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Specialty Boards Prep > Deck 2 > Flashcards

Deck 2 Flashcards

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1
Q

What are these? What do they indicate?

A

These are cholesterol clefts. They occur in many types of brain injury, and are simply an indication of chronicity.

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2
Q

What specific part of the diencephalon is the most rostral? What two important white matter tracts are located within this structure?

A

Lamina terminalis

Rostral commissure and optic chiasm

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3
Q

What are the 5 types of clinical manifestation of peripheral nerve hyperexcitability?

A
  • muscle fasciculations
  • myokymia
  • neuromyotonia
  • cramps
  • tetany
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4
Q

True or false: peripheral nerve hyper-excitability results in EMG changes that persist while under anesthesia.

A

True

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5
Q

What breed of dog is over-represented for generalized myokymia / neuromyotonia? What other disease often affects these dogs? What can precipitate signs?

A

Jack Russell terriers

Spinocerebellar ataxia (previously called hereditary ataxia)

Stress / excitement

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6
Q

Describe the differences in fasciculations, myokymia and neuromyotonia.

A

Fasciculations - single spontaneous MUAPs, results in subtle muscle rippling

Myokymia - semirhythmic bursts of MUAPs (intraburst frequencies b/w 5-150 Hz), sound like marching soldiers on EMG; also causes muscle rippling

Neuromyotonia - same as myokymia, except intraburst frequencies are 150-300Hz (faster); actually causes muscle stiffness; is waxing and waning

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7
Q

What two electrolyte disturbances can result in tetany?

A

Hypocalcemia
Hypomagnesemia

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8
Q

What are the three broad categories that can result in muscle stiffness?

How can EMG discriminate between causes of muscle stiffness?

A

CNS pathology, peripheral nerve hyperexcitability, and muscle membrane disease

EMG changes with PNH are present under anesthesia, but will abate with administration of a neuromuscular blocking agent.

EMG changes associated with CNS causes will disappear under anesthesia without the need for a neuromuscular blocking agent.

EMG changes associated with muscle disease will persist under anesthesia even after neuromuscular blocking agents.

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9
Q

What are two of the main medications used to treat myokymia / neuromyotonia? What is their purported MOA / general effect?

A

Procainamide and phenytoin, although signs can improve initially with treatment, they often progress even with treatment

They are presumed to be membrane stabilizing drugs.

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10
Q

What typically causes FOCAL myokymia?

A

Structural disease affecting involved nerve or nucleus

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11
Q

What endocrine disease in poodles has been associated with intermittent muscle cramping?

A

Hypoadrenocorticism

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12
Q

Dysfunction of this channel has been implicated in peripheral nerve hyperexcitability.

What is another possible channel that could be affected?

A

Voltage gated potassium channels (decreased function — inability to reset electrochemical gradient, resulting in sustained muscular contraction)

Voltage gated sodium channels, this time that are open for longer than normal

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13
Q

What lobe is a part of the paleopallium? What anatomic structure separates it from the neopallium?

A

Piriform lobe

Lateral rhinal sulcus

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14
Q

Define commissural, projection and association fibers

A

Commissural — fibers that cross between hemispheres

Projection — fibers that terminate in either brainstem or spinal cord

Association — fibers that stay within the cerebral hemisphere (can either be short or long)

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15
Q

What is this?

A

Cholesterinic granuloma in a horse

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16
Q

What is the term for this malformation? What species of animal is this found in? What is are two presumed causes?

A

Telencephelic anencephaly (prosencephalic hypoplasia) — where there is cranioschisis and connection of the ventricular system with this defect

Cattle

Folic acid deficiency and hyperthermia

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17
Q

What is the difference between a meningo(encephalo)cele and exencephaly?

A

A meningo(encephalo)cele is covered by skin whereas exencephaly is not.

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18
Q

What breed of cat has a meningo(encephalo)cele associated with an inherited craniofacial defect?

A

Burmese

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19
Q

What is this a picture of? What is the cause in most cases? What anatomic structure is missing in all cases? What is the other main feature of this disease?

A

Holoprosencephaly

Classic cause is ingestion of Veratum californicum on the 14th or 15th day of gestation

Corpus callosum

Cyclopian feature (ie only one eye on midline)

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20
Q

What is this a picture of? What is the most common etiology (broadly speaking)? What structures are affected v spared?

