Neuro Flashcards
1
Q
What is the name of CN I? Is it sensory or motor? What is it involved with?
A
Olfactory nerve; sensory; involved in olfaction
2
Q
What is the name of CN II? Is it sensory or motor? What is it involved with?
A
Optic nerve; sensory; allows vision
3
Q
What is the name of CN III? Is it sensory or motor? What is it involved with?
A
Oculomotor; motor; pupil/eye position, innervates majority of extraocular muscles, pupil constriction
4
Q
What is the name of CN IV? Is it sensory or motor? What is it involved with?
A
Trochlear nerve; motor; pupil/eye position, innervates superior oblique extraocular muscles
5
Q
What is the name of CN V? Is it sensory or motor? What is it involved with?
A
Trigeminal nerve; mixed function; sensory to face and eyelids, motor to masticatory muscles; 3 branches- maxillary, mandibular, ophthalmic
6
Q
What is the name of CN VI? Is it sensory or motor? What is it involved with?
A
Abducent nerve; motor; pupil/eye position, innervates lateral rectus extraocular muscle and retractor bulbi, ABDUCTS the eye
7
Q
What is the name of CN VII? Is it sensory or motor? What is it involved with?
A
Facial nerve; mixed; innervates muscles of expression, involved in taste, salivation, and lacrimation
8
Q
What is the name of CN VIII? Is it sensory or motor? What is it involved with?
A
Vestibulocochlear; sensory; controls balance and hearing
9
Q
What is the name of CN IX? Is it sensory or motor? What is it involved with?
A
Glossopharyngeal nerve; mixed; swallowing and taste, motor to swallowing muscles
10
Q
What is the name of CN X? Is it sensory or motor? What is it involved with?
A
Vagus nerve; mixed; sensation to pharynx and larynx, involved in swallowing and vocalization, recurrent laryngeal is a branch
11
Q
What is the name of CN XI? Is it sensory or motor? What is it involved with?
A
Accessory nerve; motor; innervates pharyngeal, laryngeal, and cervical muscles
12
Q
What is the name of CN XII? Is it sensory or motor? What is it involved with?
A
Hypoglossal nerve; motor; lingual muscles, involved in swallowing
13
Q
What does the dorsal rectus muscle do? What nerve supplies it?
A
Provides upward motion of the globe; oculomotor (III)
14
Q
What does the ventral rectus muscle do? What nerve supplies it?
A
Provides downward motion of the globe; oculomotor (III)
15
Q
What does the media rectus muscle do? What nerve supplies it?
A
Provides medial motion of the globe; oculomotor (III)
16
Q
What does the lateral rectus muscle do? What nerve supplies it?
A
Provides lateral motion of the globe; abducens (VI)
17
Q
What does the dorsal oblique muscle do? What nerve supplies it?
A
Provides rotation nasally and inferiorly; trochlear (IV)
18
Q
What does the ventral oblique muscle do? What supplies it?
A
Provides rotation laterally and superiorly; oculomotor (III)
19
Q
What does the retractor bulbi muscle do? What nerve supplies it?
A
Provides posterior motion of the globe; abducens (VI)
20
Q
What symptoms would you see of optic (II) nerve dysfunction? How do you test it?
A
Blindness; menace response, PLR, dazzle
21
Q
What symptoms would you see of oculomotor (III) nerve dysfunction? How do you test it?
A
Lateral strabismus, mydriasis, ptosis; eye position, PLR
22
Q
What symptoms would you see of trochlear (IV) nerve dysfunction? How do you test it?
A
Dorsomedial strabismus; move head and observe eye position
23
Q
What symptoms would you see of trigeminal (V) nerve dysfunction? How do you test it?
A
Neurotrophic keratitis; corneal reflex
24
Q
What symptoms would you see of abducens (VI) nerve dysfunction? How do you test it?
A
Medial strabismus; move head and observe eye position
25
What symptoms would you see of facial (VII) nerve dysfunction? How do you test it?
Exposure keratitis KCS; observation, palpebral reflex, STT
26
What symptoms would you see of vestibulocochlear (VIII) nerve dysfunction? How do you test it?
Spontaneous nystagmus; observation
27
Define strabismus. What are its causes?
