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4th Year Exams > Neuro > Flashcards

Neuro Flashcards

1
Q

Neuro location options for ATAXIA ONLY

A

Cerebellar or Vestibular

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2
Q

Neuro location options for PARESIS ONLY

A

Neuromuscular Disease or Lumbo-Sacral

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3
Q

Neuro location options for ATAXIA AND PARESIS

A

Spinal cord or brainstem

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4
Q

5 Finger rule components:

A

(signalment)

Onset, clinical course, lateralization, neurological localization, pain

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5
Q

Main components of a neurological exam

A 
Mentation
Gait/posture
Cranial Nerves 
Postural reactions 
Spinal Reflexes 
Palpation
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6
Q

Common causes of progressive neuropathy in young dogs

A

Immune mediated inflammation of the brain- meningoencephalitis of unknown aetiology -
Infectious diseases including bacterial infection - most commonly intracranial spread of an otitis interna, fungal cryptococcus, viral - Distemper or protozoal Neospora

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7
Q

Common fungal pathogen causing neuropathy in pet rabbits

A

Encephalitozoon cuniculi

Leads to granulomatous inflammation

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8
Q

Most common brain tumor encountered in cats

A

Meningioma

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9
Q

Two most common spinal diseases in cats

A

FIP virus myelitis
Spinal neoplasia - spinal lymphoma associated with FeLV
Both have chronic onset with progressive clinical disease usually seen in younger cats

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10
Q

What are the three functional divisions of the cerebellum?

A

Cerebrocerebellum, Spinocerebellum, & Vestibulocerebellum

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11
Q

In the differential diagnosis of the “wet eye” what do you consider to be the most important decision to make?

A

Is the wetness due to excessive lacrimation or is it an epiphora?
Basically is it increased production or decreased drainage?

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12
Q

What is the most common CSF finding from a canine patient with Steroid Responsive Meningitis Arteritis (SRMA)?

A

Neutrophilic pleiocytosis (increased cellularity with neutrophils)

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13
Q

What are common clinical signs of hydrocephalus?

A

Dome-shaped head
Behavioral changes - congenital
Open fontanel
Diverging strabismus - ventrolateral strabismus (setting sun eyes)

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14
Q

What is the difference between Type 1 and Type 2 (Hansen) intervertebral disc disease?

A

Type 1 - extrusion of the nucleus pulposus of the disc due to mineralization
Type 2 - protrusion of the annulus of the disc - usually due to hypertrophy

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15
Q

Describe a myelogram.

A

Injection of contrast into the subarachnoid space to see and analyze the spinal cord on radiographs - best used to see compressions and deviations

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16
Q

What is the typical patient with Type I IVDD (IVD extrusion)? Think about signalment and clinical presentation specifically

A

Chondrodystrophic dog breeds = Dachshunds, Basset Hounds, Beagles, Corgis, French Bulldogs. Rarely in cats
Often young to middle-aged dogs
Typically acute, more rapidly progressive, painful

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17
Q

What is the typical patient with Type II IVDD (IVD protrusion)? Think about signalment and clinical presentation specifically

A

Middle-aged or older dogs (or cats)
Often large non-chondrodystrophic breeds
Typically chronic, slowly progressive, non-painful

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18
Q

What would the gross spinal cord of a dog with steroid-responsive meningitis arteritis look like?

A

Darkened areas with hemorrhage and inflammatory lesions
Histology - Inflammatory cells will be located within the MENINGES and surround the blood vessels
** This was in 2 separate DLs so I think it’s important*

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19
Q

What are differential diagnoses in a horse with spinal ataxia?

A 
Cervical vertebral malformation/stenosis
Equine Herpes Virus (EHV1)
Equine degenerative myeloencephalopathy 
Trauma
Migrating parasites 
Equine protozoal myeloencephalitis 
Ryegrass staggers
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20
Q

Clinical signs of equine herpes virus (EHV1)?

