Tina Neurology Flashcards

Question 1

Q

Define the grades of ataxia 68

Answer

A

Grade 0-No defcits

Grade 1-Just detected at a normal gait, but worsened by backing, turning, loin pressure or neck extension

Grade 2-Defcit easily detected at normal gait and exaggerated by backing, turning, swaying, loin pressure, and neck extension

Grade 3-Defcit very prominent on walking, with a tendency to buckle or fall with backing, turning, loin pressure, or neck extension

Grade 4-Stumbling, tripping, and falling spontaneously

Grade 5-Horse recumbent

Question 2

Q

mental status

Answer

A

alert

depression;. diminished reaction

stupor: “sleeping” but reaction to sound, light, noxious stimuli
semicomatose: sleeping and partial responsiveness
comatose: no response

Question 3

Q

Cranial nerve signs present and

Seizures, blindness, dementia, delirium, mild ataxia, or weakness

Answer

A

Cerebral disease

Question 4

Q

cranial nerve signs and

Hypermetria, intention tremors, weakness

Answer

A

Cerebellar disease

Question 5

Q

cranial nerve signs and

Gait defcits, altered consciousness, tetraparesis

Answer

A

Brainstem disease

Question 6

Q

Ataxia, hypermetria, or spasticity

Rear limbs worse than front

Question 7

Q

Ataxia, hypermetria, or spasticity

Front limbs worse than rear

Question 8

Q

Ataxia, hypermetria, or spasticity

Front normal, rear abnormal

Answer

A

T-L region

Question 9

Q

Ataxia, hypermetria, or spasticity

Tail/bladder paralysis, perineal hypalgesia

Question 10

Q

Nystagmus:

clinical difference between central or peripheral lesion

Answer

A

Central lesions associated with positional nystagmus; peripheral lesions are nonpositional

Question 11

Q

A widely dilated pupil in a visual eye suggests

Answer

A

oculomotor nerve damage—there will be no direct or consensual light response

Question 12

Q

horner syndrome

Answer

A

disruption of sympathetic innervation results in pupillary constriction, ptosis of the upper eyelid, and protrusion of the nictitating membrane.

Sweating of the cranial neck extending to the base of the ear is also associated.

Question 13

Q

Elevated tail carriage is commonly seen in horses with

Answer

A

equine lower motor neuron (LMN) disease

Question 14

Q

cerebellar abiotrophy in foals is characterized by

Answer

A

symmetric ataxia with intention tremors

Question 15

Q

Vestibular ataxia is usually associated with

Answer

A

head tilt and asymmetric ataxia

Question 16

Q

Ataxia is expressed in the horse as

Answer

A

truncal sway,

weaving during walking (i.e., placing feet out of line from one step to the next),

crossing over when turning, or

pivoting on the inside limb when spun

Question 17

Q

Define paresis

Answer

A

deficiency of voluntary movement arising from a reduction in normal muscular power

Question 18

Q

UMN weakness results from disorders that affect the UMN or their axons in

Answer

A

the cerebral cortex, subcortical white matter, brainstem, or spinal cord.

Question 19

Q

Fasciculations present

UMN or LMN paresis?

Question 20

Q

Horses that demonstrate good rear limb strength standing still but are weak when walking usually have

UMN or LMN weakness?

Answer

A

UMN weakness.

This is in contrast to horses with LMN weakness, which are weak both when walking and standing still.

Question 21

Q

Spasticity is an increase in muscle tone that primarily affects

Answer

A

antigravity muscles.

Question 22

Q

Define proprioception

mediated by?

Answer

A

ability to recognize the position of the limbs, body, and head in space.

Conscious proprioception is mediated by the cerebral cortex,

unconscious proprioception is integrated by the cerebellum.

Question 23

Q

Clinical signs associated with proprioceptive loss include

Answer

A

a base‐wide stance,

truncal sway (if severe).

When spun in a tight circle, the outside limb may be abducted, the horse may pivot on the affected limb, or c_ross the rear limb over the other_

abnormal position of the limbs after coming to a stop

Question 24

Q

Schiff–Sherrington phenomenon

Answer

A

condition of increased forelimb tone and flaccid paralysis of the hind limbs and has been seen in horses, associated with spinal cord lesions between T2 and L4

Question 25

Q

Correct spinal reflexes require

Answer

A

intact sensory nerve,

spinal cord segment(s),

an intact peripheral motor nerve (LMN), and muscle.

Perception of the stimulus requires intact ascending sensory pathways

Question 26

Q

The flexor (withdrawal) reflex in the recumbent horse is tested by

In the thoracic limb, the reflex is mediated by

Answer

A

clamping the skin over the distal limb and observing for withdrawal of the limb associated with flexion of the joints.

In the thoracic limb, the reflex is mediated by

sensory fibers in the median and ulnar nerves;

spinal cord segments C6‐ T2; and

motor fibers of the axillary, median, musculocutaneous, and ulnar nerves

Question 27

Q

The biceps reflex is tested by

Answer

A

balloting the muscle belly of the biceps and brachialis muscles with a plexor and feeling for muscle contraction.

This reflex is mediated by the musculocutaneous nerves and spinal cord segments C6 and C7. It is more readily detected in foals and may be difficult to detect in adult horses

Question 28

Q

The triceps reflex is tested by

Answer

A

slightly flexing the limb, putting the triceps muscle in slight tension, then balloting the distal portion of the triceps at its point of insertion.

A positive reflex is the observation of triceps muscle contraction.

The reflex pathway tested involves the radial nerve and spinal cord segments C7‐T1.

Question 29

Q

Clinical abnormalities associated with lesions in the segment

C1–C5

Answer

A

Spastic gait, worse in rear limbs

Proprioceptive deficits

Weakness

With or without Horner’s syndrome

Question 30

Q

Clinical abnormalities associated with lesions in the segment

C6‐T2

Answer

A

Proprioceptive deficits, worse in front than rear

Weakness + Muscle atrophy, thoracic limbs

± Horner’s syndrome

Question 31

Q

Clinical abnormalities associated with lesions in the segment

T3‐L3

Answer

A

Proprioceptive deficits, rear

Normal gait, front

Rear limbs weakness

Spasticity, pelvic limbs

Question 32

Q

Clinical abnormalities associated with lesions in the segment

S3–S5

Answer

A

Urinary incontinence

Fecal retention

Hypalgesia tail and perianal

Normal thoracic and pelvic

Question 33

Q

Clinical abnormalities associated with lesions in the coccygeal segment

Answer

A

Decreased tail tone

Hypalgesia caudal to lesion

Normal front and rear limbs

Question 34

Q

Clinical signs associated with disease of the brainstem

Answer

A

Ataxia, weakness, and dysmetria, mild to moderate. Dysphagia, anisocoria, or dilated pupils possible

Question 35

Q

Predominant clinical signs of cerebral cortex lesion

Answer

A

Postural deficits, seizures, altered mentation, blindness

Question 36

Q

Menace response in foals

Answer

A

Foals are visual from birth, but the menace response is not seen until about 2weeks of age.

Question 37

Q

Differentiating neurogenic and musculoskeletal gait abnormalities

Answer

A

musculoskeletal problem:gait is regularly irregular; neuro: irr irr
neurologic disease: the abnormality apparent in all phases of the gait examination
Treatment of the horse with NSAIDs, nerve blocks and joint anesthesia useful to differentiate

Question 38

Q

Symmetrical versus asymmetrical spinal nerve damage

DDx

Answer

A

symmetrical: cervical compression, cauda equina syndrome, and EDEM

asyymetric others, especially equine protozoal myeloencephalitis (EPM)

Question 39

Q

define seizure

Answer

A

paroxysmal event that arises due to excessive discharges of the cerebrocortical neurons

Question 40

Q

define epilepsy

Answer

A

reoccurring seizures from a chronic underlying process

Question 41

Q

How to discriminate between a true seizure and merely aimless struggling from pain, anxiety, or severe orthopedic or muscle disease

Answer

A

rhythmic patterned movements are classic for seizures

In animals with a true seizure, the muscle movements are repetitive and rhythmical, while movements that are misdirected and variable may be associated with a horse or foal struggling to right themselves.

Question 42

Q

Epilepsy of genetic origin appears to be very rare in the horse and has only been documented in

Answer

A

Arabian foals with juvenile idiopathic epilepsy

Question 43

Q

The most common causes of seizures in adult horses are reported to be

Answer

A

trauma, hepatoencephalopathy, and toxicity

Question 44

Q

clinical signs of signs of increased CSF pressure

Answer

A

mydriasis

papilledema (swelling of optic nerve)

Question 45

Q

colour of CSF

adult versus foal

Answer

A

CSF of normal neonates is slightly xanthochromic (up to 10days of age) , but in older foals or adults it is consistent with prior hemorrhage and/or diffuse inflammatory conditions

Question 46

Q

Metabolic derangements causing seizures or altered state of consciousness

Answer

A

Hepatoencephalopathy

Hypocalcemia

Hyponatremia

Hypoglycemia

Hypo‐/hyperosmolality disorders

Hyperammonemia

Question 47

Q

Common iatrogenic causes of seizure or altered states of consciousness in foals and adult horses

Answer

A

Air embolism

Intracarotid injection

Postmyelography

Moxidectin overdose

Fluphenazine

Enrofloxacin overdose

Question 48

Q

define EEG

Answer

A

graphic recording of the rhythmic bioelectrical activity arising predominantly from the cerebral cortex.

Question 49

Q

prolonged or recurring seizures may result in

Answer

A

increased intracranial pressure and neuronal necrosis

Seizures in neonates may also result in reduced arterial oxygenation

Question 50

Q

mechanism of seizure control with benzodiazepines

Answer

A

All benzodiazepines hyperpolarize neuronal cells by binding to the gamma‐aminobutyric (GABA) receptor, thereby amplifying the action of GABA on chloride channels in the cell membrane.

This increased chloride conductance hyperpolarizes the neuronal cell membrane, making the cell more resistant to depolarization. The overall result is an increase in the seizure threshold and a decrease in the electrical activity of the seizure focus

Question 51

Q

diazepam in foals

Answer

A

care should be taken when administering repeated doses to foals less than 21days old because of the slower clearance of the drug reported in this age group compared with older foals and adults

Question 52

Q

diazepam in HE

Answer

A

diazepam should be used with caution in horses or foals with hepatoencephalopathy as it may exacerbate clinical signs due to the upregulation of benzodiazepine receptors

Question 53

Q

Xylazin and seizures

Answer

A

xylazine reduces cerebral blood flow after transiently increasing intracranial pressure, which may potentially exacerbate cerebral edema and worsen seizures

Question 54

Q

ACP in seizures

Answer

A

Acepromazine is contraindicated since it may reduce the seizure threshold

Question 55

Q

Medical management of repeated convulsions in neonatal foals

Answer

A

. In neonatal foals, if more than three doses of diazepam are needed over a few hours to control seizures, maintenance anticonvulsant therapy should be initiated (e.g., phenobarbital) due to their longer duration of action

Question 56

Q

Medical options for anticonvulsant maintenance

Answer

A

Options for anticonvulsant maintenance therapy include phenobarbital, bromide, phenytoin, and primidone. Phenobarbital is the drug of choice in horses.

Question 57

Q

Bioavailability and metabolization and elimination half life of Phenobarbital

Answer

A

Phenobarbital is well absorbed after oral administration, with a bioavailability close to 100% in horses .

The majority of the drug is metabolized in the liver with approximately 25% excreted as unchanged drug in horse

induces the hepatic cytochrome P450 enzyme complex, resulting in a more rapid metabolism not only of phenobarbital but also of other concurrently administered drugs. For instance, the elimination half‐life after a single oral dose of phenobarbital is reduced from 24h (initial) to 11h after 42days of treatment in horses

Question 58

Q

Suggested therapeutic serum concentration of phenobarbital in horses

Answer

A

The suggested therapeutic serum concentration in adult horses, as extrapolated from studies in humans and dogs, is 15–45µg/ml (70–175µmol/l)

an effective nontoxic therapeutic range of 5–30µg/ml in foals has been reported

Question 59

Q

Foals or adults have greater extracellular fluid volume and lower concentrations of plasma‐binding proteins?