Deviation of the globe from its normal orientation in a non-exophthalmic eye. Caused by cranial nerve deficits (III, IV, VI)
28
What function do UMN have on gait?
Gait generation, maintenance of muscle tone/posture against gravity
29
What function do LMN have on gait?
Support of weight
30
When do spinal/proprioceptive ataxia occur? What are examples?
Occur with any injury to sensory (afferent) parts of the CNS, examples include Wobblers, EPM, EDM
31
What are signs of vestibular ataxia?
Truncal sway, wide based stance, nystagmus, head tilt, circling (ex. temporohyoid osteoarthropathy)
32
Describe cerebellar ataxia
Hypermetria, usually worse in thoracic limbs, intention tremors of head, absent menace response; most common in foals; ex. cerebellar abiotrophy (Arabians)
33
Are reflexes and reactions exaggerated, normal or absent in LMN lesions?
Usually decreased to absent
34
Are reflexes and reactions exaggerated, normal, or absent in UMN lesions?
Normal to exagerated
35
What is the Mayhew scale?
Scale for neuro deficits. 0- normal; 1- neuro deficits barely detected at normal gait, worsened w/ tests; 2- neuro deficits easily detected at normal gait; 3- neuro deficits prominent at walk, buckle or fall forward w/ special tests; 4- stumbling, tripping, falling spontaneously; 5- recumbent
36
What signs will you see with cerebral cortex lesions?
Postural deficits, seizures, altered mentation
37
What signs will you see with brainstem lesions?
Ataxia, weakness, dysmetria, dysphagia, anisocoria, dilated pupils
38
What signs will you see with vestibular lesions?
Ataxia, head tilt, postural deficits pronounced
39
What signs will you see with cerebellum lesions?
Ataxia, intention tremors
40
What signs will you see with spinal cord/UMN lesions?
Paresis, ataxia, dysmetria, spasticity
41
What signs will you see with peripheral nerve/LMN lesions?
Weakness predominates, postural deficits
42
What are signs of a C1-C5 lesion?
UMN in all limbs, proprioceptive deficits and weakness in all limbs, possible Horner's syndrome, hind limbs worse than front
43
What are signs of C6-T2 lesions?
LMN in forelimbs, UMN in hindlimbs, proprioceptive deficits in hindlimbs, possible Horner's syndrome
44
What are signs of T3-L3 lesions?
Normal gait in forelimbs, UMN and proprioceptive deficits in hindlimbs
45
What are signs of L4-S1 lesions?
Normal gait in forelimbs, LMN in hind limbs
46
What are signs of sacral/S1-S3 lesions?
Urinary incontinence, fecal retention, hypalgesic tail and perineal region, decreased tail tone
47
Describe UMN paresis/weakness
Spastic paresis, hyperreflexia, delayed protraction of limbs when walking or hopping, scuffing of toes
48
Describe LMN paresis/weakness
Short-strided, similar to orthopedic disease, if diffuse, animal may collapse, tremors at rest, proprioception intact, flaccid paralysis
49
What are signs of a brachial plexus injury?
Dropped elbow, inability to bear weight, lateral deviation of shoulder, complete desensitization and flaccidity of limb
50
What are signs of radial nerve paralysis?
Inability to flex shoulder, extend limb, and fix elbow to bear weight, dorsum of foot rests on ground
51
What are common causes of radial nerve paralysis?
Anesthesia or prolonged recumbency, direct trauma from external blow collision
52
What are signs of obturator nerve paralysis? What are causes?
Splay-legged horse; can occur from dystocia or ileal or sacral fractures
53
What are signs of femoral nerve paralysis?
Inability to flex and extend stifle, inability to bear weight, crouched stance with all joints flexed
54
Describe suprascapular nerve paralysis
Atrophy of supra and infraspinatous muscles, abduction of limb during weightbearing, inability to advance shoulder, focal swelling. Called "Sweeney", caused by direct trauma, often cart horses
55
What are common neuropathic treatments?
Minimize inflammation (NSAIDs, DMSO, corticosteroids), minimize injury (stall rest, wraps/splints), limit exercise, physical therapy
56
When do horses develop menace response?
