PNS Flashcards
(156 cards)
1
Q
Which domestic species are more, and which less susceptible to botulism?
A
- Dogs, cats, and pigs are the most resistant to botulism. In affected dogs, the type C neurotoxin is most commonly involved.
- Ruminants and horses are highly susceptible, and deaths are common. Cattle are most commonly affected by the type C and D neurotoxins and horses by types B and C.
2
Q
Three proposed methods of intoxication in botulism?
A
1) ingestion of a preformed neurotoxin in a feed source.
2) in young animals, especially foals, absorption of a neurotoxin that is produced within the gastrointestinal tract from spores that have been ingested from the environmental soil. This method is referred to as toxicoinfectious botulism.
3) circulation of toxin produced by organisms growing in the anaerobic environment of an infected wound. This is wound botulism.
3
Q
What can be an exposure route for a individual dog with botulism?
A
dead birds (or other carcases)
4
Q
Mechanism of action of the botulinum toxin?
A
at the neuromuscular junction the neurotoxin binds to receptors on the axon terminal.
It translocates into the axon and interferes with the release of acetylcholine. Because this affects only neuromuscular junctions, all the clinical signs are limited to an LMN deficiency. No sensory system signs exist.
5
Q
Clinical features to help distinguish botulism from polyradiculoneuritis?
A
- Loss of external anal sphincter tone.
- Megaesophagus.
- Dysphagia.
- Paresis of the facial, eyelid and tongue muscles.
- CSF exam should be normal in botulism (and cytoalbuminergic diss in PRN)
6
Q
Which dog breeds have a familial basis for acquired myasthenia gravis?
A
- Newfoundland
- Great dane breeds
7
Q
Which receptors are targets for acquired myasthenia gravis?
A
Nicotinic ACh receptors
(Once the antibody is bound to the acetylcholine receptor, the entire unit is internalized into the muscle and is no longer available; it must be replaced by the formation of a new receptor. )
in dogs also MUSK, in cats only AcHR
8
Q
Three clinical forms of acquired myasthenia gravis?
A
(1) generalized,
(2) focal,
(3) fulminating.
9
Q
Why do dogs develop megaoesophagus commonly in comparison to cats with myasthenia gravis?
A
the esophageal muscle in dogs is striated voluntary muscle innervated by GSE neurons, and these muscle cells have acetylcholine receptors identical to those in skeletal muscle. This is in contrast to cats, who have mostly smooth muscle in their esophagus.
10
Q
Name 2 cat breeds with high incidence of acquired myasthenia gravis
A
Abyssinian
Somali
11
Q
Name a cattle breed with congenital myashenic syndrome:
A
Brahman calves
12
Q
What percentage of dogs and cats have thymoma associated MG?
A
5% dogs and 50% of cats
13
Q
Neuro findings to differentiate fulminant MG from polyradiculoneuritis?
A
Megaoesophagus and regurg to be expected with MG as opposed to PRN.
Severe atonia and hypo-areflexia to be expected with PRN as opposed to MG.
CSF exam should be normal in botulism (and cytoalbuminergic diss in PRN)
14
Q
How is the response to edrophonium test in fulminant MG
A
Usually no response (since all the ACh receptors are occupied and internalised)
15
Q
Pathogenesis of tick paralysis?
A
- The neurotoxin enters the circulation and gains access to the neuromuscular junctions, where the toxin interferes with the function of calcium in the release of acetylcholine from the axonal terminal.
- Clinical signs may occur after having been bitten by a single female tick.
16
Q
Neuro signs in tick paralysis?
A
Clinical signs occur 5 to 9 days after the tick infestation, with a rapid onset of LMN paresis starting in the pelvic limbs and spreading to the thoracic limbs. Dogs may become recumbent in 24 to 72 hours. Spinal reflexes are depressed or absent. Nociception is normal, and hyperesthesia is absent. Cranial nerve LMN signs are uncommon except for severe cases. Megaesophagus is uncommon. Death may occur as the result of respiratory paralysis in 1 to 5 days if left untreated.
17
Q
Name at least 3 infectious agents associated with polymyositis
A
- Toxoplasma gondii,
- Neospora caninum,
- Hepatozoon americanum,
- Leptospira icterohaemorrhagiae
18
Q
Name 2 PNS disorders of dogs linked to hypothyroidism (De Lahunta)
A
- myasthenia gravis
- imune-mediated polymyositis
19
Q
Which breed of dog is overrepresented with polymyositis and lymphoma?
A
Boxer dogs
In some dogs, polymyositis may precede the development of a neoplasm
20
Q
Which findings support a dignosis of snake envenoment (postsynaptic blockade of the neuromuscular junction) causing acute LMN tetraplegia and areflexia?
A
Hemolysis and hemoglobinuria
Pain swelling and erythema of the skin from the cellulitis at the site of the bite wound may be observed.
21
Q
Name 2 organophosphates which could cause a LMN tetraplegia due to blockage of the acetylcholine receptor?
A
Chlorpyrifos and fenthion
22
Q
Which drugs can be used to treat organophosphate toxicity?
A
- atropine for the muscarinic signs
- pralidoxime chloride for the nicotinic signs;
- in some toxicities, diphenhydramine may help block the action of the toxin.
