Neurology Exam 2

Front 1

List the components, and corresponding functions, of the forebrain.

Back 1

Telencephalon (the cerebrum)-responsible for cognition, intelligence, behavior, integration of senses (all 5), and motor input from the pyramidal system.
Diencephalon (thalamus and hypothalamus)-Relay and integration of sensory info except for olfactory, relay system for motor function, maintains a state of wakefulness, regulation of visceral motor activity (hypothalamus).

Front 2

List the constellation of clinical signs for forebrain disease.

Back 2

1. Cerebral syndrome: Decreased intelligence (loss of training), disorientation, behavior/attitude changes, altered mentation, seizures, head pressing. Decreased postural reactions and altered sensation on the contralateral side; circling toward the ipsilateral side.
2. Diencephalic syndrome: Altered sensation, altered mentation, behavioral changes, disorientation, seizures, narcolepsy, ataxia, loss of visceral homeostasis (autonomic functions), endocrinopathies. Decreased postural reactions, hemineglect on contralateral side. Turning toward ipsilateral side.

Front 3

Define primary, secondary, and reactive seizures.

Back 3

Primary-idiopathic epilepsy. Typically tonic-clonic seizures.
Secondary-caused by identifiable intracranial (possibly extracranial) causes.
Reactive-provoked by extracranial causes.

Front 4

Describe the typical clinical picture for idiopathic epilepsy.

Back 4

No diagnosable cause. Typically occurs in 1-5 yr old dogs. Rare in cats. Infrequent seizures that increase in frequency without treatment. Seizures typically occur at night or while sleeping.

Front 5

List the stages of seizures.

Back 5

1. Preictal-before the seizure, changes in senses or behavior (prodrome), or initial focal signs (aura).
2. Ictus-the seizure itself.
3. Postictal period-recovery after the seizure. Confusion, blindness, ataxia, somnolence, polyphagia. Can last minutes to days.
4. Interictal period-time between seizures. Neuro exam should be normal if idiopathic; abnormal if symptomatic.

Front 6

Compare and contrast generalized vs. partial seizures.

Back 6

Partial seizures: 1. Simple-motor disturbance without sensory disturbance; focal with signs reflecting location; 2. Complex-disturbance in sensorium manifest as behavioral abnormality (aka psycomotor seizures).
Generalized seizures: Both hemispheres involved; loss of consciousness. Tonic; clonic; tonic-clonic; myoclonic; or atonic.

Front 7

Describe the mechanism of action, side effects, dosing schedule, and therapeutic drug monitoring for phenobarbitol use in seizures.

Back 7

Mechanism of action: Increased neuronal reactivity to GABA (inhibitory)
Side effects: Sedation, PU/PD/PP expected, usually fade after steady state is reached. Hepatotoxicity is adverse. Will cause slight ALP elevation; decreased tT4, fT4, and increased TSH (no clinical signs). Many drug interactions.
Dosage: 2.5 mg/kg BID in cats; 2 to 5 mg/kg BID in dogs.
Therapeutic drug monitoring: 2-3 weeks after starting and any changes, every 6-12 months, or if side effect or break through seizures. Target 20-35 ug/mL (total range 15-40)

Front 8

Describe the mechanism of action, side effects, dosing schedule, and therapeutic drug monitoring for bromide use in seizures.

Back 8

Mechanism of action: Hyperpolarization of neuronal membranes
Side effects: Sedation, ataxia, PU/PD/PP, vomiting/diarrhea expected. Idiosyncratic pancreatitis or pruritic skin eruptions adverse. Can worsen renal failure. Will artifactually elevate Cl levels. TOXIC TO CATS
Dosage: 20-40 mg/kg per day in dogs. May be given SID, or split into BID or TID dosing.
Therapeutic drug monitoring: After loading dose (if used), 1 mo and 3 mo after starting treatment, every 6-12 months. Target 1-3mg/ml monotherapy, 1-2mg/ml add-on.

Front 9

Describe the mechanism of action, side effects, dosing schedule, and therapeutic drug monitoring for levetiracetam use in seizures.

Back 9

Mechanism of action: Binds to synaptic vesicle protein 2A, prevents neurotransmitter release.
Side effects: Rare
Dosage: 20 mg/kg TID
Therapeutic drug monitoring: Not considered necessary because side effects are rare, and typically not life threatening.

Front 10

Describe the mechanism of action, side effects, dosing schedule, and therapeutic drug monitoring for zonisamide use in seizures.

Back 10

Mechanism of action: Unknown, suspect blocks Ca and Na channels.
Side effects: Sedation, ataxia, GI upset expected. Idiosyncratic hepatic necrosis and proximal tubular acidosis are rare.
Dosage: 5-10 mg/kg BID in dogs, 5-10 mg/kg SID in cats. Use 10 mg/kg if add-on to phenobarb.
Therapeutic drug monitoring: Need for monitoring is controversial.

Front 11

Recognize emergency seizure situations, and describe a step-wise treatment plan for controlling emergency seizures.

Back 11

Status epilepticus and Cluster seizures are considered emergencies.
At hospital:
1. Bolus diazepam/midazolam 0.5 mg/kg at a time until seizuring stops.
2. Stabilize the patient-establish airway, give O2 if needed, PCV/Total solids/lactate/glucose assessment, correct as needed; treat hyperthermia if needed.
3. CBC/Chem and drug monitoring (if on current therapy)
4. Once stabilized start loading dose of Phenobarb (15-20 mg/kg split q6 hours over 24 hours), Bromide (500 mg/kg; split either q4-6 hours over 24 hours, or into 5 doses + maintenance dose over 5 days), Midazolam CRI (at initial bolus dose needed to stop seizures-0.5 mg/kg/hr base) if needed until loading dose of other therapy completed, or Levetiracetam (60 mg/kg IV slow bolus).
6. Propofol, pentobarbital, gas anesthesia may be used as last ditch efforts.
At home:
1. Clorazepate-given BID or TID during cluster time period for patients with established history of cluster seizure pattern.
2. Rectal diazepam (1-2 mg/kg).
3. Take to ER if not comfortable doing emergency treatments at home.

Front 12

List the components (and corresponding functions) of the brainstem.

Back 12

1. Midbrain (mesencephalon)-Organizes visual and auditory reflexes. CN III (occulomotor) and IV (troclear) originate here. Red nucleus is the major motor nucleus for quadrupeds.
2. Pons (metencephalon)-CN V (trigeminal) originates here. Pontine reticular formation helps with motor control.
3. Medulla oblongata-CN VI-XII originate here. Medullary reticular formation helps with motor control.
Primary brainstem functions (all parts): Motor control, proprioception, mentation, cardiorespiratory control, and the origination of cranial nerves (except I and II).

