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Year 4 > SA Neuro > Flashcards

SA Neuro Flashcards

1
Q

Which diagnostic tests can you use to diagnose neuro conditions?

A 
Blood, urine, faecal, microbiology 
Genetic testing
CSF
Imaging (US, radiographs, myelography, CT, MRI)
Electrodiagnostics
Muscle and nerve biopsies
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2
Q

What would you look for on a haematology test when diagnosing neuro disease?

A

Infectious and inflammatory dx
Hyperviscosity (polycythaemia)
Inclusions (lysosomal storage dx)
Thrombocytopenia

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3
Q

What would you look for on a biochemistry test when diagnosing neuro disease?

A

Liver function (bile acid stimulation test, ammonia)
Glucose and fructosamine (weakness, seizures)
Electrolytes (Na, K, Ca-weakness, seizures)
CK, AST (muscle damage)

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4
Q

Which endocrine tests may you run when investigating neuro disease (mainly for neuromuscular disease)?

A
  • Thyroid dysfunction
  • Adrenal dysfunction
  • Insulin
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5
Q

Give some markers for immune-mediated diseases

A
  • Acute phase proteins (eg C-reactive protein, good for steroid-responsive meningitis arteritis SRMA)
  • Acetylcholine receptor antibodies titres (gold standard for acquired myasthenia gravis)
  • Type IIM antibodies titres (gold standard for masticatory muscle myositis)
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6
Q

How does immune-mediated acquired myasthenia gravis work?

A

Forms circulating antibodies against Ach receptors

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7
Q

Which test would you use to diagnose myasthenia gravis?

A

Acetylcholine receptor Ab test= gold standard
Edrophonium test
IV administration of edrophonium chloride (often called tensilon) which is a fast-acting cholinesterase inhibitor
Can have false + and -

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8
Q

Give a potential problem with using the edrophonium test to diagnose myasthenia gravis
How would you resolve it?

A

Can cause a cholinergic crisis: bradycardia, salivation, miosis, dyspnoea, tremors
Give atropine

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9
Q

Which infectious diseases could cause neuro conditions in dogs?

A 
Neospora
Toxoplasma
CDV (distemper)
Cryptococcus
Tick-borne diseases
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10
Q

Which infectious diseases could cause neuro conditions in cats?

A 
FIV
FeLV
FIP
Toxoplasma
Cryptococcus
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11
Q

Why might you carry out metabolic urine screening?

A

To identify genetic diseases causing errors of metabolism
Most abnormal metabolites are concentrated in urine
Metabolic defects that produce organic acid accumulation often affect neuronal and muscle metabolism

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12
Q

Why should you always do a CSF analysis before doing a myelography?

A

The contrast material in the myelogram is irritable and will cause inflammation, which will affect the results of the CSF analysis

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13
Q

Where should you collect a CSF sample from relative to the lesion?

A

Caudal to lesion

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14
Q

When is a CSF analysis contraindicated?

A

Increased intra-cranial pressure (brain could herniate through skull)
Clotting problems (could cause bleeding into spine -> death)
Chiari-like malformations (syringomyelia)
Atlantoaxial instability or trauma

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15
Q

What shoud you never do when taking a CSF sample?

A

Aspirate

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16
Q

How much CSF should you take when obtaining a sample?

A

1ml/5kg

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17
Q

When taking a CSF sample, why should you use a plastic rather than glass tube?

A

Cells adhere to glass -> may get falsely low counts

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18
Q

What should you look at in a CSF analysis?

A

Differential cell count
Cytology
Protein
PCRs

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19
Q

What would you expect in a normal CSF sample?

A

<5 WBC/ul
No RBC
Protein <30-45mg/dl

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20
Q

What are the 2 places you can take a CSF sample from?

A

Cerebellomedullary cistern (atlanto-occipital joint) or lumbar subarachnoid space (L5-L6)

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21
Q

What position should a dog be when you take a CSF sample?

A

Lateral recumbency

Head 90 degrees, nose parallel to table

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22
Q

Where would you take a cervical CSF sample?

A

Imaginary line between occipital protuberance and wings of atlas (cerebellomedullary cystern)

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23
Q

Where would you take a lumbar CSF sample?

A

L5-L6 in dogs

L6-L7 in cats and small dogs (end of spine) (lumbar subarachnoid space)

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24
Q

What size needle should you use when taking a CSF sample?

A

Cervical: 1.5 inch needle, 21-22G
Lumbar: 1.5-3.5 inch needle, 21-22G

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25
Q

What is a pleocytosis?

