Small Animal Neurology Flashcards

Question

A word to describe only the 2 pelvic limbs being affected

Answer 1

Increased stride length Increase extensor tone (spastic) Normal/Increased reflexes Standing or walking on dorsum of foot Draggin or scuffin the dorsum of foot (nail wear)

Answer 2

Decreased stride length Decreased extensor tone (flaccid) Decreased reflexes

Answer 3

LMN- severe (rapid 5-7 days) denervation atrophy

Answer 4

None/mild occurs slowly disuse atrophy

Answer 5

Hypotonic/flaccid

Answer 6

Normal to hypertonic/spastic

Answer 7

False- they dont localize to any part of system, just describe severity

Answer 8

muscle atrophy from UMN deficit, occurs slowly disuse atrophy

Answer 9

1) Cerebellar ataxia (cerebellum) 2) Vestibular ataxia (vestibular system) 3) General proprioceptive ataxia- caudal brainstem and spinal cord

Answer 10

Hypermetria Overflexion of joints (carpi)

Answer 11

Over-reaching over extension of joints (carpi)

Answer 12

over flexion of joints (carpi)

Answer 13

Over extension of joints

Answer 14

All limbs caudal to the lesion

Answer 15

Hypermetria/overflexion of joints or hypometria/underflexion

Answer 16

True- for centra False- for peripheral

Answer 17

Symmetric but focal lesions are asymmetric

Answer 18

1) CN VII 2) Brainstem 3) Cerebellum

Answer 19

longer (over-reaching, solder marching) UMN hypermetria

Answer 20

1) Brainstem 2) Spinal cord (C1-C5, T3-L3)

Answer 21

not much, just that the nervous system isnt normal

Answer 22

1) Muscle and joint receptors 2) Nerves (LMNs) 3) Dorsal root ganglia 4) Spinal cord (dorsal column/medial lemniscus pathways) 5) Brainstem (medulla, pons, midbrain) 6) Thalamus 7) Cerebral somatosensory cortex (parietal lobe)

Answer 23

Thoracic limbs: UMN + GP ataxia Pelvic Limbs: UMN +GP ataxia

Answer 24

Thoracic limbs: LMN (no ataxia) Pelvic limbs: UMN +GP ataxia

Answer 25

Thoracic limbs: Normal Pelvic Limbs: UMN + GP ataxia

Answer 26

Thoracic limbs: normal Pelvic limbs: LMN (no ataxia)

Answer 27

Triceps Biceps Extensor carpi radialis

Answer 28

Patellar Cranial tibial Gastrocnemius

Answer 29

Coonhound paralysis

Answer 30

"Coon hound paralysis" affects predominantly the ventral (motor) nerve roots and nerves and thus causes profound weakness *Will have better sensory function (paw placement) than motor function (hopping which requires more strength0 Idiopathic or can occur following exposure to antigenic stimulation

Answer 31

contralateral

Answer 32

ipsilateral

Answer 33

Hemineglect

Answer 34

"Hemi-inattention" "Unilateral neglect" "hemi-spatial neglect"

Answer 35

Brainstem and cerebrum

Answer 36

brainstem and cerebellum

Answer 37

Mental: Altered (confusion)/ behavior change Cranial nerves: Contralateral blindness and decrease/absent menace Posture: Ipsilateral head/body turn, head press, pacing, circling Postural reactions: deficits in contralateral limbs, normal gait Normal tin increased spinal reflexes and muscle tone in contralateral limbs Sensation: contralateral facial hypoalgesia, hypoaesthesia on contralateral half body Seizures, hemi-neglect syndrom

Answer 38

Degenerative: canine cognitive dysfunction Anomalous: congenital malformation, hydrocephalus Metabolic: hepatic encephalopathy, renal encephalopathy, hyper and hyponatremia, hypoglycemia Neoplastic: extra or intra-axial neoplasia Inflammatory: meningoencephalitis of unknown origin, Toxoplasmosis, Neosporosis, FIP, FeLV) Trauma: traumatic brain injury, toxicity Vascular: Ischemic encephalopathy

Answer 39

1) CBC/Chem (including electrolytes Ca and Glucose 2) Liver function testing- Bile acid stimulation test and ammonia 3) +/- Endocrine function tests: fructosamine, insulin levels (insulioma) 4) +/- clotting function

Answer 40

1) Toxoplasma gondii 2) FIV 3) FeLV 4) Cryptococcus 5) Coccidioidomycosis

Answer 41

1) Cerebrovascular accident: to assess for an underlying cause (Cushings, Hypoproteinuria- PLN or hypertension) 2) Discospondylitis *- identify if UTI is underlying cause of infection 3) Paraparesis/ urinary dysfunction*- increased risk of UTI 4) Inborn errors of metabolism or storage disease- to assess for unusual metabolites

Answer 42

MRI - contrast required

Answer 43

1) Anesthesia 2) High cost 3) Limited availability 4) Artifacts (metal objects)

Answer 44

CSF analysis Limitations: May not be abnormal due to location (if parenchymal) or nature of lesion, can have non-specific changes, cell counts correlate with exfoliation into CSF not severity of disease

Answer 45

1) May not be abnormal due to location (if parenchymal) or nature of lesion (non-exfoliating) 2) can have non-specific changes, cell counts correlate with exfoliation into CSF not severity of disease

Answer 46

1) Increased intracranial pressure (mental status, pupil size and PLR, abnormal postures, vestibular eye movement) 2) Coagulopathy 3) Cervical (Cerebellomedullary cistern) collection contraindicated in some conditions (chiari-like malformation, AA instability, cervical trauma)

Answer 47

1 hour -differential count, cytology, protein +/- infectious disease testing

Answer 48

spinal needle, collection pots (sterile plain +/- EDTA, clippers, scrub, gloves)

Answer 49

1) Cerebellomedullary cistern 2) Lumbar cistern

Answer 50

1) Do no aspirate 2) Max volume of 1ml/5mg

Answer 51

Cerebellomedullary cistern (cistern magna)

Answer 52

cisterna magna

Answer 53

cisterna magna

Answer 54

L6-L7 (L5-L6 for larger dogs if no CSF obtained) - aim for subarachnoid space *can be more challenging to obtain CSF, more blood contamination but less risk

Answer 55

can falsely increase WBC count by 1/uL per 500 RBC protein by 1mg/dl per 1000 RBC

Answer 56

increased protein without increased WBC -Nonspecific -Extradural compression (disc compression), neoplasia, infection, vasculitis, trauma, syringomyelia, degenerative myelopathy

Answer 57

Extradural compression (disc compression) neoplasia infection vasculitis trauma syringomyelia degenerative myelopathy

Answer 58

albuminocytological dissociation

Answer 59

increased WBC in CSF

Answer 60

1) GME/ NE 2) bacterial meningitis/ meningoencephalitis 3) Fungal 4) FIP 5) Post myelography, hemorrhage, trauma, neoplasia 6) SRMA (no forebrain disease by CSF abnormalities)

Answer 61

1) GME, NE 2) CNS lymphoma 3) Viral (CDV) 4) Bacterial meningitis/ meningoencephalitis 5) SRMA (chronic)- CSF abnormalities but no forebrain disease

Answer 62

Infectious meingoencephalitis Penetrating cranial injuries Extension from otitis media/ interna *Culture of urine, blood or CSF is appropriate

Answer 63

Bacterial meningitis/ encephalitis Discospondylitis

Answer 64

Electroencephalography

Answer 65

Seizures Change in mentation Vestibular signs Circling *depends on the localization of the lesion

Answer 66

1) Meningioma (most common) 2) Glioma 3) Histiocytic sarcoma 4) Choroid plexus tumor 5) CNS lymphoma

Answer 67

1) Magnetic resonance imaging 2) Histopathology (brain biopsy or post mortem examination)

Answer 68

1) Palliative: Meningioma and glioma - prednisolone 0.25-0.5mg/kg BID initially tapering to the lowest effective dose Trilostane (pituitary) 2) Surgery 3) Radiotherapy

Answer 69

Canine Cognitive dysfunction

Answer 70

1) cerebrovascular disease 2) oxidative brain damage 3) Neuronal mitochondrial dysfunction 4) impaired neuronal glucose metabolism

Answer 71

*Slowly progressive -apparent confusion -anxiety -loss of sleep-wake style -decreased pet owner interaction Behaviors:compulsive wandering and pacing, excessive vocalization ,decreased interaction with family, attempting to pass through inappropriately narrow spaces, urinary +/- fecal incontinent, inability to recognize familar people or animals

Answer 72

Dogs >8 years old 14-35% of canine population Female and smaller dogs

Answer 73

signalment and clinical signs MRI food searching tasks

Answer 74

1) MCT diet/ diet high in carnitine, omega 3-PFA, carnitoids, Vitamin EandA (Purina neurocare or Hills b/d) 2) Selegiline (most show a positive response within the first month if they are going to improve) 3) Cognitive enrichment- new toys, regular and new walks 4) Levetiracetam (improved CNS mitochondrial function)

Answer 75

Levetiracetam

Answer 76

MCT diet/ diet high in carnitine, omega 3-PFA, carnitoids, Vitamin EandA (Purina neurocare or Hills b/d)

Answer 77

-Selegiline -Levetiracetam

Answer 78

hypernatremia

Answer 79

1) Hypovolemia- CKI, nonoliguric AKI, GI disease, burns, DM/ DKA 2) Normovolemia: Hypodypsia, fever, reduced access to water, DI 3) Hypervolemia: Hypertonic saline/ bicarbonate, hyperadrenocorticism, salt intoxication

Answer 80

1) CKI 2) Nonoliguric AKI 3) GI disease 4) Burns 5) DM/DKA

Answer 81

1) Hypodypsia 2) Fever 3) Reduced access to water 4) Diabetes insipidus

Answer 82

1) Hypertonic saline/ bicarbonate 2) Hyperadrenocorticism 3) Salt intoxication

Answer 83

*relatively rapid onset Acute: shrinkage of brain parenchyma, results in stretching and tearing of small intracranial vessels and hemorrhage Chronic (>2-3 days): Parenchyma will produce idiogenic osmoles to compensate for increased extracellular osmolarity

Answer 84

Anorexia Lethargy Vomiting Muscular weakness Behavioral change Disorientation Ataxia Seizures Coma Death

Answer 85

Hypernatremia

Answer 86

half strength or normal saline, 5% dextroses Water deficits = 0.6 x BW (kg) x [patient Na concentration / normal Na concentration] - 1) Acute: 5% dextrose Chronic: correct over 48-72 hours, should not be lowered faster than 0.5mEq/L/hr over rapid correction can lead to brain edema

Answer 87

Must be over 48-72 hours or else you can cause brain edema

Answer 88

1) Hypoadrenocorticism 2) Na losing nephropathy 3) GI fluid losses 4) Shock 5) Renal insufficiency

Answer 89

1) Hypotonic fluid admin 2) Hypothyroidism 3) Glucocorticoid insufficiency 4) Psycogenic polydipsia 5) SIADH (Syndrome of inappropriate antidiurectic secretion

Answer 90

1) Acute or chronic renal failure 2) Nephrotic syndrome 3) CHF 4) Hepatic cirrhosis 5) Accidental ingestion or injection of water