23
Q
DDs for a generalised, fast progressing LMN tetraparesis
A
- PRN
- MG
- Tick paralysis
- Botulism
- Polymyositis
- Hypokalaemic myopathy
- Organophosphate intox.
- (snake envenoment)
24
Q
Why do cats develop prominent dorsal displacement/protrusion of the scapula when the thoracic limb bears weight when walking in LMN disease?
A
presumably secondary to weakness of the serratus ventralis muscle
25
Spinal reflexes and postural reactions are normal or abnormal in animals with Hypokalaemic myopathy
usually normal
26
Which breed of cat has a recognised inherited hypokalemic myopathy?
Which gene has been implicated?
Burmese
WNK4 gene/chromosome E1
Feline hypokalemic periodic paralysis or Burmese hypokalemic periodic polymyopathy: most often with onset in 2- to 6-month-old Burmese kittens. Affected cats exhibit episodes of muscle paresis that may be diffuse, causing a crouched, short-strided gait, or localized to the cervical and proximal thoracic limb muscles.
27
Which drug can cause Hypokalemic myopathy in cattle?
mineralocorticoid drug isoflupredone (9-fluoroprednisolone acetate) for the treatment of ketosis or clostridial mastitis.
28
Name two inherited muscle disorders of labrador retrievers
1) Centronuclear (Type II Deficiency) Autosomal Recessive Polymyopathy (more common)
2) Dystrophinopathy, a Sex-Linked Recessive Muscular Dystrophy
29
What is a classical clinical sign of centronuclear Labrador polymyopathy?
The depressed or absent patellar reflex is a common clinical sign and may reflect involvement of the small striated intrafusal muscle cells in neuromuscular spindles that form the sensory component of the patellar reflex.
30
What is the prognosis of centronuclear Labrador polymyopathy?
- good prognosis for life because it is self-limiting.
- rarely progresses beyond more than 9 or 10 months and rarely causes recumbency.
31
Neurological signs with dystrophinopathy?
- vary considerably among affected dog breeds, according to the nature of the spontaneous mutation.
- short-strided gait in all four limbs, arched back, and lowered head and neck position
- decrease in range of mouth opening associated with prehension difficulties and sialosis.
- As the disease progresses, the tongue and pharyngeal muscles begin to feel enlarged between the mandibles.
- Although diffuse atrophy of most axial and appendicular muscles occurs, some of the caudal thigh muscles hypertrophy along with the diaphragm.
32
Ancillary tests to help differentiate centronuclear polymyopathy from dystrophinopathy?
marked elevation of serum muscle enzyme levels in dystrophinopathy (muscle fiber necrosis is usually severe, which results in the marked elevation of the serum enzymes CK, AST, and ALT)
33
What is the prognosis in dystrophinopathies?
It may be lethal in young puppies. Severely affected dogs have limited life spans and often develop complications associated with their cardiomyopathy.
34
Typical age of onset and breeds for exercise induced collapse (EIC)
Young adult (7 MO-2 Y)
Labrador Retriever +
Boykin Spaniel, Chesapeake Bay Retriever, Clumber Spaniel, Curly Coated Retriever, German Wire-haired Pointing Dog, Old English Sheepdog, Pembroke Welsh Corgi
35
Clinical signs of EIC
collapse
hyperthermia (up to 42,5 C)
When the dog has collapsed, the pelvic limbs are flaccid and patellar reflexes are usually absent, but the withdrawal reflexes and nociception are normal. Dogs commonly get worse in the 3 to 5 minutes after exercise is halted, perhaps related to a progressive increase in their body temperature, and severe episodes of collapse sometimes progress to involve all four limbs.
After a period of 10 to 20 minutes of rest, these dogs recover completely.
36
Gene mutation for EIC?
DNM1 (Dynamin-1)
Dynamin-1 (DNM1) is a protein that plays a key role in repackaging neurotransmitters into synaptic vesicles for release in the brain and spinal cord. DNM1 is not required for neurotransmission during low-level neurologic stimulation, but when a heightened stimulus such as intense exercise, excitement, or hyperthermia creates an increased demand for release of CNS neurotransmitters, DNM1 becomes essential for sustained synaptic transmission
37
Treatment and prognosis of EIC?
No specific treatment is available for d-EIC, but the disorder is not progressive. Affected dogs generally lead healthy lives as long as their participation in activities that trigger collapse is limited. Several dogs have died during severe episodes of collapse, so exercise should be stopped and attempts made to cool the affected dogs at the first hint of an abnormal gait.
It has been observed that affected dogs are less likely to collapse when they are exercised in water or in cold weather.
38
DDs for exercise-induced fatigue in dogs
(1) dogs that are normal on examination and
(2) those that are abnormal.
1:
cataplexy, syncope, focal seizure, movement disorder, or a nonneurological disorder (i.e., cardiac dysfunction)
myasthenia gravis, hypoglycemia, hyperkalemia, hypokalemia, muscular dystrophy, and, in Labrador retrievers, EIC
2:
myasthenia gravis, polymyopathy, muscular dystrophy, polymyositis, hypoglycemia, hyperkalemia, and hypokalemia.
39
Pathogenesis of congenital motor neuron disease (spinal muscular atrophy)?
abiotrophy of GSE neurons in the spinal cord ventral gray horn and brainstem nuclei.