Question 60

Q

Deworming horses under maintenance anti convulsive therapy

Answer

A

ivermectin, a GABA blocker, should not be given to horses and foals on anticonvulsant therapy because of the risk of breaks in seizure control that have occurred following its use

Question 61

Q

DMSO is indicated for

Answer

A

treatment of increased intracranial pressure and/or
cerebral edema,
for hypoxic‐ischemic encephalopathy and
for the acute treatment of equine protozoal myeloencephalitis (EPM).

Dimethyl sulfoxide at a dose of 1 g/kg is safe as a 10% diluted solution;

Question 62

Q

Magnesium in neurologic conditions

Answer

A

It has been suggested that magnesium sulfate, an NMDA receptor antagonist, given as an infusion, may decrease the incidence of seizures in foals suffering from hypoxic‐ischemic encephalopathy [37]. Given that magnesium sulfate improves neurologic outcome after brain impact injury in an animal model, it has also been proposed for the treatment of brain injury after head trauma in adults

Question 63

Q

Thiamine in neuro conditions

Answer

A

Thiamine administration may prevent glutamate‐ induced and NMDA receptor–mediated cell death in foals with hypoxic‐ischemic encephalopathy [62].

Furthermore, thiamine is an essential coenzyme in glucose utilization by the brain, which will further provide metabolic support [15].

Question 64

Q

Suprascapular nerve injury

Answer

A

Common Causes of Injury: Collision of shoulder with objects.

sweeney.

Eventual atrophy of supraspinatus and infraspinatus muscles. Lateral subluxation (popping) of the shoulder on weight bearing.

Answer 60

A

Often damaged in conjunction with humeral fracture; occasionally observed after recovery from general anesthesia.

Unable to bear weight on affected limb because of a lack of elbow extension. The shoulder is rested in an extended position, and the limb rests with the dorsum of the pastern on the ground.

Answer 61

A

common cause: Compression of the brachial plexus and radial nerve roots between the scapula and the ribs.

Signs of radial nerve paralysis often predominate.

Evidence of suprascapular involvement not uncommon.

Involvement of other nerves and nerve roots may be confirmed with EMG. Possible long-term atrophy of triceps. May have diffuse hypalgesia of lower limb.

Answer 62

A

common cause: External blow to the limb; occasionally observed after recovery from general anesthesia.

Unable to support weight as a result of lack of stifle extension. At a walk, the limb is advanced only with difficulty, and the stride is markedly shortened. The limb buckles due to stifle, hock, and fetlock flexion if the horse attempts to bear weight.

Quadriceps muscle will atrophy after 10–14 days. Patellar reflex is absent.

Answer 63

A

Occasionally occurs secondary to intramuscular injections, especially in foals; occasionally observed after recovery from general anesthesia.

Poor limb flexion with stifle and hock extended and fetlock flexed when the horse is not bearing weight. Weight can be supported if the foot is extended; otherwise weight is supported on the dorsal surface of the foot. Limb hypalgesia from stifle downward with the exception of the medial surface between stifle and hock.

Answer 64

A

trauma to lateral surface of the tibia/lateral side of the pelvic limb.

Frequently a component of sciatic nerve injury.

Inability to flex the hock and extend the digits. ->> drag the fetlock along the ground. Short protraction phase to the stride.

Hypalgesia laterally between hock to the fetlock.

Answer 65

A

CSF is produced as an ultrafiltrate of plasma and is actively secreted by ependymal cells of the ventricles and choroid plexus. The CSF is located in the ventricles of the brain and subarachnoid space of the spinal canal and bathes the CNS.

Answer 66

A

Jugular compression maneuver

Venous compression causes increased blood volume in the cranial cavity and compression of the CSF space, leading to increased CSF pressure. One can use jugular occlusion clinically to increase CSF pressure and facilitate collection of CSF fluid.

Answer 67

A

Pease and colleagues describe fluid collection between C1 and C2 using a lateral approach in the standing sedated horse under ultrasound guidance.

Depecker and colleagues describe fluid collection from the spinal cistern at the atlantooccipital site using parasagittal ultrasound guidance.

Answer 68

A

attaching a manometer tube with a three-way stopcock to a properly placed spinal needle, allowing the CSF to rise within it.

Answer 69

A

Hypercapnia increases cerebral blood flow in the cranial cavity, and CSF pressure and may worsen existing cerebral edema.

Answer 70

A

One must perform cell counts and cytologic evaluation within 30 minutes to avoid degeneration.

If cell counts or cytologic evaluation cannot be performed immediately, one can mix a portion of the sample with an equal volume of 50% ethanol to preserve cellular characteristics.

Answer 71

A

CSF from normal horses and foals usually contains fewer than 7 white blood cells per microliter.

Answer 72

A

Most studies show no differences in white blood cell counts in normal CSF samples obtained from the atlantooccipital space compared with samples obtained from the lumbosacral space.

Answer 73

A

Small mononuclear cells (70%–90%) and large mononuclear cells (10%–30%) predominate in equine CSF. Rarely, one may see neutrophils in horse CSF

Answer 74

A

preexisting trauma and secondary hemorrhage
increased protein concentration (150 mg/dL)
direct bilirubin leakage from serum in horses with high serum bilirubin concentration. In addition, indirect bilirubin may leak across a damaged blood-brain barrier.

Answer 75

A

increased in diseases with myelin degeneration and neuronal cell damage such as EPM, polyneuritis equi, equine degenerative myelopathy, and equine motor neuron disease.
conditions that alter blood-brain barrier permeability, such as equine herpesvirus–1.
other damage to the blood-brain barrier: serum CK can leak into the CSF and increase CSF CK activity. This increased CK activity is not associated with damaged myelin.

Answer 76

A

Collections of arachnoid villi (arachnoid granulations) are located in the venous sinus or the cerebral vein and absorb CSF. CSF absorption is related directly to the pressure gradient between the CSF and venous sinus. When CSF pressure exceeds venous pressure, these villi act as one-way ball valves, forcing CSF flow to the venous sinus.

Answer 77

A

The rate of CSF production is constant and is independent of vascular hydrostatic pressure.

Hypertonic solutions such as mannitol, when added to blood, decrease CSF production and decrease CSF pressure and edema.

Answer 78

A

Total protein concentration is higher in lumbosacral CSF compared with atlantooccipital CSF.

A difference of 25 mg/dL of protein between the atlantooccipital and lumbosacral spaces may suggest a lesion closer to the space with greater spinal fluid protein.

Answer 79

A

One can calculate the

albumin quotient (AQ) ([Albc]/[Albs] × 100) and
IgG index ([IgGc]/[IgGs] × [Albs]/ [Albc])

to determine blood-brain barrier permeability and intrathecal IgG production.

Answer 80

A

Normal total protein values range from 20 to 124 mg/dL, depending on the measuring method used

Answer 81

A

In one study, CK activity (greater than 1 IU/L) most often was associated with EPM in horses and may be helpful in differentiating compressive spinal cord disease from EPM. Furthermore, persistently increased CSF CK activity may be associated with a poor prognosis in horses with EPM.

Answer 82

A

CSF lactic acid concentration increases in eastern equine encephalomyelitis (4.10 ± 0.6 mg/dL), head trauma (5.40 ± 0.9 mg/dL), and brain abscess (4.53 mg/dL).

Lactic acid concentration may be the only CSF parameter increased in horses with brain abscess.

Answer 83

A

study of the electrical activity of the muscle

The waveforms of EMG are derived from the action potentials of the muscle fibers that are firing singly or in groups near the electrode.

f.e. to differentiate between muscle atrophy due to nerve damage versus disuse atrophy or to diagnpse early oncset laryngeal hemiplegia

Answer 84

A

Brainstem Auditory Evoked Response

evaluates the integrity of the auditory pathway from its peripheral part (cochlear nerve) to the brainstem.

It is useful in the detection of unilateral and bilateral deafness, as well as differentiation between conductive and sensorineural hearing loss.

Answer 85

A

BAERs are recognized as consisting of waves I to V in dogs, cats, and horses and are easily identified if normal

Wave I corresponds to cochlear nerve,
II to cochlear nucleus,
III to olivary nucleus,
IV to lateral lemniscus, and
V to caudal colliculus

Answer 86

A

temporohyoid osteoarthropathy,

congenital sensorineural deafness in Paint Horses,

multifocal brain disease, and

otitis media/interna.

Answer 87

A

graphic representation of the difference in voltage in microvolts between two different locations within the cerebral cortex plotted over time.

Answer 88

A

1: consists of systems designed for use in human beings. high field magnets with strengths ≥1.0 T of closed bore construction and

require the horse to be under general anesthesia.

2: consists of magnets that have been specifically designed for veterinary use. generally low field magnets with a strength in the 0.25-T range.

open bore design and can be positioned about a body part; some require general anesthesia and some only sedation. The images produced with these weaker magnets require longer scan times to obtain and are of lower resolution. Motion artifact in studies obtained on standing horses can significantly reduce image quality.

Answer 89

A

clinical manifestations of rapid excessive and/or hypersynchronous abnormal neuronal activity from the cerebral cortex that result in involuntary alterations of motor activity, consciousness, autonomic functions, or sensation

Answer 90

A

a disorder of the brain characterized by an enduring predisposition to generate epileptic seizures and by the neurobiologic, congnitive, psychological, and social consequences of this condition

Answer 91

A

condition resulting either from the failure of the mechanisms responsible for seizure termination or from the initiation of mechanisms, which lead to abnormally prolonged seizures

Answer 92

A

primary (i.e., idiopathic),
secondary (as the result of structural cerebral abnormalities), or
reactive (reaction of the healthy brain to transient systemic insult).

idiopathic (primary) : including disorders with suspected genetic etiology with no brain abnormalities

symptomatic or cryptogenic (secondary). Symptomatic epilepsies have a known cause that involves brain pathology, whereas cryptogenic epilepsies were those with unknown etiology

Answer 93

A

Epilepsy has been rarely documented in horses, except for juvenile idiopathic epilepsy in Arabian foals

Answer 94

A

neonatal maladjustment syndrome (both hypoxic-ischemic and nonhypoxic encephalopathy),

trauma, and

bacterial meningitis.

Answer 95

A

γ-Aminobutyric acid (GABA)

inhibition can be

presynaptic (release of GABA from the GABAergic nerve terminal into presynaptic nerve terminals causing a reduction of neural transmitter release) or
postsynaptic (caused by the interaction of GABA with specific postsynaptic receptors)

Answer 96

A

binds to NMDA receptors, which open sodium and calcium channels, leading to entry of these ions in the neuron and to postsynaptic depolarizations.

Answer 97

A

NMDA receptors have been implicated in the pathogenesis of seizures in infants and foals: exacerbation of intracellular calcium overload causes neuronal necrosis by activation of lytic enzyme systems and nitric oxide synthase with generation of free radicals

Answer 98

A

Just before the seizure (aura), horses might exhibit signs of anxiety and uneasiness.
During the seizure (ictus), horses might become recumbent, unconscious, and have symmetric clonic muscle contractions (contractions and relaxations of muscles occurring in rapid succession), followed by symmetric tonic muscle contractions (continuous unremitting muscle contractions).
After the seizure (postictus), horses might appear obtunded, disoriented, and blind for a few minutes, hours, or days

Answer 99

A

Benzodiazepines hyperpolarize neuronal cells by binding to GABA receptors, resulting in change of the chloride conductance pathways and making cells resistant to depolarization. The overall result is a decrease in the electrical activity of the seizure focus and an increase in the seizure threshold.

Answer 100

A

(1) facilitation of inhibitory neurotransmission via GABA receptors;
(2) inhibition of postsynaptic potentials produced by glutamate; and
(3) inhibition of voltage-gated calcium channels at excitatory nerve terminals.

Answer 101

A

phenobarbital (main active metabolite) and to a smaller extent to phenylethylmalonamide (a metabolite that might potentiate the anticonvulsant effects of phenobarbital).

Answer 102

A

inactivates voltage-dependent neuronal sodium channels, preventing depolarization of the presynaptic neuronal membrane at the excitatory nerve terminal, and thus reducing release of glutamate.