Answer 91

Acute: Osmotic gradient created, water will enter brain parenchyma cells- increasing their volume, brain edema Chronic (>2-3days): Parenchyma will actively extrude electrolytes and idiogenic osmoles

Answer 92

acute hyponatremia

Answer 93

-GI signs (nausea and vomiting) -Lethargy -Disorientation -Decreased reflexes -Seizures -Coma -Respiratory arrest

Answer 94

Sodum contain fluids - normal or hypertonic saline Na deficit= BW(kg) x 0.6 x (normal serum Na concentration - patient serum Na concentration) Acute: correct relatively quickly with normal saline Chronic: Correct slowly or you can cause cell dehydration and hemorrhage, axonal shrinkage and demyelination (Central myelinolysis)

Answer 95

Central Myelinolysis- axonal shrinkage and demyelination *cell dehydration and hemorrhage need to correct gradually over 48-72 hours should not be faster than 0.5mEq/L/hr monitor every 4 hours

Answer 96

axonal shrinkage and demyelination *cell dehydration and hemorrhage from not correcting chronic hyponatremia gradually

Answer 97

Grade 0: Asymptomatic Grade I: Mild decrease in mobility, apathy, or other Grade II: Severe apathy, mild ataxia Grade III: Combination of hypersalivation, severe ataxia, head pressing, circling, blindness Grade IV: Stupor/coma, seizures *bilaterally symmetrical

Answer 98

bilaterally and symmetrically

Answer 99

CBC: microcytosis Chem: ALT and ALP (possibly only mildy elevated in PSS) Hypoalbuminemia Hyperbilirubinemia Low urea Bile Acid Stimulation Test NH3 Abdominal Ultrasound (or CT) +/- liver biopsy

Answer 100

1) IV Fluids- restores euvolemia, reduce NH3 concentration - dilution and increases urinary excretion of both urea and NH3 2) Enemas: removes colonic contents and source of nitrogen from urease producing bacteria 3) Lactulose: favors production on NH4+ which are trapped in the colon 4) Diet: highly digestible, high biologic value protein source 5) Antibiotics- reduce number of urease producing bacteria (metronidazole or amoxicillin for 1-2 weeks) 6) Antiepileptic medication: levetiracetam

Answer 101

1) Hepatic dysfunction 2) Porto-systemic shunt *Acute liver disease is uncommon

Answer 102

Lethargy, ravenous appetite, anxiety weakness and tremors reduced vision and seizures

Answer 103

1) Severe liver disease 2) Portosystemic shunt 3) Insulinoma 4) Hypoadrenocorticism 5) sepsis 6) Pancreatic tumors 7) Glycogen storage dusease 8) Neoantal/ juvenile hypoglycemia 9) extreme exercise 10) malnutrition 11) insulin overdose 12) xylitol toxicity 13) oral hypoglycemics 14) beta blockers

Answer 104

low blood glucose check insulin at same time identify underlying cause

Answer 105

frequent feeding dextrose administration- care with insuloma

Answer 106

care dextrose administration with insulinoma

Answer 107

Microcytosis

Answer 108

ALP +ALP (mildly in PSS) Hypoalbuminemia Hyperbilirubinemia Low urea

Answer 109

hydrocephalus

Answer 110

Hydrocephalus: active dilation of ventricular system Ventriculomegaly: nonactive increase of ventricular system

Answer 111

1) Accumulation of CSF within the ventricular system (internal) 2) Accumulation of CSF within the subarachnoid space (external) 3) ObstructiveL Ventricular dilation due to a lesion causing obstruction of the CSF before it enters the subarachnoid space 4) Communicating: CSF in ventricular system communicates with the subarachnoid space 5) Due to loss of CNS parenchyma. CSF volume increases to take up the space formerly occupied by the lost parenchyma

Answer 112

toy breeds

Answer 113

-Domed shaped head and fontanelles -Obtundation, behavioral abnormalities -Difficulties in training -Decreased vision -Circling, pacing -Seizuring

Answer 114

1) MRI - periventircular hyperintensities to distinguish between ventriculomegaly and hydrocephalus 2) Ultrasound- identify large ventricles in presence of persistent fontanelle 3) CT- allows visualization of entire ventricular system - may allow identification of site of stenosis (cant tell hyperintensities)

Answer 115

Aimed at decreasing CSF production - can improve signs in short term but not effective long term 1) Glucocorticoids 2) Furosemide 3) Omeprazole 4) Acetazolamide Surgically - but can have blockage, pain, infection, mechanical failure, overshunting, or kinking

Answer 116

1) Glucocorticoids 2) Furosemide 3) Omeprazole 4) Acetazolamide

Answer 117

2 or more unprovoked seizures in >24 hours

Answer 118

behavior change circling head turn to the side of lesion loss of vision on opposite side

Answer 119

either excessive excitation or decreased inhibition glutamate - excitatory GABA- inhibitory neurons become hypersynchronized leading to a seizure

Answer 120

Prodome / Pre-ictal stage

Answer 121

Post-ictal

Answer 122

1) Pre-ictal/ prodrome 2) Aura 3) Ictal 4) Post-ictal

Answer 123

60-90 seconds peracute in onset

Answer 124

sleep or rest- seizure threshold decreases during sleep due to hypersynchrony of sleep facilitating the initiation and propagation of seizures in the parietal and occipital lobe

Answer 125

1) Generalized - both cerebral hemispheres and therefore both sides of the body - can occur alone or evolve from a focal seizure 2) Focal - lateralized or regional signs. consciousness often unimpaired. can be motor, autonomic, or behavioral.

Answer 126

Generalized seizures

Answer 127

sustained increase in muscle contraction lasting a few seconds to minutes

Answer 128

sudden, brief, involuntary contraction of a muscle or group of muscles

Answer 129

regularly repetitive myoclonus, involving the same muscle groups at a frequency of 2-3 seconds

Answer 130

sudden loss of muscle tone

Answer 131

tonic-clonic activity a sequence of movements- a tonic (sustaicned increase in muscle contraction) followed by a clonic phase (regularly repetive myoclonus, involving the same muscle groups at a frequency of 2-3 seconds

Answer 132

cats- smaller body size, able to move limbs more dramatically

Answer 133

when there is initial activation of one part of one cerebral hemisphere or region in the forebrain

Answer 134

a focal seizure where consciousness is impaired (typically focal seizures do not impair consciousness)

Answer 135

1) Motor (most common) 2) Autonomic - eg. hypersalivation 3) Behavioral

Answer 136

A seizure that is a reflex to environmental stimuli occurs in cats (late onset- 15 years) Myoclonic seizures progressing to generalized tonic-clonic seizures in some Levetiracetam to control

Answer 137

Levetiracetam

Answer 138

myoclonic seizures progressing to generalized tonic-clonic seizures

Answer 139

Narcolepsy/ cataplexy Neuromuscular collapse Syncope Movement disorder Metabolic Disorder Vestibular Disease

Answer 140

Doberman English bull dogs Boxers (ancedotally)

Answer 141

head tremors that is idiopathic. patients will stop tremoring head when you get their attention. remain conscious common in Doberman, English bulldog, and boxer

Answer 142

Paroxysmal hypertonicity found in the CKCS due to genetic abnormality remains conscious throughout can be tx with acetazolamide or benzo

Answer 143

CKCS Paroxysmal hypertonicity found in the CKCS due to genetic abnormality remains conscious throughout can be tx with acetazolamide or benzo

Answer 144

paroxysmal gluten sensitive dyskinesia that occurs in the border terrier (Canine Epileptoid Cramping) respond to a gluten free diet

Answer 145

Border terrier

Answer 146

gluten free diet often caused by a gluten sensitive dyskinesia

Answer 147

1) Reactive seizures- occurring as a natural response from the normal brain to a transient disturbance in function. concurrent neurological signs usually present Metabolic or toxic 2) Structural epilepsy- provoked by intracranial or cerebral patholgoy. concurrent neurological signs usually present. can be inflammatory, neoplastic, or traumatic 3) Idiopathic epilepsy- genetic or presumed genetic in origin. No inter-ictal neurologic signs

Answer 148

Reactive Seizures

Answer 149

Structural epilepsy

Answer 150

Idiopathic epilepsy

Answer 151

1) 2 or more seizures (24 hours apart) 2) Age of onset 6m to 6 years 3) Normal inter-ictal examination 4) No clinically significant abnormalities on minimum database, 5) Family history of IE Tier II Confidence 6) Unremarkable fasting and post-prandial bile acids 7) MRI of brain 8) CSF analysis Tier III Confidence 9) Ictal or inter-ictal EEG abnormalities

Answer 152

1) Age onset <6 months or >6 years 2) Interictal neurological abnormalities consistent with intracranial neurolocalization 3) Status epilepticus or cluster seizure 4) Previous presumptive diagnosis of IE and drug-resistance with a single AED titrated to the highest tolerable dose

Answer 153

1) Lagotto Romagnolo 2) Belgian Shepherd 3) Boerboels

Answer 154

1) Structural epilepsy or reactive seizures 2) Status epilepticus or cluster seizures 3) 2 or more seizures in a 6 month period 4) Post-ictal signs are severe and last longer than 24 hours

Answer 155

False- but drugs are used to symptomatically suppress epileptic seizures Primidone is only approved but not as affected as phenobarbital

Answer 156

Primidone not as affective as Phenobarbitone (no drugs licenced in cats)

Answer 157

1) General health of the patient 2) owners lifestyle 3) Financial limitations 4) Owner compliance with the therapeutic regimen

Answer 158

augments the inhibitory effect of GABA prolongs the chloride channel opening at GABAa receptor allows GABA to work for longer times to stop seizures

Answer 159

Initial side effects, which subside in 2-3 weeks: PU/PD, PP, ataxia) Side effects: sedation, ataxia, PU/PD. polyphagia, hepatotoxicity, hemological abnormalities (neutropenia, anemia, thrombocytopenia)

Answer 160

1) 2-3 weeks after any dose change (plain serum) 2) 6 weeks (including CBC, Chem, and ideally BAS) 3) 6 months (including CBC, Chem, and ideally BAS)

Answer 161

1) Hepatotoxicity 2) Increases metabolism of itself over time, decreasing its levels 3) Hemotological abnormalities (neutropenia, thrombocytopenia, anemia)

Answer 162

25-35ug/ml (can be effective as low as 15ug/ml)

Answer 163

Potent inducer of cytochrome P450 enzymes activity which increases ROS generation and risk of hepatic injury metabolized via hepatic microsomal enzymes- ALP and ALT elevations without hepatoxicity are common

Answer 164

via hepatic microsomal enzymes- ALP and ALT elevations without hepatoxicity are common

Answer 165

dogs with hepatic dysfunction

Answer 166

cytochrome P450 enzymes activity which increases ROS generation and risk of hepatic injury and accelerated clearing of itself over time

Answer 167

Potassium Bromide (KBr)

Answer 168

Competes with Cl- transport across nerve cell membranes and inhbits Na+ transport leading to membrane hyperpolarization which raises the seizure threshold

Answer 169

Bromide (Br)

Answer 170

Eosinophilic bronchitis

Answer 171

consistent diet

Answer 172

1) 12 weeks- when steady state is reached, use plain serum (include CBC, chem) 2) 6 months (including CBC, chem)

Answer 173

Patients with renal disease excreted unchanged in urine and undergoes tubular reabsorption in competition with chloride