(Neuronal abiotrophy most commonly affects Purkinje neurons in the cerebellum and GSE neurons in the spinal cord and brainstem. Often, multiple neuronal systems are affected. Clinical signs usually reflect the loss of those neurons most important for the animal’s ability to support weight and to generate a coordinated gait)
40
Breeds with canine and feline congenital motor neuron disease (hereditary spinal muscular atrophy)?
What about bovine?
Dogs:
- Spinal muscular atrophy of Brittany Spaniels
- Focal spinal muscular atrophy of German Shepherds
- Motor neuron disease of Rottweilers
- Multisystem chromatolytic neuronal degeneration of Cairn Terrier
- Multisystem neuronal abiotrophy of Swedish Lapland dogs
Cats:
- spinal muscular atrophy of Maine Coon
Bovine:
- Bovine spinal muscular atrophy (BSMA) of Brown Swiss cattle, Holstein, Friesian, and Red Danish breed - genetic variant of the FVT1 gene
- Blonde d'Aquitaine calves (not associated with FVT1 mutation)
41
3 forms of ongenital motor neuron disease (hereditary spinal muscular atrophy) in Brittany spaniel?
1) accelerated form: the puppies that are homozygous for the dominant gene have an accelerated form that results in clinical signs by 6 to 8 weeks of age with tetraparesis, difficult prehension, and dysphagia. By 3 to 4 months of age, the tetraparesis may progress to tetraplegia, along with severe neurogenic atrophy and associated limb deformities.
Two phenotypes are seen in the heterozygote dogs.
2) The intermediate form shows clinical signs of LMN tetraparesis at 6 to 12 months of age, and it slowly progresses to the inability to walk by 2 to 3 years of age.
3) The chronic form consists of a subtle paresis that is not observed until a few years of age and is accompanied by mild neurogenic atrophy.
42
What causes Equine motor neuron disease (EMND)
acquired disorder of adult horses that is strongly associated with an inadequate amount of vitamin E in the diet
43
Which receptors can be targeted in canine MG?
AChR
MUSK (muscle specific kinase)
(Cats no musk ab reported)
44
Proposed current classification of MG in dogs/cats
45
What percentage of dogs with generalised MG are seronegative?
2%
46
Which muscles are most affected in EMND?
Antigravity postural muscles.
These horses, without a doubt, prefer to walk rather than stand, which relates to the predilection of the MND for the GSE neurons that have the most active oxidative metabolism and that innervate the type 1 antigravity postural muscles (which require more aerobic metabolism).
The observation that affected horses “walk better than they stand” is a reliable guideline for separating EMND from virtually all other equine spinal cord diseases.
47
DDs for generalised LMN disease in horses
Subacute/chronic: EMND
Acute: botulism, exercise rhabdomyolysis, EMND
48
Ancillary procedures that help diagnose EMND?
1. extremely low serum levels of vitamin E
2. biopsy of the sacrocaudal dorsomedial muscle at the base of the tail, which is performed using a sacrocaudal epidural anesthesia, reveals denervation atrophy in this muscle, which normally consists of a large component of type 1 muscle fibers
3. In most affected horses, biopsy of the branch of the spinal accessory nerve to the sternocephalicus muscle, where it enters the muscle at the origin of its tendon near its termination on the mandible, reveals wallerian degeneration in the neuronal processes. This degeneration follows the loss of the cell bodies of these neuronal processes in the cervical spinal cord ventral gray column. However, general anesthesia is usually necessary for this procedure.
4. Fundic examination reveals a yellowish discoloration in the retina in about 30% of affected horses; it results from the accumulation of retinal lipopigment that occurs in this disease. The associated retinal degeneration is enough to be determined on electroretinography, but clinical evidence of any visual deficit has not been observed.
49
A photomicgrograph of a retina of a hors with weakness while standing is shown. What is shown in the image and what is the most likely DD?
EMND
Retina of a horse with equine motor neuron disease showing a mild excessive accumulation of lipofuscin in the pigment epithelium of the retina and in the space between that layer and the photosensitive layer.
50
Prognosis of EMND?
see image
+
also - there is a vitamin E deficiency associated myopathy (without involvement of the nerves) which respond very well to vitamin E supplementation and recover completely
51
Which gene variant causes polysacharide storage (PSSM) myopathy in horses?
The glycogen synthase gene (GYS1)
autosomal dominant
52
Types of PSSM in horses based on the gene variant?
1) gene variant present
2) gene variant not present
53
Which muscle fibers are more affected in PSSM in horses?
type 2
54
Clinical signs in horses with PSSM?
55
Prognosis of PSSM in horses?
70-75% improve to satisfactory performance with therapy
56
What can provoke episodes of HYPP in horses? (Hyperkalemic periodic paralysis)
- stress
- cold
- anaesthesia
57
Possible neuroanatomic localisations and DDS for a monoparesis of the thoracic limb
NAL: C6-T2 SCS, nerve roots, spinal nerves and their ventral branches; the brachial plexus; named nerves (depending on which additional findings are present)
DDS: PNST, intervertebral disc herniation, lymphoma, brachial plexus neuritis, chronic neuritis, brachial plexus injury/avulsion
58
At which point after brachial plexusus injury/avulsion should a leg amputation be considered if no improvement has occurred?