A

Hydranencephaly; typically caused by in utero viral infection

The neopallial cortical tissues are affected, while the basal nuclei, archipallium and paleopallium are spared

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21
Q

List the gross features involved in the complex malformation of calves

A

Sacrocaudal spina bifida
Meningomyelocele
Malformed tail
Myelodysplasia
Displacement of cerebellum and caudal brainstem into vertebral canal (up to C2)
Extension of occipital lobes ventral to tentorium cerebelli

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22
Q

What is the main pathology leading to Chiari-like malformation?

A

Early closure of the synchondroses of the ventral skull bones, resulting in shortening of the overall skull

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23
Q

What spinal cord segments are often spared from syringohydromyelia associated with COMS?

A

C1 — the syrinx doesn’t often start until the C2-3 disc space

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24
Q

What is the term for syrinx formation within the brainstem?

A

Syringobulbia

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25
Explain the occurrence of scoliosis in COMS patients?
The syrinx may interfere with the dorsal grey matter asymmetrically. On the more affected side, the syrinx causes loss of incoming GP information. Scoliosis then develops, with bending away from the side of the lesion.
26
What type of gait is common in animals with myelodysplasia? What is this presumed to be a disturbance of?
Bunny-hopping gait Lack of UMN control to the central pattern gait generators within the lumbar intumesence
27
What type of congenital malformations do Manx cats and English bulldogs get (they are similar but different)?
Manx cats — sacrocaudal spina bifida / meningomyelocele English bulldogs — lumbosacral spina bifida / meningomyelocele Both often come with some degree of myelodysplasia
28
Where is CSF produced from?
35% from the lateral/third ventricular choroid plexus 23% from fourth ventricle choroid plexus 42% from the subarachnoid space via capillaries Small amounts can also enter the ventricular system across the ependyma from vessels in the neuroparenchyma
29
What separates the vascular endothelium from the ependymal epithelium? What is different about the choroidal capillary vasculature and the rest of the CNS capillary vasculature?
A thin basement membrane AND pial meningeal cells The endothelial cells of capillaries at the choroid plexus do NOT have tight junctions (ie fenestrated)
30
Describe the biochemical features of CSF compared to blood.
CSF has more sodium, chloride and magnesium CSF has less potassium and calcium CSF has 80% less glucose CSF has much less protein (measured in mg instead of g)
31
What are two ways hyper-osmotic agents help reduce intracranial pressure?
1. Rapidly acting osmotic effect helps reduce edema /overall brain volume 2. These agents reduce rate of production of CSF from the choroid plexus
32
Rate of CSF production in dogs and cats?
Dogs — 0.05 mL/min (0.047) Cats — 0.02 mL/min (0.017)
33
At what level does the dura attach to the periosteum?
~C1-2 — rostral to this, there is no natural epidural space
34
Why does pupillary constriction occur before pupillary dilation with elevated intracranial pressure?
Constriction is thought to represent disinhibition of the parasympathetic oculomotor neurons due to damage of the prosencephalic UMNs. Dilation then represents damage to the brainstem nuclei (ie LMN dysfunction)
35
What is the primary histopathologic feature in cases of idiopathic trigeminal neuritis?
Demyelination with minimal axonal change + non-supparative inflammation
36
What three layers form the blood brain barrier?
1. Non-fenestrated capillary endothelium 2. Thick basement membrane 3. Layer of astrocytic foot processes
37
What is the ABCB1 mutation? What is its clinical significance?
Mutation in the gene encoding for the P-glycoprotein located within the cerebral endothelial cells. This protein is part of the physiologic blood brain barrier, and helps remove certain drug metabolites from the neuroparenchyma, like ivermectin. If dysfunctional, this can result in major CNS drug toxicities.
38
What constitutes the blood-CSF barrier?
Permeable vascular endothelium Basement membrane Loose layer of pial cells Cuboidal ependymal epithelium tight junctions
39
What are the anatomic landmarks used to guide lumbar CSF collection in a horse?
