Tina Neurology Flashcards

Question

Correct spinal reflexes require

Answer 1

intact sensory nerve, spinal cord segment(s), an intact peripheral motor nerve (LMN), and muscle. Perception of the stimulus requires intact ascending sensory pathways

Answer 2

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

Answer 3

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

Answer 4

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**.

Answer 5

Spastic gait, worse in rear limbs Proprioceptive deficits Weakness With or without Horner’s syndrome

Answer 6

Proprioceptive deficits, worse in front than rear Weakness + Muscle atrophy, thoracic limbs ± Horner’s syndrome

Answer 7

Proprioceptive deficits, rear Normal gait, front Rear limbs weakness Spasticity, pelvic limbs

Answer 8

Urinary incontinence Fecal retention Hypalgesia tail and perianal Normal thoracic and pelvic

Answer 9

Decreased tail tone Hypalgesia caudal to lesion Normal front and rear limbs

Answer 10

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

Answer 11

Postural deficits, seizures, altered mentation, blindness

Answer 12

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

Answer 13

* 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

Answer 14

symmetrical: cervical compression, cauda equina syndrome, and EDEM asyymetric others, especially equine protozoal myeloencephalitis (EPM)

Answer 15

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

Answer 16

reoccurring seizures from a chronic underlying process

Answer 17

rhythmic patterned movements are classic for seizures ## Footnote 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.

Answer 18

Arabian foals with juvenile idiopathic epilepsy

Answer 19

trauma, hepatoencephalopathy, and toxicity

Answer 20

mydriasis papilledema (swelling of optic nerve)

Answer 21

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

Answer 22

Hepatoencephalopathy Hypocalcemia Hyponatremia Hypoglycemia Hypo‐/hyperosmolality disorders Hyperammonemia

Answer 23

Air embolism Intracarotid injection Postmyelography Moxidectin overdose Fluphenazine Enrofloxacin overdose

Answer 24

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

Answer 25

increased intracranial pressure and neuronal necrosis Seizures in neonates may also result in reduced arterial oxygenation

Answer 26

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

Answer 27

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

Answer 28

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_

Answer 29

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

Answer 30

Acepromazine is contraindicated since it may reduce the seizure threshold

Answer 31

. 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

Answer 32

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

Answer 33

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

Answer 34

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

Answer 35

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

Answer 36

* 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;

Answer 37

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

Answer 38

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].

Answer 39

Common Causes of Injury: Collision of shoulder with objects. ## Footnote **sweeney.** Eventual atrophy of supraspinatus and infraspinatus muscles. Lateral subluxation (popping) of the shoulder on weight bearing.

Answer 40

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 41

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 42

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 43

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 44

**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 45

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 46

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 47

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 48

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

Answer 49

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

Answer 50

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 51

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

Answer 52

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 53

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

Answer 54

* 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 55

* 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 56

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 57

The rate of CSF production is constant and is i**ndependent of vascular hydrostatic pressure.** Hypertonic solutions such as mannitol, when added to blood, _decrease CSF production_ and decrease CSF pressure and edema.

Answer 58

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 59

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 60

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

Answer 61

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 62

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

Answer 63

study of the electrical activity of the muscle ## Footnote 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 64

Brainstem Auditory Evoked Response ## Footnote evaluates the i**ntegrity 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 65

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 66

temporohyoid osteoarthropathy, congenital sensorineural deafness in Paint Horses, multifocal brain disease, and otitis media/interna.

Answer 67

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

Answer 68

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 69

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 70

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 71

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 72

* **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 73

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

Answer 74

**neonatal maladjustment syndrome** (both hypoxic-ischemic and nonhypoxic encephalopathy), **trauma**, and **bacterial meningitis.**

Answer 75

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 76

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

Answer 77

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 78

* 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 79

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 80

(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 81

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

Answer 82

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 83

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

Answer 84

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 85

**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 86

Lack of REM sleep

Answer 87

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 88

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 89

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 90

paresis of the rear legs

Answer 91

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

Answer 92

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 93

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 94

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

Answer 95

increased intracranial pressure \>\> hypothalamic response to brain ischemia * hypertension * secondary baroreceptor-mediated bradycardia * irregular breathing

Answer 96

Continued elevation of intracranial pressure / reduction of cerebral blood flow results in increased sympathetic discharge (catecholamines), * myocardial ischemia and * cardiac arrhythmias.

Answer 97

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 98

oculomotorius

Answer 99

**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 100

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

Answer 101

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

Answer 102

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

Answer 103

hyperventilation (decreasing CO2 pressure in blood) CSF drainage, treatment with hyperosmolar agents or barbiturates, head elevation, and decompressive surgery

Answer 104

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 105

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 106

Recommendations now are to maintain blood glucose concentrations at 120 to 140 mg/dL in TBI. ## Footnote 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 107

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 108

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 109

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 110

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 111

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 112

worsening mental status, abnormal pupillary size or inequality indicating transtentorial herniation, or development of paresis.

Answer 113

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 114

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

Answer 115

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 116

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 117

does not occur until 4 to 5 years of age.