Around 2-3 weeks old
57
What nerves does a pupillary light reflex test?
CN II and III
58
How would you assess glossopharyngeal nerve (IX) function? What would its dysfunction look like?
Watch them eat or pass a NG tube. Dysfunction would cause dysphagia, feed material in nostrils, coughing while eating
59
How would you assess vagus nerve (X) function? What would its dysfunction look like?
Watch patient eat, slap test of thoracolaryngeal reflex, listen to respiratory noise while working. Dysfunction causes dysphagia, "roaring", larpar
60
How would you assess hypoglossal nerve (XII) function? What would its dysfunction look like?
Examine tongue for tone and symmetry, ability to retract. Dysfunction would result in failure to retract tongue and atrophy of the tongue
61
What are the parts of a gait analysis evaluation?
Walking in straight line, circling, walking with head up, walking over a curb, tail pull, walking backwards, walking up and down hill
62
What are clinical signs of Horner's syndrome? What are common causes?
Signs- miosis (constriction of pupil), ptosis (drooping of eyelid), sweating ipsilateral to lesion. Causes- extravation of irritating substance, guttural pouch disease, EPM, cervical vertebral stenotic myelopathy, trauma
63
How do you diagnose Horner's syndrome?
Clinical signs, localize the lesion, chem/gas panel may show electrolyte changes, acid base derangements, hypocalcemia or hypokalemia
64
Describe CSF analysis
Goal is to identify inflammation, trauma, neoplasia, infection, or to rule in/out specific diseases. Perform standing (LS or C1-C2) or under GA (alantooccipital)
65
Describe myelography
Antemortem diagnostic of choice for compressive spinal cord lesion, done with rads or CT under GA or standing. Administer contrast, take images in flexed, extended, and neutral positions. Can cause seizures, poor recovery, fever.
66
What is CT good for analyzing? What about MRI?
CT- skulls and cervical spine. MRI- brain and cord imaging but not feasible in horses
67
What disease is the leading cause of non-infectious spinal ataxia in horses?
Cervical vertebral stenotic myelopathy (AKA Wobbler's)
68
What are predisposing factors/causes for Wobbler's?
Congenital (occipital atlanto axial malformation in Arabians), environmental + genetic factors
69
What is the classic presentation of a Wobbler's patient?
Rapidly growing, large, history of being "clumsy", thoroughbred or warmblood
70
What are the clinical signs of Wobblers?
Spinal/proprioceptive ataxia worse in hind limbs, symmetric, UMN paresis (spasticity, delayed protraction, increased tone, exaggerated reflexes, minimal muscle atrophy)
71
What is type 1 Wobbler's?
Symmetrical overgrowth of articular processes causes dynamic compression during flexion, develops orthopedic disease, usually mid cervical (C3-C5) region in weanlings or younger horses
72
What is type 2 Wobbler's?
Asymmetrical overgrowth either by direct bony compression or soft tissue hypertrophy, seen in mature horses at C5-C6, C6-C7
73
How is Wobbler's diagnosed?
Neurological examination, radiographs. Calculate sagittal ratios and look for abnormal ossification, malalignment, or degenerative joint disease
74
What are sagittal ratios?
Measurements used to identify compression of cord (based on rads)
75
What findings in a myelogram would suggest Wobblers?
Complete attenuation of ventral contrast column, at least 50% attenuation of dorsal contrast column
76
Describe medical/conservative treatment of Wobblers
Young horses- restrict exercise, restrict protein and carbs (to slow growth rate), alterations in copper and zinc, add vitamin E supplementation. Adults- corticosteroid injections, HA supplementation
77
Describe surgical treatment of Wobblers
Ventral stabilization "basket" surgery to stop repetitive trauma to spinal cord. Best candidates are young horses with 1-2 lesions and short duration of clinical signs. Takes 6mos to 1 year to recover, full effects may not be seen until that time. Expect 1-2 grades improved.
78
What is the relationship between vitamin E levels and equine motor neuron disease?
Negative- less vitamin E= more risk
79
Describe the clinical signs of equine motor neuron disease?