A

An increased cel count, usually WBCs

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26
Q

For which conditions may you see a neutrophilic pleocytosis in a CSF sample?

A 
(Increased neutrophils)
SRMA (steroid-responsive meningitis arteritis)
Bacerial infection
Granulomatous meningitis
Necrotising encephalitis 
Fungal
FIP
Post-myelography, haemorrhage, trauma, neoplasia
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27
Q

For which conditions may you see a mononuclear pleocytosis in a CSF sample?

A 
Granulomatous meningitis
Necrotising encephalitis 
CNS lymphoma
Viral (distemper)
Bacterial and steroid-responsive meningitis arteritis
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28
Q

For which conditions may you see a mixed pleocytosis in a CSF sample?

A 
Granulomatous meningitis
Bacterial and steroid-responsive meningitis arteritis
Fungal
Protozoal
Non-inflammatory disease (infarction)
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29
Q

For which conditions may you see an eosinophilic pleocytosis in a CSF sample?

A 
(Uncommon)
Eosinophilic meningitis
Fungal
Protozoal
Parasitic
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30
Q

What is myeography?

A

Administration of contrast agent to subarachnoid space to outline the spinal cord
Highlights space-occupying lesions as deviations or thinning of contrast column

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31
Q

CT is good for diagnosing what?

A

Trauma
Haemorrhage and middle ear disease
Fair for tumours and IVDD

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32
Q

What is electrodiagnostics?

A

Recording of electrical activity of muscles or neuronal structures
Can be spontaneous or in response to stimulation

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33
Q

What is electromyography (EMG)?

A

Records spontaneous muscle electrical activity
Normal muscle at rest is electrically silent
Destabilisation of the muscle cell membrane results in spontaneous discharge and so identifies damaged or denervated muscles and lesions

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34
Q

What do nerve conduction velocities (NCV) do?

A

Evaluate peripheral nerve function by stimulating a nerve at 2 different locations and recording:

  • Amplitude of response (strength)
  • Latency of response (how long it takes to get there-to calculate velocity)
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35
Q

What do velocities and amplitude represent on an nerve conduction velocity test?

A

Velocities: myelin
Amplitude: axon

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36
Q

What do repetitive nerve stimulation tests do?

A

Evaluate neuromuscular junctions (eg myasthenia gravis)

If amplitude decreases by >10%, suggestive of disease

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37
Q

What do F wave tests do?

A

Evaluate nerve roots and proximal part of peripheral nerves

Lost/delayed F waves if nerve roots are damaged

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38
Q

What do electroencephalography (EEG) tests do?

A

Record spontaneous electrical activity in cerebral cortex. 5-12 electrodes on head.
Good for:
-Detecting seizures
-Localising seizure focus
-Monitoring response to AEDs (automated external defibrillators) in cases with epilepsy
-Brain death

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39
Q

What do brainstem auditory evoked response (BAER) tests do?

A

Screening tool for detection of congenital sensorineural deafness
Determines hearing threshold in adults
Assess neural lesions on CNVIII or brainstem
Assess for brain death

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40
Q

Why do we take muscle and nerve biopsies when diagnosing neuro disease?

A

Mainly to differentiate between inflammatory and non-inflammatory (metabolic, degenerative) disaese

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41
Q

How big should a muscle biopsy be?

A

0.5 x 0.5 x 1.0cm

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42
Q

How big should a nerve biopsy be?

A

1/3 the width for 1cm

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43
Q

Which nerve is commonly biopsied?

A

Peroneal nerve (cranial tibia mucsle) (easily identified, is both motor and sensory)

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44
Q

Give some neurological deficits of the forebrain

A
  • Altered mental status (depressed/disorientated)
  • Contralateral blindness (decreased menace but normal PLR)
  • Normal gait
  • Circling (ipsilateral), head turn, head pressing, pacing
  • Reduced postural responses in contralateral limb (tells you the lesion is rostral to midbrain)
  • Normal to increased spinal reflexes and muscle tone
  • Seizures, behavioural changes, hemineglect syndrome
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45
Q

How would you identify the location of a lesion using postural reactions?

A
  • Lesions rostral to the midbrain (eg forebrain) -> contralateral reduced responses
  • Lesions caudal to the midbrain (eg SC) -> ipsilateral reduced responses
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46
Q

Give some neurological deficits of the midbrain

A
  • Depression, stupor, coma
  • Cranial nerve deficits, possible vestibular signs
  • Paresis of all or ipsilateral limbs
  • Possible decerebrate rigidity
  • Reduced postural responses in all/ipsilateral limbs
  • Normal to increased spinal reflexes and muscle tone
  • Resp or cardiac abnormalities
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47
Q

Opisthotonus with hyperextension of

all four limbs reflects a lesion where?