Adverse effects of phenytoin include

prolonged depression in foals, as well as

mild atrioventricular block and

decrease in blood pressure in adults.

Answer 103

A

potential adverse effects include excessive sedation, respiratory depression, bradycardia, hypotension, and hypothermia in neonatal foals.

Answer 104

A

Horses sleep an average of 3 to 4 hours per day with multiple phases of rest and sleep (polyphasic sleepers) throughout a 24-hour period.

Duration of lateral recumbency during nighttime has been reported to be 2% to 9% and 5% to 15% in wild and stabled horses, respectively

Answer 105

A

wakefulness,

drowsiness: one pelvic limb primed

slow wave sleep: horses can sleep standing with the head held low or in sternal recumbency if safe and comfortable. Many horses in this stage display a second atrioventricular block

REM sleep: loss of muscle tone. In addition to rapid eye movements, twitching, blinking, flaring nostrils, and even limb stretching might be observed

Answer 106

A

Lack of REM sleep

Answer 107

A

Imipramine, a tricyclic antidepressant drug, has been recommended to control narcolepsy and cataplexy.138 The drug blocks the uptake of serotonin and norepinephrine and decreases REM sleep. Oral administration (250– 750 mg) produces inconsistent results

Answer 108

A

Physostigmine is an anticholinesterase drug given at 0.05 to 0.1 mg/kg slowly intravenously that might precipitate a cataplectic attack within 3 to 10 minutes after administration in affected horses.

not recommended: untoward effects such as colic and cholinergic stimulation. lack of positive response to physostigmine does not rule out a diagnosis of narcolepsy

Answer 109

A

Trauma to the CNS - accounting for 22% to 24% of neurologic disorders.

Traumatic brain injury (TBI) was reported in 23% to 44% of cases, and

spinal cord injury (SCI) was reported in 56% to 77% of cases.

Answer 110

A

paresis of the rear legs

Answer 111

A

in a study 44% of injury was rearing and falling backward, resulting in poll injury

Answer 112

A

serious injury occurs to the basilar bones (bones composing the base of the skull like basisphenoid bone)

as a result of strong traction forces from the rectus capitis ventralis muscles

less common: fracture of the bones on the side and base of the calvarium such as the petrous temporal, squamous temporal, and parietal bones

Answer 113

A

defined as the presence of gas within any intracranial compartment (intraventricular, intraparenchymal, subarachnoid, subdural, and epidural).

Pneumocephalus was diagnosed by radiographs or CT in horses after trauma to the head with suspected or confirmed fractures to the sinuses.

No clinical neurologic signs were noted.

Answer 114

A

Brain swelling after TBI because of edema formation and hematoma formation within the skull are the most common causes of increased intracranial pressure

Answer 115

A

increased intracranial pressure

>> hypothalamic response to brain ischemia

hypertension
secondary baroreceptor-mediated bradycardia
irregular breathing

Answer 116

A

Continued elevation of intracranial pressure / reduction of cerebral blood flow results in

increased sympathetic discharge (catecholamines),

myocardial ischemia and
cardiac arrhythmias.

Answer 117

A

Although α2-agonists may transiently cause hypertension, which may potentiate intracranial hemorrhage, xylazine has been found to cause a minor decrease in cerebrospinal pressure in normal, conscious horses and is considered a safe sedative to use in horses with head trauma if the head is not allowed to drop too low that it could affect physiologic changes in intracranial pressure.

Answer 118

A

oculomotorius

Answer 119

A

Apneustic or erratic breathing reflects a poor prognosis, and bilaterally dilated and unresponsive pupils indicate an irreversible brainstem lesion.

Apneustic: abnormal breathing pattern characterized by deep , gasping inspiration with a pause at full inspiration followed by a brief insufficient release

erratic breathing: rapid shallow breathing

Answer 120

A

a decorticate posture, characterized by rigid extension of neck, back, and limbs

Answer 121

A

dysfunction of multiple cranial nerves in addition to depression and limb ataxia and weakness

Answer 122

A

one study showed that only 50% of bony fractures of the calvarium were confirmed radiographically

Answer 123

A

hyperventilation (decreasing CO2 pressure in blood)

CSF drainage,

treatment with hyperosmolar agents or barbiturates,

head elevation, and

decompressive surgery

Answer 124

A

Hyperventilation reduces the partial pressure of carbon dioxide in blood and subsequently leads to cerebral vasoconstriction. Reduced cerebral blood volume reduces intracranial pressure. However, cerebral vasoconstriction may lead to reduction of cerebral blood flow to ischemic levels.

Answer 125

A

no difference in outcomes between administering albumin versus normal saline in the intensive care unit. Furthermore a post hoc follow-up study demonstrated a higher mortality rate in TBI patients that were treated with albumin compared with those treated with saline.

Answer 126

A

Recommendations now are to maintain blood glucose concentrations at 120 to 140 mg/dL in TBI.

neurointensivists have shown that intensive insulin therapy increases markers of cellular distress in the brain and suggest that s_ystemic glucose concentrations of 80 to 110 mg/dL are too low in TBI and may lead to cerebral hypoglycemia_.

Answer 127

A

Fever is extremely common after TBI, and it has been well documented in animal models and in human beings to negatively affect outcome after TBI (e.g., by augmenting secondary injury mechanisms).1

Answer 128

A

Corticosteroids are no longer recommended for use in TBI following results of studies showing no benefit of these drugs and results of the CRASH trial that showed increased mortality in adults who received methylprednisolone after TBI

Answer 129

A

Ketamine is not recommended as part of a balanced anesthesia regimen in intractable seizures afetr TBI because it increases cerebral blood flow and intracranial pressure.

Answer 130

A

5 to 10 mg/kg IV to effect is reported to be useful. The major adverse effect of barbiturates is hypotension, especially if mannitol and furosemide have been administered, so they must be used with caution and adequate blood pressure monitoring.

Barbiturates should be reserved for those cases in which elevated intracranial pressure is refractory to other treatments.

Answer 131

A

The permeability of the blood-brain barrier to sodium is low. Hypertonic saline produces an osmotic gradient between the intravascular and the interstitial-intracellular compartments, leading to shrinkage of brain tissue and subsequent reduction of intracranial pressure. It augments volume resuscitation and increases circulating blood volume, mean arterial blood pressure, and cerebral perfusion pressure.

(4–6 mL/kg) over 15 minutes

Answer 132

A

worsening mental status,

abnormal pupillary size or inequality indicating transtentorial herniation, or

development of paresis.

Answer 133

A

Hyperosmolar therapy, which includes mannitol or hypertonic saline, is frequently used in human patients to reduce intracranial pressure. Both of these treatments appear effective at reducing intracranial pressure, and there does not appear to be a clinically significant difference between the two with regard to mortality or neurologic outcomes.1

Answer 134

A

trauma to or fractures of the cervical vertebrae are the most common

Answer 135

A

injury to the cranial cervical (C1–C3) and caudal thoracic (T15–T18) regions.

In fact, fracture of the axial dens with atlantoaxial subluxation is most commonly seen in foals less than 6 months of age

Answer 136

A

occipital-atlantoaxial region,

the caudal cervical region (C5–T1), and

the caudal thoracic region.

Reports also exist of injuries at the lumbosacral and coccygeal regions.

Answer 137

A

does not occur until 4 to 5 years of age.

Answer 138

A

spinal cord ischemia

Answer 139

A

refers to the deleterious cellular effects of excess glutamate and aspartate stimulation of ionotropic (f.e. NMDA) and metabotropic (glutamate rec) receptors -> intracellular calcium increase +++

Extracellular concentrations of both of these excitatory amino acids are increased after acute SCI, which occurs through release from damaged neurons, decreased uptake by damaged astrocytes, and through depolarization-induced release.

Answer 140

A

after acute SCI a phase of spinal shock can occur in which profound depression is noted in segmental spinal reflexes caudal to the level of the lesion, even though reflex arcs are physically intact.

Answer 141

A

extensor hypertonus is present in otherwise normal thoracic limbs in patients with severe cranial thoracic lesions.

Answer 142

A

Cord injury typically results in damage that is worse in the large myelinated motor and proprioceptive fibers compared with the smaller or nonmyelinated nociceptive fibers. Therefore ataxia and loss of proprioception and motor function will occur before the loss of deep pain.

Answer 143

A

xanthochromia and mild to moderate increased total protein concentrations. CSF analysis may be normal, especially in very acute or chronic cases.

Answer 144

A

impaired ventilation, bradycardia, and hypotension. This is particularly the case in lesions cranial to C5 (respiratory center affected) and cranial to T2 (origin of sympathetic outflow = thoracolumbar spinal cord).

Answer 145

A

free radical scavenging but may include decreased catecholamines and glutamate, as well as decreased apoptosis-related cell death.

Answer 146

A

physiologic: turning the head to the left
pathologic: lesion on the right

Answer 147

A

bc of ipsilateral extensor tonus and contralateral flexor tonus that act as an adaptive mechanism against gravity by catching the body and preventing a fall in the direction of vestibular stimulation

Answer 148

A

oculocephalic reflex

Answer 149

A

The slow phase is controlled by vestibular input, and the fast phase is a function of the brainstem.

Answer 150

A

Facialis

Vestibulocochlearis

symphathetic innervation

Answer 151

A

Central vestibular disease has similar clinical signs, but proprioceptive deficits are a distinguishing sign from peripheral vestibular disease. Other signs of central vestibular disease include

involvement of other cranial nerves,
alterations in mentation,
cerebellar disease, and
dysconjugate and/or positional nystagmus. The presence of vertical nystagmus is only observed with central vestibular disease

Answer 152

A

medial strabismus

Answer 153

A

Blindfolding a horse with compensated vestibular disease results in ataxia and a head tilt

Answer 154

A

one cannot induce physiologic nystagmus by rapid manipulation of the head

Answer 155

A

If no improvement of facial nerve deficits occurs within 3 to 4 months after the onset of disease, the prognosis is poor for recovery. If one notes even mild improvement in the first 4 months, facial nerve function might return.

Answer 156

A

Regardless of initial cause, inflammation induces bony proliferation at the articulation of the stylohyoid bone with the petrous temporal bone, resulting in loss of the joint space and fusion of the temporohyoid joint. The hyoid apparatus is attached to the tongue and larynx; fusion of the temporohyoid joint results in impaired flexibility of the unit. A stress fracture of the petrous temporal bone, the stylohyoid bone, or both might result from eating, vocalization, or any activity associated with normal tongue movement

Answer 157

A

CT of the skull followed by endoscopy of the pharynx and guttural pouch

Answer 158

A

Stabilization of the horse and decreasing inflammation near the fracture site
Treatment with broad-spectrum antimicrobials for either extension of a possible otitis interna-media or secondary infection in the hemorrhage that follows the fracture
Treatment of exposure keratitis and keratoconjunctivitis sicca (parasymp fibers of the facial nerve influence tear production)
Surgical procedures to remove pressure on the temporohyoid articulation to decrease pain and to decrease the likelihood of repeated petrous temporal bone fracture

Answer 159

A

partial stylohyoid ostectomy

ceratohyoidectomy

Answer 160

A

damage to the vestibular and facial nerves. Profuse aural hemorrhage or loss of CSF from the external ear canal frequently is observed.

Answer 161

A

renal failure

Degeneration of the hair cells within the peripheral receptor organs of the auditory and vestibular system

Answer 162

A

alterations in the range of gait

Answer 163

A

haracterized by a head tilt away from the lesion and nystagmus with the fast phase toward the lesion, is apparent with unilateral lesions involving the cerebellar peduncle

Answer 164

A

Cerebellar abiotrophy -> apoptosis of Purkinje cells

Abiotrophy in the nervous system refers to premature degeneration of neurons caused by some intrinsic abnormality in their structure or metabolism

commonly in arabians

Answer 165

A

inherited as an autosomal recessive trait

Answer 166

A

foals less than 1 year of age

occurs most frequently in 1- to 6-month-old foals.

Adult-onset cerebellar abiotrophy has been reported twice

Answer 167

A

intention tremor of the head, vertical or horizontal,

or

hypermetric forelimb gait

Generally, gait abnormalities are symmetric, although in a Welsh Cob and Arabian cross foal the initial signs were characterized by a stiff motion in the left front limb

Answer 168

A

no change in mentation.