6 weeks (de Lahunta) or if allodyinia with automutilation has occurred
59
DDs for monoparesis in the horse?
- Equine protozoal myelitis,
- PNST,
- lymphoma,
- polyneuritis equi,
- other neoplasms
- radial nerve injury after anaesthesia
60
What is the cause of Equine protozoal myelitis?
- Sarcocystis neurona (most cases): endemic form in USA
- Neospora hugeshi: sporadic form worldwide
61
Common CSF findings in polyneuritis equi
- Pleocytosis (non-suppurative)
- Elevated protein
62
Prognosis in polyneuritis equi?
poor, continual care is necessary to ensure elimination of feces and urine.
63
Clinical signs of polyneuritis equi?
Atonia, areflexia, and analgesia of the tail, anus, and perineum.
Rectal impaction
Protrusion of penis
Analgesa of the skin of the penis
Rarely:
1) pelvic limb gait abnormalities (when the sciatic nerve is involved)
2) cranial nerve involvement (VII, VIII, and, less often, V is seen in some horses)
64
Which lesions are involved in the compression in Cauda equina syndrome (degenerative lumbosac. disease) of dogs?
1) Proliferation of annulus fibrosus dorsally
2) Bony proliferation of the body of L7 and S1
3) DJD of the articular processes
4) hypertrophy of the lig. flavum and dorsal long. ligament from dorsal
65
What is "Limber tail syndrome"?
also called acute caudal myopathy or swimmers tail or cold tail
a disorder of the muscles in the tail that has been described in hunting dogs, especially pointers and Labrador retrievers.
66
Lesions in neosporosis of young dogs?
Neosporosis may affect the nervous system at any age, but for reasons that are not known, this protozoan has a predilection for the lumbosacral spinal nerve roots (radiculitis) of young dogs.
Lesions also are present in these spinal cord segments (myelitis) and in the pelvic limb muscles (myositis), but the spinal nerve lesions are the most extensive
67
Main lesions in neosporosis of the adult dog?
CNS - usually cerebellum
68
What is "swimmer puppy syndrome"?
- developmental abnormality that occurs at a critical period of growth when a normal puppy is just starting to be able to stand and walk. It is the result of a disparity in growth between the muscles and the bones and soft tissues.
- usually large puppies that lack the strength to stand. As they struggle to stand, their limbs progressively become abducted. This places excess weight on their sternums, and that causes an excessive curvature or bowing of the ribs, resulting in a flattened thorax. In an attempt to stand in this abducted position, the flailing limbs make the puppy appear as if it were swimming—hence the name of the syndrome. In time, secondary joint deformities and ankylosis may occur.
- breeders who are aware of this condition have learned to prevent the problem by hobbling the puppies by loosely tying their limbs together to prevent the abduction and by providing nonskid surfaces during this critical growth period. Providing a bed of deep, soft material such as blankets may be helpful. This is not a neurologic problem or a primary muscle disorder. One or more within a litter may be affected.
69
Pathogenesis of feline ischemic/traumatic polyomyelomalacia?
1) severe abdominal compression, as would occur if run over by an automobile, causing a thrombosis or prolonged vasospasm of the lumbar arteries and ischemic poliomyelomalacia.
2) traumatic swelling of the hypaxial muscles may have compromised the blood flow in the lumbar arteries that course through these muscles to access the spinal cord.
3) This spinal cord lesion may be produced experimentally in dogs, cats, and laboratory animals by ligating the aorta at or cranial to the level of the renal arteries.
70
Which breed of calves was reported with poliomyelomalacia at about 10 days of age?
Ayrshire calves
71
Most likely diagnosis?
5 YO Dachshund, tetraplegia with loss of nociception which started as pelvic limb weakness 3 days prior.
Dorsal view of the entire spinal cord of a 4-year-old dachshund with ascending-descending myelomalacia.
72
Lesions of which SC location usually does not trigger ascending-descending myelomalacia?
Cervical lesions
73
Proposed pathophysiology of ascending-descending myelomalacia?
- vascular compromise primarily and may be the result of a sudden vasospasm of all the parenchymal arterioles.
- the vasospasm or the necrosis may be the result of the sudden release into the parenchyma of biologic amines such as glutamate, norepinephrine, dopamine, histamine, and serotonin.
- varying degrees of hemorrhage are associated with this necrosis.
74
Diabetes and hypothiroidism most commonly cause neuropathy/paresis of which nerve?
Tibial nerve (most common in the cat).
The resultant tarsal overflexion causes a plantigrade posture.
Diffuse neuromuscular paresis (and in some cases Horner syndrome also may be present) associated with diabetes in cats and dogs, resulting in tetraparesis is seen more rarely.
Hypothyroid neuropathy is believed to result from the decrease in adenosine triphosphatase activity that is needed for axonal transport. It may affect the tibial nerves, the recurrent laryngeal nerves, the facial or vestibular nerves, and possibly the vagal nerves to the esophagus. Only a very small number of dogs with chronic hypothyroidism develops a neuropathy and exhibits clinical signs.
75
Which disease could cause a skipping type gait and with a posture evident in the image (lexed posture of the tarsus and the severe atrophy of the caudal crural muscles)
Dancing doberman disease
(Inherited neuropathy/myopathy of Doberman Pinschers)
76
Which disease could cause a skipping type gait and this posture in a Leonberger?
