Neurology Flashcards
1
Q
What signs will you see with a C1-C5 lesion
A
UMN thoracic limbs
UMN pelvic limbs
2
Q
What signs will you see with C6-T2 lesions
A
LMN thoracic limbs
UMN pelvic limbs
3
Q
What signs will you see with T3-L3 lesions
A
Normal thoracic limbs
UMN pelvic limbs
4
Q
What signs will you see with L4-caudal lesions
A
Normal thoracic limbs
LMN pelvic limbs
5
Q
With spinal cord lesions, what is the order of functional loss
A
1) Proprioception
2) Weakness/ataxia
3) Voluntary motor
4) Bladder
5) Nociception
6
Q
What is the last thing to go with spinal cord lesions
A
Nociception
7
Q
What does the pelvic withdrawal reflex test
A
Sciatic (L6-S1 segments)
8
Q
What does th thoracic withdrawl reflex test
A
all thoracic limb peripheral nerves (C6-T2)
9
Q
What nerve does the patellar reflex test
A
Femoral (L4-L6)
10
Q
What nerve does the cranial tibial reflex test
A
Peroneal / Fibial (L6-L7)
11
Q
What nerve does the gastrocnemius reflex test
A
Tibial (L7-S1)
12
Q
What nerve does the biceps reflex test
A
Musculocutaneous (C6-C8)
13
Q
What nerve does the triceps reflex test
A
Radial (C7-T2)
14
Q
What nerve does teh extensor carpi radialis reflex test
A
Radial (C7-T2)
15
Q
What is Schiff-Sherrington Syndrome
A
occurs with severe T3-L3 myelopathies
Persistent severe extension of thoracic limbs
-due to disinhibition of extensor motor neurons in cervical intumescence
-Border cells (L1-L5) send axons cranially to cervical intumescence to inhibit extensor motor neurons
*When held in standing position, the thoracic limbs is normal
16
Q
Schiff-Sherrington Syndrome occurs with myelopathies at what level
A
severe T3-L3 myelopathies
17
Q
What do you see with Schiff-Sherrington Syndrome
A
Persistent severe extension of thoracic limbs (severe T3-L3 myelopathies)
-due to disinhibition of extensor motor neurons in cervical intumescence
-Border cells (L1-L5) send axons cranially to cervical intumescence to inhibit extensor motor neurons
18
Q
T/F: With Schiff-Sherrington syndrome, When held in standing position, the thoracic limbs is normal
A
True
19
Q
What is afferent of cutaneous trunci reflex
A
Afferent (sensory) - sensory dematome at level of pinch
20
Q
What is the efferent of cutaneous trunci reflex
A
C8-T1integration
lateral thoracic nerves to cutaneous trunci muscle
21
Q
T/F: cutaneous trunci absence is where the lesion is
A
false - its close but there is some different
travels from sensory dermatome to C8-T1 then goes back via lateral thoracic nerves to cutaneous trunci muscles
22
Q
What will you see with UMN bladder dysfunction
A
Hypertonicity caudal to the lesion
-Increased external (pudendal nerve) and internal (hypogastric nerve) urethral sphincter tone
23
Q
What nerve contracts the external urethral sphincter
A
Pudendal (S1-S3)
24
Q
What nerve contracts the internal urethral sphincter
A
Hypogastric (L1-L4)
25
What will you see with a LMN bladder
Decreased to absent reflex
Hypotonic / flaccid bladder muscle tone
very easy expression
26
What will you see with a UMN bladder
Normal to increased reflexes
Normal to hypertonic / spastic firm bladder
difficult expression
27
Hansen Type 1- chondroid degeneration typically affects what animals
Typically young, chondrodystrophic breed
28
What causes Hansen Type 1- chondroid degeneration
1) normal gelatinous nucelous pulposus (NP) loses water binding capacity and loss of Gags
2) Loss of hydroelastic properties and ability to withstand pressure
3) Progresses to calcification
4) Abnormal NP contents extrude through weakened annulus into veretebral canal
29
What dogs typically get Hansen Type 2 - fibroid degeneration
any breed but typically large non chondrodystrophic breeds
-German shepherd most common
Dogs typically >7 years old
30
What causes Hansen Type 2 - fibroid degeneration