Front 13

For the following tests of cranial nerves, list the afferent and efferent nerves and the effector muscles: Palpebral, Corneal, Pupillary Light Reflex, Vestibulo-ocular reflexes, Facial sensation, Gag reflex.

Back 13

1. Palpebral-afferent, opthalmic branch of CN V; efferent, CN VII; effector, orbicularis oculi muscle.
2. Corneal-Afferent,ophthalmic branch of CN V; efferent, CN VI; effector, retractor bulbi muscle.
3. PLR-afferent, CN II; efferent, CN III; effector-sphincter muscle of the pupil.
4. Vestibulo-ocular-
5. Facial sensation-
6. Gag reflex-

Front 14

List the cranial nerves that control the following: Muscles of mastication, eye position (list the type fo strabismus found with a deficit).

Back 14

Muscles of mastication: Mandibular branch of the trigeminal nerve (V).
Eye position:
1. Oculomotor (III)-ventrolateral strabismus
2. Trochlear (IV)-rotation ("4th nerve palsy", only noticeable if pupil is not round)
3. Abducent (VI)-medial strabismus

Front 15

List the ways vision is assessed on a neurologic examination.

Back 15

1. Visual placing
2. Cotton ball tracking
3. Obstacle course (both lit and dim).
4. Pupil size and symmetry
5. PLRs
6. Dazzle reflex
7. Corneal reflex
8. Manace response (learned integrated response, not a reflex).

Front 16

Using PLRs, neurolocalize blindness at the level of the:
1. Optic nerve
2. Optic tract
3. Occipital lobe

Back 16

1. Optic nerve-ipsilateral mydriasis, blindness, and negative PLRs in the affected eye.
2. Optic tract-Contralateral mydriasis, blindness, and negative PLRs.
3. Occipital lobe-symmetric pupils and normal PLRs, with blindness contralateral to the lesion.

Front 17

Describe sympathetic innervation to the eye and know the signs of Horner's syndrome in small animals.

Back 17

Sympathetic innervation originates in the thoracic spinal cord, goes through the cervicothoracic and middle cervical ganglia, synapses in the cranial cervical ganglion, post ganglionic fibers join CN IX then CN V.
Primary effectors are the orbitalis muscle, smooth ciliaris muscle, and dilator pupillae.
Clinical signs: Ptosis (droopy eyelid), miosis, enophthalmos, and elevated nictitans. May also see periphreal vasodilation, anhydrosis/hypohydrosis on the nasal planum of cattle, or sweating in horses.

Front 18

Describe the functions of the cerebellum.

Back 18

Regulates rate, range and force of motor activity:
1. Coordinates and smooths movements
2. Regulates muscle tone both at rest and during motion
3. Plays a role in UMN support of the body against gravity
4. Coordinates vestibular function.

Front 19

List the clinical signs of cerebellar syndrome.

Back 19

1. Cerebellar ataxia/dysmetria
2. Intention tremors
3. Decerebellate rigidity-opisthotonus, extended thoracic limbs and flexed pelvic limbs
4. Increased muscle tone
5. +/-hyperactive reflexes
6. Delayed postural reactions followed by exaggerated response
7. Possible vestibular syndrome

Front 20

Describe the functions of the vestibular system.

Back 20

1. Special proprioception-sense of the body in space.
2. Conscious perception of balance.
3. Coordination of eye, neck, and limb position relative to head position.
4. Perception of gravity and the body's orientation relative to gravity.

Front 21

Compare and contrast (neurolocalize) the following: peripheral vestibular syndrome, central vestibular syndrome, and paradoxical vestibular syndrome.

Back 21

Peripheral (inner ear, peripheral nerve): Ipsilateral head tilt, rolling, falling, circling; contralateral nystagmus fast phase; may cause Horner's syndrome and/or facial paralysis.
Central (brainstem): Same as peripheral vestibular syndrome, but will also have ipsilateral postural reaction deficits! If nystagmus is vertical or positional, lesion is almost always central.
Paradoxical (cerebellar): Contralateral head tilt, falling, rolling; Ipsilateral postural reaction deficits and nystagmus fast phase.

Front 22

Describe the typical signalment, onset, and progression of congenital brain disease.

Back 22

Signalment: <6 months of age, typically brachycephalic breeds.
Onset: Slow onset from birth
Progression: None or slow, most damage is done in-utero.

Front 23

Describe CSF dynamics, including: production, flow, and absorption.

Back 23

CSF produced constantly in the choroid plexus.
Flow: lateral ventricles->interventricular foramina->third ventricle->mesencephalic aqueduct->fourth ventricle->lateral apertures->subarachnoid space->dorsal over the cerebellum and cerebrum or down the central canal of the spinal cord
Absorption occurs through the arachnoid villi in the venous sinuses and cerebral veins.

Front 24

Apply the knowledge of CSF flow dynamics to the pathogenesis of hydrocephalus.

Back 24

Obstruction of CSF flow or decreased absorption of CSF during embryonic development causes expansion of the ventricles into the cerebral tissue. Decrease in cerebral tissue is responsible for forebrain signs. MRI is best diagnosis. Omeprazole or pred can be used to decrease CSF production, or a ventriculoperitoneal shunt may be placed to reduce continued pressure in the ventricles, but damage cannot be reversed (no reversion of signs).

Front 25

Apply the knowledge of CSF flow dynamics to the pathogenesis of intracranial arachnoid cysts.

Back 25

Split in the arachnoid membrane during embryogenesis allows CSF to form a cyst; common in the quadrigeminal cistern. Causes forebrain signs. Associated with small breed dogs. MRI used to diagnose. Omeprazole to decrease CSF production; Surgery to either place cystoperitoneal shunt, or fenestrate the cyst entirely.

Front 26

Apply the knowledge of CSF flow dynamics to the pathogenesis of Chiari-like malformation.

Back 26

Occipital hypoplasia compresses the cerebellum and causes it to herniate into the foramen magnum, decreasing CSF flow. This results in hydro- or syringomyelia formation. Phantom scratching, Scoliosis, and cervical myelopathy are the most common signs; seizures, deafness, and facial nerve paralysis have also been reported. MRI is the best diagnosis. Gabapentin and omeprazole may be used to decrease CSF flow and manage neurologic signs. Foramen magnum decompression may also be done, but relapse is common.

Front 27

Understand the disease progression of congenital degenerative disorders such as lysosomal storage disease and cognitive dysfunction syndrome.