Leonberger inherited neuropathy (distal polyneuropathy)
77
Which disease could cause a posture like this in this breed? (Tibetan mastiff)
hypertrophic neuropathy affecting the tibial nerves.
78
An autosomal recessive inherited giant axonal neuropathy that occurs in which dog breed?
German shepherd
79
Which nerve is commonly injured in calf due to dystocia related manual assistance?
Femoral nerve (L 4,5)
- the femoral nerves are at risk for being injured when a dystocia due to a “hip lock” leads to vigorous overextension of the hips when the extraction of the calf requires manual assistance.
This overextension puts traction on the femoral nerve or its roots. Most publications describe hemorrhages or disruption of the femoral nerve where it emerges from the iliopsoas muscle to enter the quadriceps femoris.
- If the injury is mild, spontaneous recovery may occur in a 2- to 4-week period.
80
Causes of a plantigrade posture?
1. A tibial nerve dysfunction with denervation of the tarsal extensor muscles: the gastrocnemius and the superficial digital flexor (diabetes, hypothyroidism)
2. rupture of the gastrocnemius and the superficial digital flexor tendons
3. A rupture of part or all of the common calcanean tendon
4. A fracture of the calcaneus
5. A disruption of the long plantar ligament
81
DDs for this posture?
An 8-year-old doberman pinscher with an overflexed left tarsus caused by rupture of the tendon of insertion of the gastrocnemius muscle at the calcaneus. Note the flexion of the digits from the stress placed on the intact superficial digital flexor tendon.
82
What causes this type of gait in horses?
Stringhalt
a hyperactivity of flexors of hips, stifle, tarsus, and digit aided by the reciprocal apparatus. It involves a disorder of the central pattern generators of spinal cord segments L4 through S2, their roots, spinal nerves, spinal ganglia, femoral, sciatic, fibular, and tibial nerves.
83
Which 2 forms of stringhalt exist?
1) sporadic/classic form - affects individual horses with a sudden onset, unilateral or bilateral, with no associated CNS or PNS lesions.
2) epidemic form pastured horses where false dandelion (flatweed, catsear, Hypochaeris radicata) is present. 3-4 weeks on a pasture. This form of stringhalt is related to a dying-back axonopathy of branches of the sciatic nerves in the pelvic limbs. Neurogenic atrophy occurs in crural muscles.
84
Aetiology of "stiff lamb syndrome"?
The most common muscle disorder in young ruminants and foals is the myopathy and rhabdomyolysis associated with vitamin E and selenium deficiency.
85
DDs for neck ventroflexion in a cat
hypokalemia,
thiamin deficiency,
hyperthyroidism,
myasthenia gravis,
diabetes mellitus,
polymyositis,
organophosphate toxicity
86
Breed and gene mutation in feline hypokalemic periodic polymyopathy
Burmese cats
WNK4 on chromosome E1
87
Which nucleus houses the GSE bodies of the CN III?
motor nucleus of the oculomotor nerve in the rostral mesencephalon at the level of the rostral colliculi.
The nucleus is adjacent to the midline within the ventral portion of the central grey substance that surrounds the mesencephalic aqueduct. This nucleus is rostral to the motor nucleus of the trochlear nerve and caudal to the parasympathetic nucleus of the oculomotor nerve.
88
What is the function of the medial longitudinal faciculus in regard to the nerves innervating the extraocular muscles?
- interconnects the oculomotor, trochlear, and abducent GSE neurons that innervate the extraocular muscles to permit coordinated conjugate movements of the eyes.
89
Where does the CN III leave the cranial cavity and which muscles does it innervate?
Orbital fissure
Dorsal, medial, ventral rectus.
Ventral oblique.
Levator palpebrae supperioris.
90
Where are the GSE cell bodies of the CN IV located?
motor nucleus of the trochlear nerve is adjacent to the midline in the ventral portion of the central gray substance that surrounds the mesencephalic aqueduct at the level of the caudal colliculi.
It is caudal to the larger motor nucleus of the oculomotor nerve.
91
Where does the CN IV exit the cranial cavity and which muscles does it innervate?
Fissura orbitalis (in some horses trochlear foramen).
Contralateral dorsal oblique muscle.
92
Where are the GSE cell bodies of the CN VI located?
Motor nucleus of the abducent nerve in the rostral medulla.
This is a small nucleus at the level of the medulla where the caudal cerebellar peduncle merges with the cerebellum. It is adjacent to the midline and floor of the fourth ventricle.
93
Where does the CN VI exit the cranial cavity and which muscles does it innervate?
Orbital fissure.
Rectus lateralis, retractor bulbi.
94
In which direction do the dorsal and ventral oblique muscles rotate the eye?
- dorsal oblique will intort the eyeball, or rotate the dorsal portion medioventrally toward the nose,
- ventral oblique will extort the eyeball or rotate the dorsal portion lateroventrally away from the nose.
95
Write the pathway tested with the physiologic nystagmus:
sensory receptors in the inner ear -> CN VII -> vestibular nucleus (medulla oblongata) -> rostrally via the medial longitudinal fasciculus to the abducent, trochlear, and oculomotor nuclei -> corresponding nerves
96
Which diseases most commonly cause CN IV dysfunction in cats and which in horses/cattle? What about dogs?