Answer 174

unknown MOA

Answer 175

Levetiracetam (Keppra)

Answer 176

Those with kidney disease (renal excretion)

Answer 177

blocks propagation of epileptic discharges

Answer 178

Zomisamide

Answer 179

Imepitoin (Pexion)

Answer 180

FIP FIV FeLV Toxoplasmosis

Answer 181

1) Meningioma 2) Lymphoma 3) Glioma

Answer 182

we do not think that it has the same genetic basis as with dogs (called epilepsy of unknown cause)

Answer 183

Hippocampal necrosis up to 30% of cats which seizure -Clusters and complex focal seizures- hypersalivation and lipsmacking

Answer 184

1-5 years of age seizures last 1-3 minutes

Answer 185

Hypoglycemia Hepatic encephalopathy Intoxication

Answer 186

can occur in up to 30% of cats which seizure clusters and complex focal seizures that present with hypersalivation and lipsmacking

Answer 187

fulminant hepatic necrosis

Answer 188

Heinz Body anemia

Answer 189

lower starting (2mg/kg) and loading (12-15mg/kg) in cats because less likely to get sedation

Answer 190

eosinophilic bronchitis

Answer 191

less likely to achieve remission Decreased survival time more likely to be euthanized

Answer 192

2 or more seizures within 24 hours

Answer 193

Seizures lasting >5 minutes >2 seizures without full recovery

Answer 194

1) Cluster seizure: 2 or more within 24 hours 2) Status Epilepticus: Seizure lasting >5 minute or >2 seizures without full recovery *Irreversible neuronal damage occurs after 30-60 minutes

Answer 195

1) Seizure lasting >5 minutes or 2) >2 seizures without full recovery

Answer 196

it can occur after 30-60 minutes due to failure of mechanisms that usually stop an isolated seizure (abnormal excessive excitation or ineffective inhibition) -Excessive glutamate release -Excitotoxic cell injury

Answer 197

1) Stage 1: Increased autonomic activity- tachycardia, hypertension, hyperglycemia 2) Stage 2: Irreversible neuronal damage (after 30 minutes)- hypotension, hypoglycemia, hyperthermia, hypoxia

Answer 198

tachycardia hypertension hyperglycemia

Answer 199

hypotension hypoglycemia hyperthermia hypoxia

Answer 200

1) Idiopathic epilepsy 2) Toxicity 3) Metabolic disease 4) Neoplasia 5) CNS inflammatory disease 6) Trauma

Answer 201

STOP THE SEIZURE 1) Diazepam 1-2mg/kg per rectum (0.5mg/kg IV) 2) Midazolam 0.2mg/kg intranasalaly -GET the history

Answer 202

-When, how many -Before, during and after -Autonomic signs -Other abnormalities -Any pre-existing disease -Medication -Access to toxins

Answer 203

IV catheter placement Examination Baseline blood work- minimum: GLucose, sodium, calcium, PCV, Hepatic +/- renal function In existing epileptics: Serum levels of antiepileptic drugs

Answer 204

1) Phenobarbital 2.5mg/kg q12h 2) If clusters of status (or futher seizure activity over the next few hours: Phenobarbital IV loading 3) If further seizures - Levetiracetam loading (60mg/kg)

Answer 205

1) Diazepam- interacts with plastic and light 2) Midazolam - not in hepatic dysfunctions, dogs in SE may become refractory 3) Propofol- 6mg/kg IV bolus followed by 6mg/kg/h care heinz body anemia in cats , use preservative free formation

Answer 206

1) Hepatic dysfunction 2) Dogs in status epilepticus may become refractory

Answer 207

CARE- heinz body anemia use preservative free formation

Answer 208

1) Heart rate and respiratory rate 2) Blood pressure (systolic >90mmHg (MAP 70-80mmHg) 3) urine production 1-2 ml/kg/hr 4) Oxygenation/ventilation- pulse oximetry >95%; end tidal CO2 35-40mmHg 5) Temperature 6) Neurological examination- allow assessment for signs of improvement or eterioration 7) If on infusion assess pharyngeal tone- if risk of aspiration- intubate

Answer 209

1) Altered GABA A receptor subunit expression 2) NMDA receptor activation is the major mediator of excitotoxicity - increased calcium entry into cells, increased duration of status in rodents *Need NMDA receptor antagonist (ketamine) to stop maintenance phase and neuroprotective

Answer 210

There is altered GABA A receptor subunit expression and NMDA receotir activator is major mediator of excitotoxicity Ketamine is an NMDA receptor antagonist to stop the maintenance phase alongside dexmedetomidine

Answer 211

other AEDs

Answer 212

Sympathetic nervous system 1) Thoracolumbar region (Hypogastric nerve) 2) Somatic component- Pudendal nerve

Answer 213

1) Hypogastric nerve (thoracolumbar region) 2) Pudendal nerve (somatic)

Answer 214

Parasympathetic system Cranial-sacral region - Pelvic nerve

Answer 215

Micturition - cranial sacral region

Answer 216

B-receptor: Stimulation relaxes muscle to store urine a- receptor: Stimulation constricts internal urethral sphincter (smooth muscle) *Promotes storage of urine)

Answer 217

ACh receptor 1) Sensory and motor to the external urethral sphincter 2) Stimulation constricts external urethral sphincter *Promotes storage of the urine

Answer 218

Constriction

Answer 219

relaxation of detrusor constriction of the internal urethral sphincter

Answer 220

contract the detrusor to evacuate urine *Sensory branch to complete an emptying reflex arch

Answer 221

to complete an empyting reflex arch and prevent over contraction of detrusor

Answer 222

1) Pudendal nerve (somatic) leads to contraction of external sphincter muscle 2) Hypogastric nerve (L1-L4) via a receptor contracts internal sphincter muscle 3) Inhibition of pelvic nerve to detrusor muscle to allow relaxation 4) As bladder fills, pressure stimulates pelvic nerve sensory fibers which relay to B-receptors to relax further 5) Brain stem micturition centers facilate and modulate these activityes

Answer 223

1) Pelvic nerve sends sensory info up the brain stem, cerebellum, cerebrum 2) Activation of micturition via UMN pathways in pons and medulla; descends via spinal cord 3) Inhibition of L1-L4 sympatheics (B receptors on detrusor, a receptors on internal sphincter muscle 4) Inhibition of pudendal n to relax external sphincter 5) Facilitation of pelvic nerve to contract detrusor m *Part of coordination of these nerves is mediated reflexively within the sacral segments and from sacral to lumbar segments -> reflex bladder contractions

Answer 224

1) Brainstem: Loss of communication/coordination with micturition center 2) Spinal cord: loss of communication or coordination with micturition center or specific nerves based on lesion location 3) Cauda equina: Pelvic or pudendal nerve damage 4) Cerebral or cerebellar disease (rare)- loss of comm with micturition, loss of voluntary control 5) Neuromuscular disease- dysautonomia, other peripheral nerve, detrusor muscle, or NMJ effects (rare) 6) Detrusor-urethral dyssnergia: lack of coordination between detrusor contraction and urethral relaxation

Answer 225

Detrusor-urethral dyssnergia

Answer 226

a form of neurogenic bladder dysfunction where there is a lack of coordination between detrusor contraction and urethral relaxation

Answer 227

1) Primary bladder pathology: a) Myopathic bladder disease- Detrusor atony or bladder rupture b) Mechanical outflow obstruction (Urolithiasis, neoplasia/polyps, prostatic disease, urethral stricture, extraluminal compression 2) Behavioral, environmental a) Pain upon urination b) Hospitalized cats or dogs unwilling to urinate c) Posture- orthopedic or neurologic disease 3) Pharmacologic effects: opiates, antidepressants, anticholingers

Answer 228

a) Myopathic bladder disease- Detrusor atony or bladder rupture b) Mechanical outflow obstruction (Urolithiasis, neoplasia/polyps, prostatic disease, urethral stricture, extraluminal compression

Answer 229

a) Pain upon urination b) Hospitalized cats or dogs unwilling to urinate c) Posture- orthopedic or neurologic disease

Answer 230

1) Opiates 2) Antidepressants 3) Anticholinergics

Answer 231

it is likely compromised to a similar degree in the muscles of the lower urinary tract

Answer 232

LMN: decreased to absent UMN: Normal to increased- can account for overflow

Answer 233

LMN: Hypotonic, flaccid bladder UMN: Normal to hypertonic/spastic firm bladder

Answer 234

LMN: very easy UMN: can be difficult

Answer 235

These are all LMN signs leading to the inability to contract the detrusor muscle and dribbling due to inability to constrict sphincters *L4-S3 spinal lesion

Answer 236

Hypotonicity of pelvic and pudendal nerve leading to decreased external urethral sphincter tone and decreased detrusor strength 1) Inability to contract detrusor muscle 2) Dribbling due to inability to constrict sphincters

Answer 237

Hypertonicity caudal to lesion leading to increased external urethral sphincter tone and increased resting tone to the detrusor muscle 1) Loss of higher level coordination of detrusor/sphincter 2) Detrusor cannot overcome resistance from external urethral sphincter

Answer 238

1) Loss of nerve function leading to poor detrusor contraction and poor internal sphincter control 2) Intact central integration- aware bladder is full and attempts to urinate *Stanguria, dysuria, with large residual volume

Answer 239

1) Bacterial infection/ cystitis from residual volume remaining, (higher incidence of IVDD dogs) 2) Urine scald from overflow dribbling or reflex contractions 3) Bladder atony- from prolonged distension (>24-48 hours) 4) Bladder rupture- uncoommon with functional problems and more of concern with mechanical obstruction (or during expression)

Answer 240

Where there is stretch injury to the detrusor muscle leading to the detrusor muscle cells not functioning dysfunction due to 1) inability to contract detrusor 2) May have some overflow dribbling from prolonged distension >24-48 hours

Answer 241

when the bladder is distended to the point of overstretching the muscle UMN dysfunction: protective mechanism local reflex arc to release small amounts of urine LMN dysfunction: tone of sphincters is reduced leaving an open pathway for urine to leak out (Not over-distension but may indicate incomplete emptying which can lead to UTI and continuous leaking can lead to severe urine scalding and cutaneous infections)

Answer 242

Shortterm: Prevent infections, detrusor atony, and urine scald Longterm: Treat underlying cause of dysfunction and improve function

Answer 243

1) Evacuate bladder 2-4 times a day via manual expression or catherization (intermittent or indwelling) 2) Skin care: keep skin clean and dry, frequent baths, baby powder, ointments to protect skin, absorbent bedding

Answer 244

Pros: inexpensive, can be performed by some owners Cons: Usually only evacuate 50% of volume, stressful for patient, abdominal soreness, risk for bladder rupture

Answer 245

Pros: Able to completely empty bladder, less likely to induce infection than with indwelling Cons: Cost/labor intensive, irritation to bladder and urethral walls, difficult to perform by some owners

Answer 246

Pros: able to completely empty bladder, less laborious, less irritation to urinary tract than intermittent, less stressful to patient Cons: Cost, infections more common, avoid while patient on antibiotics, irritation to bladder and urethral walls, can only be maintained in hospital

Answer 247

a-antagonist: Phenoxybenzamine, Prazosin Striated muscle relaxants: Valium Parasympathomimetics (ACh stim)- Bethanecol A-agonist: PPA, estrogen

Answer 248

a-antagonists like Phenoxybenzamine or Prazosin to block the alpha mediated constriction of the internal sphincter

Answer 249

a-antagonists like Phenoxybenzamine or Prazosin

Answer 250

alpha antagonist used to relax internal urethral sphincter 48-72 hour onset activity

Answer 251

Prazosin has short onset of activity Phenoxybenzamine (48-72 hours to onset of activity)

Answer 252

alpha-antagonist used to relax internal urethral sphincter

Answer 253

Internal: Phenoxybenzamine, Prazosin External: Diazepam- striated muscle relaxation (short duration)

Answer 254

Diazepam (Valium)

Answer 255

Parasympathomimetics (ACh) like Bethanechol to promote voiding by contraction of the detrusor and relaxation of trigone and sphincter

Answer 256

pelvic nerve

Answer 257

pudendal nerve

Answer 258

a parasympathomimetic drug used to treat urinary retention when obstruction is absent stimulates detrusor contraction short onset of activity Also stimulates contraction of external urethral sphincter

Answer 259

contraction of the detrusor and external urethral sphincter muscle

Answer 260

These patients are easily expressed Do they need medications?