Trembling, muscle fasciculations, weight shifting, base narrow stance, low head carraige, elevation in tail ("elephant on ball stance"), excessive recumbency, muscle atrophy, weight loss despite appetite, not ataxic- walk better than they stand
80
How is Equine motor neuron disease diagnosed?
Measure serum or muscle vitamin E, examine retina, muscle biopsy of sacrocaudalis dorsalis medialis- look for neuro atrophy of type 1 oxidative fibers, definitive diagnosis
81
What is the prognosis and treatment for equine motor neuron disease?
Treatment leads to improvement over 6 weeks in 40% of cases. 40% cases have permanent disfiguration, 20% have continued atrophy. Treat with vitamin E supplementation (must be active alpha tocopherol 5000-7000 IU/day)
82
What is the most common cause of peripheral vestibular disease in horses?
Temporohyoid ostearthropathy (THO)
83
Describe the process and signs of temporohyoid ostearthropathy (THO)
Acute onset of peripheral vestibular disease and/or facial nerve paralysis caused by bony proliferation of articulation of stylohyoid and petrous temporal bones leading to fusion of the joint
84
What are potential causes of THO?
Extension of inflammation and infection from otitis media/interna, guttural pouch infection, repetitive trauma, nonseptic osteoarthritis, aging change
85
How is THO diagnosed?
DV view radiographs, endoscopy to visualize stylohyoid bone, CT/MRI for best image, necropsy
86
Describe the medical treatment of THO
Stabilize and provide supportive care, anti-inflammatories, antibiotics (if potential joint infection or otitis), treat the eye
87
Describe surgery for THO
Stylohyoid ostectomy (bone can grow back), ceratohyoidectomy- procedure of choice, basihyoid-ceratohyoid disarticulation
88
What is the difference between equine degenerative myelopathy (EDM) and neuroaxonal dystrophy (NAD)?
Cell body and axons in the brain and spinal cord undergo degeneration in both, EDM is more widespread, NAD is subset of EDM
89
What are clinical signs of EDM and NAD in young horses?
Symmetric ataxia, UMN weakness, may have depressed mentation, absent menace response, base-wide stance, no muscle atrophy, normal tail tone/perineal sensation
90
What are clinical signs of EDM and NAD in adult horses?
Ataxia (subtle), rapid behavioral change
91
How are EDM and NAD diagnosed?
Increased pNfH on CSF or in blood, low vitamin E levels, postmortem examination
92
How are EDM and NAD treated/prevented? What is the prognosis?
Vitamin E supplementation!! Prognosis poor, not reversible
93
What group of clinical signs are described by cauda equine syndrome?
Urinary/fecal incontinence, decreased tail tone, analgesia of tail, hypalgesia in perineal region, pelvic limb deficits
94
What are causes of cauda equine syndrome?
Inflammatory (polyneuritis equi- auto-immune?), EPM, epidural abscess, EHM, toxic, neoplastic, traumatic (broken tail, secondary to tail block)
95
What breed is predisposed to epilepsy?
Egyptian Arabians
96
What are infectious causes of seizures?
Bacterial meningitis, brain abscess, verminous encephalitis, EEE/WEE/VEE, WNV, rabies
97
What are traumatic causes of seizures?
Skull fracture, basisphenoid fracture, blunt head trauma
98
What are neoplastic causes of seizures?
Brain tumor, insulin producing tumor -> hypoglycemia
99
What are toxins that can cause seizures?
Moldy corn, castor bean, Jimsonweed, nightshade, hemlock, milkweed
100
What are metabolic and miscellaneous causes of seizures?
Hypoglycemia, hypocalcemia, hepatic encephalopathy, hypoxic ischemic encephalopathy, cholesteatic granuloma, pituitary adenoma in PPID
101
How are seizures treated in horses?
Short-term control- midazolam or diazepam. Long-term control- KBr, phenobarbital, Keppra, treat underlying cause if obvious. Dont' ride horse.
102
What are systems to evaluate in a down horse?
Musculoskeletal, GI, CV, neuro, metabolic
103
How should you approach a down horse? What is the prognosis?