involves progressive thickening of the dorsal annulus fibrosis & (fibrous collagenization of NP)
*rarely calcified
Protrusion dorsally into vertebral canal
31
With Hansen Type 2 - fibroid degeneration, there is protrusion which way **
dorsally into the vertebral canal
32
What is conservative treatment of IVDD
1) Crate rest 4-6 weeks
2) Bladder management
3) Prevent continued extrusion through ruptured AF
4) Adjunctive therapy
-Steroids or NSAIDS
-Muscle relaxants
-Opioids
-Gabapentin / Amantidine
-Acupuncture
-PE
33
What surgery do you typically do for intervertebral disc disease
hemilaminectomy to remove the compression
34
T/F: surgery if IVDD results in instant recovery
False
-secondary spinal cord trauma / injury takes time to heal
-surgical decompression just allows healing to begin
functional recovery takes weeks to months
35
Where might the lesion be if the patient has a stiff, short strided thoracic limb gait
C6-T2
LMN on thoracic limbs
UMN on pelvic limbs
36
What nerve is associated with the biceps reflex
Musculocutaneous C6-C8
-Biceps brachi
-Brachialis
-Coracobrachialis
37
What are the clinical signs of Horner's syndrome
-Sympathetic denervation to the eye
-Miosis
-Ptosis
-Enophthalmos
-Prolapse of nictitans
38
Horner's syndrome occurs with damage to
T1-T3
39
How do you treat nerve sheath tumors
1) Amputation +/- hemilaminectomy
2) Radiation therapy may be of benefit
3) Adjunctive chemotherapy
4) Analgesics are mainstay of palliative treatment
40
T/F: nerve sheath tumors are locally invasive, life-threatening tumors regardless of benign vs malignant status
True
41
What maximizes chance of nerve ssheath tumor resection
early diagnosis
-dont over interpret arthritis; may be concurrent
-rely on neurological exam finidngs
42
How come you get increased patellar reflex with sciatic nerve dysfunction
Normally antagonistic response is gone
this leads to hyperreflectivity
(femoral nerve is fine)
43
Where does degenerative myelopathy typically occur
T3-L3 signs
-GP ataxia / UMN paraparesis
-Normal to increased tone and reflexes in the pelvic limbs
*Not painful
degenerative process ascends and descends in the spinal cord
44
What exam findings will you see with forebrain disease
1) Behavior/ altered mentation
2) Contralateral blindess (absent menace)
3) Ipsilateral head turn, body turn, head pressing, circling
4) Contralateral postural reaction deficits
5) Seizures
6) Contralateral or truncal hypoesthesia
45
What are the different ways to describe mentation changes (forebrain dysfunction)
1) Dull- neurologic or non-neurologic, awake not alter to surroundings, not interested in normal stimuli
2) obtunded: dull and slow to respond but will response appropriately , neurologic
3) Stuporous: unresponsive to normal stimuli, responsive to strong stimuli
4) Comatose: unconscious. cannot be aroused, even with noxious stimuli
Others: abnormal behaviour, disoriented, delirious
46
neurologic or non-neurologic, awake not alter to surroundings, not interested in normal stimuli
Dull
47
dull and slow to respond but will response appropriately
neurologic in origin
obtunded
48
unresponsive to normal stimuli, responsive to strong stimuli
stuporous
49
unconscious. cannot be aroused, even with noxious stimuli
comatose
50
Forebrain dysfunction produces postural reaction deficits on the
contralateral side to lesion
51
Forebrain dysfunction produces menace and nasal stim deficits on the
contralateral side to lesion
52
Forebrain dysfunction produces facial or truncal hypoesthesia on the
contralateral side to the lesion
53
Why do patients with forebrain disease have postural reaction, menace, nasal stim, and facial and/or truncal deficits
all require somatosensory processing in cerebral cortex
-parietal and occipital cognitive association areas
54
T/F: forebrain dysfunction produces normal gait
True- has normal to minimal
NO ataxia!