Answer 261

Not typically with neurogenic dysfunction could be used in LMN dysfunction to increase internal sphincter need to be cautious about outflow

Answer 262

No- can occur after 24-48 hours after overdistention

Answer 263

contralateral limbs

Answer 264

Contralateral blindness and decreased/absent menace

Answer 265

CN III- XII affected

Answer 266

deficits in all 4 or ipsilateral limbs

Answer 267

tetraparesis/ paralysis ipsilateral hemiparesis/ paralysis possibly opistotonus or decerebrate rigidity

Answer 268

1) Intention tremor - head and eyes 2) Hypermetria, truncal ataxia, broad stance 3) possible decerebellate rigidity

Answer 269

delated initiation then exaggerated dysmetric response

Answer 270

ipsilateral to the lesion

Answer 271

cerebellum lesion where there is head tilt and circling contralaterally to the lesion dysmetria, head tremor, truncal sway postural deficits ipsilateral to lesion but contralateral to the head tilt

Answer 272

1) Neoplastic* - primary extra or intraaxial, or secondary 2) Infectious * Meningoencephalitis of unknown origin, Rabies, distemper, toxoplasma, neospora, FIP, bacterial 3) Traumatic brain injury

Answer 273

diffuse and symmetrical

Answer 274

idiopathic, noninfectious CNS diseases Immune mediated, possibly genetic predisposition 1) Granulomatous meningoencephalitis (GME) 2) Necrotising meningoencephalitis (NME) 3) Necrotising leukoencephalitis (NLE)

Answer 275

1) Granulomatous meningoencephalitis (GME) 2) Necrotising meningoencephalitis (NME) 3) Necrotising leukoencephalitis (NLE)

Answer 276

Toy and terrier breeds 4-8 years of age

Answer 277

Pugs, YT, maltese, chihuahuua <4 years of age

Answer 278

Pugs, YT, maltese, chihuahuua <4 years of age

Answer 279

1) MRI- can help determine the type, based on location and 2) CSF 3) Brain biopsy- used to definitive diagnosis

Answer 280

forebrain, brainstem, cerebellum grey and white matter

Answer 281

asymmetrical, multifocal, forebrain loss grey/white matter definition

Answer 282

asymmetrical cerebral white matter and brainstem

Answer 283

Combination of immunosuppressive treatment -Prednisolone +/- immunosuppressive medication (Cytarabine or Cyclosporin) -Add in symptomatic treatment (e.g anticonvulsants)

Answer 284

Cytarabine or Cyclosporin

Answer 285

abnormal CSF at 3 months post treatment

Answer 286

False -CSF is predictive of relapse

Answer 287

Grave 25-33% die within 1 week of diagnosis and median survival of 26 days but if they live 3months after, they have very low risk of death due to MUO lower life if seizuires, alterned mentation, or foramen magnum herniation

Answer 288

False- does not typically cause intracranial signs only neck pain

Answer 289

6-18 year old dogs Goldens, Bernese, Wirehaired pointers, Boxer, Beagle (Beagle Pain Syndrome)

Answer 290

Acute: Pyrexia, Lethargy, neck pain, neurological examination is WNL Chronic: unusual - repeated episodes of neck pain, neurological examination can be abnormal C1-T2, +/- pyrexia and lethargy

Answer 291

abnormal C1-T2

Answer 292

1) MRI 2) CSF- neutrophilic pleocytosis 3) Infectious disease testing 4) Consider spinal radiographs to rule out AA sublux, trauma, discospondylitis +/- thoracic and abdominal imaging, echocardiography

Answer 293

1) 4-6 months of slowly tapering steroids 2) analgesia (typically for 1 week)

Answer 294

neutrophilic pleocytosis

Answer 295

rule out AA sublux, trauma, discospondylitis

Answer 296

lymphoma - diagnosis based on MRI changes CSF has low sensitivity for identification of lymphoblasts

Answer 297

False- low sensitivity for identification of lymphoblasts Diagnosis is based on MRI changes but can look like MUO

Answer 298

1) Hemangiosarcoma 2) Lymphoma 3) Carcinoma - prostatic, mammary 4) Malignant melanoma

Answer 299

Dry form* Immune mediated vasculitis causing vasogenic edema, hemorrhage, and thrombosis predilection for brainstem, 4th ventricle, and spinal cord

Answer 300

1) Brainstem 2) 4th ventricle 3) Spinal cord

Answer 301

Feline Infectious Peritonitis (FIP)

Answer 302

<2 years old (often ~8months) but occasionally seen in older

Answer 303

Localization T3-L3 myelopathy, central vestibular syndrome and multifocal CNS -Paraparesis -Nystagmus -Seizures

Answer 304

Localization T3-L3 myelopathy, central vestibular syndrome and multifocal CNS (commonly brainstem, 4th ventricle, spinal cord)

Answer 305

Difficult to diagnose as dry form (no ascites) 1) CSF PCR/ serum titers of FCoV (titers of 1:640 or higher may indicate FIP) 2) Signalment, history 3) MRI 4) Histopath

Answer 306

1) Remdesivir 2) Antiviral nucleoside analogue GS-441524 for 12 weeks (neurological require higher doses) - Not FDA approved 3) Corticosteroids may help reduce inflammation and edema 4) Symptomatic/supportive care

Answer 307

grave to poor depends on treatment available and response to treatment

Answer 308

Neospora Meningoencephalomyelitis

Answer 309

paresis/paralysis head tilt head tremors seizures

Answer 310

MRI CSF PCR Serum antibody titres Increased CK and AST (given muscle changes)

Answer 311

1) Clindamycin /TMPS +Pyrimethamine 2) Anti-inflammatory corticosteroids to reduce associated inflammation 3) Symptomatic treatment 4) PT if muscle involvement

Answer 312

before anyone handles the patient, obtain an accurate vaccine history 1) Ask specifically when vaccines were given 2) Any neurological signs in an unvaccinated patient should be considered a rabies suspect (typically ascending LMN signs)

Answer 313

1) Inoculation of muscle via bite wound 2) Infects nerve endings 3) Retrograde transport up nerves (without a viremic phase) 4) Ascends spinal cord to brain 5) Spreads down CN VII, IX, to salivary glands 6) Destroys LMNs along pathway of ascent =ascending LMN paresis *Nonsuppurative polioencephalomyelitis and craniospinal neuritis

Answer 314

because it destroys the LMNs along pathway of ascent

Answer 315

Dogs and cat: 3 weeks to 6 months Humans: 3 weeks to several years

Answer 316

10 days (usually die within 20 days of shedding virus)

Answer 317

Prodromal stage (2-3 days): behavior change, fever, pruritis at site of exposure then progresses to either -Furious form: forebrain dysfunction, hyperesthesia, photophobia, seizures, aggression, if doesnt die from seizures then can progress to dumb stage -Dumb form: ascending LMN paralysis, limbs +/- cranial nerve LMN signs, dropped jaw, choking, dysphagia, dyspnea (CN V, IX-XII)

Answer 318

Prodromal stage (lasts 2-3 days)

Answer 319

Furious form

Answer 320

Must remove brain to submit for testing 1) Intracytoplasmic neuronal inclusion bodies (Negri bodies) 2) Positive immunohistochemistry and PCR *Protection when removing head- can be spread via aerosol

Answer 321

Negri bodies

Answer 322

1) Young dogs (Polioencephalomyelopathy) non-inflammatory grey matter disease Forebrain signs: seizures, myoclonus 2) Mature dogs (>1 year) Leukoencephalomyelopathy inflammatory demyelinating disease of white matter brainstem, cerebellum, and spinal cord with central vestibular/cerebellar +/- spinal cord signs

Answer 323

leukoencephalomyelopathy inflammatory demyelinating disease of white matter brainstem, cerebellum, and spinal cord with central vestibular/cerebellar +/- spinal cord signs

Answer 324

polioencephalomyelopathy non-inflammatory grey matter disease Forebrain signs: seizures, myoclonus

Answer 325

-History/clinical signs -Viral inclusion bodies of skin and brain biopsy -PCR -CSF cytology: elevated protein and mononuclear pleocytosis -Titers mainstay of diagnosis: IgG and IgM

Answer 326

Unvaccinated and unexposed

Answer 327

Previous vaccination

Answer 328

Recent vaccine or recent infection

Answer 329

Active CNS infection

Answer 330

Recent vaccination

Answer 331

An elevated CSF IgG means that there is an active CNS infection *false + if there is blood contamination *

Answer 332

Steroids- may reduce inflammation and can also reduce viral clearance No definitive treatment other than symptomatic or supportive treatment

Answer 333

Poor few cases stabilize and recover

Answer 334

1) Hematogenous 2) Direct invasion- inner ear, eyes, nasal sinus, osteomyelitis, trauma 3) CSF

Answer 335

usually acute CNS signs -obtundation and CN deficits are most common neck pain (~30%) pyrexia (~50%)

Answer 336

1) MRI 2) CSF analysis- increased protein concentration and pleocytosis, bacteria 3) CSF/ blood culture positive 15-30%

Answer 337

increased protein concentration and pleocytosis, bacteria

Answer 338

antibiotics +/- surgical drainage guarded prognosis

Answer 339

Diffuse and symmetrical

Answer 340

organophosphates pyrethrin lead ivermectin metaldehyde tremorgenic mycotoxins medications (antidepressants, amphetamines, metronidazole

Answer 341

depend on type of toxin approx 40% all reactive seizures due to toxins often GI, CV, or respiratory signs muscle tremors and fasciculations often seen

Answer 342

progressive increases in intracranial pressure

Answer 343

traumatic brain injury (TBI)

Answer 344

It can be from either or both (hemorrhage secondary to skull fracture

Answer 345

Primary: occurs at the time of the traumatic incident leading to direct mechanical damage Secondary: Occurs in minutes to days following trauma, leading to biochemical changes - what we treat as these factors contribute to rising ICP

Answer 346

Primary brain injury

Answer 347

Secondary brain injury

Answer 348

it is a common and potentially deadly development of TBI pressure exerted within the skull by intracranial components

Answer 349

Cerebral Perfusion Pressure (CPP)

Answer 350

CPP = MAP - ICP If ICP increases, you are going to have a rise in MAP to combat that