A

Brainstem

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48
Q

Give some neurological deficits of the cerebellum

A
  • Normal mentation
  • Ipsilateral menace deficit, normal vision, possibly vestibular signs
  • Possibly decerebellate rigidity (hyperextended FLs, spastic flexion of hips)
  • Intention tremors
  • Truncal ataxia, broad-based stance, hypermetria
  • Delayed then hypermetric postural responses
  • Normal spinal reflexes and muscle tone
  • Rarely increased frequency of urination
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49
Q

Hyperextension of the forelimbs and spastic flexion of the hips reflects a lesion where?

A

Cerebellum

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50
Q

What is meant by ‘white shakers’?

A

-Idiopathic cerebellitis, idiopathic tremor syndrome
-Mostly small breeds, young dogs
-Fine tremor, worse with stress/excitement
+/- head tilt/decreased menace/ leaning and falling, ataxia

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51
Q

How do you diagnose white shakers?

A

CSF-mildly inflammatory

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52
Q

How do you treat white shakers?

What is the prognosis like?

A

Corticosteroids for 4-6 months +/- other immunosuppressive drugs
Good prognosis, may relapse

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53
Q

What are the 3 main methods of infection of bacterial meningitis?

A
  • Haematogenous
  • CSF
  • Direct invasion (eg inner ear, eyes, bite wounds)
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54
Q

Give some clinical signs of bacterial meningitis

A

Usually acute:

  • Obtundation and cranial nerve deficits
  • Neck pain
  • Pyrexia
  • Neutrophilia (50% of cases)
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55
Q

How would CSF be affected by bacterial meningitis?

A
  • Increased protein concentration
  • Pleocytosis (increased lymphocytes)
  • Phagocytosed organisms (rare)
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56
Q

How do you treat bacterial meningitis?

A
  • Antibiotics
  • Surgical drainage
  • Guarded prognosis
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57
Q

Give some clinical signs of increased intracranial pressure

A
  • Altered mental status: obtunded, stupor, coma
  • Altered pupil function: anisocoria, miosis, mydriasis
  • Posture: decerebrate or decerebellate
  • Bradycardia and hypertension (Cushing’s reflex)
  • Physiological nystagmus
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58
Q

What is the oculocephalic reflex?

A
  • When you move head, eyes should follow

- May be absent in comatose patients with brainstem dysfunction eg head trauma

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59
Q

How should you treat a patient with head trauma?

A
  • ABC
  • Oxygenation
  • Restore blood pressure
  • Fluid therapy (avoid glucose)
  • Analgesia
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60
Q

How would you treat raised intracranial pressure?

A
  • Mannitol (decreases blood viscosity) followed by crystalloid fluid therapy to prevent dehydration eg normal 0.9% saline (CI in hypovolaemia)
  • Or hypertonic saline (4mg/kg 7.5% as slow bolus) (CI in hyponatremia)
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61
Q

Give some general care you should consider when treating a patient with head trauma

A
  • Keep head elevated
  • Avoid jugular compression
  • Turn every 4-6 hours
  • Catheterise bladder
  • Nutritional support (tube feeding)
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62
Q

What should you not give to patients with head trauma?

A

Corticosteroids

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63
Q

What is hydrocephalus?

A

Abnormal dilation of the ventricular system within the cranium

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64
Q

Which kinds of dogs are affected by hydrocephalus?

A

Toy breeds, young age

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65
Q

Give some clinical signs of hydrocephalus

A
  • Domed head
  • Persistent fontanellae
  • Abnormal behaviour
  • Cognitive dysfunction
  • Seizures
  • Obtundation
  • Circling/pacing
  • Vestibular signs
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66
Q

How do you treat hydrocephalus?

A
  • Medical: corticosteroids, furosemide, anti-epileptic drugs

- Surgical: ventriculoperitoneal shunt (drains fluid from ventricles into abdomen)

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67
Q

What is lissencephaly?

Which breeds are predisposed to it?

A
  • No development of gyri and sulci

- Llasa apso, Korat cats

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68
Q

Give some clinical signs of lissencephaly

A

-Seizures and behavioural changes

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69
Q

What are hydronencephaly and porencephaly?

A

Presence of cerebral cavities, usually communicating with subarachnoid space and/or lateral ventricles

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70
Q

Give the clinical signs of hydronencephaly and porencephaly

A
  • 1st few months: circling, abnormal behaviour

- Up to a few years: seizures

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71
Q

What is hepatic encephalopathy?