55
What are the top infectious disease differentials for forebrain disease in cats
-Toxoplasma gondii
-FIV
-FeLV
-FCoV
56
What are the different types of intracranial neoplasias
-Meningioma
-Glioma
-Histiocytic sarcoma
-Choroid plexus tumor
-CNS lymphoma
57
What are the signs of vestibular disease
1) Ataxia- lean, list, fall or roll. loss of balance
2) Head tilt
3) Circle
4) Hemiparesis / postural reaction deficits (central only)
5) Nystagmus
6) Strabismus
7) Horner's syndrome
8) Facial nerve paresis/paralysis
58
T/F: you can see facial paresis /paralysis with vestibular disease
True - both peripheral and central
59
Peripheral Vestibular Disease
Nystagmus: ___________
Fast phase: _________
Head tilt________ from lesion
Stabismus: _________ from lesion
PR deficits: _______
CN deficits: _______
Peripheral Vestibular Disease
Nystagmus: Horizontal, rotary
Fast phase: away rom lesion
Head tilt: toward lesion from lesion
Stabismus: ipsilateral from lesion
PR deficits: No
CN deficits: CN VII (facial)
60
Central Vestibular Disease
Nystagmus: ___________
Fast phase: _________
Head tilt________ from lesion
Stabismus: _________ from lesion
PR deficits: _______
CN deficits: _______
Central Vestibular Disease
Nystagmus: Horizontal, rotary, vertical
Fast phase: away
Head tilt toward from lesion
Stabismus: usually ipsilateral from lesion
PR deficits: Yes- always on the side of lesion
CN deficits: V-VII, IX, X, XII
61
Paradoxical Vestibular Disease
Nystagmus: ___________
Fast phase: _________
Head tilt________ from lesion
Stabismus: _________ from lesion
PR deficits: _______
CN deficits: _______
Paradoxical Vestibular Disease
Nystagmus: Horizontal, rotary, vertical
Fast phase: toward
Head tilt away from lesion
Stabismus: usually contralateral from lesion
PR deficits: Yes- always on side of lesion
CN deficits: NO
62
What type of nystagmus can central and paradoxical vestibular disease have, in addition to horizontal and rotary
Vertical nystagmus
63
In both peripheral and central vestibular disease, the fast phase of nystagmus is ______ from the lesion
away
64
In peripheral vestibular disease, head tilt is _______ the lesion
toward
65
In central vestibular disease, head tilt is _______ the lesion
toward
66
In paradoxical vestibular disease, head tilt is _______ the lesion
away
67
Central vestibular disease always has
Postural reaction deficits on the side of the lesion
also typically has other cranial nerves affected (aside from CN VII and CN VIII)
68
Causes of peripheral vestibular disease
-Otitis media/interna
-Idiopathic vestibular disease
-Congenital vestibular
-Hypothyroidism
-Feline inflammatory polyps
-Aural neoplasia
-Trauma
-Toxic (aminoglycosides)
69
What causes paradoxical vestibular disease
cerebellar involvement
-lack of inhibition
causes:
head tilt away
fall/leaning away
fast phase nystagmus towards
postural reaction deficitis on same side of lesion
70
What does vestibular ataxia look like
off-balance
wide based stance
leaning to one side of the body
71
what branch of trigeminal innervates the masticatory muscles
mandibular
72
What are the 3 branches of trigeminal nerve
Mandibular
Ophthalmic
Maxillary
73
What are your top differentials for acute generalized tetraparesis
1) Botulism
2) Tick paralysis
3) Polyradiculoneuritis
4) Myasthenia gravis (acquired)
74
Botulism is almost aways accompanied with
GI signs - vomiting and diarrhea
75
Lower motor neuron disease occurs where
-Spinal cord segments
-Nerve root
-Peripheral nerve
-Neuromuscular junction
-Muscle
76
What is the goldstandard for myasthenia gravis diagnosis
Acetylcholine Receptor Antibody (AChR Ab) test
<0.6nmol/L Normal serum titer
>0/6nmol/L positive serum titier, diagnostic of acquired myasthenia gravis
77
failure of NMJ due to reduction of number of function nicotinic acetlycholine receptors
acquired myasthenia gravis
78
What 4 diseases can caise LMN tetraparesis/plegia
Coonhound
Botulism
Tick Paralysis
Myasthenia gravis
79
What are the clinical signs of myasthenia gravis
1) LMN tetraparesis
2) Dysphagia
3) Megaesophagus
4) Facial weakness
5) Aspiration pneumonia
6) Urinary retention
*Normal spinal reflexes
80
T/F: dogs with myasthenia gravis have normal spinal reflexes *
True
81
T/F: botulism can cause megaesophagus
true
82
What LMN tetraparesis/plegia disease has CSF with albuminocytologic dissociation
Coonhound paralysis
83
T/F: dogs with myasthenia gravis have normal CSF
true
84
What is nerve conduction study for myasthenia gravis