Answer 118

spinal cord ischemia

Answer 119

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 120

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 121

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

Answer 122

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 123

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

Answer 124

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 125

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

Answer 126

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

Answer 127

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 128

oculocephalic reflex

Answer 129

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

Answer 130

Facialis Vestibulocochlearis symphathetic innervation

Answer 131

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 132

medial strabismus

Answer 133

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

Answer 134

one cannot induce physiologic nystagmus by rapid manipulation of the head

Answer 135

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 136

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 137

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

Answer 138

1. Stabilization of the horse and decreasing inflammation near the fracture site 2. Treatment with broad-spectrum antimicrobials for either extension of a possible otitis interna-media or secondary infection in the hemorrhage that follows the fracture 3. Treatment of exposure keratitis and keratoconjunctivitis sicca (parasymp fibers of the facial nerve influence tear production) 4. Surgical procedures to remove pressure on the temporohyoid articulation to decrease pain and to decrease the likelihood of repeated petrous temporal bone fracture

Answer 139

partial stylohyoid ostectomy ceratohyoidectomy

Answer 140

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

Answer 141

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

Answer 142

alterations in the range of gait

Answer 143

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 144

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 145

inherited as an autosomal recessive trait

Answer 146

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 147

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 148

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 149

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 150

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

Answer 151

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 152

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 153

decrease in the cerebellar-to-whole brain weight ratio most prominent finding is the widespread loss of Purkinje neurons

Answer 154

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

Answer 155

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 156

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 157

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 158

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 159

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 160

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 161

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

Answer 162

* 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 163

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 164

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 165

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 166

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 167

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 168

1.3% to 2% of Thoroughbred horses

Answer 169

(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 170

between 12 and 23 months of age

Answer 171

* symmetric ataxia, * upper motor neuron paresis, and * dysmetria, which are usually worse in the pelvic limbs than thoracic limbs

Answer 172

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 173

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

Answer 174

Adverse reactions: one third of horses undergoing myelography, mortality rate of 2%, most common complications: worsening of neurologic grade and **seizures**

Answer 175

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 176

**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 177

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 178

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 179

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 180

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 181

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 182

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 183

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 184

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 185

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 186

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

Answer 187

superoxide dismutase, catalase, glutathione peroxidase (that contains _selenium_), **α-tocopherol (vitamin E)**, and **ascorbic acid (vitamin C)**

Answer 188

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 189

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 190

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 191

natural RRRα-tocopherol (nonacetate) form of vitamin E

Answer 192

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 193

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 194

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 195

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 196

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 197

* **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 198

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 199

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 200

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 201

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 202

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 203

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 204

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 205

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 206

1. clinics 2. A **key part of the diagnosis of EPM is ruling out other conditions that may be present;** 3. 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 207

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 208

* 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 209

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 210

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 211

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 212

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 213

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 214

**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 215

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 216

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 217

* 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 218

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 219

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 220

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

Answer 221

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

Answer 222

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 223

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 224

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 225

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

Answer 226

* 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 227

* 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 228

Tetanus (C. tetani toxins)

Answer 229

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 230

most countries of southeast Asia has extended to India, Pacific islands, and northern Australia.

Answer 231

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 232

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 233

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 234

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 235

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 236

Many horses will improve within 3 to 7 days of displaying clinical signs. If s**ignificant 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 237

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

Answer 238

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 239

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 240

**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 241

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 242

Diagnosis is made through serology such as **Western blot, ELISA**, IFAT; virus isolation; IMHC; and RT-PCR.

Answer 243

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 244

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 245

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

Answer 246

**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 247

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 paralysi**s, ataxia, shifting lameness with hyperesthesia, self-mutilation of an extremity, flaccid tail and anus, and urinary incontinence.

Answer 248

**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 249

**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 250

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 251

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 252

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 253

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 254

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 255

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 256

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

Answer 257

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 258

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 259

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 260

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 261

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 262

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 263

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 264

(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 265

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 266

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 267

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 268

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 269

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 270

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 271

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 272

(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 273

BoNT/B and BoNT/C

Answer 274

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 275

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 276

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 277

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 278

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 279

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 280

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 281

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 282

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 283

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 284

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 285

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 286

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 287

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

Answer 288

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 289

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 290

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

Answer 291

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 292

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 293

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 294

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 295

Acute, subacute, and chronic forms of EGS are recognized

Answer 296

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 297

**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 l**arge quantities of nasogastric reflux**. * Affected horses are hypovolemic, and the reduced circulating volume may cause death from cardiac failure.

Answer 298

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 299

The course of the disease is **weeks to months**. **Cachexia**, with the development of a **“tucked up” appearanc**e, is the most prominent clinical abnormality in horses with chronic EGS. ## Footnote **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 300

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 301

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

Answer 302

**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 303

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 304

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 305

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 306

**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 307

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 308

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 309

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 310

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 311

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 312

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 313

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 314

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 315

* **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 316

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

Answer 317

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 318

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 319

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 320

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 321

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 322

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 323

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 324

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 325

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 326

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 327

renal granulomatous lesions encapsulating the nematodes ## Footnote In contrast, all three cases reported to date in foals showed no renal involvement but did show pulmonary granulomata.

Answer 328

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 329

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 330

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 331

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 332

**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 333

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 334

**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 335

UMN of sympatheticus if only ataxia: Cervical spinal cord injury or compression With other cranialnerve sogns: Space occupying brainstem lesion

Answer 336

preganglionic LMN sympathetic trunc brachial plexus trauma, neoplasi cranial thoracic or jug vein infection?

Answer 337

postganglionic LMN sympthetic trunc DD orbital trauma or gutt pouch disease

Answer 338

central vestibular disease