A

Ascending paresis/ataxia
Pyrexia
Bladder incontinence
Tail paresis

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21
Q

Where does EHV1 harbor within the CNS to make it a lifelong disease?

A

Trigeminal ganglion

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22
Q

Describe what is seen with dynamic stenosis of cervical vertebral malformation type 1.

A

Paresis and ataxia - all 4 limbs
With neck flexion and hyperextension - the vetebrae move excessively –> cord compression
Affects C3-C5
Seen most frequently in young animals

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23
Q

Describe what is seen with absolute stenosis of cervical vertebral malformation type 2.

A

Paresis and ataxia - all 4 limbs
Osseous changes in the vertebrae that acuse spinal cord compression
Usually affects OLDER horses
Affects C5-C7

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24
Q

Differential diagnoses for dog with exercise intolerance and regurgitation

A

Myasthenia Gravis
Botulism
Hypoadrenocorticism
Polymyositis

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25
Q

Describe the diagnostic tests for myasthenia gravis?

A
  1. Edrophonium chloride challenge = TENSILON RESPONSE TEST -Edrophonium is short acting anticholinesterase drug that increases AcH concentration in the NMJ - If the dog has myasthenia gravis - this will show a marked imorovement in muscle strength and exercise tolerance for a few minutes
  2. Nicotinic acetylcholine receptor antibody serology = most specific and sensitive test for myasthenia gravis - tests for circulating antibodies against the nicotinic ACH receptors
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26
Q

What would be an ideal treatment plan for diagnosed myasthenia gravis?

A
  1. Supportive care - preventing aspiration pneumonia, fluids if regurgitating often, GIT drugs - prokinetics to speed up the movement of food, nutritional support - feed from a height
  2. Anticholinesterase drugs
  3. Immunosuppressive drugs
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27
Q

What are the main sources of infection from Clostridium Botulism?

A

Forage poisoning - feed material with preformed toxin - soil contamination or air got into it
Wound botulinum - anaerobic wounds contaminated by the botulinum spores
Toxico-botulinum- usually seen in young foals caused by an infection in the GIT and production of the toxin –> absorption

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28
Q

How does botulinum toxin cause clinical signs?

A

Botulinum toxin acts at the neuromuscular junction by inhibiting the release of Acetyl choline vesicles at the presynaptic membrane. Without ACh, the nerve signal is not passed to the post synaptic muscle membrane.

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29
Q

What are the clinical signs associated with each of the 3 main forms of grass sickness (chronic, acute, subacute)

A

Thought to be from an enteric Clostridium botulinum toxin
Chronic= Weight loss, dysphagia, patchy sweating, muscle fasciculations, variable tachycardia, paretic stance.
Sub-acute = Dysphagia, colic (often impactions), sweating, muscle fasciculations, tachycardia
Acute = Severe, sudden onset colic with small intestinal distension and nasogastric reflux, death by gastric rupture

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30
Q

What are the clinical signs of equine motor neuron disease?

A 
Usually caused by chronic vitamin E deficiency leading to free radical damage and attack of type 1 fibers in muscles of posture/core strength 
"Horse on a drum" stance 
Low head carriage 
muscle fasciculations = twitches 
Patchy sweating
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31
Q

How to easily differentiate between tetanus and exertional rhabdomyolysis?

A

Blood sample and test for CK activity

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32
Q

Both botulism and tetanus are caused by clostridial toxins. So why does botulism cause a flaccid paralysis whereas tetanus causes a spastic paralysis?

A

Botulinum toxins work at the NMJ
Tetanus acts at the spinal cord after being tracked up from the motor neurons - they inhibit the inhibiting NTs from “renshaw cells” –> excitation

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33
Q

Dog comes in seizuring, what do you do?