Back 27

Lysosomal storage disease-interrupted metabolic pathway causes products to build up in neurons. Will be normal at birth; often present first with cerebellar dysfunction, then progressive multifocal to diffuse encephalopathy.
Cognitive dysfunction syndrome-Pathophysiology not well understood, multifactorial. Progressive, non-specific forebrain signs; occurs in older dogs and cats. Often involves brain atrophy. Treat with selegiline, diet, and environmental enrichment.

Front 28

Recognize the clinical picture typical of metabolic encephalopathy.

Back 28

Diffuse, global encephalopathy. Signs include: decreased mentation, head pressing, blindness, seizures, +/- abnormal neurologic examination.

Front 29

List the common causes of metabolic and nutritional encephalopathy.

Back 29

1. Hepatic dysfunction-probably due to hyperammonemia.
2. Renal dysfunction-hyperosmolality, neural dehydration.
3. Hypoglycemia-Brain can only use glucose; transport into brain requires minimum glucose concentration.
4. Hyperthyroidism-hypertension/stroke
5. Hypothyroidism-dec neuronal O2 consumption, myxedema coma, atherosclerosis/stroke
6. Cushing's-hypertension/stroke, pituitary macroadenoma compressing other brain tissue.
7. Diabetes mellitus-hyperosmolarity/brain dehydration.
8. Acid/base derangements-resp acidosis->CO2 enters brain->inc cerebral blood volume->intracranial hypertension.
9. Thiamine deficiency-dec ATP production in the brain.
10. Hyper or hypocalcemia-alters excitability of neuronal membrane (hyper=dec; hypo=inc).

Front 30

Understand the pathophysiology of sodium derangements (and their too-fast correction) causing encephalopathy.

Back 30

1. Acute hypernatremia-neuronal dehydration; stretching/tearing of vessels as brain shrinks.
2. Chronic hypernatremia-rapid correction results in water imbibition and cytotoxic edema of the brain.
3. Acute hyponatremia-brain tissue becomes hyperosmolar to blood->cerebral edema.
4. Chronic hyponatremia w/rapid correction-axonal shrinkage, damage to oligodendrocytes causes demyelination.

Front 31

Know what is the most common sign of neurotoxicosis.

Back 31

Seizures!

Front 32

Compare and contrast the clinical features of meningiomas and gliomas.

Back 32

Meningioma: Occur more often in female dogs, long nosed breeds over represented; more common in male cats. Located extra-axial or outside the brain. Distinct margins, uniform contrast enhancement with dural tail sign on MRI.
Glioma: Most common in brachycephalic breeds. Can be astrocytic or oligodentrocytic. Intra-axial location, no distinct margins, nonuniform contrast enhancement.

Front 33

Describe the treatment options and goals (prognosis if known) for intracranial neoplasms.

Back 33

Meningiomas: Full surgical removal occasionally successful in cats. Debulking and radiation-Good prognosis (1-3 yrs).
Gliomas: Surgical debulking and radiation-moderate prognosis (6-12 mo).
Choroid plexus tumors: Papilloma-may be able to completely remove (curative), if not, recurrence is common. Carcinoma-often metastasizes, poorer prognosis. Not radiation sensitive.
Pituitary gland tumor: typically adenomas. Radiation therapy-good prognosis (1-2 yrs); surgical resection is rare.
Trigeminal nerve sheath tumor: Radiation therapy.

Front 34

Compare and contrast clinical features of GME, NME, and NLE.

Back 34

GME: Young to middle aged, small breed dogs; females more common. Abrupt onset, progressive. Signs typically localize to the caudal brainstem and cervical spinal cord; can be focal or disseminated. Also an optic form-targets optic nerve and chiasm. CSF analysis-marked pleocytosis and elevated protein; MRI-lesions in white matter.
NME: Most common in early adulthood; Pugs, Maltese, and Chihuahuas. Signs localize to the forebrain (seizures!). MRI-lesions in the grey matter/white matter junction.
NLE: "Yorkie encephalitis", middle-aged, small breed dogs. Signs localize to the brainstem. MRI-areas of cavitation in the white matter.
Treatment for all 3 types is Pred or other immunosuppressive therapy.
Prognosis: Good short term with GME; Poor to grave with NME and NLE.

Front 35

Describe the four types of canine distemper virus infections.

Back 35

1. Myoclonus-repetitive, rhythmic muscle contractions.
2. Grey matter disease-seizures in young dogs.
3. Demyelinating disease-mature dogs.
4. General encephalitis-behavioral changes, circling, blindness in older dogs.

Front 36

Know the clinical features of FIP in the CNS.

Back 36

Causes spastic paresis, ataxia nystagmus, and loss of balance (cerebellomedullary).

Front 37

Know the common causes of infectious encephalitis.

Back 37

Rickettsial:
1. Rocky mountain spotted fever
2. Ehrlichiosis
3. Salmon poisoning-neorickettsia helminthoeca
Fungal:
4. Cryptococcus neoformans
5. Blastomyces dermatitidis
6. Histoplasma capsulatum
Protozoal:
7. Toxoplasma gondii
8. Neospora caninum
Viral:
9. Distemper (dogs)
10. FIP (cats)

Front 38

Recognize the typical clinical picture of vascular encephalopathy.

Back 38

Middle-age to older animals
Brachycephalic dogs predisposed to "global ischemia"
Cerebellar infarcts common in small breed dogs.
Acute to peracute onset of clinical signs. Signs will reflect location of vascular injury. Recovery from neurologic signs tends to be rapid, with good prognosis

Front 39

List possible underlying etiologies for hemorrhagic and ischemic stroke.

Back 39

Hemorrhagic: Systemic hypertension, coagulopathies, congenital vascular defects (rare).
Ischemic: Cardiac disease, hypercoagulable states (Cushing's dx, renal dx), increased blood viscosity (lipemia), infectious diseases, atherosclerosis (rare in animals), and feline ischemic encephalopathy (associated with cuterebra).

Front 40

List the components of Cushing's reflex, and understand the pathophysiology of this response.

Back 40

1. Systemic hypertension
2. Reflex bradycardia
CPP=MAP-ICP. Normal is 70. If ICP increases MAP must increase also to maintain CPP at 70.

Front 41

Understand the differences between primary and secondary brain injury.

Back 41

Primary-Trauma resulting in contusions, lacerations, and skull fractures.
Secondary-Failure of Na/K pump ultimately results in cytotoxic edema, free radical damage, cell membrane damage, and tissue acidosis due to anaerobic metabolism. End result is increased intracranial pressure->herniation and compression->changes in breathing pattern, ocular changes, and changes in mentation status/coma. May also result in decerebrate rigidity (all limbs rigid, opisthotonus, and depressed mentation).

