sleep deprivation in the horse:
Fear, pain, too compromised (COPD), geriatric horses in the hospital
98