Lateral: tuber sacrale Cranial: spinous process of L6 Caudal: spinous process of S2 (S1 is too short to feel Then draw a line between the tuber coxae and that should get you close.
40
Normal levels of CSF protein in cats, dogs, cattle and horses?
Cats: <20 Dogs: 25-30 Cattle: 40 Horses: 80
41
What is the concentration of iodinated contrast agent that should be used for myelography?
No greater than 240 mg/mL
42
Which ventricle is the most susceptible to becoming enlarged in cases of obstructive hydrocephalus?
Lateral ventricles
43
This disease in cattle causes a secondary communicating obstructive hydrocephalus via what means.
Vitamin A deficiency via dural fibrosis
44
What is the presumed cause of congenital hydrocephalus in many small breed dogs?
Mesencephalic aqueductal stenosis secondary to abnormal fusion of the rostral colliculi. Often, this happens early on in utero, but then the aqueduct becomes patent by the time of birth / imaging.
45
What is the fancy term for a head, neck, and body turn?
Pleurothonus, typically occurs ipsilateral to a prosencephalic lesion
46
What are the vertebral formulae for the major domestic species?
47
Which spinal nerve contributes the most to the femoral nerve?
L5
48
What are the spinal nerves the contribute to the fibular and tibial nerves?
Fibular —L6 and L7 Tibial — L7 and S1
49
What is the sensory innervation to the first digit of the hind paw?
Femoral nerve via its continuation as the saphenous nerve
50
List the spinal cord segments involved in the named nerves coming from the brachial plexus.
Suprascapular - C6-7 Subscapular - C6-7 Musculocutaneous - C6-8 Axillary - C7-8 Radial - C7-T1(2) Median - C8-T1 Ulnar - C8-T1
51
What is the difference between primary and secondary demyelination?
Primary — disease that directly affects the myelin / its production (ie distemper virus) Secondary — loss of myelin secondary to loss of axonal integrity
52
Describe the process of Wallerian degeneration
- nerve is damaged - axon degenerates distal to damaged segment - secondary demyelination occurs - Schwann cells proliferate, forming Büngner bands to guide reinnervation - Axonal buds form, growing at ~1mm/day - (hopefully) reinnervation is eventually established
53
Traditionally, how long does it take to see EMG changes following denervation?
5-10 days
54
What distinguishes myotonia from complex repetitive discharges? What disease process is commonly results in CRDs?
CRDs have an abrupt onset and ending, and do not wax or wane. They are generated by a group of damaged cells. Cushing’s often results in CRDs. Myotonia is generated by individually damaged myocytes, and has a waxing and waning EMG pattern.
55
Offer an explanation as to why acute idiopathic polyradiculoneuritis does not result in megaesophagus.
AIPN is caused by an immune system attack against the ventral roots. The cranial (internal) portion of accessory nerve (which supplies innervation to the esophagus) doesn’t really have ventral roots to be attacked. This is in contrast to other LMN diseases like botulism and myasthenia gravis that routinely result in megaesophagus.
56
True or false: the immune system target in acute idiopathic polyradiculoneuritis can either be the myelin or the axon, and cases where it is the axon have a quicker recovery.
False — the first part of the statement is true, but myelin focusing forms typically recover faster due to the ability of the Schwann cells to proliferate.
57
How does botulinum toxin cause clinical signs?
Once it gains access to the body, the toxin gains access to pre-synaptic axons at the NMJ. Once in the nerve terminal, it cleaves SNARE proteins which are responsible for vesicle exocytosis. This means less ACh containing vesicles are released. This affects all NMJs, so we often see megaE, poor perineal and CN deficits. It can also cause autonomic signs because of the cholinergic blockade in those neurons.
58
What are two cat breeds that are predisposed to myasthenia gravis? Why do cats less commonly get megaesophagus with MG?
Abyssinian Somali Only the proximal third of the cat esophagus contains striated muscle, with the rest being smooth muscle.
59
What percentage of dogs and cats with MG have a mediastinal mass?
Dogs — 5% (3.4% in the classification paper) Cats — 25% (52% in the classification paper)
60
What is a unique drug toxicity in cats that results in myasthenia gravis?
Methimazole toxicity
61
What are the common ticks in North America that result in tick paralysis? Australia?