Answer 351

Cerebral blood flow (CBF)

Answer 352

fluctuations in CVR to compensate for changes in CPP

Answer 353

True 1) chemical factors- PaO2, PaCO2, nitric oxide 2) myogenic factors 3) Neurogenic factors- parasympathetic vs sympathetic

Answer 354

Increase PaO2: vasoconstriction Decrease PaO2: vasodilation

Answer 355

Increase PaCO2: vasodilation Decrease PaCO2: vasoconstriction

Answer 356

Increases in nitric oxide cause vasodilation and increased delivery of blood

Answer 357

50-150mmHg

Answer 358

Cerebral perfusion pressure

Answer 359

keeps CBF constant over a MAP range (50-150 mmHg)

Answer 360

Brain parenchyma CSF arterial and venous blood Fixed calvarial volume

Answer 361

Intracranial compliance (Monroe Kelly Doctorine)

Answer 362

functional and intact blood brain barrier trauma disrupts autoregulation and affects CPP

Answer 363

Cushing Reflex

Answer 364

1) Raised ICP 2) Reduced CPP 3) reduced CBF 4) Raised PaCO2 (makes ICP worse) 5) Medullary Vasomotor center initiates sympathetic stimulation 6) Arterial hypertension detected by carotid baroreceptor 7) Vagal stimulation leading to bradycardia

Answer 365

1) foramen magnum herniation 2) Rostral transtentorial herniation 3) Caudal transtentorial herniation 4) Transcalvarial/ herniation through a calvarial defect (fontanelle, fracture) 5) Subfalcine herniation

Answer 366

after 72 hours swelling will stabilize and begin to resolve over time

Answer 367

after 72 hours swelling will begin to resolve if you can get patients past the 72 hour mark, they will get better

Answer 368

Resuscitate and re-evaluate* -ABCs (airway, breathing, cardiovascular) -Quick assessment tests- PCV, total solids, Azostix, Blood glucose -AFAST/TFAST -Immediate assessment for hypo/hyperthermia, hypovolemic shock, hypoxemia (PaO2 <90mmHg) and hypotension (sysBP <120 mmHg) -Modified Glasgow Coma Score

Answer 369

used to evaluate patient's motor activity, brainstem reflexes, and level of consciousness helps with prognosis

Answer 370

Assess for extent of injuries -Nervous system (vertebral fractures/luxations, etc) -Other body functions Complete physical assessment- neuro and orthopedic Additional blood work Radiographs Imagin?

Answer 371

False- should not be used in when to decide when yo euthanize a patient

Answer 372

-Tachycardia (early) -Bradycardia (later) -Ventricular arrhythmias- catecholamine release (if CPP is extremely low) resulting in myocardial ischemia -Abnormal respiratory rate and/or pattern -Deteriorating neurologic function -Cushing reflex - bradycardia (<60bpm) in face of systemic hypertension (>250mmHg)

Answer 373

HR: <60bpm Systemic Hypertension >250mmHg

Answer 374

No- this reflex is helping them. if you bring down the blood pressure they will suffer the consequence

Answer 375

It needs to be at a 30-45 degree angle *Maximizes venous return without impairment of arterial flow to brain Decreases ICP *Avoid jugular compression - which inhibits venous return from the brain and increases ICP further

Answer 376

30-45 degree angle Maximizes venous return without impairment of arterial flow to brain Decreases ICP

Answer 377

it inhibits venous return from the brain and increases ICP further

Answer 378

fluid resuscitation maintain MAP 80-120mmHg to ensure CPP >60mmHg Avoid overhydration- which can exacerbate cerebral edema

Answer 379

Yes- do not volume limit fluids to victims of severe head trauma

Answer 380

PaO2 >90mmHg PaCO2 >30mmHg

Answer 381

CONSCIOUS 1) facemask- used temporarily; tend to stress patients 2) Oxygen cage/hood: generally ineffective; get rapidly depleted when opened, these patients need close observation 3) Nasal cannula or oxygen catheter (flow rate 100ml/kg/min) is preferred- apply lidocaine to avoid patient sneezing during placement- valsalva maneuvers can increase ICP 4) Transtracheal oxygen cather- 50ml/kg/min UNCONSCIOUS 1) Intubate and ventilation 2) Mechnical ventilation +/- tracheostomy tube

Answer 382

Nasal cannula or oxygen catheter (flow rate 100ml/kg/min) is preferred- apply lidocaine to avoid patient sneezing during placement- valsalva maneuvers can increase ICP

Answer 383

Apply lidocaine *Valsalva maneuvers can increase ICP

Answer 384

100 ml/kg/min

Answer 385

1) Increases intravascular osmolality; result in osmotic shift of edema fluid (intracellular) into intravascular space 2) Decreases blood viscosity and reflex vasoconstriction 3) Free-radical scavening 4) Reduction in CSF production

Answer 386

Contraindication: 1) Hypovolemia 2) Electrolyte abnormalities 3) Use caution in renal failure/insufficiency or heart failure Some concerns over reverse osmotic shift, dehydration, and AKI due to renal vasoconstriction but if given appropriately this is unlikely

Answer 387

Patients with renal failure/insufficiency or Heart failure

Answer 388

Reserved for severe head trauma patient 1) MGCS <8 2) Deteriorating neurologic patient 3) Failing to respond to other treatment 4) Positive initial response to initial mannitol dose

Answer 389

to avoid reverse osmotic shift, AKI, etc Reserved for hemodynamically stable patient

Answer 390

Improved hemodynamic status via volume expansion and positive inotrope effects Contraindications: significant sodium derangements (hyponatremia) and dehydration

Answer 391

1) significant sodium derangements (esp hyponatremia) 2) dehydration

Answer 392

Increases osmotic gradient across BBB Volume expansion Increases cardiac output and blood pressure

Answer 393

you can minimize adverse effects like respiratory depression and breakthrough pain allows for better control and titration of effect Options: opiates, gabapentin, NMDA antagonists and injectable NSAIDs

Answer 394

False- they are detrimental

Answer 395

may exacerbate hyperglycemia which promotes anaerobic glycolysis and increases lactic acid concentration and increases secondary injury effects *Doesnt increase true perfusion on does vasodilation

Answer 396

surgical removal of bone to reduce ICP by enlarging cranial vault

Answer 397

May help to decrease ICP by lowering CO2 (vasoconstriction) Maintain PaCO2 between 30-35mmHg to decrease CBF and ischemia Not practical in a non-anesthetized non-intubated patient

Answer 398

may be indicated in most severe cases of head trauma, refractory to other therapies used in hemodynamically stable patients

Answer 399

False- it is thought to decrease ICP however prognosis declined during rewarming phase * do not actively warm patient who are hypothermic but no not actively cool them

Answer 400

Level of consciousness Presence or absence of brain stem reflexes Age and general physical status Presence and extent of other concurrent injuries

Answer 401

the trend in the first 48 hours is more valuable than an isolated neurological evaluation Almost linear relationship between socre and probability of survival within the first 48 hours High score = high probability of survival Low score = unlikely to survive MGCS of >8 is associated with 50% chance of survival

Answer 402

Hyperglycemia

Answer 403

Coagulopathies- DIC Pneumonia Fluid /electrolyte abnormalities (CDI) sepsis seizures (intraparenchymal hemorrhage if around time of trauma or if months to years after trauma= development of glial scar seizure focus

Answer 404

1) Cerebellar ataxia (cerebllum) 2) Vestibular ataxia (vestibular system) 3) General proprioceptive (GP) ataxia (caudal brainstem and spinal cord)

Answer 405

Dysmetria (hypermetria, hypometria) Rate: Onset of voluntary movement (protraction) is delayed followed by bursty movements Range: Greater movements of the limbs in all ranges of motion Force: Limb raised too high in protraction (excessive joint flexion) and forcefully returned to ground (excessive joint extension) Truncal sway Base-wide stance/gait Multiplanar intention tremor (dysmetria of head and neck)

Answer 406

both can be seen but hypermetria is more common

Answer 407

coordinates voluntary movements and regulates skilled movements: such as rate, range, and force

Answer 408

1) Cerebrocerebellum 2) Spinocerebellum (vermis) 3) Vestibulocerebellum

Answer 409

1) cerebrocerebellum: coordinates voluntary movements and regulates skilled movements: such as rate, range, and force 2) Spinocerebellum (vermis): coordinates truncal and limb movements (muscle tone and unconscious proprioception 3) Vestibulocerebellum: regulates posture and equilibrium balance

Answer 410

coordinates truncal and limb movements (muscle tone and unconscious proprioception

Answer 411

regulates posture and equilibrium balance

Answer 412

the cerebrocerebellum is responsible for voluntary movements and regulating skilled movements with rate, range, anf force therefore damage to this part will result in dysmetria and intention tremor

Answer 413

it coordinates truncal and limb movements so it would lead to hypermetria and hypertonus (spasticity) leading to thoracic limb hyperextension and pelvic limb hip flexion) decerebellate posture)

Answer 414

it regulates posture and equilibrium/balance so damage to this would result in disequilibrium, wide based gait and nystagmus

Answer 415

The diffuse cerebellum is impacted, can be -Degenerative -Congenital (anomalous/malformation) -Metabolic -Neoplasia -Inflammatory

Answer 416

Feline Cerebellar Hypoplasia

Answer 417

lack of cerebellar development due to in utero infection of feline embryos with feline panleukopenia virus

Answer 418

at birth -apparent at onset of locomotion -cerebellar ataxia- symmetric truncal sway, intention tremor, and hypermetria/dysmetria

Answer 419

none cats compensate- clinical signs may even improve slightly with time

Answer 420

at birth -apparent at onset of locomotion -cerebellar ataxia- symmetric truncal sway, intention tremor, and hypermetria/dysmetria

Answer 421

1) Cerebrocerebellar signs: Dysmetria and intention tremor 2) Spinocerebellar signs: hypermetria and spasticity; decerebellate posture 3) Vestibulocerebellar signs: Disequilibrium

Answer 422

False- there is no loss of any single function just a general inadequacy of motor responses as the cerebellum is a regulator of movement

Answer 423

normal cerebellum at birth but progressive disease with gradual loss of cells clinical signs appear from 2 to 36 months with varying progression Autosomal recessive: Kerry Blue Terriers, Gordon Setters, Rough-coated collies also Arabian horses

Answer 424

Kerry Blue Terriers, Gordon Setters, Rough-coated collies Arabian horses

Answer 425

1) Breed- Kerry blue terriers, gordon setters, rough-coated collies 2) Clinical history- gradual onset of 2 to 36 months 3) DNA testing for some breeds 4) Family history

Answer 426

Hypoplasia: Abnormal at birth, never fully developed, non-progressive Abiotrophy: normal at birth, degeneration over weeks to months, progressive

Answer 427

This is an issue with the right cerebellum- the menace deficit is due to the pathway going through the cerebellum due to acute nature, think vascular (infarct) and also neoplasia (from age)

Answer 428

because the menace pathway goes through the cerebellum so therefore there will be menace deficit ipsilateral to lesion

Answer 429

based on the underlying disease if identified- kidney, CV (hypertension, valvular disease), infection, coagulopathy Supprotive care

Answer 430

ipsilateral

Answer 431

Cerebellum does not initiate motor activity- paresis is not a sign of pure cerebellar dysfunction there is likely damage to cerebellum, brainstem +/- C1-C5 spinal cord