One almost never observes nystagmus, which has been reported in only one case of abiotrophy in a Gotland pony.

A menace reflex frequently is absent or diminished.

Answer 169

A

Signs are generally progressive for several months after diagnosis. Once the animal has reached maturity, the condition becomes static, although mild improvement has been observed

Answer 170

A

The signs of characteristic ataxia and head tremor without weakness in Arabian, part-Arabian, or Gotland pony foals

Answer 171

A

The CBC and serum biochemistry profile are normal in affected foals.

Usually, there are no abnormalities in CSF and, if present, are not specific like elevation in TP and CK

Answer 172

A

a typical history and the clinical signs of

intention tremor,
lack of menace,
failure to blink to bright light, and
ataxia

in Arabian, part-Arabian, or Gotland pony foals.

The signs of characteristic ataxia and head tremor without weakness in the appropriate breed are nearly pathognomonic.

Answer 173

A

decrease in the cerebellar-to-whole brain weight ratio

most prominent finding is the widespread loss of Purkinje neurons

Answer 174

A

Photomicrograph of the cerebellum from a 9-month-old foal with cerebellar abiotrophy. The decreased number of Purkinje neurons is notable.

Answer 175

A

No treatment exists for cerebellar abiotrophy. As noted previously, signs may be progressive until the foal reaches maturity. Signs may stabilize or improve slightly with time.

Answer 176

A

progressive degenerative cerebellar condition recognized in the northwest part of New Caledonia that causes mild to severe ataxia

signs:

ataxia, which is most prominent in the pelvic limbs;
toe dragging
wide-based stance.

As the disease progresses, horses might have difficulty rising.

*The signs are primarily referable to involvement of the cerebellum; however, weakness likely is caused by brainstem or spinal cord involvement. Nystagmus is not observed. Ataxia is progressive over 3 to 4 years until the horse dies or is euthanized.

Answer 177

A

Mild cerebellar atrophy might be apparent on gross examination of the brain. Histologically, severe depletion of Purkinje neurons is evident throughout the cerebellum.238 Purkinje neurons might contain lipofuscin pigment and vacuoles. Moderate to severe lipofuscin pigmentation of neuron cell bodies occurs throughout the brain and spinal cord. Although lipofuscin accumulation might be considered a normal variation of aging, the degree of pigment accumulation is far more severe than that in horses of similar age

Answer 178

A

The pathogenesis of this disease is unknown.

no genetic component

accumulation of lipofuscin pigment and association with free-ranging horses suggest a metabolic disorder, perhaps resulting from toxicity.

Answer 179

A

characterized by a midline defect of the cerebellum and cystic dilation of the fourth ventricle, which separates the cerebral hemispheres.

Frequently, all or portions of the cerebellar vermis fail to form, and the corpus callosum may be absent.

The condition is rare in horses and has been observed in Thoroughbred and Arabian foals.

Answer 180

A

Foals with this syndrome might be abnormal neurologically from birth, with

difficulty rising,
seizures, and
absence of the suckle reflex.
forehead might be domed excessively.

as the foal ages:

Ataxia,
nystagmus,
aggression, and
difficulty in training might persist.

Answer 181

A

Diagnosis generally is made at postmortem examination; however, one case was diagnosed antemortem using CT

Answer 182

A

Cerebellar abiotrophy in arabians
Dandy-Walker syndrome
Cerebellar hypoplasia (single case report, foal)
Bilateral focal cerebellar cortical hypoplasia (single case report, adult)
cerebellar dysplasia (single case reports in adults and foals)

Answer 183

A

Unlike in many other large animals, no infectious agents have the cerebellum as their primary target;

Occasionally, disseminated Streptococcus equi subsp. equi infection (bastard strangles) may result in a cerebellar abscess (one report of successful surgical drainage + penicillin
infection and migration with Halicephalobus gingivalis with eosinophilic inflammation (two case reports)

Answer 184

A

can cause a number of clinical abnormalities, including cerebellar ataxia.251

Severe poisoning: incoordination, dysmetria, and gross head nodding in the experimental setting.

(Associated clinical signs: lethargy, anorexia, exudative dermatitis, laminitis.)

Lesions in the cerebellum : focal atrophy and cellular depletion in the granular layer with little to no involvement of Purkinje cells.
neuronal necrosis and gliosis in the cerebrum, lymphocytic perivascular cuffing, and swollen axons in the spinal cord.

Diagnosis of methylmercurial poisoning can be based on clinical signs and measurement of mercury in the liver and kidney.

Answer 185

A

chronic progressive equine movement disorder of unknown etiology

Gait patterns of shivering were characterized in one study as (primarily in the pelvic limbs but might progress to thoracic limbs)

(1) hyperextension when backing and lifting the limb,
(2) hyperflexion and abduction during backward walking,
(3) shivering hyperflexion with abduction during backward walking, and
(4) shivering-forward hyperflexion including intermittent hyperflexion and abduction with forward walking
signs usually begin at less than 5 years of age and progress in the majority of cases (74% reported in one study)

Answer 186

A

shivers is characterized by end-terminal neuroaxonal degeneration in the deep cerebellar nuclei, which results in context-specific hypermetria and myoclonus

Horses with shivers are significantly taller (mean 173 ± 6.2 cm) with a higher male-to-female reatio (3:1) than a control population

Answer 187

A

cervical vertebral compressive myelopathy: young, well-fed, rapidly growing horses.

Analysis of over 800 horses with CVCM confirmed what previous studies have shown:

males (stallions and geldings) and
Thoroughbreds, Tennessee Walking Horses, and Warmbloods
ranged from less than 6 months to less than 7 years of age

Answer 188

A

1.3% to 2% of Thoroughbred horses

Answer 189

A

(1) dynamic vertebral compressions, whereby the spinal cord compression is intermittent and occurs when the cervical vertebrae are flexed (more cranial vertebral) or extended (more caudal vertebrae)
(2) static compressions, in which spinal cord compression is continuous regardless of cervical position.
- important for imaging studies because significant flexion or extension may be necessary to demonstrate dynamic compressions.

Answer 190

A

between 12 and 23 months of age

Answer 191

A

symmetric ataxia,
upper motor neuron paresis, and
dysmetria,

which are usually worse in the pelvic limbs than thoracic limbs

Answer 192

A

Thoracic limb deficits are usually less severe than pelvic limb deficits because of the more superficial location of pelvic limb spinocerebellar proprioceptive tracts in the spinal cord.

Answer 193

A

arthritis of the articular processes of the caudal (C5–T1) cervical vertebrae, and articular process osteophytes are the most commonly seen radiographic lesions.

Answer 194

A

Adverse reactions: one third of horses undergoing myelography,

mortality rate of 2%,

most common complications: worsening of neurologic grade and seizures

Answer 195

A

Myelography has traditionally been considered the gold standard antemortem diagnostic test; however, sagittal diameter ratio analysis may be more sensitive and specific than myelography, at least if the 50% or 2-mm reduction of the dorsal contrast medium myelographic rules are used

More recently a technique has been described for cervical vertebral canal endoscopy during which a flexible videoendoscope with an external diameter of 4.9 mm is introduced into the subarachnoid space dorsal to the spinal cord.2

P638

Answer 196

A

Stall rest, glucocorticoids, DMSO, and other antiinflammatory drugs may provide transient improvement in clinical signs in horses with CVCM, especially if acute exacerbation of disease secondary to trauma is seen.

Ventral intervertebral fusion using a stainless steel fenestrated basket or threaded cylinder can allow expansion of the vertebral canal, atrophy of articular enlargements, and resolution of some or all the clinical signs in selected cases.

In a controlled field study, in which growing foals with CVCM were fed a diet restricted in protein and energy (65%–75% of National Research Council recommendations), clinical signs and radiographic lesions resolved in some foals and significantly improved in others.271 A positive effect of dietary modification and changing the rate of growth is likely to be seen only in young horses less than 1 to 2 years of age.11

Answer 197

A

33 were euthanized after diagnosis, and of the remaining horses 30% had at least one racing start. Horses were more likely to race if they had a neurologic grade less than 1 in the thoracic limbs and less than 2 in the pelvic limbs.1

Answer 198

A

a group of neurodegenerative diseases described in human beings and animals that are characterized by dystrophic alterations of neurons and axons and development of spheroid bodies.

In the horse, equine degenerative myeloencephalopathy (EDM) is considered a more severe form of equine neuroaxonal dystrophy (ENAD) where CNS lesions are thought to be on a continuum, with EDM lesions being more widely distributed than those seen in ENAD

Answer 199

A

EQUINE NEUROAXONAL DYSTROPHY/ EQUINE DEGENERATIVE MYELOENCEPHALOPATHY is a noncompressive, diffuse, symmetric, degenerative neurologic disease characterized by symmetric ataxia, weakness, and dysmetria in young horses of many breeds and both genders.

Answer 200

A

varies from less than 1 month to several years, with most horses manifesting signs within the first year of life

recent evaluation of a group of 88 horses with neurologic deficits suspected to be secondary to ENAD/EDM showed that 42% of the horses were older than 3 years at the time of examination;

Answer 201

A

Signs are referable to upper motor neuron and general proprioceptive deficits:

symmetric ataxia,
weakness, and
dysmetria,
most notably hypometria (spasticity),

of all four limbs, often worse in the pelvic limbs.3,287

Signs may begin in the pelvic limbs and progress to the thoracic limbs.

Answer 202

A

a recent evaluation of 88 horses with suspected ENAD/EDM found

60% of those horses to have an abnormal mentation ranging from quiet to obtunded, and

38% had a decreased or inconsistent to absent menace without loss of vision.

In addition, the presence of a pigment retinopathy in 4 out of 10 related Warmblood horses that had clinical signs of ENAD/EDM was recently demonstrated

Answer 203

A

The disease is considered not or very slowly progressive, and most horses stabilize at around 3 years of age. Horses do not recover from this neurodegenerative condition.

Answer 204

A

Pedigree analyses support a genetic cause for increased susceptibility to α-tocopherol deficiency with subsequent development of NAD/EDM; however, the mode of inheritance of NAD/EDM has been difficult to ascertain. From previous studies the mode of inheritance was most likely considered to be an autosomal dominant one

Currently, it is hypothesized that the genetic variant of ENAD/EDM is a susceptibility locus, and the amount of α-tocopherol received by a foal during the first year of life may play a role in determining the final phenotype

Answer 205

A

the imbalance between production of prooxidants and the antioxidant defenses.

ROS (e.g., superoxide anion, hydrogen peroxide, hydroxyl radical) are formed during the reduction of oxygen to water in normal cellular metabolism . Aerobic cells have antioxidant defense mechanisms that protect them from oxidative stress. - Brain very vulnerable

Another source of ROS is through the metabolism of excitatory amino acids and neurotransmitters such as glutamate and aspartate. When present in excess, excitatory amino acids can trigger a series of events including an increase in intracellular calcium, which can lead to the production of free radicals and subsequent neuronal damage and death. Other sources of free radicals that arise from brain metabolism include cytochrome P-450 electron transport, monoamine oxidase activity, and endogenous guanidine compounds.

Answer 206

A

Lipid peroxidation of cellular membranes and the direct oxidation of amino acids leading to inactivation of enzymes, receptors, and structural proteins

Answer 207

A

superoxide dismutase, catalase, glutathione peroxidase (that contains selenium),

α-tocopherol (vitamin E), and

ascorbic acid (vitamin C)

Answer 208

A

Insufficient vitamin E may result in oxidative damage and lipid peroxidation of cell membranes and may therefore cause

accumulation of lipopigment.
Accumulation of lipofuscin-like pigment is a common feature of experimentally induced vitamin E deficiency in rats and monkeys and in human and equine motor neuron disease.
Lipofuscin accumulation in the CNS of ENAD/EDM-affected horses has been reported,283,290,299 and the amount exceeds the amount found in age-matched controls

Answer 209

A

Definitive diagnosis of ENAD/EDM can be made only with histopathologic examination of the spinal cord and brainstem. Antemortem diagnosis is based on clinical signs and ruling out other neurologic diseases (especially CVM and EPM). In ENAD/EDM, CSF analysis and cervical spinal radiographs are usually within normal limits, although increased CSF creatine kinase (CK) levels have been found in horses affected with EDM.40 Measuring serum/plasma α-tocopherol concentrations may be unreliable when the animal is examined after the critical deficient period.