This wasn’t on the notes, I just researched it in case it comes up in the long papers

A

1) Diazepam IV (if you can’t put IV cath in then give it rectally)
2) If diazepam doesn’t work give it Phenobarbitol (loading dose) or Levicetaram (might be preferred because doesn’t cause obtundation but more expensive)
3) If again this doesn’t work give propofol
IN THE MEANTIME PROVIDE O2 WITH A MASK/FLOW BY
- The dog has stopped seizuring-
5) IV Fluids (correct hypernatremia, hypocalcemia, hypoglycemia) but take blood sample first!
6) cool down if TRP> 40C
7) keep on Phenobarbitol after seizure has stopped to prevent recurrence
8) Intubate for O2 administration if patient doesn’t have a gag reflex (heavily sedated)
9) while the patient is resting elevate the head at 30 degrees (decrease intracranial pressure)
10) administer mannitol, then furosemide if suspecting increased intracranial pressure (these patients are hypertensive and bradycardic)

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34
Q

What are the definitions for Epilepsy, Cluster seizures and Status epilepticus?

A

Epilepsy= 2+ unprovoked seizures, more than 24h apart
SE= seizure activity for more than 5 min. seizures can be convulsive (tonic clonic movement) or non-convulsive (patient is unconscious)
Cluster seizure= 2+ seizures within 24h with a normal interictal period (recovery in between episodes)

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35
Q

What’s the drug of choice for cluster seizures?

A

Levitiracetam

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36
Q

Phases of a seizure

important to know while you take history. Owners might confuse epilepsy for syncope or something else

A

1) AURA (dog hypersalivating, anxious, altered sensory activity)
2) ICTAL (seizure episode. focal or generalized, symmetrical or asymmetrical)
3) POST-ICTAL (drowsy, confused, aggressive, increased drinking)

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37
Q

Why is it important to diagnose idiopathic epilepsy? Even if the dog has only had 1 episode?

A

60% of IE patients will have a status epilepticus episode in their life (dangerous!) so they should be on anti-epileptic therapy

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38
Q

Types of generalized seizures

A

Tonic - increased muscle tension-
Clonic - prolonged repetitive muscle contraction-
Myoclonic - jerky contractions-
Atonic - flaccid-

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39
Q

Types of epilepsy

A

IDIOPATHIC - patient normal in the intrictal period, no neuro deficits, metabolically normal, between 6mo and 6y of age, generalized sizures-
STRUCTURAL - these tend to be asymmetric + neuro deficits in the interictal period and present focal asymmetric seizures - structural brain lesion
REACTIVE - response to toxin or metabolic issue like HE, generalized seizure, symmetric neuro deficits in the interictal period -

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40
Q

Types of focal seizures

A

Autonomic - drooling, diarrhea..-
Sensory - aggression, vocalization, tail chasing…-
Motor

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41
Q

Confidence levels in diagnosing IE

A

Tier I: dog signalment fits, metabolic screening (including BA, T4, B12), physical and neuro exam - may have family history of IE as well
Tier II: Diagnostic imaging MRI and CSF analysis
Tier III: EEG

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42
Q

Events that can mimic epilepsy

A
  • syncope
  • acute vestibular syndrome
  • narcolepsy
  • movement disorders (hypertonicity and others)
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43
Q

Neurolocalization for seizures

A

FOREBRAIN!!

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44
Q

What is the therapeutic range for Phenobarb concentration in the blood? Why is it important that it stays within this range?

A

15-35 ug/ml

Causes hepatotoxicity and other nasty side effects like pancytopenia

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45
Q

What is first line epilepsy tx in a healthy dog?

What about a dog with hepatic compromise?

A

Phenobarb is first line in healthy patients.
Imepitoin can be used in patients with hepatic compromise but it’s not as effective as phenobarb
If a patient has severe seizures and hepatic compromise then consider doing low dose phenobarb + KBr

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46
Q

How many days does it take each drug to reach plasma steady state?
Why do you need to know?