Answer 432

1) Cerebrum (basal nuclei and cortical grey matter) 2) Brainstem (e.g red nucleus) (Cerebellum is not important for motor initiation, strength, or mentation)

Answer 433

benign condition of episodic uncontrolled head tremors that start and stop spontaneously Breed: Boxers, bulldogs, dobermans unknown cause usually doesnt respond to tx action-related postural tremor

Answer 434

geriatric tremors that develop a high frequency postural tremor of pelvic limbs only evident when the dog is standing movement obilterates tremor benign and treatment is not required

Answer 435

occurs/worsen during purposeful movement slow (low frequency) and coarse (high amplitude) disappear at rest Etiology: cerebellum and tracts more common in diffuse cerebellar diseases

Answer 436

intention tremor

Answer 437

a tremor seen at rest* diffuse inflammatory CNS disease of unknown etiology- thought to be autoimmune disorder acute onset, intention tremor of the head, limbs, and/or body worsens with exercise, stress, and excitement disappears during sleep typically affects young, mature, small breed dogs also called idiopathic generalized tremor syndrome (IGTS), idiopathic cerebellitis, white shaker syndrome

Answer 438

Corticosteroid-Responsive Tremor Syndrome (CRTS)

Answer 439

diffuse inflammatory CNS disease of unknown etiology thought to be autoimmune disorder

Answer 440

Seen at rest * worsens with exercise, stress, excitement *Acute onset, intention tremor of the head, limbs and/or body disappears during sleep

Answer 441

1) History + Signalment- generalized robotic tremors with no structural brain lesions * 2) CSF analysis- minimal to moderate nonsuppurative (lymphocytic) pleocytosis 3) Histopath- postmortem: mild nonsuppurative meningoencephalitis (lymphocytic perivascular cuffs in meninges, parenchyma or choroid plexus)

Answer 442

-Generalized robotic tremors -Decreased menace response -Head tilt -Nystagmus -Ocular tremors (opsoclonus) -ataxia

Answer 443

Immunosuppressive doses of corticosteroids (1mg/kg q12hrs) taper dose 25-50% every 4 weeks

Answer 444

good for complete recovery relapses may occur

Answer 445

neuromuscular disease

Answer 446

Reflexes reduced/absent Atrophy of muscles Tone reduced (RAT)

Answer 447

peripheral nerve deficit

Answer 448

neuromuscular junction deficit

Answer 449

muscle deficit

Answer 450

all nerves of the thoracic limbs C6-T2 sciatic of pelvic (L6-S1)

Answer 451

musculocutaneous (C6-C8)

Answer 452

radial (C7-T2)

Answer 453

Radial (C7-T2)

Answer 454

Femoral (L4-L6)

Answer 455

Fibular nerve (L4-L7)

Answer 456

Tibial nerve (L7-S1)

Answer 457

Mentation: WNL CN: WNL/LMN TL tone and reflexes: LMN PL: tone and reflexes: LMN Gait/Posture: flaccid tetraparesis/plegia, exercise intolerance , narrow stance

Answer 458

-Tetraparesis, exercise intolerance and collapse -Stiff/Stilted gait with reduced stride length, bunny hopping, may fatigue -Narrow based stance -Tremors/fascicultions -Regurgitation/altered esophageal motility -Myalgia -Dysphonia -Reduced reflexes and tone -Muscle atrophy

Answer 459

Neuropathy

Answer 460

junctionopathy

Answer 461

muscular dystrophy

Answer 462

congenital myopathies

Answer 463

hypothyroidism hypoadrenocorticism hyperadrenocorticism hypokalemia

Answer 464

myasthenia gravis immune mediated polymyositis tick paralysis toxoplasma neospora botulism FIV FeLV polyradiculoneuritis idiopathic trigeminal neuropathy idopathic facial nerve paralysis

Answer 465

2M Ab (disease specific autoantibody)

Answer 466

1) AChR Ab (disease specific autoantibody) - gold standard 2) Neostigmine response test 3) repetitive nerve stimulation 4) thoracic radiographs 5) Clinical signs

Answer 467

for acquired and some congenital Myastenia gravis cases IV administration of neostigmine- prolongs action of acetylcholine at the NMJ, slower onset but longer duration of action compared to edrophonium beware: cholingeric crisis: Bradycardia, salivation, miosis, dysponea, tremors- have an intubation kit on stand-by and atropine drawn up (esp in cats)

Answer 468

cholingeric crisis: Bradycardia, salivation, miosis, dysponea, tremors- have an intubation kit on stand-by and atropine drawn up (esp in cats)

Answer 469

Neostigmine

Answer 470

Electromyography

Answer 471

identifying denervated muscles extent and severity treatment monitoring

Answer 472

Motor nerve conduction velocity

Answer 473

repetitive nerve stimulation

Answer 474

Superficial easily identified MIXED motor and sensory nerve (e.g common peroneal)

Answer 475

Formalin fixed (for inflammation and fibrosis) Fresh and frozen

Answer 476

1) Superficial easily idnetified mixed motor sensory nerve (common peroneal) 2) Fascicular biopsy- third to half of the nerve width and 1cm in length to minimize deficits 3) Keep straight, but not stretched 4) Fix in formalin

Answer 477

1) Triceps brachii lateral head (distal 1/3) 2) Biceps femoris 3) Vastus lateralis (distal 1/3) 4) Cranial tibial (proximal 1/3) 5) Masticatory muscle- frontalis and temporalis

Answer 478

used for masticatory muscle myositis temporal muscle - white and shiny aponeurosis, normally very thick but if severely atrophied identification can be challenging make sure you get down to the bone ideally fresh and fixed

Answer 479

due to reduced neuromuscular transmission 1) Congenital- genetic defect (autosomal recessive) 6-8 weeks of age Dogs- jack russell terrier, english springle spaniel, smooth haired mini dachi, labrador Cats- sphinx + devon rx 2) Acquired- immune mediated >6months at diagnosis Predisposed breeds- Akitas, terriers, scottish terries, german shorthaired pointers, chihuahua Ab target AChR on postsynaptic membrane leading to receptor blockage +/- endplate destruction or paraneoplastic

Answer 480

1) Immune mediated: Antibody targets AChR on postsynaptic membrane leading to receptor blockage +/- endplate destruction 2) Paraneoplastic- thymoma in up to 52% of MG in cats 3) Cats on thiourylene for hyperthyroid (carbimazole, methimazole)

Answer 481

Thymoma thymoma in up to 52% of MG in cats

Answer 482

Dogs- jack russell terrier, english springle spaniel, smooth haired mini dachi, labrador Cats- sphinx + devon rx

Answer 483

Predisposed breeds- Akitas, terriers, scottish terries, german shorthaired pointers, chihuahua Cats: Abyssinian

Answer 484

Megaesophagus

Answer 485

1) Generalized- most common 2) Fulminant- acute onset rapidly progressive 3) Focal- approx 40%: facial, pharyngeal, laryngeal, megaesophagus *But megaesophagus in approx 90% of cases

Answer 486

True- only about 15% of cases with cats

Answer 487

abyssinian

Answer 488

If they are on thiourylene medication for hyperthyroidism -Carbimazole -Methimazole

Answer 489

-Weakness: usually episodic improving with rest -Regurgitation, vomiting -Ptyalism -Coughing -Dysphagia -Collapse -Nerve weakness/ paralysis(Fatiging palpebral and patellar reflexes)

Answer 490

-rapid onset and progression of profound muscle weakness -marked respiratory distress -regurgitation -inability to ventilate

Answer 491

AChR Antibody test 2% false negative

Answer 492

1) Acetylcholinesterase Inhibitors- Pyridostigmine PO or Neostigmine IM (short acting) 2) Immunosuppressive sometimes - corticosteroids, will falsely lower AChR titers 3) Thymectomy (if indicated) 4) Supportive care - postural feeding for megaesophagus

Answer 493

guarded to poor (approx 30% do not respond to tx) Worse prognosis if aspiration pneumonia, fuliminant MG, regurgitation, High AChR antibody spontaneous remission in some 59-89% cases

Answer 494

similar to Guillian-Barre syndrome in humans Dogs> cats (West Highland White and Jack Russel) or bengal cats Inflammation of nerves and nerve roots due to idiopathic, post vaccine, and contact with racoons (7-12 days prior) suggested to be immune-mediated cause or possible association with campylobacter and raw feeding most pathology in ventral spinal roots- primary demyelination and axonal degeneration in severe forms

Answer 495

Dogs- any breed or age but west highland white terriers and jack russels at increased risk

Answer 496

nerves and nerve roots most pathology in the ventral spinal roots (primary demyelination and axonal degeneration)

Answer 497

bengal cats

Answer 498

Idiopathic - immune mediated? Post vaccine? 7-12days post contact with racoons? Raw food w campylobacter?

Answer 499

acute onset, rapidly progressive (usually over days, can be over hours) -Progressive non-ambulatory flaccid tetraparesis (starting with pelvic limb and progresses to thoracic limb, can affect respiratory muscles -Markedly reduced motor function- absent reflexes -Dysphonia (loss of bark) -Retain tail wag -Usually pure motor deficits (CN not affected other than mild facial paresis, no sensory deficitis -Hyperaesthesia reported *Natural disease progression, prolonged if axonal damage

Answer 500

1) Clinical signs 2) CSF analysis - albuminocytological dissociation: normal cell count and increased protein 3) Electrodiagnostics: Elevated F-ratio, Increase F latency or absent F wave, changes present 6-7 days after onset of clinical signs

Answer 501

1) Physiotherapy 2) Supportive care 3) Analgesia if painful (Gabapentin, Acetaminophen, NSAID) 4) Human IV Immunoglobulin if available

Answer 502

fair but guarded if respiratory depression

Answer 503

Dermacentor variables and andersoni (female tick saliva) Ixodes holocyclus (Australia)

Answer 504

Female tick saliva contains a neurotoxin that interferes with ACh release at the NMJ (presynaptic) Signs occur 5-9 days after tick infestation

Answer 505

Signs occur 5-9 days after tick Infestation 1) rapidly progressive ascending paresis- initially pelvic limbs progressing to recumbency in 24-72 hours 2) Spinal reflexes decreases or absent 3) Hypotonia Nociception= normal rarely CN involvement Decreased bark +/- respiratory difficulty may result in respiratory paralysis and death

Answer 506

1) Identify ticks (multiple) 2) Clinical signs 3) Electrodiagnostics - RNS increment as Botulism

Answer 507

Flaccid paralysis - neurotoxin that interferes with ACh release at the NMJ (presynaptic)

Answer 508

removal of ticks via direct removal or dip animal in insecticide soln, frontline or other

Answer 509

Recovery in 24-72 hours

Answer 510

exotoxin produced by Clostridium botulinum (likely ingestion of contaminated food) toxin absorbed from gut acts to block vesicle fusion with presynaptic membrane and ACh release

Answer 511

1) Nicotinic ACh synapses (junctionopathy): acute onset- rapidly progressive (2-3 days) tetraparesis may affect cranial nerves- jaw tone, facial paralysis, gag reflex, megaesophagus 2) Muscarinic ACh synapses (dysautonomia) - urinary dysfunction, GI dysmotility, mydriasis, reduced tear production 3) GI signs