Cats: vertical pupils -> lateral deviation of the pupils.
Otitis media-interna.
Cattle/horses: horisontal pupils, dorsomedial strabismus.
Polioencephalomalacia (thiamin deficiency).
Dogs: round pupils so the rotation of the eyeball can not be appreciated except with a fundic exam.
97
Dysfunction of which CN is shown in the image?
Trochlear nerve CN IV
98
What is a vestibular strabism?
is a ventrolateral strabismus that is observed in some positions of the head when the vestibular system is affected by a lesion. The strabismus is ipsilateral to the vestibular system lesion. It may be differentiated from an oculomotor nerve strabismus because it is not present in all positions of the head, and when testing for normal (physiologic) nystagmus, the affected eye adducts as well as the opposite eye. A strabismus related to a GSE neuronal lesion is present in all positions of the head. This is in contradistinction to a positional strabismus related to vestibular dysfunction
99
Which breed of cat can show a mild billateral medial strabism?
Siamese cats
Strabismus may also occur with some congenital anomalies in the architecture of the central projections of the visual system. A mild bilateral medial strabismus is observed in Siamese cats. This breed has a higher portion of retinal ganglion cell neurons whose axons cross at the optic chiasm and project to the contralateral lateral geniculate nucleus.
100
Which 2 neoplasms most commonly affect cranial nerves in the middle cranial fossa?
Meningiomas and germ cell neoplasia
101
What is the cavernous sinus syndrome?
Also called the middle cranial fossa syndrome. Clinical signs of neoplasms or other disease processes that cause a mass effect located here that affect cranial nerves III, IV, and VI and the ophthalmic and maxillary nerves from cranial nerve V
102
Which nucleus houses the cell bodies of the GSE CN V?
Motor nucleus of CN V (pons)
This nucleus is found at the level of the middle and rostral cerebellar peduncles, just rostral to where all three cerebellar peduncles merge with the cerebellum.
103
Which muscles are innervated by the CN V mandibular branch? What is the exit point of the mandibular branch?
masseter,
temporal,
pterygoid,
rostral digastricus,
mylohyoideus,
tensor veli palatini
tensor tympani
Foramen ovale
104
Which nerves innervate the digastric muscle?
- rostral belly: mandibular branch of CN V
- caudal belly: CN VII
105
Pathogenesis of idiopathic trigeminal neuropathy?
bilateral nonsuppurative trigeminal neuritis.
An inflammatory disease that is believed to be an autoimmune disorder. A direct viral infection cannot be excluded, nor can an indirect infection that provides an antigen in common with cranial nerves. In an autopsy study of one affected dog, this inflammatory lesion was in all components of the trigeminal nerve bilaterally, including the ganglia. Demyelination was prominent, and axonal degeneration was rare, indicating that this was predominantly a primary demyelination. Numerous lymphoplasmacytic perivascular cuffs and many macrophages engulfing the degenerate myelin were seen.
106
Two most common neoplasia to affect the trigeminal nerve?
malignant NST
lymphoma
107
Name one disease of ruminants and one for horses which cause encephalitis that involves the motor nuclei of the trigeminal nerve bilaterally and causes paresis or paralysis of the muscles of mastication that results in an open mouth that cannot be closed to prehend food.
Listeria monocytogenes in ruminants
Sarcocystis neurona in horses
108
Why does a thick, ropy/foamy saliva accumulate around the lips and nose in dogs with billateral trigeminal lesions?
The change in the consistency of the saliva likely reflects dysfunction of the trigeminal nerve and denervation of the ipsilateral major salivary glands.
Supportive evidence of this change in the consistency of the saliva is seen when the patient drinks from a bowl. Often there is thick, ropy/foamy saliva left in the water bowl.
* The trigeminal nerve is a conduit for the distribution of postganglionic parasympathetic innervation to structures of the head. Parasympathetic innervation to the salivary glands is provided by preganglionic parasympathetic neurons of the facial and glossopharyngeal nerves
109
Which nucleus houses the GSE cell bodies of the CN VII?
Facial nucleus in the rostral medulla.
This well-defined nucleus is ventrolateral in the medulla, midway between the pyramid medially and the spinal nucleus of the trigeminal nerve laterally, caudal to the trapezoid body and the level of attachment of the caudal cerebellar peduncle to the cerebellum
110
Where does the CN VII leave the cranium?
Stylomastoid foramen
The facial nerve accompanies the vestibulocochlear nerve into the internal acoustic meatus of the petrosal portion of the temporal bone. The facial nerve is more dorsal; it enters the facial canal within the temporal bone and emerges through the stylomastoid foramen.
111
Which muscles are innervated by the GSE CN VII?
relatively thin muscles of the ear, eyelids, nose, cheeks, and lips
+
caudal portion of the digastric muscle
112
Why do most dogs an cats experience no ear drop in cases of facial paralysis?
because the ear cartilage is taut enough to keep the ear erect despite the paralysis of the ear muscles
113
Why is the consistency of saliva altered in some animals in cases of facial nerve paralysis?
when there is a lesion that affects the facial nerve or its GVE nucleus due to denervation of the salivary glands
114
Dysfunction of which nerve is shown here?
complete R CN VII (ear, nose)
115
Dysfunction of which nerve is shown here?