Front 42

Describe the mechanisms of action of mannitol and hypertonic saline.

Back 42

Mannitol-produces osmotic gradient in the vascular space, pulls water from the brain. Also free radical scavenger.
Hypertonic saline-Produces osmotic gradient in the vascular space to pull water from the brain. Also helps resotre intravascular volume. Commonly combined with hetastarch.

Front 43

List the clinical signs associated with myopathic syndrome.

Back 43

Generalized weakness
Exercise intolerance
Stiff/stilted gait
Body/limb tremors
Muscle atrophy or hypertrophy-depending on stage
Myalgia
Limited joint movement (contracture)
Regurgitation or altered esophageal motility
Ventroflexion of head and neck (cats!)
Trismus-inability to open the mouth
No sensory abnormalities

Front 44

List the clinical signs associated with Junctionopathies/diffuse lower motor neuron disease.

Back 44

Generalized neurogenic muscle atropy
Ascending flaccid paralysis
Decreased to absent spinal reflexes (LMN signs everywhere)

Front 45

List the clinical signs associated with motor neuropathy vs. sensory neuropathy.

Back 45

Motor neuropathy: flaccid paresis/paralysis, neurogenic muscle atrophy, hypotonia, hyporeflexia/areflexia, muscle fasciculations
Sensory neuropathy: changes in sensation, paresthesia may lead to self mutilation, proprioceptive/postural deficits, hyporeflexia/areflexia, NO muscle atrophy.

Front 46

Contrast the classes of peripheral nerve injury and their associated prognoses.

Back 46

1. Neurapraxia-transient lack of nerve function with little or no structural damage. Good prognosis.
2. Axonotmesis-Damage to the axon, but basement membrane intact; allows for regrowth of the nerve. Prognosis guarded to good.
3. Neurotmesis-Complete transection of nerve, no ability to regrow. Prognosis grave.
Note: all of these look the same clinically at first, it can take up to a week for neural atrophy to develop.

Front 47

Congenital muscular dystrophies

Back 47

Cause: deficient or abnormal myofiber cytoskeletal proteins.
Clinical signs: Progressive muscle atrophy-commonly affects the muscles of the throat; stilted gait, bunny-hopping; exercise intolerance and myalgia.
Diagnosis: Muscle biopsy; EMG-bizarre, high frequency discharges.
Treatment: None.

Front 48

Labrador Retreiver Myopathy

Back 48

Cause: autosomal recessive defect in yellow and black labs.
Clinical signs: Stilted gait with bunny hopping. Onset at 6 wks to 7 mo of age
Diagnosis: Muscle biopsy and EMG
Treatment: None, but dogs typically stabilize by 12 mo of age, and live relatively normal lives.

Front 49

Hypokalemic myopathy (cats)

Back 49

Cause: hypokalemia causes cells to be hyperpolarized and refractory to depolarization and contraction.
Clinical signs: Neck ventroflexion, stiff gait
Diagnosis: Hypokalemia
Treatment: Correct the cause of hypokalemia, provide supplementation.

Front 50

Cushing's myopathy

Back 50

Cause: mechanism unknown
Clinical signs: stiff gait, esp in pelvic limbs; weakness, muscle atrophy.
Diagnosis: specific waveform on EMG, must have Cushing's
Treatment: Treat the Cushing's, prognosis guarded to good for return of normal function.

Front 51

Masticatory muscle myositis

Back 51

Cause: autoimmune disease targeting the muscles of mastication
Clinical signs: Acute onset, painful swelling of masticatory muscles, trismus, fever, atrophy if chronic.
Diagnosis: Antibody titers against type IIM fibers.
Treatment: Immunosuppressive therapy.

Front 52

Autoimmune polymyositis

Back 52

Cause: Exact mechanism unknown.
Clinical signs: Generalized weakness, worsening with exercise; myalgia.
Diagnosis: Muscle biopsy
Treatment: Immunosupressive therapy.

Front 53

Infectious myositis

Back 53

Cause: Toxoplasma and neospora are most common; also: clostridium, leptospira, sarcocystis, hepatozoon, ehrlichiosis, and RMSF.
Clinical signs: Toxo and Neospora will cause rigid pelvic limb extension.
Diagnosis: Serology or muscle biopsy.
Treatment: depends on causative agent.

Front 54

Tetanus (mimics a myopathy)

Back 54

Cause: Tatanospasm toxin released by C. tetani-enters motor nerve and CNS, blocks inhibitory signs.
Clinical signs: Muscle stiffness, contraction of facial muscles, sawhorse stance.
Diagnosis: Based on history and clinical signs
Treatment: Wound care if wound can be found, Penicillin, antitoxin available that will bind toxin not yet in CNS but prone to causing anaphylaxis.

Front 55

Ischemic neuromyopathy (aortic thromboembolism)

Back 55

Causes: Thromboembolism at the aortic bifurcation.
Clinical signs: pelvic limb dysfunction, rectal hypothermia, cool paws, cyanotic nail beds, analgesia of the digits and tarsal area.
Diagnosis: History, finding underlying etiology (HCM in cats, metabolic disease in dogs), ultrasound to find clot, elevated CK.
Treatment: Surgical removal, antithrombotic agents (heparin), address underlying issues.
Prognosis: Guarded

Front 56

Congenital myasthenia gravis

Back 56

Cause: reduction or absence of ACh receptors (not produced). Common in JRTs, fox terriers, samoyeds, and mini dachshunds.
Clinical signs: Unable to walk, early onset
Diagnosis: Response to anticholinesterase drugs
Therapy: Anticholinesterases may help, but remission is unlikely.

Front 57

Acquired myasthenia gravis

Back 57

Cause: Antibodies bind to ACh receptors and either block or destroy them.
Clinical signs:
1. Generalized-exercised induced weakness, better after rest. Normal tendon reflexes.
2. Focal-weakness of the muscles in the head and neck; megaesophagus, dysphonia, dysphagia.
3. Acute, fulminant-Rapid progression of weakness including the muscles of respiration.
Diagnosis: Antiacethylcholine receptor antibody test; Tensilon test; EMG; Muscle biopsy; Also a good idea to do rads for megaesophagus.
Treatment: Anticholinesterases, immunosuppressive therapy, treat any GI motility signs

Front 58

Botulism

Back 58

Cause: Ingestion of C. botulinum TOXIN, blocks ACh release at the neuromuscular junction.
Clinical signs: Ascending flaccid paralysis, cranial nerve deficits, opposite of SLUD signs.
Diagnosis: no definitive diagnosis available, based on history and clinical signs.
Treatment: Supportive care, will recover if given enough time.