A

Cause that’s when you need to check plasma levels of the drug in case of ineffective seizure control
Phenobarb = 14d
KBr = 120d (slow mf)
Imepitoin = 1-2 d

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47
Q

What mechanism is responsible for anti-epilepsy tx failure?

A

p-glycoprotein efflux pumps in the BBB.
These are ATP dependent pumps that pump out drugs from the brain. If the gene encoding them (MDR-1) is overexpressed -> drugs don’t work
Collies have common MDR-1 mutation -> so ivermectin and other drugs can cause CNS toxicity at lower dose

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48
Q

What are some considerations with KBr as antiepileptic tx?

A
  • never a sole treatment, only add-on
  • renally excreted
  • put these patients on fluids-> they will start seizuring agin (because increased KBr excretion)
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49
Q

Dog in status epilepticus comes in? What drug do you choose to control seizure?

A

Phenobarb (not diazepam) because phenobarb needs less GABA to work (SE depletes GABA)

50
Q

How do you differentiate from paradoxical vestibular syndrome and the other vestibular dysfunctions?

A

Head tilt away from the side of postural reaction deficits.

Postural deficits on the left side-> means there is a L side lesion of the cerebellum -> L side of cerebellum stops inhibiting L brainstem vestibular nuclei -> increase input from the L side of vestibular system -> increased extensor tone on the left -> head tilts to the right. BOOM.

51
Q

What vestibular syndrome is more likely with concurrent Horner syndrome or facial paralysis (CN7)?

A

peripheral vestibular

52
Q

What vestibular syndrome is more likely with concurrent CN6 to 12 deficits (dysphagia, dysphonia)?

A

central vestibular (all the nuclei are close to each other in the brainstem)

53
Q

What endocrinopathy can cause vestibular syndrome?

A

Hypothyroidism

54
Q

What nutritional deficiency in cats often causes neurological signs?

A

Thiamine deficiency

55
Q

What pathogens do you have to consider when you suspect infectious causes of neurological disease in cats?

A

Toxoplasma, FIP, cryptococcus, FeLV, FIV

56
Q

What pathogens do you have to consider when you suspect infectious causes of neurological disease in dogs?

A

Neospora, distemper, bacterial spread from otitis interna

57
Q

What commonly administered antibiotic can cause toxicity to the brainstem?

A

Metronidazole. Acute onset, progressive signs.

58
Q

Diagnostic work-up for PERIPHERAL VESTIBULAR DISEASE:

A
  • Did you give an ototoxic drug?
  • If not, look inside the ear for evidence of otitis media
  • if no otitis media and tympanic membrane intact consider idiopathic/vascular cause of vestibular disease (can do an MRI to be sure)
  • if there is otitis media and abnormal tympanic membrane -> myringotomy -> take a sample for cyto from the bullae
  • if cyto reveals bacteria/fungi -> treat -> has the vestibular disorder resolved?
  • if cyto is sterile, or no response to AB/antifungal -> do an MRI (see if there is MUO, neoplasia, polyp or other structural abnormality)
59
Q

Toxins that may cause seizures

A 
Xylitol (indirectly, causes hypoglycemia)
Metaldehyde
Organophosphates
Lead
Ethylene glycol

And mycotoxins, theobromide from chocolate, and permethrin

60
Q

What vascular conditions can cause neurological signs?

A
  • Polycythaemia
  • hyperviscosity (increased globulins)
  • thromboemboli
  • hypertroglyricedemia
  • hypertension (ALWAYS measure BP in cats + do a fundic exam - which is also useful to evaluate FIP infection)
61
Q

Why is it reasonable to do urinalysis in a dog that presents with generalized symmetrical seizures?

A

To look for ammonium biurate crystals.

25% of dogs with PSS have these crystals

62
Q

What dog breed is overrepresented for brain tumors?

A

Boxers! They often get gliomas

63
Q

What kind of neurotransmitter is used by the cerebellum?