Stay on dorsal side, get TPR. Do neural exam, CBC/chem, blood gas, UA, CSF, imaging. Maintain horse in sling for short-term or flip every 2-6 hours. Prognosis is POOR
104
Describe the lifecycle of Sarcocystis neurona
Opossums ingest sarcocysts from intermediate host, sarcocysts reproduce in GI tract, sporocysts are shed in feces and contaminate feed and water. Horse is aberrant host, ingests sporocysts which form sarcocysts in muscle and somehow migrate to CNS
105
What are risk factors for developing EPM?
>5 years old, warmbloods, living in the south
106
What are the clinical signs of EPM?
Can be acute or insidious, varied signs based on location of sarcocysts- ataxia, asymmetry, atrophy, inconsistent lameness, LMN signs, brainstem signs, CN involvement
107
What are differential diagnoses for EPM?
Wobblers, EEE/WEE/VEE/WNV/EHM, neuroborrelliosis, ortho disease, hepatic encephalopathy, neoplasia, trauma, THO
108
What helps differentiate EPM horses from horses with other diseases?
Lack of fever, typically not painful, mentation changes are uncommon, horses are generally pretty happy
109
How is EPM diagnosed?
Neuro exam with neurolocalization (often multifocal), serology (only useful if negative), CSF analysis, response to therapy, ruling out other diseases
110
What is the most accurate test for EPM?
SAG 2, 4/3 ELISA serum:CSF ratio; ratio <100 consistent with antibody production and active infection
111
How is EPM treated?
With ponazuril or diclazuril- both safe, effective, expensive ($1000/month), treat until signs resolve. Can also use folate inhibitors (sulfonamide/pyrimethamine) but less effective. May be more effective if used together. Additionally can use anti-inflammatories or immune stimulants
112
Describe rabies and its 3 phases
Arbovirus, ZOONOTIC, reportable. Reservoir- mammals. Phase 1- centripetal, days to weeks, enters CNS and replicates in limbic system, adjacent structures, and spinal cord. Phase 2- spreads to highly vascular organs (ex. salivary glands). Phase 3- centrifugal, unknown
113
What is the incubation period for rabies in horses? What are the common clinical signs of the different forms?
Incubation period 2-6 weeks. Most common complaints are lameness and colic. Paralytic form- ascending paralysis, loss of tail/anal tone, ataxia. Brainstem/dumb form- dysphonia, dysphagia, pharyngeal paralysis, head tilt, blidness, drooling. Cerebral/furious form- aggression, photophobia, hydrophobia, hyperesthesia, circling, roaring, bruxism, convulsions, depression
114
How is rabies diagnosed in horses?
IFAT on brain tissue, negri bodies on histopathology
115
What kind of viruses are WEE/EEE/VEE? Where are they found? Who carries them?
Togavirus (zoonotic, reportable). Carried by rats, birds, snakes, mosquitoes. EEE- SE USA, WEE- Western US and midwest, VEE- northern SA, central America, Mexico
116
What clinical signs are associated with EEE/WEE/VEE?
Initial hyperexcitability progressing to somnolence, depression, recumbency, blindness
117
How is EEE/WEE/VEE diagnosed?
CSF- neutrophilic to mononuclear pleocytosis, increased protein, antigen specific antibody detection on CSF or serum
118
Describe the prognosis of EEE/WEE/VEE
Poor, EEE worst, then VEE, then WEE, tend to have residual neuro deficits
119
How are EEE/WEE/VEE prevented?
Vaccines are cross-protective, control mosquitoes
120
What kind of virus is West Nile virus?
Flavivirus, zoonotic, not contagious between horses
121
How is WNV carried?
Carried by birds with mosquitoes as vectors. Horses and humans are dead end hosts. Peak season is September-November.
122
What clinical signs are associated with WNV?
Ataxia, abnormal gait, muscle/muzzle fasciculations, depression, recumbency, +/- mild/mod fever
123
How is WNV diagnosed?
IgM capture ELISA on CSF or serum, PCR on tissue
124
How is WNV treated?
Supportive care, mannitol (reduce brain edema), corticosteroids, WNV specific immunoglobulin
125
What is the prognosis for WNV?
70-80% survival, poor prognosis if recumbent, residual signs possible
126
How is WNV prevented?
Vaccinate!
127
Where is equine herpesvirus latently stored?