Front 59

Tick paralysis

Back 59

Causes: Exact mechanism is unknown, but caused by saliva of gravid female Dermacentor ticks. Tick must be attached for 5-9 days.
Clinical signs: Rapidly ascending paraparesis, progressing to quadraparesis.
Diagnosis: Find the tick!
Treatment: Remove the tick (including mouth parts), Supportive care until recovered.

Front 60

Acute idiopathic polyradiculoneuritis

Back 60

Cause: autoimmune?
Clinical Signs: Rapidly ascending quadriplegia, +/-respiratory paralysis; Can still wag, urinate, and deficate!?
Diagnosis: EMG, CSF
Treatment: Supportive therapy and physical rehabilitation. Steroids do NOT help.

Front 61

Chronic inflammatory demyelinating polyneuropathy

Back 61

Cause: ??? Occurs in mature dogs and cats.
Clinical signs: Ascending LMN paresis, abnormal proprioception and reflexes
Diagnosis: Nerve biopsy
Treatment: Steroids

Front 62

Protozoal polyradiculoneuritis

Back 62

Cause: Toxoplasma or Neospora
Clinical signs: Pelvic limb extention
Diagnosis: Serology
Treatment: Based on organism

Front 63

Trigeminal neuritis

Back 63

Cause: idiopathic, nonsuppurative inflammation of the motor branch of V.
Clinical signs: Acute inability to close the jaw.
Diagnosis: None-classical appearance
Treatment: Supportive care and physical therapy (opening and closing the mouth). This is self-limiting

Front 64

Diabetic neuropathy

Back 64

Cause: Possibly change in vasculature around the nerves.
Clinical signs: Plantigrade stance, muscle atrophy
Diagnosis: Diagnose DM
Treatment: Treat diabetes and most cases will revert.

Front 65

Hypothyroid neuropathy

Back 65

Cause: unknown
Clinical signs: Cranial nerve V, VII, and VIII dysfunction; laryngeal paralysis, megaesophagus, LMN paresis/paralysis of all limbs.
Diagnosis: Hypothyroid dog with neuropathy.
Treatment: Correct the hypothyroidism.

Front 66

Delayed organophosphate toxicity (neuropathy) in cats

Back 66

Cause: Chronic exposure to OPs
Clinical signs: decreased proprioception, reflexes, and paraparesis
Diagnosis: History, decreased serum cholinesterase activity
Treatment: 2PAM

Front 67

Vincristine induced neuropathy

Back 67

Cause: vincristine administration
Clinical signs: Paraparesis, ataxia, depressed reflexes.
Diagnosis: history of vincristine administration
Treatment: Resolves after drug withdrawal.

Front 68

Dysautonmia (neuropathy)

Back 68

Causes: Unknown, but suspected toxic or infectious because of geographic and seasonal predilection.
Clinical signs: Variable parasympathetic or sympathetic dysfunction
Diagnosis: Miosis after dilute pilocarpine administration; improved ability to urinate after low dose bethanechol
Treatment: Supportive depending on signs.
Prognosis: Poor.

Front 69

Insulinoma neuropathy

Back 69

Cause: Insulinoma, pathogenesis unknown.
Clinical signs: Diffuse LMN signs
Diagnosis: Diagnose the insulinoma
Treatment: As for insulinoma

Front 70

Nerve sheath tumor neuropathy

Back 70

Causes: nerve sheath tumor, most often affects CN V or the brachial plexus.
Clinical signs: CN V-atrophy of the masticatory muscles; Brachial plexus-Unilateral limb atrophy, can lateralize if the mass is close enough to compress the spinal cord; Horner's syndrome.
Diagnosis: find the tumor
Treatment: ??

Front 71

Brachial plexus avulsion (neuropathy)

Back 71

Cause: Trauma, hit by car is most common.
Clinical signs: LMN atrophy, LMN reflex deficits, +/-Horner's syndrome
Diagnosis: Based on clinical signs, +/-EMG
Treatment: Physical therapy, limb amputation if animal is self-mutilating.

Front 72

Tail avulsions (neuropathy)

Back 72

Most common in cats

Front 73

Injection injury neuropathy

Back 73

Siatic nerve most commonly affected.
More common in young-less muscle mass.
May be from needle puncture, drug toxicity, pressure from hematoma formation, or scarring around the nerve.

Front 74

Bovine Spongiform Encephalopathy

Back 74

Etiology: REPORTABLE. Prion disease, spread by ingestion of infected meat or bone meal. Incubation period is months to years, fatal 2 wks to 6 mo after onset of signs.
Clinical signs: insidious onset; increased apprehension, hyperesthesia, incoordination.
Diangosis: Histology of brain tissue (medulla oblongata @ level of the obex)
Treatment: None
Control: Illegal to feed meat, blood, or bone meal to cattle in the US.
Prognosis: Fatal

Front 75

Rabies (in Cattle)

Back 75

Etiology: REPORTABLE. 3 forms; incubation period 2 wks to 6 mo, depending on distance of inoculation site from CNS. Most animals die within 10 days of onset of clinical signs.
Clinical signs: hindlimb ataxia, weakness; CONSTANT STRAINING +/-RECTAL PROLAPSE.
Diagnosis: Submit brain for FA.
Treatment: None
Control: Vax available, but not labeled for cattle. Economically not useful.
Prognosis: Fatal

Front 76

Pseudorabies in Cattle

Back 76

Etiology: REPORTABLE. Primary host is pigs (including wild pigs), requires close contact to spread. Incubation 4-7 days, duration of illness 8 hrs to 3 days.
Clinical signs: Severe pruritis. Sudden death may occur without clinical signs.
Diagnosis: Histopathology on tissue samples from areas of most intense pruritis.
Treatment: None
Control: Limit exposure between swine and cattle.
Prognosis: Fatal

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Listeriosis (cattle)

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Clinical signs: Unilateral CN deficits in the caudal cranial nerves (V-XII)-Ptosis, dropped ear, more open nostril, dysphagia, tongue may protrude from one side of mouth. Head-pressing, circling, stuck in corners.
Diagnosis: Often based on clinical signs and response to therapy. CSF=mononuclear pleocytosis. Can sometimes be cultured from CSF.
Treatment: Oxytetracycline, or Penicillin for 1-4 weeks. Fluids should be given if animal cannot swallow.
Etiology: Caused by Listeria monocytogenes. Cases tend to be sporatic; associated with improperly stored silage, can also be found in feces and milk which may contaminate vegetation.
Prognosis: Survival good if treated promptly, but may have permanent neuro deficits.