A

GABA, so the cerebellum can only send inhibitory signal

64
Q

Signs of cerebellar dysfunction

A
  • dysmetria (hypermetria)
  • intention tremors (animal struggles with UMN control of LMN)
  • hypertonia (loss inhibitory signal to UMN)
  • broad-base stance
  • delayed postural reactions
  • menace deficit with normal PLR
  • vestibular signs (if lesion on the flocculonodular lobe)
  • decerebellate posture (if lesion in the rostral lobe)
65
Q

What structures does the menace response “test”?

A

CN 2, thalamus, forebrain, brainstem, cerebellum, CN 7

66
Q

Neurolocalization of mental status alteration

A

Forebrain or brainstem (ARAS)

67
Q

How do you distinguish decerebrate from decerebellate posture?

A

Decerebrate is always unconscious

68
Q

If you suspect a patient has vestibular disease, how can you elicit pathological nystagmus?

A

Turn the patient on their back (sudden position change)

69
Q

CSF shows mononuclear pleocytosis with increased protein, what is the most likely cause of neuro signs?

A

Inflammation. Increased protein due to leaky vessels

70
Q

Do you expect paresis with cerebellar dysfunction?

A

No! Cerebellum doesn’t control LMN, it only controls UMN which in turn control LMN. If anything these guys have increased muscle tone (loss of UMN inhibition)

71
Q

Neurolocalization of behavioral changes

A

Thalamus

72
Q

Clinical signs of forebrain dysfunction

A
  • altered mental status
  • seizures (contralateral if focal)
  • hemi-neglect syndrome (contralateral)
  • decreased motor function (contralateral)
  • compulsive, WIDE circling
  • pleurothotonous (head+body turn) towards the lesion
  • PROPRIOCEPTIVE ATAXIA (but spinal reflexes normal)
  • decreased facial sensation
73
Q

Would a cerebellar lesion cause absent PLR?

A

Nope

74
Q

What cranial nerves carry parasympathetic fibres?

A

3, 7, 9, 10

75
Q

What CN innervate extraocular muscles? what dysfunctions do you end up with?

A

3,4,6
Abducens -> medial strabismus
Trochlear -> dorsolateral strabismus
Oculomotor -> ptosis, dilated pupil, ventrolateral strabismus

76
Q

Most common brain tumor in cats

A

Meningioma

77
Q

What region of the medulla receives the impulse from the forebrain for gait generation?

A

Red nucleus (contralateral brain)

78
Q

What are possible causes of CN7 dysfunction?

A
  • idiopathic neuropathy (pretty common in dogs)
  • hypothyroidism
  • middle ear infection (+/- vestibular signs)
79
Q

Why can cats get a D shaped pupil?

A

dysfunction of one of the two ciliary nerves, commonly caused by lymphoma

80
Q

1st order Horner syndrome

A

Lesion in the tectotegmental spinal tract (runs from midbrain deep into brainstem and spinal cord)
These guys present ataxia, paresis, and other intracranial signs

81
Q

2nd order Horner syndrome

A

Lesion in the C6-T2 region (cervical area) and brachial plexus
These guys usually have a mass in the cervical lesion or some kind of forelimb dysfunction (like reduced reflexes)

82
Q

3rd order Horner syndrome

A

Lesion at the level of the skull.

These guys can present with middle/inner ear disease, facial paralysis, vestibular dysfunction

83
Q

What drug combo is commonly used in intracranial immune mediated conditions?

A

Prednisolone and cytarabine (great BBB penetration)

Cytarabine - anti-metabolite

84
Q

Most common cause of trigeminal dysfunction?

A

Idiopathic neuropathy

85
Q

What cranial nerve can be affected by a cervical lesion?

A

Hypoglossal -> droopy tongue

86
Q

What cranial nerves control gag reflex?

A

9 and 10

87
Q

How do you differentiate between proprioceptive, vestibular and cerebellar ataxia?