Answer 512

True they are resistant

Answer 513

acts to block vesicle fusion with presynaptic membrane and ACh release

Answer 514

1) Clinical signs 2) Electodiagnostics- Increment 3) Toxin in feed or mouse inoculation

Answer 515

they can exacerbate the NMJ blockade

Answer 516

No aminoglycosides or tetracyclines - can exacerbate NMJ blockade

Answer 517

supportive care -bladder management -AP- care (no aminoglycosides or tetracyclines) -recumbent care -ME management -physical therapy

Answer 518

depends on the severity of signs most dogs recover in 1-3 weeks poor if impaired ventilaton or aspiration pneumonia

Answer 519

Radiculoneuritis and Myositis -pelvic limb hyperextension (usually with one limb and progresses to the other) -ascending paralysis of the pelvic limbs with muscle contracture and arthrogryposis

Answer 520

Radiculoneuritis and Myositis -pelvic limb hyperextension (usually with one limb and progresses to the other) -ascending paralysis of the pelvic limbs with muscle contracture and arthrogryposis

Answer 521

1) Clinical signs- radiculoneuritis and myositis 2) CK/AST 3) serology 4) PCR- on blood and CSF 5) EMG and muscle biopsy

Answer 522

Clindamycin / TMPS + Pyrimethamine physical therapy

Answer 523

contractures is present or when end stage disease

Answer 524

auto antibodies to 2M myosin isoform (found only in muscles of mastication)

Answer 525

1) Temporalis 2) Masseter 3) Pterygoid 4) Digastric

Answer 526

dogs juvenile form in CKCS

Answer 527

1) acute signs - swollen and painful masticatory muscles 2) exophthalmos 3) Bilateral masticatory muscle atrophy * 4) Trismus (due to pain or fibrosis)

Answer 528

1) Imaging- muscles and TMJ to rule out TMJ abnormalities, craniomandibular osteopathy, osteomyelitis or neoplasia 2) CK 3) 2M antibodies 4) EMG 5) Temporal muscle biopsy

Answer 529

Prednisolone +/- other immunosuppression Physical therapy Prognosis is good if treated early and aggressively to get the jaw moving

Answer 530

immune mediated, usually idiopathic Dogs> cats (Newfoundland, boxer, GSD, labrador, golden retriever) Clinical signs: variable- acute or chronic -pyrexia, stiffness, non-ambulatory tetraparesis, reluctance to move, lowered head carriage, myalgia, muscle atrophy, exercise intolerance, fatigue +/- esophageal involvement (regurgitation)

Answer 531

variable- acute or chronic -pyrexia, stiffness, non-ambulatory tetraparesis, reluctance to move, lowered head carriage, myalgia, muscle atrophy, exercise intolerance, fatigue +/- esophageal involvement (regurgitation)

Answer 532

1) CBC, Chem, CK (acute disease- CK and AST are typically elevated +++ and inflammatory leukogram 2) +/- T4/TSH and ACTH depending on clinical suspicion 3) Electrodiagnostics- marked EMG abnormalities, normal MNCV 4) Muscle biopsy 5) Rule out infectious disease and neoplasia with abdominal ultrasound

Answer 533

prednisolone +/- other immunosuppressives analgesia relapse can occur, monitor clinical signs and rpt CK

Answer 534

Gram + Obligate anaerobe

Answer 535

1) Wound- anaerobic conditions and infection 2) Production of neurotoxin tetanospasmin 3) Toxin spreads hematogenously or locally 4) binds to NMJ and undergoes retrograde axonal transport to neuronal cell body 5) Binds irreversibly to presynaptic sites of inhibitory neurons 6) PRevents the release of glycine and GABA 7) Failure to inhibit motor reflexes 8) Prolonged muscle contraction

Answer 536

binds to NMJ and undergoes retrograde axonal transport to neuronal cell body Binds irreversibly to presynaptic sites of inhibitory neurons Prevents the release of glycine and GABA Failure to inhibit motor reflexes Prolonged muscle contraction

Answer 537

formation of new axon terminals

Answer 538

Horse > Human > dog > cat > birds

Answer 539

5-10 days after wound or surgical procedure you will begin to notice dramatically increased muscle tone and rigidity- most noticeable in the extensor muscles can be up to 3 weeks in cats because they are less susceptible

Answer 540

5-10 days after wound or surgical procedure Generalized- whole body (head and neck first then body and limbs) -Stiff and stilted gait -Tail base stiff -Rusus sardonicus and trismus: involvment of the facial muscles -Opistotonus -Tetany: auditory, visual or tactile stimuli -Muscle pain -Urinary retention -Seizures can develop *Autonomic nervous system syns may occur after 1-2 weeks: increased parasympathetic tone more common (bradycardia and bradyarrhythmia) and GI and urinary dysfunction Localized: one or 2 limbs closest to wound or paraspinal muscles- most common in cats: signs progress from extremity more proximally

Answer 541

one or 2 limbs closest to wound or paraspinal muscles- most common in cats: signs progress from extremity more proximally

Answer 542

Autonomic nervous system syns may occur after 1-2 weeks: increased parasympathetic tone more common (bradycardia and bradyarrhythmia) and GI and urinary dysfunction

Answer 543

Risus sardonicus is a facial expression that involves a sustained spasm of the facial muscles that creates a distorted grin, raised eyebrows, and an anxious expression seen in tetanus

Answer 544

1) Clinical signs 2) Identification of wound or recent surgery 3) CBC/ Chem (Usually normal, aside from possible increased CK)

Answer 545

-Monitor and supportive care: dark area with minimal sound (ear plugs), adequate bedding, nutrition and fluid intake (consider PEG or E tube due to dysphagia), enema or catheter, monitor temp -Prevention of more toxin formation/binding -Control of muscle rigidity/ analgesia (Benzodiazepine CRI =/- chlorpromazine/ acepromazine) -Anti-toxin administration: only affects free toxin -Wound debridement -Antibiotics *Recovery dependent on development of new axonal terminals - 2 week delay before clinical improvement

Answer 546

hyperthermia may occur due to sustained muscle contraction

Answer 547

1) Anti-toxin administrations - only affects free toxin, usually equine antitoxin (human can also be used), IV is ideal bc SQ takes 2-3 days to reach therapeutic levels but anaphylaxis is possible (test dose first) 2) Wound debridement- identify, clean, and debride. CARE- nail bed infections, mastitis, post OVH/ other reproductive tract infections 3) Antibiotics - Metronidazole for at least 10days

Answer 548

Metronidazole for at least 10 days

Answer 549

Anaphylaxis is possible Test dose 0.1-0.2ml intradermal/subcutaneous- monitor injection site for 30minutes then 100-1000 units/kg (max 20,000 units) antitoxin Equine antiserum IV bolus over 30minutes, can also be given SQ or IM

Answer 550

Benzodiazepine CRI +/- chlorpromazine/ acepromazine other meds if no improvement: phenobarbitone, propofol (may need ventilation support), opioids, methocarbamol, magnesium sulfate remember analgesia but be careful because you might increase respiratory depression

Answer 551

guarded- dependant on presenting severity several weeks to months for a full recovery (2 week delay for clinical improvement) dogs 40-50% fatality

Answer 552

acute onset facial nerve paralysis -unilateral (most common) or bilateral -absent palpebral, present vision -facial droop- ear, lip, muzzle, eyelid -facial sensation present *Corneal ulcer can develop due to exposure keratitis (normal teat production) or if parasympathetic portion damaged reducing tear production +/- vestibular signs (70% dogs)

Answer 553

due to exposure keratitis (normal teat production) or if parasympathetic portion damaged reducing tear production

Answer 554

both nerves run side by side and through the ear

Answer 555

Rule out other causes 1) CBC/Chem and T4/TSH 2) MRI +/- contrast enhancement of affected facial nerve otherwise normal 3) CSF= normal v albuminocytological dissociation 4) STT and fluorescein for corneal ulcer

Answer 556

artificial tears

Answer 557

Resolution within 6-8 weeks (average of 45 days) if it is going to occur 15% no recovery of facial nerve function 45% hemifacial contracture

Answer 558

bilateral masticatory muscle atrophy

Answer 559

Dogs > cats

Answer 560

inflammation within trigeminal nerves and ganglia bilaterally

Answer 561

leads to bilateral masticatory muscle atrophy Dogs > cats due to inflammation within trigeminal nerves and ganglia bilaterally Clinical signs: acute onset- paresis/parlysis of masticatory muscles bilaterally -> drooped jaw (most. common cause of inability to close the mouth) Hormal gag and tongue tone and movement Horner's or facial paresis can be seen sensory deficits in up to 30% of cases

Answer 562

*Acute onset* 1) Paresis / paralysis of masticatory muscles bilaterally -> dropped jaw (Most common cause of inability to close the mouth) 2) Normal gag and tongue tone and movement 3) Horner's or facial paresis can be seen (possibly more common with neoplasia or neuritis as the cause of trigeminal signs_ 4) Sensory deficits in up to 30% of cases

Answer 563

Acute onset

Answer 564

idiopathic trigeminal neuropathy (as opposed to masticatory muscle myositis the jaw is closed and fixed- unable to open)

Answer 565

CBC, Chem, T4/TSH MRI CSF need to rule out neuritis and trigeminal nerve sheath tumor

Answer 566

Supportive Care- physiotherapy, tape muzzle to allow eating Usually resolves in around 3 weeks NO change in time to recovery with corticosteroids

Answer 567

unilateral masticatory muscle atrophy

Answer 568

Trigeminal Nerve Sheath Tumor (~50%) other neoplasia if no changes on MRI- infectious/inflammatory, traumatic, idiopathic (30%)

Answer 569

1) Neurogenic atrophy of masticatory muscles (unilateral) 2) Possible abnormal sensation (face rubbing, absent palpebral, absent corneal reflexes) 3) Progression to involve other cranial nerve and brainstem functions if neoplastic

Answer 570

Dependent on the cause If trigeminal nerve sheath tumor- RT, prednisolone (palliative) neuritis- consider steroids

Answer 571

Neuropraxia

Answer 572

prognosis: good and few days recovery temporary nerve damage - conduction block no disruption of the nerve or myelin sheath

Answer 573

Axonotmesis

Answer 574

Prognosis: Variable- axonal growth= 1-4mm/days (slow recovery) Disruption of the axon Intact basal lamina and myelin sheath

Answer 575

Neurotmesis

Answer 576

Prognosis: partial recovery is possible but complete recovery is unlikely partial or complete transection of nerve (axon and supporting structures)

Answer 577

Neuropraxia > Axonotmesis > Neurotmesis

Answer 578

Chronic progressive paraparesis leading to symmetrical platigrade stance, hyporeflexia and distal pelvic limb muscle atrophy

Answer 579

a chronic progressive paraparesis (symmetrical plantigrade stance) with hypreflexia Distal pelvic muscle atrophy but the thoracic limbs can be affected in time sensory changes

Answer 580

Insulin Appropriate diet

Answer 581

1) Hyperglycemia 2) Fructosamine 3) Electrodiagnostics- abnormalities along entire length of peripheral nerves and nerve roots 4) Muscle and nerve biopsy

Answer 582

if treated early- neurological improvement may take several weeks to months

Answer 583

It can lead to a chronic progressive paraparesis symmetrical plantigrade stance hyporeflexia distal pelvic limb muscle atrophy