Dermacentor variabilis and dermacentor andersoni Ixodes holocyclus
62
Name 8 causes of acute neuromuscular disease
Myasthenia gravis Acute idiopathic polyradiculoneuritis Botulism Tick paralysis Polymyositis Snake envenomation Organophosphate toxicity Hypokelamic myopathy MASH POT B
63
What are the two most common cranial nerve deficits encountered in acute idiopathic polyradiculoneuritis?
Dysphonia and facial weakness
64
What is one unique sign of neuromuscular disease in the cat? Why does this happen?
Dorsal protrusion of the scapulae Weakness of the serratus ventralis muscle
65
Name three differentials for the juvenile / young Labrador with neuromuscular dysfunction (breed specific).
- centronuclear autosomal recessive polymyopathy - muscular dystrophy - exercise induced collapse (although this presents much differently than the first two)
66
In muscular dystrophy patients, which muscles undergo pseudohypertrophy and which undergo true hypertrophy?
Pseudohypertrophy — tongue, pharyngeal muscles, and diaphragm True hypertrophy — cranial belly of the sartorius
67
What is the genetic defect associated with exercise induced collapse?
Genetic defect in the coding of the protein known as dynamin-1. DMN-1 is responsible for repackaging neurotransmitters into synaptic vesicles.
68
What is the pathogenesis behind motor neuron disease? What is the alternative name for this disease? What species can develop an acquired form of this disease?
Abiotrophy of the ventral horn neurons, and subsequent LMN dysfunction. Spinal muscular atrophy Horses, via Vitamin E deficiency
69
Name three diagnostic tests that can help diagnose acquired equine MND
1. Serum levels of Vitamin E (should be low) 2. Muscle biopsy of the sacrocaudal dorsomedial muscle near tail base (should show denervation) 3. Biopsy of the spinal accessory nerve (should reveal Wallerian degeneration)
70
Damage to which of the nerve roots in particular results in miosis? Ptosis / third eyelid elevation?
Miosis occurs with T1 damage Ptosis / third eyelid elevation occurs with T2-3 damage
71
Describe the type of gait abnormality seen with infraspinatus muscle contracture Describe the gait abnormality seen with a suprascapular neuropathy
External rotation of the thoracic limb, with internal rotation of the elbow (pictured). Some flipping of the paw. No gait deficits with suprascapular neuropathy, just muscle atrophy
72
What provides the sensory innervation to the prepuce versus the penis?
Prepuce — genitofemoral nerve (L3-4) Penis — dorsal nerve of penis (S1-3, continuation of pudendal nerve)
73
What are the classic clinical signs of polyneuritis equi? What other nerves are occasionally involved? Presumed pathogenesis?
Urinary / fecal incontinence Tail paresis / paralysis Rarely gait deficits reflective of sciatic dysfunction Cranial nerves 7,8 and occasionally 5 Auto-immune; lymphoplasmacytic infiltration of affected nerve roots
74
True or false: tail paresis / paralysis indicates disease within the vertebral canal
True — since the course of the spinal nerves supplying the tail have such a short extra-vertebral canal course, it is very unlikely that enough will be damaged external to the canal to cause clinically apparent tail weakness
75
Describe the clinical features of acute caudal myopathy. Presumed pathogenesis?
Tail that is held horizontally for a few inches, and then drops, limp, after that. Typically self-resolving after a few days. Thought to be a type of compartment syndrome — excessive use of tail (ie after swimming) results in swelling of the muscle. The muscle swells within tight fascial sheath, and then ischemia occurs to the muscles.
76
What type of organism is this?
This is a protozoal organism, specifically Neospora caninum
77
What are the two proposed pathogenic mechanisms in feline traumatic poliomyelomalacia?
Vasospasm of the lumbar arteries Hemorrhage / swelling of hypaxial mm, resulting in lumbar artery compression
78
What intoxication causes these changes? In what species?
Selenium toxicity in pigs, resulting in symmetric diffuse poliomyelomalacia of the ventral grey horn
79
Common cause of sciatic neuropathy in birds
Renal adenocarcinoma The kidney is elongated in the bird, and is just ventral (anterior?) to the origin of the sciatic.
80
What type of inherited neuropathy does the leonberger breed get? What is the proposed human equivalent?