Trigeminal ganglion
128
What are the three forms of equine herpesvirus 1?
Respiratory- young horses, most common. Abortion- late term. Neurologic disease- EHM, least common, biggest concern.
129
What are the signs of equine herpes myeloencephalopathy (EHM)?
Fever, ataxia, generally worse in pelvic limbs, "dog sitting", urine dribbling, decreased tail tone, fecal retention
130
How is EHM diagnosed?
PCR of nasopharyngeal swab or whole blood in EDTA test of choice, ELISA and VN also available
131
Describe the treatment and prognosis for EHM
Supportive care, anti-inflammatories (NSAIDs, corticosteroids), antivirals (valacyclovir), prognosis decent for non-recumbent horses
132
What should you do during an outbreak of EHM?
Isolate and test suspected cases, report suspected cases, quarantine until results available, generally 21-28 days after no new cases
133
Why should you vaccinate against equine herpesvirus 1 when it doesn't protect against myeloencephalopathy?
Can still reduce duration of viremia and reduce nasal shed
134
Describe Clostridium tetani
Gram positive obligate anaerobe, exists in spore form, has three toxins- tetanospasmin, hemolysin, nonspasmogenictoxin. Tetanospasmin is the toxin that causes clinical signs.
135
How is tetanus transported within the body?
Bacteria proliferates in areas with low oxygen tension (wounds), binds to peripheral nerve terminals, is transported within axon and across synapses until it reaches CNS where it is taken up in the axon by endocytosis and blocks the release of GABA
136
What are the clinical signs of tetanus?
Diffuse, symmetric hypertonicity and hyperresponsiveness of all muscle groups, third eyelid prolapse, saw horse stance, tachycardia, dysphagia
137
What is a differential diagnosis for tetanus?
Hypocalcemia- causes tetany in horses, flaccid paralysis in cattle
138
What is the treatment for tetanus? What is it's prognosis?
Metronidazole, procaine penicillin, hyperbaric oxygen therapy, tetanus antitoxin, muscle relaxants, supportive care. Mortality ~75%
139
Where do the four types of Clostridium botulinum endotoxin occur?
Type A- West of Rockies; Type B- mid-Atlantic; Type C- FL, CA, AZ, NE, Canada; Type D- rare
140
Describe the pathophysiology of Clostridium botulinum
Blocks ACh release, toxin is taken up into vesicle, acidification leads to toxin being pushed into cytoplasm, toxin cleaves SNARE proteins and prevents cells from releasing vesicle neurotransmitter
141
What are the three different Clostridium botulinum syndromes?
Forage poisoning- ingestion of pre-formed toxin (adult horse); Wound botulism- castration site, injection site, umbilicus; Toxicoinfectious- ingestion of spores that proliferate in GI tract and produce toxin, seen in foals
142
What are the clinical signs of botulism?
Diffuse, flaccid paralysis, LMN weakness rather than ataxia, dysphagia, slow to eat or retract tongue, constipation, urine dribbling, bladder distension, mydriasis, ptosis, slow PLR, loss of corneal sensation/palpebral reflex
143
How is botulism diagnosed?
Difficult- "grain test"- can a horse finish 8oz of grain in <2 minutes? Or finding toxin in feed, GI contents, or wounds.
144
How is botulism treated?
Neutralize circulating toxin, use type B/C plasma or polyvalent plasma, debride wounds, provide supportive care and nutritional support
145
What is the vector of lyme disease?
Ixodes ticks vector it (Borrelia burgdorferi)
146
What clinical signs are associated with neuroborreliosis/Lyme disease?
Lethargy, anorexia, pyrexia, ataxia, hyperesthesia, uveitis, polysynovitis, neck pain, poor performance, tremors, weight loss, mentation changes
147
How is neuroborreliosis/lyme disease diagnosed?
Definitively on histopathology (ID of organisms in CNS tissue). Seroprevalence is so high that test is not helpful.
148
How is neuroborreliosis treated?
Minocycline can be used, maybe oxytetracycline- successful treatment rare, prognosis poor
149
How is neuroborreliosis prevented?
Tick control, deer eclusion. Can use topical cypermethrin, permethrin, pyrethrins, or piperonyl butoxide