R buccal branches of CN VII
paralysis limited to the right nose and lip muscles caused by compression of the buccal branches of the facial nerve at the ramus of the mandible after prolonged lateral recumbency for surgery
116
What is stanchion paralysis?
cattle that struggle vigorously may also injure the auricular branches of the auriculopalpebral nerves and cause ipsilateral ear droop and loss of ear motion. This injury is referred to as stanchion paralysis.
117
Why is there rhythmic movement of the dorsomedial superior eyelid in some animals with vestibular nerve dysfunction?
This presumably occurs secondary to the close association between the facial nucleus and vestibular system. A branch of the palpebral branch of the auriculopalpebral nerve (facial nerve) innervates the levator anguli oculi muscle, which is responsible for this eyelid movement.
118
Dysfunction of which nerve is shown here?
CN VII (GVE fibers)
A 9-year-old Cavalier King Charles spaniel with facial paralysis. There also is keratoconjunctivitis sicca and hyperkeratosis of the nasal planum secondary to a loss of parasympathetic general visceral efferent innervation to the lacrimal gland and nasal planum, respectively.
119
Which drug is associated with laryngeal paralysis in horses?
In Arabian foals, organophosphate anthelmintic haloxon starting at 2 days of age.
Chronic lead poisoning in horses causes a polyneuropathy that includes the recurrent laryngeal nerves and results in laryngeal paresis
120
Name some canine breeds with inherited forms of laryngeal paralysis
- Bouvier des Flandres (4-6 MO)
- Dalmatians,
- bull terriers,
- Siberian husky, sled-dogs (Husky cross)
- Leonberger
- Rotweiler
121
Pathogenesis of canine idiopathic laryngeal paralysis
a dying-back axonopathy that predominantly affects long neurons such as those in the recurrent laryngeal and sciatic nerves.
122
Typical breeds for canine idiopathic laryngeal paralysis
Labrador retrievers,
Saint Bernards, Newfoundlands,
Rottweilers, and
Chesapeake Bay retrievers.
123
Causes of feline laryngeal paralysis?
Unilateral paresis may follow injury to the carotid sheath during venipuncture, dog bites, or thyroid surgery.
Infiltrative lymphoma may cause unilateral or bilateral laryngeal paresis.
124
Where are the GSE neuronal cell bodies of the CN XII located?
The motor nucleus of the hypoglossal nerve in caudal the medulla
125
Where does the CN XII leave the cranial cavity and which muscles does it innervate?
Hypoglossal canal
- the extrinsic tongue muscles (styloglossus, hyoglossus, and genioglossus),
- the intrinsic tongue muscles,
- the geniohyoideus
126
Name some diseases in domestic animals to cause CN XII dysfunction
All: botulism
Dog: unilateral, extraparenchimal lesion involving the CN XII nerve roots
Horse: unilateral, almost pathognomonic for Sarcocystis neurona
Cattle: bilateral paresis/paralysis of the tongue, L. monocytogenes encephalitis
127
Name the species, CN affected and most likely working diagnosis
Dog, R CN XII
extraparenchimal lesion involving the CN XII nerve roots
128
Name the species, CN affected and most likely working diagnosis
Cattle: billateral paresis/paralysis of tthe tongue, L. monocytogenes encephalitis
129
Name some diseases that affect GSE-LMN of both spinal and cranial nerves:
Botulism: dysphagia, facial paresis, and jaw and tongue paresis
Myasthenia gravis: facial and laryngeal paresis, esophageal muscle paresis.
North American tick paralysis and polyradiculoneuritis in dogs usually cause only mild facial paresis.
Polyneuritis equi may cause facial paresis.
Diffuse autoimmune polymyositis may include masticatory and pharyngeal muscles, causing dysphagia of the esophagus and regurgitation.
130
In which cases can prosencephalic lesions cause cranial nerve defficits?
as a result of a sudden interference with the UMN corticonuclear pathways that are involved in voluntary efforts that require cranial nerve GSE-LMN activity.
Cattle -> dysphagia may occur with severe acute prosencephalic hemorrhagic necrosis caused by Histophilus somni vasculitis
Horses, dysphagia may follow the sudden destruction of cerebral white matter, a leukoencephalomalacia caused by “moldy corn poisoning.” (Fumonisin B1, fungus Fusarium moniliforme)
131
Where are most of the lesions in listerial encephalitis located?
Which cranial nerve deficits are most commonly seen?
Medulla and pons -> L. monocytogenes gains acces thru nerve endings in the oral cavity -> enter the brain thru CN V
Various combinations of facial paralysis and vestibular ataxia with a head tilt are the most common cranial nerve signs
132
What is shown here?
Atrophy of the gluteal muscles on the right side (cranial gluteal nerves)
Equine protozoal neuritis
133
What is show here? Horse.
Nerve affected and most likely DD?
Atrophy of the right side of the tongue, CN XII R nucleus.
134
Where are the parasympathetic preganglionic GVE-LMN neruonal cell bodies located?
Sacral SCS - lateral grey column
135
What is the pelvic plexus?
hypogastric nerve (ganglionic axons) + pelvic nerve (preganglionic axons) + prostatic/vaginal artery
136
Which nerve (and which receptors) innervate the detrusor muscle?