It is a dying back neuropathy that classically results in laryngeal paralysis and sciatic neuropathy initially. Charcot-Marie-Tooth polyneuropathy
81
What is the nerve / muscle is affected in ‘dancing Doberman’ neuromyopathy?
Tibial nerve and caudal crural muscles — some dogs have evidence of just neuropathy while others have evidence of just a myopathy.
82
What are the first signs of rabies if an animal is bitten in the pelvic limb?
LMN pelvic limb signs often occur first due to a poliomyelitis. This will typically progress to overt encephalitis signs within a few days.
83
What types of nerve injury are cattle at risk for during dystocia (calf and mother)?
Calf — femoral nerve damage Mother — obturator nerve damage, and potentially fibular nerve damage
84
Where is the fibrous band in a German Shepherds with fibrotic myopathy? How does it result in their characteristic gait?
Starts at the pelvis, runs caudomedially associated with the semitendinosis, semimembranosus and gracilis muscles, and inserts on the proximomedial tibia. When the limb is being protracted (swing phase) and the hip joint is being flexed, this caudally located band resists flexion of the hip, and stops this flexion early. Since it is more medially located, it causes the knee to internally rotate during the swing phase and causes the foot to be placed down more medially (axially) than normal.
85
Four (and a bonus fifth) differentials for a pelvic limb plantigrade posture.
- tibial neuropathy - rupture of common calcanean tendon - calcaneus fracture - disruption of long plantar ligament - proximal gastrocnemius tendon rupture (like off of the femur)
86
What part of the common calcanean tendon is ruptured and what part is intact to result in a plantigrade stance with flexed digits? Why do the toes flex?
Ruptured part is the gastrocnemius component, while the intact part is the superficial digital flexor tendon. Overflexion at the hock adds tension to the intact SDFT.
87
What is this horse demonstrating? What are the two forms of it?
Stringhalt Primary stringhalt is idiopathic, and no abnormalities are identified on histopathologic examination. Secondary (aka epidemic) stringhalt is associated with plant ingestion, specifically “false dandelion” and is common in Australia; this actually causes a dying-back neuropathy in the sciatic nerves.
88
What disease process can result in severe hypertonia in goats? What is a classic BW finding?
Vitamin E / selenium deficiency Severe CK elevation
89
List 7 ddx for cervical (ventro)flexion in a cat
1. Hypokalemia 2. Thiamin deficiency 3. Hyperthyroidism 4. Myasthenia gravis 5. Diabetes mellitus 6. Polymyositis 7. Organophosphate toxicity
90
What are two diseases in LA that can result in drop jaw seconds to an encephalitis damaging both motor nuclei of CN V?
Listeria in ruminants and EPM (sarcocystis neurona) in horses (pictured)
91
Put these four nuclei from rostral to caudal: - motor nucleus of CN IV - GSE motor nucleus of CN III - Pretectal nucleus - Parasympathetic motor nucleus of CN III
- Pretectal nucleus - Parasympathetic motor nucleus of CN III - GSE motor nucleus of CN III (level of rostral colliculi) - GSE motor nucleus of CN IV (level of caudal colliculi)
92
What muscle does the oculomotor nerve innervate that results in ptosis?
Levator palpebrae superioris
93
What is the medial longitudinal fasciculus and where is it located?
It is a white matter tract within the brainstem that connects the vestibular nuclei with the motor nuclei of CNN III, IV and VI. Is it located on midline just medial to these motor nuclei and just ventral to the ventricular system.
94
Name these structures.
95
Name these structures
96
Name these structures.
97
Name these structures
98
In what disorder is trochlear nerve palsy most frequently encountered? Describe the appearance of an eye with trochlear nerve palsy.
Thiamin deficiency in ruminants causing a polioencephalomalacia. “Extorsion” is the common word people use — dorsal part is rotated laterally and ventral part is rotated medially.
99
What is the name of this foramen? What are the other names of the foramen where the other trigeminal branches exit?
Oval foramen Ophthalmic branch leaves via the orbital fissure, and the maxillary leaves the skull via the round foramen —> alar canal —> rostral alar foramen
100
Dysfunction of what muscle is responsible for the development of middle ear effusion? What is it innervated by?
Tensor veli palitini Mandibular branch of CN V

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