Answer 210

A

r, it should be noted that a single serum α-tocopherol sample may not adequately reflect the true vitamin E status of the horse, because up to 12% variation in concentrations can occur normally

less than 1.5 mg/ mL= deficient

Answer 211

A

natural RRRα-tocopherol (nonacetate) form of vitamin E

Answer 212

A

Oral supplementation with vitamin E to genetically susceptible foals in the first year of life may reduce the incidence and severity of disease. Typically animals are supplemented at 1000– 2000 IU/450 kg/day of vitamin E.

Additionally, one study reports improvement of clinical signs after gaining access to fresh grass

Answer 213

A

Vitamin E toxicity associated with supplementation in horses has not been reported, and the risk is considered minimal in horses

however, adverse effects have been reported with doses greater than 10 times NRC requirements

Answer 214

A

Although clinical signs of ENAD/EDM typically appear to stabilize by 2 to 3 years of age, affected horses are neurologically abnormal and often unfit for any performance activity. Generally, horses with ENAD/EDM do not progress to a state of recumbency. Severely affected horses usually have an earlier age of onset and rapid disease progression, whereas mildly affected horses usually have a later age of onset and the disease has a less rapid course

Answer 215

A

the majority of cases are because of infection with S. neurona

Another protozoan parasite (Neospora hughesi) has also been shown to be a cause of EPM in the horse;

Answer 216

A

Horses in the United States

high seropositive incidence to S. neurona: 15% to 89%,
- increases with increasing age,
- in areas with less freezing days
low seroprevalence against N. hughesi: less than 3% to 10%.

Answer 217

A

exposure to opossums (south and north america)
- higher risk for disease in the fall
housing:
- decreased risk with pasture housing
- increased risk with increased numbers of horses
- increased with straw or corn stalks bedding compared to wood
- decreased at operations that stored feeds in rodent-proof containers.
type of use: used for prim racing > used primarily for pleasure.
Breed : Thoroughbreds, Standardbreds, and Warmblood horses > Quarter Horses.
Age: Young horses > older ones
recent transportation increased odds of disease.
Region: twice as likely to have EPM if they resided in
- Kentucky, Michigan, Missouri, New Jersey, New York, Ohio, Pennsylvania, and Tennessee.

Answer 218

A

All horses are susceptible to the development of EPM, but epidemiologic surveys have suggested that the average age of affected horses is approximately 4 years.3

Answer 219

A

EPM is a disease of the Western Hemisphere, with cases reported from many states within the United States, as well as Canada, Mexico, Panama, Argentina, and Brazil.

Answer 220

A

S. neurona is not transmitted horizontally among horses, nor can it be transmitted to horses from nonequine intermediate hosts. Antibodies against S. neurona in foals before suckling have been reported but current evidence indicates that transplacental or lactogenic transmission of S. neurona is very uncommon or absent

several recent studies indicate that N. hughesi can be transmitted transplacentally in horses

Answer 221

A

definitive host is the opossum, whereas the intermediate hosts are skunks, raccoons, and armadillos, among others

Several species of animals and birds have been reported to exhibit signs similar to those in horses with EPM.

the horse is an aberrant or dead-end host

Answer 222

A

needs 2 hosts: definitive (=opossum) and intermediate

opossum eats Sarcocystis spp.>> contains bradyzoites that are released:

produce sporulated oocysts by sexual reproduction in the gut wall of the appropriate predator? or definitive host.

Infective sporocysts or oocysts only released by definitive host via feces

intermed host: infected oro-fecally, non-sexual sporulation through infected endothelium>>> development of Sacocystis in the muscle -> intermediate host HAS TO BE EATEN to spread disease

intermediate: racoon, otter, cat

dead end or aberrant host: horse - not all horses develop neuro disease

(so seropositivity is not diagnostic)

treatment: 20 mg/kg sulfadiazine SID or BID

prognosis: most improve and small percentage recover completely, 10-20% relapse within 2yrs

Answer 223

A

evidence for the role of physiologic stress is found in the observation that stressed horses develop more severe clinical signs than naturally infected (nonstressed) horses.

however, the interaction is complex and not fully understood at this time

Answer 224

A

we don’t know. suspicion:

Mouse studies : importance of CD8+ T cells (also called cytotoxic T cells) in protection against S. neurona encephalopathy in that species; it is presumed to be similar in horses.

Endothelitis and meningoencephalitis developed in CD8 knockout mice after challenge with S. neurona.

Answer 225

A

Clinical signs are variable, which reflects the random distribution of the lesions that may occur within the CNS.

Neurologic examination typically reveals asymmetric ataxia, weakness, and spasticity involving all four limbs.

The presence of ataxia, asymmetry, and atrophy (the “three A’s of EPM”) suggests multifocal or diffuse disease, which is characteristic of, although not pathognomonic for, EPM.

Answer 226

A

clinics
A key part of the diagnosis of EPM is ruling out other conditions that may be present;
Immunodiagnostic testing of serum and CSF should be conducted to confirm intrathecal antibody production against S. neurona or N. hughesi. (Western Blot might decrease detection of blood contamination antibodies)

most recent studies suggest the surface antigen designated SAG2 ELISA serum:CSF titer ratio, should be utilized for antemortem testing for EPM

Answer 227

A

The prognosis for horses diagnosed with EPM appears to be similar regardless of the treatment used, because most reports suggest an approximate improvement rate of 60% to 75% with the standard therapy.

Answer 228

A

Ponazuril: successful treatment in 60% of treated animals, success defined as improvement by at least one neurologic grade. A 90-day relapse rate of 8% after the termination of treatment was found.
diclazuril: improvement in 58% of the treated animals, when given for 28 day

the majority of horses with EPM are treated for a longer period of time, generally 6 to 8 weeks or longer if clinical improvement is still apparent.313 Attempting to treat until the horse is negative on immunodiagnostic testing is currently not recommended

Answer 229

A

Practical approaches including not feeding off the ground, providing separate sources of fresh water for horses and preventing wildlife access to horse pastures, paddocks, and stalls may also help reduce the incidence of protozoal infections in horses

Intermittent use of coccidiostatic and coccidiocidal drugs is another approach used to prevent EPM although more studies are needed

Answer 230

A

uncommon neurologic disease of all equine species that is characterized by tail and anal sphincter paralysis, often accompanied by cranial and peripheral nerve damage.

Answer 231

A

The cause of this disease is unknown.

Evidence suggests that the immune system is involved because horses with polyneuritis equi have circulating antibodies to P2 myelin protein, which is present in rats with experimental allergic neuritis

Answer 232

A

Although the disease manifests itself in two forms, signs are generally slow and progressive:

(1) the acute or early signs include hyperesthesia of the perineal or head regions (or both), and
(2) in the chronic form, horses show paralysis of the tail, anus, rectum, and bladder. Paralysis often is accompanied by fecal and urinary retention, urinary scalding of the pelvic limbs, and penile paralysis in male horses

Answer 233

A

cranial nerve involvement is reported primarily to affect cranial nerves V, VII, and VIII

A head tilt, ear droop, lip droop, and ptosis are common signs

Answer 234

A

Colic caused by fecal retention may be the primary sign when one initially examines horses with polyneuritis equi. Fecal retention leads to an impaction caused by the flaccid anal sphincter, often accompanied by an atonic, distended bladder.

If the clinician sees these signs in the acute or hyperesthetic form, they usually progress to hypalgesia or anesthesia. An area of hyperesthesia might surround the area of anesthesia

Answer 235

A

The definitive diagnostic test is a postmortem examination.

Blood works may show signs of chronic inflammation, CSF changes unspecific

Some horses with clinical signs exhibit circulating serum antibodies to P2 myelin.491,497 However, the presence of this antibody is only weakly supportive of the diagnosis because the same antibody has been detected in horses with EHV-1 and equine adenovirus infections

Answer 236

A

primary: damaged extradural nerve roots (st also intradural nerve roots)

granulomatous lesions with various degrees of inflammation and ionflamm cell infiltration

>>> myelin degeneration,

>>>subsequent axonal degeneration,

>>> thickening of the epineurium, endoneurium, and perineurium with proliferation,

>>>replacement by the fibrous tissue

The most severe lesions are in the cauda equina

Answer 237

A

symmetric muscle atrophy and
weight loss with significant weakness, sweating, and muscle fasciculations.
LMN affected:
- usually not ataxic,
- walk better than they stand.
denervation atrophy of both muscle fiber types (1 and 2) with a predominance of type 1 muscle fibers.
diagnosis:
- spinal accessory nerve biopsy or
- sacrocaudalis dorsalis muscle biopsy.
- any muscle containing both fiber types is useful for diagnosis.

Answer 238

A

The most important differential diagnosis is trauma to the sacrococcygeal area of the spinal canal, which can be differentiated by radiography of the area looking for fractures or displacements.

EPM is the second most common disease in the differential diagnosis of polyneuritis equi

EHV-1 myeloencephalitis

verminous myeloencephalitis

EMND

Answer 239

A

The primary therapy is palliative. No treatment for the disease is known. Removing feces from the rectum and evacuating the bladder are usually necessary. If cystitis caused by bladder distention occurs, systemic antibiotics might be indicated. Some attempts have been made at treating the inflammation with corticosteroids, but the effects have been short lived

Answer 240

A

The prognosis is poor. Some animals might be maintained for a few months.

Answer 241

A

also known as Scandinavian knuckling syndrome, is characterized by acute onset of bilateral pelvic limb digital extensor dysfunction and knuckling. no ataxia

Answer 242

A

The disease has been described in horses of various breeds during the months from December to April in Sweden, Norway, and Finland. The estimated prevalence of disease on farms in Norway and Sweden is 27% with a case fatality rate of 29%.

Answer 243

A

The exact etiology of disease is unknown but suspected to be forage-related toxicity.

Histologic lesions consist of inflammatory demyelinating polyneuropathy and intracisternal Schwann cell inclusions.

Answer 244

A

The neuromuscular system is composed of motor units.

A motor unit consists of a single lower motor neuron, its axon and supportive cells (Schwann cells), neuromuscular junction, and all the muscle fibers innervated by the motor neuron.

Answer 245

A

presynaptic (axonal terminal), synaptic (synaptic space), and postsynaptic (muscle membrane) regions.

Answer 246

A

Botulism (C. botulinum toxins A, B, C, D)
Drugs (e.g., aminoglycosides, tetracyclines, antiarrhythmics, anticholinesterases)
Hypermagnesemia
Hypocalcemia
Tick paralysis (females of Ixodes holocyclus [Australia], Dermacentor sp. [USA])

Answer 247

A

Envenomations (e.g., black widow spider [Latrodectus matans, alpha-latrotoxin])
Hypomagnesemia
Hyperkalemic periodic paralysis
Myasthenia gravis–like Myotonic disorders
Tick myotonia (Otobius megnini),
myotonia congenital/dystrophica
Snake envenomation (rare: coral snake, rattlesnake)

Answer 248

A

Tetanus (C. tetani toxins)

Answer 249

A

Flaviviridae: Flavivirus

The genus Flavivirus has at least 70 viruses.

Of importance in equine species are

Arthropod-borne (e.g., Culex spp.): Japanese encephalitis, St. Louis encephalitis (rare!), West Nile,

tick-borne (Ixodes spp.): Powassan, and louping ill viruses.

Answer 250

A

most countries of southeast Asia

has extended to India, Pacific islands, and northern Australia.

Answer 251

A

Indirect specigic JE antibody IgM detection via ELISA (1w after infection)

Diagnostic confirmatory tests include serologic assays to detect immune response:

neutralizing test,
complement fixation,
hemagglutination inhibition, and
ELISA tests

or direct virus isolation from tissue of the centra nervous system (infectious!!!!) ot blood and CSF very early in the disease

The disease has a high mortality rate of 10% to 40%, with 40% to 70% of survivors having permanent neurologic deficits.6

Answer 252

A

WNV is generally transmitted via bite from infected mosquitoes. There are several species of mosquito capable of acquiring the virus after feeding in infected vertebrate amplifying hosts (most common birds and bats), but the most important in the United States include Culex genus (C. pipiens, C. restuans, C. salinarius, C. tarsalis).