decremental response with supramaximal stimulation
85
What CN signs are present with tick paralysis
Dysphonia
LMN tetraparesis
86
What nerve conduction results are seen with tick paralysis
mild decrease in CMAP amplitude
87
How do you diagnose tick paralysis
1) Identification of ticks
2) Exclusion of other NM diseases
3) Mild decreases in CMAP amplitude
88
What ticks cause tick paralysis
female tick saliva has neurotoxin
Dermacentor variables and andersoni
89
What are the CN signs of botulism
-LMN tetraparesis/plegia
-Dysphonia
-Megaesophagus
-Mydiasis
-Decreased PLRs
others:
-Decreased mentation
-Urinary retention/ incontinence
-GI signs
90
T/F: CSF of botulism is normal
true
91
What does EMG of coonhound paralysis show
spontaneous activity
92
What nerve conduction results is seen with botulism
Decreased CMAP amplitude
Incremental response with supramax stim
93
What nerve conduction results do you see with Coonhound
Decreased CMAP amp
Slow F-wave latencies and ratios
94
What causes acute polyradiculoneuritis (APRN)
immune mediate cause is suspected
can be idiopathic, post vaccine, or secondary to contact with racoons (7-12d prior), camplyobacter and raw feeding
95
Steroid Responsive Meningitis Arteritis (SRMA) typically causes
only neck pain
does not typically cause neurological deficits or intracranial signs
96
What diseases does meningoencephalomyelitis of unknown origin (MUO) encompass
1) Granulomatous meningoencephalitis (GME) - focal, multifocal, ocular
2) Necrotizing meningoencephalitis (NME)
3) Necrotising leukoencephalitis (NLE)
97
What kinds of animals typically get granulomatous meningoencephalomyelitis (GME)
middle aged (4-8 years)
female
small breed (toy and terrier)
but any age, gender, size possible
98
What causes granulomatous meningoencephalomyelitis (GME)
unknown etiology
immune mediated
T-cell hypersensitivity
99
What are the clinical signs of granulomatous meningoencephalomyelitis (GME)
clinical signs reflect the location of the lesion
-Brain (cerebrum, brainstem, cerebellum)
-Spinal cord
-Eye- optic neuritis
100
What are the three forms of granulomatous meningoencephalomyelitis (GME)
focal
multifocal
diffuse
101
How do you diagnose granulomatous meningoencephalomyelitis (GME)
-signalment
-history
-MRI (best)
-CSF- pleocytosis, elevated protein
-lack of infectious agent
-histopathology
102
What does CSF of granulomatous meningoencephalomyelitis (GME) show
normal in 3-57% of cases
-pleocytosis
-elevated protein
103
How do you treat granulomatous meningoencephalomyelitis (GME)
1) Immunosuppression
-Steroids
-Cytosine arabinoside
-Procarbazine
-CCNU
-Cyclosporine
2) Sympotmatic:
-Anti-convulsants
-Consider concurrent antibiotics pending titer results
104
What is the prognosis of granulomatous meningoencephalomyelitis (GME)
focal form has a better prognosis
diffuse form may not respond to treatment
105
What are the two forms of necrotizing encephalitis
1) Necrotising meningoencephalitis (NME): grey/white matter disease
-Pug
-Maltese
2) Necrotising leukoencephalitis (NLE): white matter
-Yorkie, Chihuaha, Pomeranian, Boston Terrier, Shih Tzu
106
MUO that affects forebrain, brainstem, cerebellum
grey AND white matter
Granulomatous meningoencephalitis (NME)
107
white matter affected (asymmetrical)
-Yorkie, Chihuaha, Pomeranian, Boston Terrier, Shih Tzu
Necrotizing leukoencephalitis (NLE)
108
grey/white matter disease
-Pug
-Maltese
Necrotizing Meningoencephalitis (NME)
109
GME affects ______ breeds of ______ years
NME and NLE affects _______ breeds of ______ years
GME: toy and terrier 4-8 years
NME/NLE:: pug, YT, Maltese, Chihuaha <4years
110
What signs might you see with Necrotizing Encephalitides (NME/NLE)
acute onset
forebrain signs: seizures, circling, postural reaction deficits
111
How do you diagnose Necrotizing Encephalitides (NME/NLE)
1) Histopath for definitive diagnosis
2) Presumptive: signalment, history, clincal progression, MRI, CSF (elevated protein, mononuclear pleocytosis)
3) Lack of infectious etiology
112
What will you see on CSF of Necrotizing Encephalitides (NME/NLE)
CSF (elevated protein, mononuclear pleocytosis)
113
How do you treat Necrotizing Encephalitides (NME/NLE)
1) Immunosuppression
-Steroids
-Cytosine arabinoside
-Procarbazine
-CCNU
-Cyclosporine
2) Sympotmatic:
-Anti-convulsants
-Consider concurrent antibiotics pending titer results
114
What is the prognosis of Necrotizing Encephalitides (NME/NLE)
grave 4-6 months
NME worse (can die within days)
115
Is NME or NLE worse
NME - can die within days