Answer 584

Progressive weakness with muscle atrophy and decreased reflexes -Facial nerve paresis -Laryngeal paralysis -Megaesophagus -Peripheral vestibular disease

Answer 585

Low tT4 and fT4 Elevated TSH

Answer 586

thyroid hormone replacement neurological response may take 6 months

Answer 587

thromboembolism -> ischemic damage to muscle and the nerve If >30 minutes -> pathological damage Cats> Dogs feline aortic thromboembolism (FATE)- cats with cardiomyopathy

Answer 588

Cats > Dog Caused by feline aortic thromboembolism (FATE) or dogs with renal disease

Answer 589

-Paresis/ paralysis -Hyoreflexia -Firm muscles: painful on palpation -Cyanotic nail beds -decreased to absent femoral pulses

Answer 590

1) CBC/Chem 2) CK- elevated 3) K+ elevated (due to metabolic waste from cells) 4) Identification of clot- ultrasound vs CT *Look for underlying cause like FATE (cats) or renal disease (dogs)

Answer 591

poor prognosis can treat underlying cause and give Aspirin, Plavix

Answer 592

Cats (rarely in dogs)

Answer 593

1) Reduced intake 2) Increased loss (chronic renal failure) 3) Congenital predispositions (Burmese cats)

Answer 594

*Acute onset * -Stiff and stilted gait -Muscle weakness -Cervical ventroflexion -Muscle pain

Answer 595

1) CBC/Chem: Serum K+ <3.5mmol/L , check for chronic renal failure and hyperthyroidism, CK due to muscle fiber necrosis 2) muscle biopsy

Answer 596

Oral supplementation (may need IV supplementation initially- CARE of cardiac monitoring) Prognosis is good if potassium is supplemented and primary cause is treated

Answer 597

Thoracic Limbs: UMN Pelvic Limbs: UMN

Answer 598

Thoracic Limbs: LMN Pelvic Limbs: UMN

Answer 599

Thoracic Limbs: Normal Pelvic Limbs: UMN

Answer 600

Thoracic Limbs: Normal Pelvic Limbs: LMN

Answer 601

UMN: normal to increased LMN: decreased to absent reflexes and tone

Answer 602

normal to increased

Answer 603

decreased to absent reflexes and tone

Answer 604

proprioception

Answer 605

nociception

Answer 606

1) Proprioception 2) Weakness (paresis) 3) Motor (plegia) 4) Bladder 5) Nociception *Recovery occurs in reverse order

Answer 607

1) Nociception 2) Bladder fxn 3) Motor (plegia) 4) Weakness (paresis) 5) Proprioception

Answer 608

1) Nucleus pulposus 2) Annulus fibrosus

Answer 609

young, chondrodystrohpic breeds

Answer 610

1) young, chondrodystrohpic breeds has a nucleus pulposus which loses water binding capacity and GAGs 2) Progresses to calcification 3) Nucleus pulposus extrudes through the annulus fibrosus (rapid progression) into the spinal cord

Answer 611

T11-L2 because there is no intercapital ligament caudal to T10

Answer 612

there is no intercapital ligament caudal to T10

Answer 613

Myelography

Answer 614

Computed Tomography (CT)

Answer 615

MRI- consistently more accurate than myelography and CT for determining the site and side of lesion able to see normal discs and calcified discs Cons: expensive and takes a lot of time

Answer 616

-peracute transverse T3-L3 lesions -severe thoracic limb extension -due to disinhibition of extensor motor neurons in the cervical intumescence (border cells in L1-L5) -Normal TL gait when held up *Often present with spinal shock (PL hypotonia and decreeased withdrawl reflex)

Answer 617

due to disinhibition of extensor motor neurons in the cervical intumescence (border cells in L1-L5)

Answer 618

fibroid degeneration that is a chronic form where the annulus fibrosis gets thicker over time and there is a protrusion

Answer 619

Schiff-Sherrington Syndrome - due to disinhibition of extensor motor neurons in the cervical intumescence *Peracute transverse T3-L3 lesions

Answer 620

with peracute transverse T3-L3 (often with Schiff-Sherrington Syndrome) Will look like LMN (pelvic limb hypotonia) and decreased withdrawl reflext can persist 10-14 days

Answer 621

paraplegia with loss of deep pain sensation

Answer 622

1) Crate rest 4-8 weeks ** most important 2) Bladder management 3) Prevent continued extrusion through ruptured AF 4) Adjunctive therapy- steroidal or NSAID, methocarbamol, opiods (tramadol), gabapentin/ amantidine, acupuncture, physical therapy

Answer 623

Crate rest for 4-8 weeks

Answer 624

Dogs with cervical intervertebral disc disease -Consider surgery in even more mild cases

Answer 625

when it is a cervical disc herniation- they do not usually respond well to conservative management

Answer 626

-Persistent/ recurrent pain -Unresponsive to conservative therapy -if loss of nociception (within 24-48 hours) -Cervical IVDD *Surgery may offer a more complete and faster recovery and lower probability of recurrence at that site

Answer 627

*Remove compression* -Hemilaminectomy -Ventral slot for cervical discs *Surgery does not result in instant recovery as secondary spinal cord trauma/injury takes time to heal *surgical decompression allows healing to begin *functional recovery takes weeks to months

Answer 628

Large non-chondrodystrophic (any breed) german shepherd age >7 years

Answer 629

Progressive thickening of the dorsal annulus fibrosis (rarely calcified) Protrusion into the vertebral canal

Answer 630

MRI- the discs are rarely calcified so it will not be picked up by radiograph of CT

Answer 631

caused by thickening of the dorsal annulus fibrosis and protrusion into vertebral canal rarelt calcified occurs in large non-chondrodystrophic breeds german shepherds treat with conservative and surgery but lower surgery prognosis than Type I

Answer 632

a stroke to the portion of the spinal cord via disc material leading to an ischemic injury to the spinal cord acute and initially very painful non-progressive localizes to the area of cord affected

Answer 633

Treatment: supportive, physical therapy prognosis: good if improvement begins within 2 weeks grave is LMN with no deep pain

Answer 634

MRI- see spinal cord (CT cant see spinal cord) area of hyperintensity where ischemic area is

Answer 635

Acute Noncompressive nucleaus pulposus extrusion (ANNPE)

Answer 636

Acute Noncompressive nucleaus pulposus extrusion (ANNPE) *Distinguish the two on MRI.

Answer 637

Discospondylitis

Answer 638

hematogenous or from bladder infection

Answer 639

usually due to bacteria (Staphylococcus, Streptococcus, Brucella canis) or fungus (Aspergillus)

Answer 640

medium to giant breed dogs young to middle aged

Answer 641

PAIN (often severe) alone or findings consistent with site of infection

Answer 642

acute to subacute to chronic *Pain spinal hyperesthesia systemic signs- fever, inappetance, decreased mentation reluctance to mvoe

Answer 643

1) radiography (take 3 weeks from clinical signs) 2) urinalysis and culture 3) CBC/ Chem 4) Blood cultures 5) Brucella canis serology if intact male 6) Fluoroscopy gioded FNA of disc 7) MRI

Answer 644

with a broad spectrum antibiotic (based on cultur e or empirically with cephalosporins) *8-12 months (long treatment) Need analgesics

Answer 645

degenerative disease of the spinal cord (similar to ALS) axon and myelin degeneration within the spinal cord no known etiology or inflammatory component on histopathology seen in german shepherds, boxers, corgis onset usually after 7 years of age Insidious onset, slowly progressive over 6-12 months no pain or inflammation associated signs: Non-painful, T3-L3 signs (GP ataxia. UMN paraparesis with normal to increased tone and reflexes in pelvic limbs)

Answer 646

german shepherds boxers corgis

Answer 647

True - axon and myelin degeneration within the spinal cord

Answer 648

NON-PAINFUL T3-L3 signs -GP ataxia/ UMN paraparesis -Normal to increased tone and reflexes in the pelvic limbs *Degenerative process ascends and descends in the spinal cord

Answer 649

1) Diagnosis of exclusion (T3-L3 signs with normal MRI and CSF analysis) 2) DNA test: SOD1 genetic mutation

Answer 650

no definitive treatment -only proven effective therapy is physical therapy

Answer 651

SOD1 genetic mutation

Answer 652

Lumbosacral Syndrome

Answer 653

german shepherds middle-aged to older

Answer 654

general term referring to degenerative joint disease at L7-S2 -Stenosis secondary to bony proliferation, articular process proliferation and ligamentous hypertrophy and type II disc protrusion commonly middle aged to older german shepherds

Answer 655

lumbosacral syndrome

Answer 656

1) Stenosis secondary to bony proliferation 2) articular process proliferation 3) ligamentous hypertrophy 4) type II disc protrusion

Answer 657

favorable with decompressive surgery (dorsal laminectomy) conservative therapy may help in some cases -analgesics -physical therapy -+/- steroids or NSAIDs

Answer 658

Caudal Cervical Spondylomyelopathy -general term for compression of the cervical spinal cord

Answer 659

1) Young great danes, borbels, and mastiffs: degeneration and thickiening of the articular processes +/- laminae leading to dorsolateral compression of the cervical spine, usually no disc generation 2) Older Doberman Pinschers: type 2 disc protrusion and hypertrophy of the articular processes, ligamentum flavum and the dorsal longitudinal ligament leading to dorsal and ventral compression of the cervical spinal cord

Answer 660

young great danes, mastiffs, borbels

Answer 661

older doberman pinschers

Answer 662

luxation of C2 dorsal to C1 1) Congenital malformation of C2 (hypoplastic or aplastic dens) 2) Trauma of dens, rupture of ligaments Diagnosis: lateral radiograph- do not flex head and do awake so that normal muscle tone with help guard neck Treatment: conservative therapy, some dogs recover, recurrence is possible and fusion does not occur Surgery: goal to fuse C1-C2

Answer 663

Lateral radiograph to see the luxation of C2 dorsal to C1 *DO NOT FLEX HEAD do radiographs awake so that normal muscle tone with help guard neck

Answer 664

Conservative therapy: some dogs recover, recurrence is possible, fusion does not occur surgical therapy to fuse C1-C2, not always advantageous

Answer 665

toy breeds dogs typically < 1 year old spontaneous onset or mild trauma

Answer 666

*Luxation of C2 dorsal to C1 1) Congential malformation of C2- hypoplastic or aplastic dens, toy breeds <1 year with spontaneous or mild trauma 2) Trauma of dens, rupture of ligaments

Answer 667

Diffuse neuromuscular

Answer 668

Paresis Paralysis/plegia

Answer 669

Vestibular General Proprioceptive Cerebellar

Answer 670

Is the patient ambulatory

Answer 671

Yes! Starting treatment is advised in the event of Structural epilepsy or metabolic seizures Status epilepticus or cluster seizures 2 or more seizures in a 6 month period Post-ictal signs are severe or last longer than 24 hours As this patient has had 3 seizures within 2 months, treatment would be advised.

Answer 672

Zonisamide

Answer 673

Levetiracetam

Answer 674

Phenobarbitone

Answer 675

Potassium Bromide

Answer 676

1) Structural epilepsy or metabolic seizures 2) Status epilepticus or cluster seizures 3) 2 or more seizures in a 6 month period 4) Post-ictal signs are severe or last longer than 24 hours

Small Animal Neurology Flashcards

(746 cards)