Answer 253

A

Because transmission is via vectors, transmission could be seasonal in temperate regions and year-round in subtropical regions. Intense virus activity in the United States begins in July, with a peak incidence in September and October.506,620 A drop in ambient temperature with soft frost usually results in a rapid decrease in reporting activity

Answer 254

A

Most horses seroconvert without clinical disease after infection with WNV. However, approximately 8% to 10% of infected naïve horses develop clinical disease with neurologic signs.623 Neurologic signs usually develop 5 to 22 days post infection.

Answer 255

A

affects predominantly the brainstem

sometimes weakness + muzzle twitching

The most common clinical signs are

weakness (94–100%),
ataxia (72%),
altered mentation (67%),
fever early in disease (65%),
fasciculations (61%),
cranial nerve deficits (44%),
ercumbency (30%).
Other common signs include anorexia (47%) and bruxism (20%)

Answer 256

A

Many horses will improve within 3 to 7 days of displaying clinical signs.

If significant improvement, full recovery within 1 to 6 months can be expected in 90% of patients.

Residual weakness and ataxia appear to be common, with long-term loss of the use of one or more limbs infrequently described. Mild to moderate persistent fatigue on exercise has been observed.

Answer 257

A

e.g., Halicephalobus gingivalis, Setaria spp., Strongylus vulgaris

Answer 258

A

Most diagnostic laboratories use the

WNV IgM capture ELISA (MAC) for actual confirmation of disease

(increases in IgM rarely occur after vaccination).

The sensitivity and specificity of this test are 81% and 100%

Horses develop a very intense IgM response on exposure to WNV that lasts approximately 6 weeks.

POST MORTEM: PCR, culture, and immunohistochemistry in tissues of the CNS

Answer 259

A

Flaviviruses cause

polioencephalomyelitis (inflammation of the gray matter) with lesions

that increase in number from the diencephalon through the hindbrain and frequently increase in severity caudally through the spinal cord.

Answer 260

A

progressive severe immune-mediated nonsuppurative meningoencephalitis.

Natural infection in horses results in peracute, acute, or subacute meningoencephalitis leading to death in 1 to 4 weeks of affected animals.

In endemic areas (Germany), the prevalence of disease is estimated to be 12%.

Answer 261

A

Specific neurologic signs are variable but may include

slow-motion eating,

chewing motions of the mouth,

head pressing, somnolence and stupor, hyperexcitability, fearfulness, aggressiveness, hypokinesia, abnormal posture, hyporeflexia, head tilt, neurogenic torticollis, and inability to swallow.

Answer 262

A

Diagnosis is made through serology such as Western blot, ELISA, IFAT;

virus isolation; IMHC; and RT-PCR.

Answer 263

A

Spitzmäuse = reservoir

infizierte Tiere exkret virus: augensekret, nasensekret, urin

not all seropositive horses develop disease

(inkubationszeot kann sehr lang sein also vll abtrennen von seropositiven tieren von neg?)

The virus gets access to nasal mucosa and migrates to olfactory bulbs via axonal transport mechanisms.

The virus has tropism for the limbic system, particularly the hippocampus, but also migrates centrifugal to the peripheral nervous system.

(absondern von anderen Pferden, Depression, Schreckhaftigkeit, speicheln)

Answer 264

A

The most common route of transmission of the virus is

via saliva-contaminated wounds or bites

from a wild carnivorous or insectivorous bat carrying the virus

Answer 265

A

The incubation period is usually between 14 and 90 days, but it could be longer, up to a year.

Answer 266

A

No signs are pathognomonic for rabies infection in horses. There is usually a prodromal phase on which signs are often overlooked or not appearing as neurologic in origin.

Clinical signs on presentation vary and range from lameness to sudden death.

Hyperesthesia, ataxia, behavior change, anorexia, paralysis or paresis, and colic have been reported as initial clinical signs.

One rarely finds a bite wound, and the horse might or might not be febrile. The site of inoculation and its proximity to the CNS influence what clinical signs one observes

Answer 267

A

First, in the cerebral or furious form, one might see aggressive behavior, photophobia, hydrophobia, hyperesthesia, self-mutilation, straining, muscular tremors, convulsions, and blindness

Second, in the brainstem or dumb form, one commonly sees obtundation, anorexia, head tilt, circling, excess salivation, facial and pharyngeal paralysis (giving the name of “hydrophobia”)

paralytic or spinal form, one sees progressing ascending paralysis, ataxia, shifting lameness with hyperesthesia, self-mutilation of an extremity, flaccid tail and anus, and urinary incontinence.

Answer 268

A

Fluorescent antibody testing of tactile hair follicles of facial skin taken on biopsy

or from corneal epithelium might help diagnose rabies antemortem.

The fluorescent antibody technique detects the rabies virus antigen in these tissues. However, a negative test does not exclude rabies as a differential diagnosis

Answer 269

A

Large intracytoplasmic eosinophilic inclusions within neurons and ganglion cells,

pathognomonic for rabies

However, in 15% to 30% of confirmed rabies cases, Negri bodies are not present in histopathologic sections, especially if the animal died or was euthanized early in the disease process

Answer 270

A

The mouse inoculation test is the most accurate method for diagnosing rabies virus infection but requires 5 to 6 days to complete. The mouse inoculation test involves the injection of suspect brain or salivary gland tissue homogenates intracerebrally in mice and observation of clinical and neurologic signs or death

Answer 271

A

Currently, there are three inactivated

(tissue culture– derived products with an adjuvant)

vaccines licensed for rabies to be administered intramuscularly.

The American Association of Equine Practitioners recommends that all horses in the United States be vaccinated against rabies.

Answer 272

A

Equine motor neuron disease (EMND) is an acquired neurodegenerative disease of adult horses that has been reported in North and South America, Japan, and Europe

The disease affects primarily the motor neurons in the spinal cord ventral horn cells and brainstem and leads to characteristic clinical signs, including generalized neuromuscular weakness and neurogenic muscle atrophy

Answer 273

A

EMND occurs in adult horses 2 years and older with a mean age of onset of clinical signs of 9 years.704 The risk for EMND increases with age, peaking at around 15 years.

Answer 274

A

Clinical signs reflect motor denervation of skeletal muscles. Muscle wasting despite a normal or ravenous appetite, trembling or muscle fasciculations, and excessive recumbency are the predominant signs of EMND, and each of these was shown to be present in greater than 90% of 77 cases.

Answer 275

A

Muscle wasting is most noticeable in the quadriceps, triceps, and gluteal areas. Onset of muscle wasting usually occurs before the other clinical signs do, but sometimes signs of muscle weakness are seen in normally muscled horses

Answer 276

A

Ataxia is not a clinical sign of EMND. A horse with EMND is said to move better than it stands.

Answer 277

A

EMND predominantly affects type I fibers, in contrast to denervating diseases in other species

Motor neurons supplying the type I fibers have a higher oxidative activity and thus may be more susceptible to oxidative injury.

Answer 278

A

The clinical signs of neuromuscular weakness result from the generalized denervation muscle atrophy found in horses with EMND. Oxidative stress is believed to be the underlying mechanism for development of EMND, either through a deficiency in antioxidant elements, such as vitamin E, and/or an excess of prooxidant elements such as copper and iron

A chronic vitamin E deficiency is thought to be the most important contributor

Answer 279

A

NAD/EDM develops in genetically susceptible animals if vitamin E deficiency occurs during the first year of life,279,723 whereas EMND occurs in adult horses after an extended period of vitamin E deficiency

Clinical signs and histopathologic findings are very different in these two diseases

Answer 280

A

biopsy of the sacrocaudalis dorsalis muscle - histopathologic examination of this muscle reveals changes consistent with denervation muscle atrophy and scattered muscle necrosis

The plasma vitamin E concentration is consistently low (less than 1 μg/mL); however, a 2006 case report described a horse with EMND that had normal serum vitamin E concentrations and was hypothesized to have developed the disease secondary to high tissue iron concentrations

Answer 281

A

Treatment with vitamin E has been associated with improvement of clinical signs in about 40% of cases within 6 weeks of treatment, of which many horses can make a near full recovery in 3 months

The prognosis is poor for return to performance and guarded for life. Although no published investigations exist regarding the survival rate and follow-up of horses with EMND, horses with EMND generally have been shown to follow one of three possible clinical courses.502 Approximately 20% of horses continue to deteriorate, and the severe weakness and excessive recumbency necessitate humane euthanasia. In approximately 40% of horses, clinical signs appear to stabilize; however, these horses do not regain muscle mass and may develop severe gait abnormalities. Continued clinical abnormalities frequently lead to euthanasia within 1 year of onset of clinical signs. The third group of horses (approximately 40%) show dramatic improvement after treatment with vitamin E, and many may regain a normal muscle mass. These horses may remain stabilized, that is, appear normal, for 1 to 6 years or more; however, many relapse, resulting in euthanasia.

Answer 282

A

C. tetani is a large gram-positive bacillus and is an obligate anaerobic spore former. It is part of the normal flora of the intestinal tract of humans and animals and can be readily isolated from the intestinal tract and feces of a wide range of animals

Answer 283

A

Under anaerobic conditions, C. tetani spores germinate and produce three exotoxins: tetanolysin, tetanospasmin, and nonspasmogenic toxin. Tetanospasmin is the most powerful and most important clinically

Answer 284

A

(1) binding to the neuronal cell membrane; (2) internalization by endocytosis; and (3) the intracellular blockade of neurotransmitter release.

tetanospasmin blocks the postsynaptic inhibitory signal of the spinal cord motor neurons by preventing release of the inhibitory neurotransmitters glycine and GABA. This disinhibition leads to continued stimulation of motor and reflex arcs, which results in the characteristic muscular spasms and contractions, hyperesthesia, and eventually convulsions, respiratory arrest, and death seen in patients with tetanus.

Answer 285

A

Tetanospasmin is poorly absorbed across mucous membranes, is destroyed by gastric juices, and is unable to cross the placenta as result of its high molecular weight.

Answer 286

A

Tetanus is manifest as hypertonia of the striated muscles, with clonic paroxysmal muscular spasms superimposed. Muscular activity may be increased to the point that rectal temperature becomes markedly elevated. Clinical signs may be generalized or localized. Localized tetanus involves muscular rigidity and spasms in the vicinity of the infected wound. With time, this usually progresses to a more generalized tetanus affecting the entire body; however, the initial manifestation of tetanus is most often generalized rather than localized

Answer 287

A

From the three reports available on survival of equine tetanus, the oldest describes a case fatality rate of 75%, with previous vaccination strongly associated with survival.745 Two other reports describe a mortality rate of 68%746 and 59%

Answer 288

A

There is no definitive antemortem test for tetanus. There are also no postmortem findings pathognomonic for the disease. Finding microscopic evidence of the bacteria or its toxin at the site of a wound is an unreliable diagnostic indicator. A biologic assay for antemortem diagnosis is possible in some cases by injecting infected material into the tail base of mice and observing for onset of clinical signs

Answer 289

A

The binding of tetanospasmin to the Renshaw cells via ganglioside receptors is almost irreversible. Recovery is slow and does not occur until new interneuronal synapses develop to replace those that were inactivated by toxin. Therapeutic management of clinical cases of tetanus is centered around the following five goals:

Elimination of the Source of the Toxin: Penicillin is the drug of choice for eliminating the vegetative form and is recommended to be administered at high dosages. Metronidazole is indicated for deep and contaminated wounds because it is able to penetrate necrotic tissues without losing efficacy.

Neutralizing Unbound Toxin: Administration of 1500 U of antitoxin to unvaccinated horses provides immediate passive protection lasting approximately 3 weeks (achtung theilers disease)

Relief of Pain and Control of Neuromuscular Derangements: Phenothiazine drugs. Diazepam has glycine mimetic effects and potentiates release of GABA, an inhibitory neurotransmitter. The combination of benzodiazepines and α2-agonists such as xylazine may also be very effective in controlling muscle spasms.