A

Proprioceptive - often the animal is also paretic. Occurs with a forebrain lesion. Stride length is inconsistent, the animal has no idea where its paws/limbs are
Vestibular- falling, rolling, head tilt, nystagmus…
Cerebellar - the animal has balance but movements are exaggerated, tremors, increased tone.

88
Q

UMN vs LMN paresis

A

UMN damage -> spastic (increased tone) paresis

LMN damage -> flaccid paresis

89
Q

What spinal cord segment is compromised in Schiff Sherrington posture?

A

T3-L3 segment. Border cells in L1-L7 travel cranially to the C2-C6 segment.

90
Q

List all the reflexes to test during a neuro exam. If abnormal, what is the localization?

A

PLR
Vestibulo-ocular
Palpebral
Corneal

Localization = brainstem

91
Q

What responses can you test in a neuro exam that require consciousness? If all of these are abnormal, what is the likely neurolocalization?

A

Facial sensation
Vision
Menace
Proprioception

Localization = forebrain

92
Q

What is the most important prognostic indicator in spinal injuries?

A

Nociception (not the same as withdrawal reflex tho!!!)

Do not test nociception if the animal has voluntary movement and proprioception intact.

93
Q

What plant causes Thiamine deficiency in ruminants? What consequence does the deficiency have?
What are other ways ruminants develop this pathology?

A

Braken fern!!
Causes tan, symmetrical multifocal depression in the cerebrum -> POLIOENCEPHALOMALACIA
Causes intracranial swelling and compression. Clinical signs are severe.
Ruminants can also get it after excessive grain intake

94
Q

List viruses that can cause congenital cerebellar hypoplasia in cows and sheep

A

BVD, Border disease, Schmallenberg

95
Q

What is the most common agent causing meningitis in pigs?

A

Strep suis = Glasser’s disease

This is a disease affecting serosal surfaces (peritoneum, pleura, meninges, joints…)

96
Q

Cow presents with facial paralysis and a protruding third eyelid.
What is the neurolocalization?
What is the most common pathogen that affects this area in cattle?

A

Brainstem.

Listeria monocytogens.
Commonly acquired from spoiled silage

97
Q

How do you distinguish a meningioma from an astrocytoma in a PM?

A

Meningioma -> extra-axial, well-demarcated, compressing mass

Astrocytoma -> intra-axial (arises within spinal cord/cerebrum), hemorragic

98
Q

Cow appears stiff, aggressive, overexcited and has fasciculations. What are your top differentials?
How can you differentiate between them?

A
  • Hypomagnesemia (although likely to be recumbent)
  • (hypocalcemia less likely but treatment is the same as hypomagnesemia)
  • BSE (NOTIFIABLE!!)
  • ketosis

Drench with MgCa and propylene glycol. If she doesn’t respond to treatment call APHA

99
Q

Why is it important that the farmer’s dog doesn’t shit in the pasture?

A

Cows can pick up neospora from it, sheep can pick up coenurosis (CNS tenia)

100
Q

How do you differentiate between Ataxia vs Lameness vs Weakness in horses?

A
  • Ataxia: gait it irregularly irregular +/- circling
  • Lameness: gait is regularly irregular. Always check feet
  • Weakness: horse reluctant to move.
101
Q

Horse presents flaccid tail, colon impaction and urinary incontinence. Where is the lesion in the CNS?

A

Sacral spinal cord.

102
Q

How can you differentiate whether horse is weak due to systemic disease or myopathy?

A

Run bloods. Specifically look at AST and CK (muscle enzymes). they will be increased in myopathies

103
Q

Neurolocalization of Horner syndrome in a horse that also presents with unilateral sweating

A

Brainstem

104
Q

What are the main clinical features of steroid responsive meningitis arteritis?