Pelvic nerve (parasympathicus) -> muscarinic cholinergic (ACh)
Hypogastric nerve (sympathicus) -> beta adrenergic (noradrenaline)
137
Where are the sympathetic preganglionic GVE-LMN neruonal cell bodies located?
lateral gray column of T1-4(5) SCS
138
Where do the preganglionic sympathetic fibres synapse with the ganglionic ones (for bladder innervation)?
Caudal mesenteric ganglion (from there the hypogastric nerves leave the ganglion)
139
Where do the postganglionic sympathetic fibres synapse? (bladder innervation)
1) cell bodies of the parasympathetic ganglionic neurons (which have alpha 2 adrenoreceptors) - whilst the sympathicus is active, the parasympathicus is inhibited
2) internal blader sphincter (Alpha-1 adrenoreceptors)
3) detrusor muscle (beta adrenergic receptors)
140
Which nerve innervates the urethralis muscle (external sphincter of the bladder)?
Pudendal nerve (GSE-LMN cell bodies) - S1-3 SCS
nicotinic cholinergic receptors
141
Where are the dendritic zones of the GVA neurons for bladder innervation located, and which type of receptors are they? Which nerve do they course thru to reach the SC?
wall of the bladder and urethra
mechanoreceptors (A-delta) - respond to strech and distension
Pelvic nerve to the S1-3 SCS thru dorsal segmental roots
Their cell bodies are in the sacral spinal ganglia
142
Where are the centers for micturition located?
Pontine reticular formation
143
Which neuro signs are expected with a lesion of the S1-3 SCS or nerve roots?
- LMN bladder
- atonic external anal sphincter
- absent perineal reflex
- hyp/analgesia of the perineum
144
What kind of urinary issue would we expect with a cerebral lesion?
Cerebral lesions do not directly interfere with the functioning of the micturition centers in the brainstem but may cause a loss of learned habits of micturition. The patient may exhibit normal urination but without regard to where it is performed. Be aware that this incontinence may mimic a urinary bladder and urethra (lower urinary tract) disorder or behavioral issues, especially in cats.
145
What kind of urinary issue would we expect with a cerebellar lesion?
Normally, the cerebellum has an inhibitory effect on micturition, and cerebellar lesions may cause increased frequency of urination, but this complaint is rarely recognized. (other cerebellar signs like ataxia would predominate)
146
Innervation of the colon/rectum/sphincters (autonomic)
The sympathetic innervation to the descending colon and rectum is inhibitory, whereas it is facilitatory to the internal anal sphincter. The sacral spinal cord segment GSE-LMN innervates the striated external anal sphincter muscle via the sacral plexus and the caudal rectal branch of the pudendal nerve.
147
Which nerve branch of the CN VII provides the parasumpathetic innervation?
Major petrosal nerve - it leaves the facial nerve before it exits the stylomastoid foramen
Lesions of the facial nerve that occur after it emerges from the stylomastoid foramen cannot affect this parasympathetic innervation!!!!!
148
What is dysautonomia? Which anatomic structures are affected?
Horses - grass sicknes
Cats - Key-Gaskell syndrome
diffuse disorder of the GVE-LMN
degenerative lesions are seen in GVE ganglia, incl. enteric components, but also some spinal ganglia
149
Clinical signs of dysautonomia in dogs and cats
- mydriasis unresponsive to light,
- protrusion of the third eyelid,
- dry oral and nasal mucosae, dry eye
- dysphagia,
- megaesophagus,
- vomiting, diarrhea or constipation,
- fecal or urinary incontinence,
- bradycardia.
150
Which disease is suspected based on the image?
susp. dysautonomia
paradoxic ocular signs with dilated, unresponsive pupils (parasympathetic denervation) and bilateral protrusion of the third eyelids and smaller palpebral fissures (sympathetic denervation).
151
Which disease would you suspect in a dog with a bouncy gait (excessive overflexion of the limbs + abduction), wide based posture, normal withdrawal reflexes, reduced patellar reflexes with normal weight bearing and normal muscle tone/mass of the quadriceps?
Sensory ganglioradiculitis
152
Pathological findings in canine ganglioradiculitis?
Nonsuppurative lymphoplasmacytic inflammation of multiple cranial and spinal nerves and spinal nerve ganglia that extends into the dorsal roots of the latter +/- inflammation of the trigeminal ganglion
153
What is neurotrophic keratitis
lesions that affect the ophthalmic nerve branch of the trigeminal nerve and deafferent the cornea may result in degenerative changes in the cornea (oedema and erosion).
154
Where are the dendritic zones of the GVA system? The cell bodies?
viscera of body (dendritic zones)
spinal and cranial ganglia (cell bodies)
155
Functions of GVA vs. SVA?
GVA: body temperature, blood pressure, gas concentration and pressure, and movement of viscera.
SVA: taste and smell.
156
Cranial nerves with GVA axons?
Head/neck:
- CN VII from middle ear and blood vessels of the head;
- CN IX from caudal tongue, pharynx, carotid body, and carotid sinus;
- CN X from pharynx and larynx.
Thorax/abdomen:
branches of vagus and sympaticus