Supportive Care

Generation of Active Immunity to Tetanus Toxins

Answer 290

A

Unfortunately, the concentration of tetanus toxin required to cause overt neurologic disease is insufficient to generate a protective immunologic response. Therefore at the initiation of treatment for tetanus, all horses should be immunized with tetanus toxoid to initiate a protective antibody response. An antibody response may take 2 to 4 weeks to develop.

Answer 291

A

In foals, tetanus-specific IgG antibodies inhibiting the foal’s response to tetanus toxoid are passively transferred via colostrum. High titers of IgGa, IgGb, and IgG(T) subisotypes were detected in postsuckling serum samples collected from foals born to mares that had received booster doses of multicomponent vaccines during the past 2 months of gestation. In addition, antibody response to vaccination of younger foals has been shown to be poor, necessitating multiple doses of toxoid. Current recommendations are to vaccinate foals born to vaccinated mares at 4 to 6 months of age with boosters 4 to 6 weeks later and a third vaccine at 10 to 12 months of age. Vaccination for foals born to unvaccinated mares should begin at a younger age: the current recommendations are to start at 1 to 4 months of age with a booster 4 weeks after the first dose and a third vaccine 4 weeks after the second dose.

Answer 292

A

(1) food-borne botulism (so ingestion of toxins)
(2) toxicoinfectious botulism, (means eating the bacterium with production of toxins in the GI tract - mainly neonates bc in adults it is killed by digestion) and
(3) wound botulism.

Answer 293

A

BoNT/B and BoNT/C

Answer 294

A

BoNT/A and B botulism are associated with forage,

whereas BoNT/C botulism is associated with decomposing carcasses.

Ravens have been shown to serve as transport vectors by feeding off a decomposing animal carcass and then transporting the toxin to the feed buckets or feed troughs of horses up to 1.5 miles distant from the decomposing carcass.

Answer 295

A

There are six phylogenetically distinct groups of BoNT producing clostridia:

Clostridium botulinum groups I–III,
Clostridium argentinense group IV, and
some strains of Clostridium baratii and Clostridium butyricum

that produce seven serotypically distinct BoNTs (serotypes A–G).

Investigators have shown that there are now more than 40 different BoNTs

Answer 296

A

Toxicoinfectious botulism, or “shaker foal syndrome,” is usually associated with BoNT/B and occurs in foals between 2 weeks and 8 months of age. The syndrome is similar to what is seen in human infants whereby spores are ingested, germinate, and produce toxin once in the gastrointestinal tract.

Under normal circumstances, the intestinal flora of adult animals and humans inhibits the intestinal proliferation of BoNT-producing clostridia, thereby limiting the occurrence of toxicoinfectious botulism to neonates.

Answer 297

A

Wound botulism occurs in horses when BoNT/B-producing clostridia infect a wound, germinate, proliferate, and release toxin under anaerobic conditions. In adult horses, wound botulism has been associated with an injection abscess and castration, and in foals, it has been diagnosed in conjunction with infected umbilical remnants and an infected limb wound.

Answer 298

A

Endemic foal botulism is thus considered to occur from ingestion of spores present in contaminated soil. Toxin can be detected in the feces of approximately 30% to 40% of foals with botulism but only during the acute clinical phase.

Answer 299

A

BoNTs cross the intestinal epithelial barrier, disperse in extracellular fluid, and enter the lymphatic system and the blood circulation where they can remain for many days.

They are unable to cross the blood-brain barrier.

BoNTs are very specific and only bind to peripheral nerve terminals, particularly those of skeletal and autonomic cholinergic nerves.

BoNTs act presynaptically at the peripheral cholinergic neuromuscular junction and result in the inhibition of neurotransmitter (acetylcholine) release and consequent neuroparalysis

Answer 300

A

The diagnosis of botulism is difficult and frequently is based on compatible clinical signs of acute onset of flaccid paralysis, weak or poor eyelid tone, poor tail tone, slow or difficult eating, and dysphagia, as well as a compatible history of possible exposure to toxin.

Answer 301

A

BoNT intoxication results in diffuse, symmetric, flaccid paralysis and loss of muscle strength.

The disease usually affects motor nerves with high efferent traffic, resulting in weakness, dysphagia, and poor muscle tone. Usually generalized weakness, dysphagia, or both are the first clinical signs detected by observant horse owners. Early in some cases the owners will note prolongation of the time the horse takes to eat its grain, or they will note abdominal discomfort and colic.

Mydriasis and ptosis are observed early in the disease process, as well as a sluggish pupillary light response. Reduced tongue tone and slow tongue retraction are characteristic early signs of botulism that typically occur before the onset of obvious muscle weakness.

Once the toxin is bound, improvement in clinical signs is achieved after sprouting of the presynaptic axon terminal and subsequent formation of a new synapse

Answer 302

A

Generally, the clinical signs appear from 24 hours up to 17 days after exposure.

The incubation period may be associated with inoculum size, which suggests that the shorter the incubation, the more severe the disease.

Answer 303

A

Foals are typically bright and alert when they are lying down, but when they stand will develop fine muscle fasciculations that progress to severe muscle trembling, hence the term “shaker foal syndrome,” before the foal stumbles and falls down. Foals are too weak to lie down in a normal fashion, yet they fall down.

Answer 304

A

Vital signs are typically normal in the early stages, but heart rate and respiratory rate increase once the horse is recumbent, depending on the amount of struggling that occurs.

Answer 305

A

one of the following:

(1) detection of BoNT in serum, gastrointestinal contents, or from a wound;
(2) detection of BoNT and/or BoNT-producing clostridial spores in the feed and/or gastrointestinal contents in addition to compatible clinical signs; or
(3) detection of an antibody response in a convalescent patient

The current gold standard test for botulism is the mouse bioassay -> low sensitivity in adult horses (32%) and foals (53%) but high specificity (97% in adults and 100% in foals).759 These results indicate that a positive result is highly suggestive of botulism but that negative results do not exclude the diagnosis.

Quantitative real-time PCR assays for BoNT genes alternatively

Answer 306

A

prompt administration of specific or multivalent antitoxin to bind circulating BoNT. A single dose of antitoxin is considered to be sufficient (30,000 IU for a foal and 70,000 IU for an adult horse) because that should provide passive protection for more than 60 days

nursing care

In severely affected foals or adults with respiratory failure, mechanical ventilation is indicated.

Answer 307

A

antimicrobials can potentiate neuromuscular blockage (aminoglycosides, tetracyclines, and procaine penicillin) and should be avoided.

Answer 308

A

A recent review of 92 cases of botulism in adult horses showed that overall survival was 48% (in older studies 10-30).

Survival was significantly better for horses that arrived standing (67%) and even higher (95%) for horses that remained able to stand throughout hospitalization.

Treatment with antitoxin increased the odds of survival significantly, with treated patients being four times more likely to survive.

Horses in which treatment is initiated after they are recumbent only have a 13% chance of survival.

FOALS:

review of 30 foals that were less than 6 months of age showed a survival of treated cases of greater than 96%. All foals, except one mildly affected one, received botulism antitoxin.

one study: mechanical ventilation, survival in treated foals was 87.5%.

Answer 309

A

Type B botulism is preventable by vaccination using type B toxoid, which was initially developed to prevent disease in newborn foals. The current USDA-approved available product is a killed (toxoid) vaccine directed against C. botulinum type B

(1) providing safe and high-quality feed; (2) properly storing animal feed; (3) inspecting water sources for dying of dead small animals and birds; (4) avoiding spreading poultry litter that contains birds or dead animals on pastures; and (5) avoiding use of poultry litter as bedding material.

Answer 310

A

Equine grass sickness (EGS) is an acquired degenerative polyneuropathy that predominantly affects the neurons of the autonomic and enteric nervous system.

Answer 311

A

The disease predominantly affects the prevertebral and paravertebral ganglia of the autonomic nervous system and enteric neurons (myenteric and submucosal plexuses) and is therefore characterized as a dysautonomia;

however, given the fact that neuronal degeneration has also been identified in the brain and spinal cord of horses with EGS, the disease is likely better termed a multisystem neuropathy.

Answer 312

A

Horses with EGS are generally young adults between 2 and 7 years of age.780 No gender predilection is apparent, but a study in Scotland found that there may be an increased susceptibility to EGS in native Scottish breeds

Answer 313

A

botulism

EPM;

EMND;

EHV-1 myeloencephalopathy;

WNV;

rabies;

several toxins such as lead, ionophore drugs, yew, and yellow star thistle;

low blood calcium; and

hyperkalemic periodic paralysis.

Answer 314

A

There is a strong association between EGS and grazing. Numerous epidemiologic studies have been performed over the years, and besides grazing, other consistently reported risk factors for development of the disease are

age,
recent movement to new pasture or premises, and
time of year, with most cases occurring in spring and early summer

Answer 315

A

Acute, subacute, and chronic forms of EGS are recognized

Answer 316

A

Most horses are depressed, anorexic, dysphagic, and tachycardic.

The dysphagia is likely caused by cranial nerve dysfunction and possibly esophageal dysfunction and is recognized by drooling of saliva, feed material in the nares, impacted feed material in the buccal pouches, and difficulty drinking.
The drooling of saliva seen in EGS may also be caused by excessive salivation, which has been reported in some forms of human dysautonomia.
Contributors to the tachycardia include increased adrenaline and noradrenaline and removal of vagal inhibitory input.
Ptosis, sweating, and muscle fasciculations can also be present in all forms of EGS.

Answer 317

A

acute onset of gastrointestinal ileus within generally less than 48 hours.

Signs of abdominal pain are mild to moderate and are caused by gastric and small intestinal distention. Considering the degree of gastrointestinal distention, the severity of abdominal pain is usually less than would be expected. Examination per rectum reveals small intestinal distention and often a mild secondary impaction of the large colon.
Typically these cases produce large quantities of nasogastric reflux.
Affected horses are hypovolemic, and the reduced circulating volume may cause death from cardiac failure.

Answer 318

A

The course of disease is 3 to 7 days, and clinical signs are similar but less severe than in acute EGS.

Horses with subacute EGS do not develop gastric or small intestinal distention, and nasogastric reflux is usually absent.

Horses with subacute EGS often have large colon or cecal impactions.

Answer 319

A

The course of the disease is weeks to months. Cachexia, with the development of a “tucked up” appearance, is the most prominent clinical abnormality in horses with chronic EGS.

progressive myasthenia, demonstrated by a base-narrow stance, leaning back against walls and weight shifting of the limbs. Unlike in botulism and equine lower motor neuron disease where horses spend more time recumbent, this is not the case in horses with EGS. Furthermore, in EGS muscle fasciculations are also present when animals are lying down, which is typically not the case in botulism or equine lower motor neuron disease.

Answer 320

A

Specific histopathologic findings characteristic of neuronal degeneration include chromatolysis, loss of Nissl’s substance, eccentricity or pyknosis of the nuclei, neuronal swelling and vacuolization, accumulation of intracytoplasmic eosinophilic spheroids, and axonal dystrophy.

lesions are more severe in the autonomic ganglia (cranial cervical, stellate, celiacomesenteric) and enteric nerves

-> The most severe lesions are found in the myenteric and submucosal plexuses of the ileum, and less severe changes occur in the celiacomesenteric ganglion.

Answer 321

A

Multiple experimental studies over the past decades have failed to identify the causative agent or agents of EGS.

Answer 322

A

No noninvasive definitive test exists to obtain an antemortem diagnosis of EGS.

only lab abnormalities: Acute phase proteins and fibrinogen concentrations are significantly higher in horses with EGS compared to those with intestinal tract obstructions.

Other ancillary diagnostic tests that may be helpful include evaluation of esophageal motility by endoscopy or contrast imaging, electrodiagnostic testing, and the use of

0.5% phenylephrine applied to the cornea to confirm the presence of smooth muscle paralysis underlying the ptosis (ptosis should temporarily disappear).