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Thromboembolic Meningoencephalitis of cattle (TEME)

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Clinical signs: Acute onset-sleepiness, anorexia, staggering, fever, depression, blindness, seizures, partial paralysis of multiple cranial nerves.
Diagnosis: Inflammatory leukogram, CSF=neutrophilic pleocytosis. High titers for Hemophilus somni.
Treatment: Antibiotics, fluid therapy, anticonvulsants as necessary.
Epidemiology: Caused by gram neg Hemophilus somni. May also cause pneumonia and polyarthritis. Occurs in feedlot cattle, more during winter months in colder climates.
Control: Vaccinate in areas where common.
Prognosis: Good if not recumbent. Neurologic form has low morbidity but high mortality.

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Meningitis in cattle

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Clinical signs: Depression, fever, diarrhea, navel ill, arthritis, sinusitis, and otitis. Hyperesthesia, stiff neck, seizures, blindness, ataxia with spasticity. Spinal reflexes normal to hyper.
Diagnosis: CSF tap=neutrophilic pleocytosis, culture and sensitivity can be helpful.
Treatment: Antibiotics-ceftiofur recommended because penetrates BBB.
Etiology: Occurs most in neonates that have failure of passive transfer. May be bacterial, viral, fungal, or protozoal. E coli and Salmonella most common.
Control: Insure adequate colostrum (4L dairy, 2L beef).
Prognosis: Poor.

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Pituitary Abscess in cattle

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Clinical signs: acute and rapid progression. Head and neck extension, depression, head-pressing, asymmetric CN deficits, dysphagia, anisocoria, no PLRs, mydriasis, facial paralysis.
Diagnosis: CSF=elevated WBC and protein.
Treatment: None
Etiology: Typically caused by Arcanobacterium pyogenes. May originate from infection of the head/face.
Prognosis: Poor-typically fatal.

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Brain Abscess in cattle

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Clinical signs: Slower onset and progressive, asymmetric signs based on location of the abscess.
Diagnosis: CSF=neutrophilic pleocytosis, but could be normal.
Treatment: Antibacterial therapy WITH surgical drainage.
Etiology: Adult or young cattle with a history of pyogenic disease. Previous dehorning and sinusitis increase risk. Caused by Arcanobacterium pyogenes most often. Neuro deficits will be from compressive effect of abscess.
Prognosis: Very poor without surgical drainage and long term antibiotics.

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Tetanus in cattle

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Clinical signs: Progressive muscular rigidity, becomes worse with stimuli. May progress to respiratory paralysis and death.
Diagnosis: No definitive diagnosis.
Treatment: Debride wounds and treat would locally with penicillin. Tetanus antitoxin and toxoid. Systemic antibiotics. Muscle relaxants and other supportive care.
Etiology: Caused by neurotoxins produced by Clostridium tetani, found in soil and feces.
Control: Vaccine is available, use in problem herds.
Prognosis: High mortality, some recovery with treatment and support, but can be costly.

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Botulism in cattle

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Clinical signs: progressive, ascending muscular hypotonia.
Diagnosis: Demonstrate toxin in serum, up to 6 days after onset of clinical signs.
Treatment: Antitoxin, type specific, good for early stages. Supportive care. Abx only if ingestion of actual bacteria is suspected (not just preformed toxin).
Etiology: Caused by Clostridium botulinum toxin. Bacteria does not have to be present. Incubation is 1-7 days. Sensory nerves and CNS are NOT affected. Most often associated with accidental inclusion of animal carcasses into hay or silage.
Prognosis: Fatal

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Nervous coccidiosis of cattle

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Clinical signs: Ataxia and tremors with periods of normalcy; may have seizures-opisthotonos, tonic-clonic movement, medial strabismus, snapping of the eyelids.
Diagnosis: None specific. Intestinal coccidiosis usually precedes the neurologic form.
Treatment: Sulfonamides and anticoccidial drugs. Neuro signs may persist for some time after treatment.
Etiology: Occurs most often in feedlot cattle during the winter months.
Control: Control measure the same as for intestinal coccidiosis.
Prognosis: Poor

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Polioencephalomalacia of cattle

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Clinical signs: Acute onset of central blindness, +/-dorsomedial strabismus; ataxia, tremors, recumbency.
Diagnosis: Most often based on history and response to thiamine. CSF=mononuclear pleocytosis and elevated protein. Necropsy-swollen, yellow tinged cerebrum; will fluoresce under UV light.
Treatment: Thiamine; response should occur in 1-2 days.
Etiology: Usually young cattle (6-12 mo), or any age small ruminant. More common in feedlots. Secondary to ruminal acidosis, diets high in sulfates, thiamine deficient diets; amprolium may predispose.
Control: Moderate carb diet, supplement with thiamine in problem herds.
Prognosis: Excellent if treated early.

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Salt poisoning in cattle

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Clinical signs: Ataxia, lethargy, depression, wandering, head pressing, blindness, aggressiveness, seizures.
Diagnosis: History of lack of water; serum and CSF sodium levels will be markedly elevated.
Etiology: Caused by overload of salt (rare) or lack of water intake (common). Hypernatremia leads to cerebral edema.

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Viamine A deficiency in cattle

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Causes central blindness, most common in calves.
Blindness is not reversible.

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Lead poisoning in cattle

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Clinical signs: Diffuse cerebral disease-aggression, central blindness most common; also convulsions, wandering, head pressing, opisthotonos.
Etiology: Most common neuro-toxicosis in cattle. More frequent in young, but any age. Look for junk piles!
Diagnosis: Basophilic stippling and nucleated RBCs, whole blood lead levels. Lead levels detectable in urine after EDTA treatment confirms.
Treatment: Ca-EDTA, thiamine, magnesium sulfate laxatives (bind lead in the GI)
Prognosis: Fair with early, aggressive treatment.

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Delayed organophosphate toxicosis in cattle

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Clinical signs: Pelvic limb weakness, flaccid paralysis.
Etiology: Waste oils used as lubricants, hydraulic/transmission oils, pesticides, anthelmintics.
Diagnosis: suppressed cholinesterase levels.
Treatment: None

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Hydrocephalus/Hydrancephaly

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Congenital defect-domed skull, dull mentation.
Acquired form has been associated with Blue Tongue.
No economically successful treatment

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Cerebellar hypoplasia

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Clinical signs: Base-wide stance intention tremors present at birth. Will not have mentation/attitude changes.
Etiology: BVD is the most common agent (mom infected during gestation), affected animal can be PI.
Treatment: None
Control: Vaccinate females prior to breeding.