A
  • common in young patients
  • animal is pyrexic
  • cervical pain (low head carriage)

proprioception will be intact!!!! disorders affecting only the meninges do not cause proprioceptive deficits

105
Q

Do you expect a dog with degenerative myelopathy to be painful?

A

No. The spinal cord has no pain receptors.

106
Q

What kind of lesion do decreased reflexes in all 4 limbs suggest?

A

Neuromuscular.

If the spinal cord was involved you would have decreased reflexes either in the thoracic or pelvic limbs, not both.

107
Q

Horse in the UK presents with ataxia and paresis. What are your top differentials?

A

1) cervical vertebral malformation. super common.
take rads to verify, you either see subluxation of the vertebrae (type 1) or osteoarthitic changes (type 2)
2) EHV.
These horses have paresis that starts from pelvic limbs and progresses to the thoracic limbs. May see other resp signs or history may be suggestive
3) Equine Degenerative Myoencephalopathy
suspect if the horse is young and has no access to pasture (vit E deficiency). Also in these horses the pelvic limbs are waaay more affected than thoracic
4) trauma

108
Q

After the neuro exam you find that a dog has T3-L3 myelopathy. What’s important to do?

A

Check the bladder!! Most of these patients can’t empty it -> it will rupture

109
Q

What are the only two spinal diseases that have a peracute onset and that get progressively better on their own?

A
  • Fibrotic thromboembolism
  • Acute Non Compressive Nucleus Polposus Extrusion

Only way to differentiate is with MRI.

110
Q

What would you recommend to the owner of a horse that suffers recurrent episodes of rhabdomyolysis?

A
  • high fat/low carb diet (rice bran, oil..)

- regular exercise (must be put on a walker every day)

111
Q

What are the muscle enzymes that may be elevated in myopathies? When does their peak occur?

A

CK - 6h post exercise

AST - 24 h post exercise

112
Q

Why is acute rhadbomyolysis an emergency? How do you treat it?

A

myoglobin is toxic to the nephron.
Must treat with fluids and diuretics to encourage excretion. Also is very painful so opioids should be administered (avoid NSAIDs for nephrotoxicity)

113
Q

What is the difference between Becker and Duchenne muscular dystrophy?

A

Becker is the milder form

114
Q

What are the most common myopathies in horses? What are the risk factors for each?

A
  • Atypical myopathy: horse at pasture ingests sycamore or acer leaves
  • Muscle strain injury: any horse that just got injured. return to exercise should be gradual and controlled
  • Exhausted Horse Syndrome: unfit horse that gets overexercised in hot weather
  • Sarcolemmal Na pump myopathy in quarter horses
  • Ryanodine receptor myopathy in quarter horses-> malignant hyperthermia
115
Q

Clinical signs of sacrocaudal luxation

A

Flaccid tail
fecal and urinary incontinence

Differentiate from cauda equina: SCL patients are not commonly lame

Definitive diagnosis made with rads

116
Q

Prognostic indicator for patients with sacrocaudal luxation?

A

Perianal sensation and tone. If present-> higher chance of regaining continence in the next week or two

117
Q

Clinical signs of cauda equina syndrome

A
  • pelvic limb lameness/paresis (with no ataxia)
  • lameness that gets worse with exercise (patients with OA experience the opposite, their lameness get better as they keep moving)
  • +/- flaccid tail
  • +/- fecal and urinary incontinence
  • +/- platigrade stance (with extended hock during reflex test)
118
Q

Risk factors for developing degenerative lumbosacral stenosis

A
  • presence of transitional vertebrae
  • vertebral osteochondrosis (defect in ossification)
  • osteoarthritis (osteophyte formation)
  • any other congenital abnormality that causes vertebral misalignment
119
Q

What is the supportive medical management for degenerative neuromuscular diseases?

A

NSAIDs + gabapentin, cage rest, nursing care

120
Q

A “two engine gait” is most characteristic of what spinal cord lesion?

A

C6-T2

4th Year Exams (8 decks)

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