A definite antemortem diagnosis can only be made following histopathologic examination of enteric ganglia (mostly ileum)

Answer 323

A

Recently histopathologic examination of gustatory papillae via a lingual biopsy technique was evaluated in postmortem specimens of horses with EGS and was shown to have a sensitivity of 100% and a specificity of 98.2%.803

This approach has the potential to offer a valuable and cost-effective means of antemortem disease confirmation but requires further prospective validation.

Answer 324

A

The most important differential diagnoses for acute EGS are a

small intestinal strangulating lesion and
duodenitisproximal jejunitis.

Clinical signs and neuronal lesions in chronic EMND and chronic EGS may be similar, and these similarities have led to the speculation that these two diseases are related. Further examination, however, reveals important differences such as the fact that EMND occurs in older horses that have not had access to pasture, and EGS occurs in young horses with access to pasture. EGS sometimes occurs along with EMND

Answer 325

A

The case fatality rates for acute and subacute EGS are 100%.

Horses with chronic EGS often are euthanized because of weakness, inability to stand, and emaciation; however, when given appropriate care at a referral hospital, approximately 40% to 50% of horses may survive long term.

Answer 326

A

transmission of B. burgdorferi through the bite of infected hard ticks (Ixodes spp.).

In the Eastern and Midwestern United States the vector is the b_lacklegged tick or deer tick_, Ixodes scapularis (formerly I. dammini), whereas in the Western United States the vector is the western blacklegged tick, I. pacificus.

In Europe the sheep tick, I. ricinus, is the vector of Lyme borreliosis.

Answer 327

A

The disease has a seasonal prevalence and is most common in spring, summer, and fall, with a peak incidence in June and July.

In some climates such as California, ticks might be active throughout the year

Answer 328

A

Clinical signs associated with Borrelia burgdorferi in horses, as in human beings, are often nonspecific and involve multiple body systems.

chronic weight loss,
sporadic lameness,
laminitis,
lowgrade fever,
swollen joints,
muscle tenderness,
anterior uveitis,
encephalitis, and
abortion.

Answer 329

A

Infection with Borrelia burgdorferi is common but rarely results in neuroborreliosis.

Neurologic signs could be variable. These signs might include

behavioral changes,

hyperesthesia,

hyperreactivity,

gait abnormalities,

cranial nerve deficits,

neck stiffness,

muscle atrophy and

muscle tremors or fasciculations

Answer 330

A

The diagnosis of Lyme disease is often difficult. History of tick exposure or living in a Lyme disease–endemic area is helpful; when combined with the identification of clinical signs and the elimination of other diseases, this information allows the clinician to make a presumptive diagnosis.

Answer 331

A

Blood tests are of limited value; however, ELISA, kinetic ELISA, Western blot testing, and PCR on blood samples and synovial fluid from suspect animals have been evaluated

Western blot used to be the gold standard

see AEEP testing guidelines

Answer 332

A

Borrelia burgdorferi organisms are capable of nonspecifically activating monocytes, macrophages, and synovial lining cells, as well as natural killer cells, B cells, and complement, leading to production of host proinflammatory mediators. These proinflammatory mediators seem to localize in joints, leading to chronic arthritis and lameness.

Answer 333

A

Recommended treatment includes oxytetracycline (6.6 mg/ kg IV every 24 hours) or doxycycline (10 mg/kg PO every 12 hours).827 Treatment can be started with tetracycline for 1 week followed with doxycycline for 3 to 4 weeks. Ceftiofur (2.2–4.4 mg/kg IV every 12 hours) has also been evaluated.827 In animals infected with B. burgdorferi, a rapid clinical response (2–4 days) is expected with tetracyclines. In some horses the clinical signs might show an initial worsening as a response to toxins released after death of the organisms.

Answer 334

A

no vaccine

daily grooming with removal of ticks, along with the use of tick repellents that contain permethrin.

Keeping pastures mowed and removing brush and woodpiles makes the environment less hospitable for rodents, which in turn decreases the tick population.

Answer 335

A

Disorders of the Oral Cavity: Dental disorders Pharyngeal lesions Tongue or gingival lesions Buccal ulceration
Disorders of the Eyes: Abnormalities affecting vision Cysts, masses, foreign bodies, cataracts Nasolacrimal duct disorders
Disorders of the Ear: Otitis Ear ticks (Otobius megnini) Mites Mass lesion–neoplasia, abscess, granuloma Foreign body
Upper Airway Disorders Nasal passages–e.g., masses Rhinitis (allergic, vasomotor) Sinuses–masses, exudate, sinusitis Guttural pouch disease Laryngeal disorders
Disorders of the Skull: Fractures Neoplastic lesions Temporomandibular joint disorders Temporohyoid osteoarthropathy Other disorders of the hyoid apparatus
Neurologic Abnormalities Trigeminal neuralgia Equine protozoal myeloencephalitis Photic headshaking
Cervical Pain Osteoarthritis Neuropathy Myositis
Behavior Stereotypical behavior Classical conditioning response Avoidance behavior
Objections to Rider or Tack Bridle, bit, browband fit and comfort Rider actions or interference Excessive head and neck flexion

Answer 336

A

Mean age of onset is typically 7 to 9 years, and Thoroughbreds and geldings appear to be overrepresented in some studies

Answer 337

A

Headshaking can be seasonal or nonseasonal.

Early literature suggested an increased incidence of headshaking during the warmer months of the year, and a later study indicated that the peak periods of onset were spring and early summer.

Studies have found that 64% and 59% of headshaking horses are affected seasonally, with the majority developing signs in the spring or early summer

Answer 338

A

Trigeminal nerve involvement is supported by the observations that some horses improve after blocking the

infraorbital nerve (part of the maxillary branch) and that most horses improve after
caudal nasal nerve, a branch of the maxillary nerve commonly referred to as the posterior ethmoidal nerve (branch of ophthalmic nerve).

Answer 339

A

Cyproheptadine, an antihistamine and serotonin antagonist with anticholinergic effects, has been used (0.3 mg/kg PO twice daily) to treat headshaking horses, resulting in improvement in 5 of 7 horses in one study838 and 43 of 61 horses in another.832 Horses that respond do so within 1 week, and some might respond within 24 hours. Cyproheptadine also works as a calcium channel blocker in addition to blocking serotoninmediated pain as a proposed mechanism of action.

Answer 340

A

Cyproheptadine has also been used with carbamazepine (4–8 mg/kg PO q 6–8 h), resulting in 80% to 100% improvement in seven of nine cases, with horses responding within 3 to 4 days.

Answer 341

A

Carbamazepine is a sodium channel–blocking antiepileptic drug and is the drug of choice for treating trigeminal neuralgia in human beings.850 Carbamazepine alone was reported to be effective in headshaking horses, but results were unpredictable.831 The elimination half-life of carbamazepine in the horse is less than 2 hours, making sustaining therapeutic concentrations difficult; the drug is therefore of more benefit diagnostically than therapeutically in headshaking horses

Answer 342

A

Blockade of the infraorbital nerve might improve some horses and might identify candidates for infraorbital neurectomy. However, results of infraorbital blockade and infraorbital neurectomy do not correlate, and infraorbital neurectomy is not a recommended procedure because of neuroma formation, self-trauma, risk of infection, low success rate, and recurrence of pain that might require a second surgery

A high percentage of horses improve after blockade of branches of the maxillary nerve, and sclerosis of this nerve results in temporary improvement in some horses.8

Answer 343

A

An owner survey found that nose nets that cover the nostrils with mesh and include a drawstring or elastic band that applies pressure to the upper lip resulted in some improvement in 70% of headshaking horses and that 70% or more improvement occurred in about 30% of the horses

Answer 344

A

More recently, a study investigated the neuromodulation of the trigeminal nerve by using percutaneous electrical nerve stimulation under sedation. Horses tolerated well the procedure, which proved to be safe and minimally invasive and provided pain relief in the short to medium term (months).

Answer 345

A

Antemortem diagnosis is often impossible; however, a high index of suspicion might be warranted for certain clinical signs (acute onset or rapidly progressive asymmetric, focal, or multifocal brain or spinal cord signs)

Answer 346

A

The likely route of entry is through nasal and oral mucosa, followed by possible hematogenous spread to organs with high vascularization such as the brain, spinal cord, and kidneys

Organisms affecting the CNS have been reported to have a predilection for the basilar, pituitary region of the brainstem

Answer 347

A

renal granulomatous lesions encapsulating the nematodes

In contrast, all three cases reported to date in foals showed no renal involvement but did show pulmonary granulomata.

Answer 348

A

The meningeal worm Parelaphostrongylus tenuis causes neurologic disease in horses ranging in age from 6 months to 9 years.

signs: scoliosis (observed in 90% of reported cases), with progressive gait deficits. Scoliosis is most common in the cervical area.

Answer 349

A

One should consider verminous encephalomyelitis in all cases of acute or progressive asymmetric disease of the spinal cord, cerebrum, cerebellum, or brainstem.

only brain involvement :
- equine togaviral encephalomyelitis,
- rabies,
- equine protozoal myelitis (EPM),
- trauma,
- cerebral abscess or basilar epidural empyema,
- bacterial meningitis, hepatic encephalopathy, neoplasia, and leukoencephalomalacia.
limited to spinal cord
- EPM,
- EHV-1 myeloencephalopathy,
- trauma,
- WNV meningoencephalitis,
- EDM,
- trauma, spinal osteomyelitis or discospondylitis, vertebral fracture, and neoplasia.
auda equina syndrome,
- polyneuritis equi,
- sacral or coccygeal fracture,
- EPM,
- EHV-1 myeloencephalopathy,
- sorghum or Sudan grass toxicity, epidural abscess from tail blocking, and neoplasia.

Answer 350

A

CSF analysis in cases of parasitic encephalomyelitis can be normal; however, CSF changes are common and include xanthochromia, increased protein, and neutrophilic and mononuclear pleocytosis, but eosinophils rarely occur

Answer 351

A

Antemortem diagnosis might be possible in those cases in which renal or bony involvement is detected and nematodes are identified in biopsies of the affected tissues.

Additionally, a PCR-based diagnostic test has been developed for confirmation of Setaria encephalomyelitis in goats, sheep, and horses. This test is based on specific amplification of Setaria spp. filarial DNA from a blood sample from the host.

Answer 352

A

often unrewarding.

None of the cases reported in the literature has responded favorably to antiinflammatory drugs and anthelmintics. In one horse with a Halicephalobus gingivalis granuloma limited to the prepuce, therapy with ivermectin and diethylcarbamazine was successful.

Specific antiparasitics suggested for treating verminous encephalomyelitis include benzimidazole compounds (oxfendazole, thiabendazole, fenbendazole, and mebendazole), diethylcarbamazine and ivermectin for the treatment of nematodes, and organophosphates with caution (trichlorfon and dichlorvos) for the treatment of warble fly larvae. Although ivermectin is effective against most equine parasites, it might not be the best choice because of its delayed method of killing, which might take as long as 10 to 14 days.

Answer 353

A

quite uncommon in horses.

In one Australian survey of 450 horses, with neurologic disease, the prevalence of neurologic disease secondary to neoplasia was less than 2%.

Answer 354

A

seasonal disorder

in late fall through early spring.

caused by ingestion of the mycotoxin fumonisin B1, a metabolite of Fusarium moniliforme.

Two clinical syndromes

more common neurologic syndrome characterized initially by incoordination, aimless walking, intermittent anorexia, lethargy, obtundation, blindness, and head pressing. These signs might be followed by hyperexcitablity, belligerence, extreme agitation, profuse sweating, and delirium. Recumbency and clonic-tetanic seizures might occur before death.
Less commonly, horses develop a hepatotoxic syndrome with swelling of the lips and nose, somnolence, severe icterus and petechiation of mucous membranes, abdominal breathing, and cyanosis

Answer 355

A

UMN of sympatheticus

if only ataxia: Cervical spinal cord injury or compression

With other cranialnerve sogns: Space occupying brainstem lesion

Answer 356

A

preganglionic LMN sympathetic trunc

brachial plexus trauma, neoplasi cranial thoracic or jug vein infection?

Answer 357

A

postganglionic LMN sympthetic trunc

DD orbital trauma or gutt pouch disease

Answer 358

A

central vestibular disease

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Tina Neurology Flashcards

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