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Spastic paresis (Elso heel)

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Clinical signs: spastic contracture of muscles and extension of stifle and tarsal in one or both hind limbs; often have sawhorse stance in front limbs.
Treatment: Tibial neurectomy may treat palliatively until animal can be finished and taken to slaughter.
Control: Do not use affected cattle for breeding, genetic component.

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Spinal fractures, luxations, and trauma in cattle

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Clinical signs: Vary by location.
Treatment: Anti-inflammatories and glucocorticoids.
Prognosis: Good to poor depending on severity of signs.

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Vertebral body abscess in cattle

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Clinical signs: knuckling and weakness of the rear legs.
Diagnosis: CSF-neutrophilia; necropsy is confirmatory.
Treatment: None-little efficacy
Prognosis: Poor

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Peripheral nerve disorders in cattle

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Neurolocation:
1. Brachial plexus-weakness or pralysis of front limb, dropped shoulder.
2. Radial nerve-a. distal: dragging dorsal aspect of hoof; b. proximal: non-weight bearing
3. Siatic-paralysis of rear limb, often recumbent.
4. Obturator-splay legged in rear, may be non-weight bearing. Often occurs concurrently with siatic.
5. Peroneal nerve-mild to severe knuckling in rear.
6. Tibial nerve-hock overflexed, fetlock partially flexed, still bearing weight on bottom of foot. "Drop hock"
7. Femoral nerve-semiflexion and non-weight bearing on rear limb.
Treatment (All): ASAP with anti-inflammatories. Dexamethasone is best, use meloxicam in pregnant animals.
Control: Anticipate possible causes (prolonged lateral recumbancy, dystocia, injections, etc).

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Components of Equine Neuro Exam

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1. Distant observation of gait, mentation, behavior, head position, etc.
2. History/Signalment-many age, breed, sex, and use associated diseases. Ask owner about behavior and mentation changes; onset, rate of progression, and duration of signs; housing environment; health of other horses; presence of wildlife/parasites.
3. Physical Exam-other signs of systemic disease; also look for symmetry, atrophy, swelling, pain, sensation, and presence of tremors or myoclonus.
4. Cranial nerve exam-similar to dogs and cats.
5. Gait examination-Walk, trot, circle, head held up while moving, up/down incline, backing, and over obstacles. Observe for weakness, spacticity, hypermetria, and ataxia. May also have to do a concurrent lameness exam. Attempt to differentiate from musculoskeletal problems.
6. Other tests-proprioception, sway reaction, hopping, tail/anal tone, abnormal sweating, reflex testing (recumbent animal only).

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What is the grading scale used during gait examination in horses?

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0. No deficits
1. Deficits barely perceptible, or noticed on head elevation
2. Deficits noted at a walk
3. Deficits noted at rest and walking, falls with special testing.
4. Falls or nearly falls at normal gait.
5. Recumbent

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What signs would lead you to suspect neurologic deficits in a horse as opposed to musculoskeletal issues?

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2 or more gait deficits
Ataxia present (always neuro in origin)
Behavior or mentation changes
Cranial nerve signs
Note: Can have simultaneous neuro and musculoskeletal problems.

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What additional diagnostic tests can be done to evaluate neurologic disease in horses?

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CSF tap-collected from either the LS junction or the Atlanto-occipital joint. Analysed for color, cellularity, protein concentration, albumin and IgG concentrations, and specific antibody titers.
Plain radiographs-evaluate the skull, cervical spinal cord, and distal limbs.
Myelography-identify cervical spinal cord compression.
CT/MRI-good for limb, skull, brain, and cervical lesions. Limited by the size of the machine vs. size of the animal.
Electroencephalography-cerebral lesions.
Electromyography-LMN deficits.
Clin Path: CBC/Chem (metabolic/systemic causes), Vit E/Selenium, Ammonia (hepatic or colitis induced encephalopathy).
Necropsy

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West Nile Virus in horses

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Cortical disease
Epidemiology: Birds act as reservoirs and amplification hosts, transmitted by mosquitoes, horses and humans are dead end hosts.
Clinical signs: fever, depression, and anorexia in uncomplicated infection. Muscle fasciculations in the face and neck, weakness, ataxia, dysmetria, CN deficits, and corticals signs. May cause sudden death.
Diagnosis: IgM capture ELISA on serum or CSF
Treatment: Supportive care, fluids, abx, NSAIDs and osmotic agents. Hyperimmune plasma may be used.
Prevention: Vaccination

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Eastern, Western, and Venezuelan equine encephalitis

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Cortical disease
Epidemiology: Birds are primary reservoir (also small rodents for VEE), transmitted by mosquitoes, humans and horses are dead end hosts. In VEE, horses develop enough viremia to spread by direct contact.
Clinical signs: Biphasic fever, hyperexcitability, depression, recumbency, blindness, propulsive walking, head pressing, ataxia.
Diagnosis: IgM and IgG detection in serum or CSF.
Treatment: Fluids, abx, NSAIDs, nursing care.
Prevention: Vaccination

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Equine Herpesvirus Myeloencephalopathy (EHM)

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Cortical disease
Epidemiology: Caused by the neurotropic strain of EHV-1, which is more contagious and likely to reach the CNS. Spread by aerosol of respiratory secretions that may spread up to 30-40 ft.
Clinical signs: Caused by vasculitis with thrombosis, hypoxia and ischemia adjacent to CNS tissue. Fever, URT signs, hind limb ataxia/weakness, weak tail tone, incontinence, +/-CN deficits.
Diagnosis: CSF tap-xanthochromia, inc. protein, EHV-1 CSF titer. PCR of nasal secretions (swab).
Treatment: Supportive, abx, NSAIDs, antivirals.
Control: Vaccination (decreases viral shedding); rapid and strict quarantine of animals with a fever, and quarantine of the facility for at least 3 weeks after the last horse has a fever.

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Rabies in horses

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Cortical disease
Epidemiology: Infection typically from bite wound, incubation period 9 days to 1 year, potentially zoonotic.
Clinical signs: There are no specific signs, therefore rabies should be considered in any neurologic horse.
Diagnosis: Immunofluorescent antibody test at necropsy.
Treatment: None
Control: Vaccinate! If exposed, quarantine vaccinated horses for 45 days and rebooster immediately, and quarantine unvaccinated horses for 6 months and vaccinate at the end of the quarantine period.

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Idiopathic epilepsy of Egyptian Arabian Foals

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Cortical disease
Epidemiology: Inherited disease, onset between 2 days to 6 months of age
Clinical signs: Seizure. Often unobserved by owner, and horse presents for trauma or blindness. Signs are typically self-limiting, and disappear at 1-2 years of age.
Diagnosis: Rule out other causes of seizures in foals-hypoglycemia, septicemia, hypoxic ischemic encephalopathy, meningitis.
Treatment: Acute-diazepam, midazolam, or IV phenobarb. Chronic-Phenobarb or KBr. Treat for at least 6 months then wean off gradually to see if symptoms have resolved.

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Narcolepsy of horses

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Cortical disease
Epidemiology: Most common in ponies and mini horses. Episodes are typically triggered by benign/relaxing activity.
Clinical signs: Uncontrolled episodes of cataplexy and sleep, animal may be asleep for seconds to minutes and may or may not become recumbant.
Diagnosis: Rule out other causes of sudden collapse. Physostigmine test will precipitate an attack.
Treatment: Imipramine (tricyclic antidepressant)

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Sleep deprivation in horses

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Cortical disease
Epidemiology: Caused by anything that prevents REM sleep from occuring (stress, pain, etc).
Clinical signs: excessive daytime sleepiness and collapsing episodes. Often mistaken for narcolepsy.

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Cerebellar abiotrphy of horses

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Cerebellar disease
Epidemiology: Occurs in Arabians, Arabian crosses, Gotland ponies, and Oldenburg horses. Premature degeneration of neurons in the cerebellum, occuring between 1-6 months of age.
Clinical signs: Wide base stance, ataxia, stiff gait, hypermetria, intention tremors. Will progress until the horse reaches maturity, then stabilize.
Diagnosis: Rule out other causes.
Treatment: None. Depending on severity, horse may be fine as a pet, but will never be rideable.

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Basisphenoid-basioccipital fractures of horses

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Brainstem/CN disease
Epidemiology: Occurs most frequently due to rearing over backwards and striking the poll of the head. Causes damage to the medulla and pons.
Clinical signs: Head tilt, ptosis, ataxia, spacticity, intention tremors. Can cause death due to resp failure if resp centers are damaged.
Diagnosis: Neuro exam, history of trauma, radiographs.
Treatment: Anti-inflammatories, supportive care, thiamine, vitamin E.

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Temporal hyoid osteoarthropathy of horses

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Brainstem/CN disease
Epidemiology: chronic inflammation of the stylohyoid bone, and surrounding structures in the gutteral pouch.
Clinical signs: ear rubbing, head tossing, abnormal chewing, performance problems, pain on palpation; cranial nerve deficits develop later in the disease.
Diagnosis: Endoscopy of the gutteral pouch, radiographs, CT/MRI.
Treatment: Broad spectrum abx, NSAIDs, supportive care, and treatment of auxiliary lesions due to CN deficits (eg. corneal ulcers due to facial nerve paralysis).

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Botulism in horses

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Epidemiology: Three types-forage poisoning (common in adults), wound botulism (rare), toxicoinfectious botulism ("shaker foal syndrome").
Clinical signs: Loss of tongue tone, lowered head carriage, dysphagia/slow eating, gerneralized and symmetrical muscle weakness. Can cause sudden death due to resp. failure.
Diagnosis: Rule out other diseases. May find toxin in serum, plasma, GI contents, or wounds (difficult).
Treatment: Botulism antitoxin before recumbent, Penicillin, Hyperimmune plasma, Nursing care, +/-mechanical ventilation (helps most often in foals).
Prevention: Vaccinate

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Equine protozoal myelitis

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Epidemiology: Sarcocystis neurona (Neospora hughesi in the West US). Horses ingest sporocysts in feed, hay, bedding, and pasture.
Clinical signs: Focal or multifocal lesions, signs vary by location. Most common-ASYMMETRICAL muscle atrophy, weakness, ataxia, vague lameness, or spacticity. May cause cranial nerve signs.
Diagnosis: Clinical signs and rule out other causes, response to treatment. SAG-1 ELISA and other immunodiagnostic tests on CSF may help, but false negs and pos are common.
Treatment: Ponazuril, Diclazuril, or Sulfadiazine pyrimethamine. Anti-inflammatories, vit E.
Control: Vaccination (questionable efficacy), prevent contamination of feed, bedding, and pasture.

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Cervical vertebral stenotic myelopathy (equine "wobblers")

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Epidemiology: Narrowed/stenotic canal due to malformation of the cervical vertebra. Has genetic and environmental factors.
Clinical signs: Symmetric ataxia, paresis, spasticity. Hindlimbs will be affected prior to and worse than the forelimbs. Onset is often before 1 year of age, or at the beginning of training.
Diagnosis: Radiographs, sagittal ratio decrease may help confirm. Myelogram.
Treatment: Conservative-reduce exercise and reduce growth rate (reduce calories, provide adequate minerals); if young, this may allow time for vertebral development to "catch up". Surgical-works best for cases of mild to moderate clinical signs and short duration; will only improve clinical signs by one grade, so reserved for grade 1-2 cases.

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Tetanus in horses

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Epidemiology: Most commonly associated with deep penetrating wounds. C. tetani is found in soil and as a GI commensal. Tetanospasm toxin blocks inhibitory neuron pathways.
Clinical signs: Diffuse hypertonicity of striated muscle.
Treatment: Abx, tetanus antitoxin, muscle relaxants, nursing care.
Prevention: Vaccination.

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Equine Degenerative Myeloencephalopathy (EDM)

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Epidemiology: Progressive degeneration of the neurons. Genetic predisposition in many breeds.
Clinical signs: insidious to acute onset of symmetric ataxia and paresis of the trunk and limbs. Typical onset is before 1 year of age.
Diagnosis: Associated with low serum vit E, but no definitive diagnostic test antemortem.
Treatment: Supplementation with vit E, may or may not cure completely.
Prevention: Supplement with vit E if familial predisposition, lack of access to green pasture, or if other horses on the farm have been affected.

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Equine motor neuron disease

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Epidemiology: Associated with low vit E. Spontaneous, progressive, sporatic disease.
Clinical signs: Acute muscle weakness without atrophy or progressive muscle atrophy, trembling, lowered head carriage, stand with feet camped in.
Diagnosis: Low plasma/serum vit E levels are suggestive. Biopsy of tail head muscle or spinal accessory nerve.
Treatment: Vit E supplementation.
Prognosis: Guarded

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Polyneuritis equi

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Epidemiology: Etiology is unknown but suspected to be immune mediated following some infective/invasive trigger.
Clinical signs: Progressive paralysis of the tail, anus, rectum, and bladder, symmetrical hind limb weakness.
Diagnosis: Rule out other causes.
Treatment: Supportive care and NSAIDs.
Prognosis: Poor.