A

Liver dysfunction -> toxins in blood -> brain dysfunction

-Caused by acute liver failure or congenital portosystemic shunt

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72
Q

Give some clinical signs of hepatic encephalopathy

A

Mostly signs of forebrain dysfunction:

  • Seizures
  • Circling, head-pressing
  • Abnormal behaviour
  • Mentation changes (obtundation)
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73
Q

How do you diagnose hepatic encephalopathy?

A
  • Blood ammonia levels
  • Bile acids
  • Liver US or CT
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74
Q

How do you treat hepatic encephalopathy?

A
  • Lactulose (reduces absorption of ammonia from gut)
  • Antibiotics
  • Restricted protein diet
  • Anti-epileptic drugs
  • Surgery
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75
Q

Give the clinical signs of hypocalcaemia

A
  • Muscle spasm and cramping
  • Muscle twitching, trembling, stiffness
  • Mental depression
  • Tonic-clonic spasm
  • Episodic rigidity
  • Tetraparesis
  • Seizures
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76
Q

Give the clinical signs of hypercalcaemia

A
  • Muscle spasm and cramping, muscle twitching -Trembling
  • Mental depression
  • PU/PD
  • Constipation
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77
Q

Give some causes of hypernatremia (high blood sodium)

A
  • Excess water loss
  • Excess salt intake
  • Insufficient water intake
  • Brain abnormalities
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78
Q

Give the clinical signs of hypernatremia (high blood sodium)

A

-Changes in mentation and seizures

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79
Q

How do you treat hypernatremia (high blood sodium)?

A

Correct sodium levels slowly over 48-72 hours

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80
Q

What is a storage disease?

A
  • Defect of a lysosomal hydrolase enzyme
  • Accumulation of storage substrates within the cytoplasm (mainly of neurons) -> cellular dysfunction -> diffuse neurological dysfunction -> progressive -> death
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81
Q

How do you manage storage diseases?

A
  • No treatment

- Symptomatic treatment eg anti-epileptic drugs, anti-anxiety drugs

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82
Q

Give some causes of hypoglycaemia

A

Insulinoma, hepatic dysfunction

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83
Q

Give some clinical signs of hypoglycaemia

A
  • Anxiety, lethargy, depression
  • Ravenous appetite, exercise intolerance
  • Tremors, visual deficit, seizures, coma
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84
Q

How do you diagnose hypoglycaemia?

A

Blood glucose <3mmol/L and clinical signs

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85
Q

How do you treat hypoglycaemia?

A
  • Direct administration of glucose in emergency
  • Frequent feeding in chronic cases
  • Treat underlying cause
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86
Q

Give some primary neoplasms of the brain

A
  • Intra-axial glial cell tumours

- Extra-axial meningiomas, choroid plexus tumours

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87
Q

How do you diagnose brain tumours?

A
  • MRI (sometimes CT)

- CSF analysis (to rule out inflammatory disease)

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88
Q

How do you treat brain tumours?

A
  • AEDs (anti-epileptic drugs)
  • Anti-inflammatory dose of corticosteroids to reduce cerebral oedema
  • Surgery +/- radiotherapy
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89
Q

What is Lafora’s disease?

A
  • Neuronal glycoproteinosis
  • Progressive myoclonic epilepsy
  • Jerking (myoclonic) which is induced by flashing lights, sudden sounds and movements
  • Wire-haired Dachshund and Basset Hound; rare
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90
Q

How do you treat Lafora’s disease?

A
  • Antioxidant-rich diet
  • Avoid starchy/sugary treats
  • Treat epilepsy symptomatically (eg KBr)
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91
Q

Give some clinical signs of vestibular disease

A
  • Head tilt (ipsilateral)
  • Vestibular ataxia and wide-based stance
  • Nystagmus
  • Leaning and falling, sometimes tight circling
  • Positional strabismus
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92
Q

Is a vertical nystagmus normally caused by a defect in the central or peripheral vestubular system?

A

Central

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93
Q

What is a cerebrovascular accident?

A
  • Stroke

- Rapid loss of brain function due to a disturbance in blood supply to the brain

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94
Q

What are the 2 types of cerebrovascular accident (stroke)?

A
  • Ischaemic (majority; results from aterial/venous obstruction)
  • Haemorrhagic (results from rupture of blood vessels)
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95
Q

How do you diagnose a cerebrovascular accident (stroke)?

A

MRI

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96
Q

Give some concurrent medical conditions that could lead to a cerebrovascular accident (stroke)?

A
  • CKD
  • Hypertension
  • Hyperadrenocorticism (Cushings)
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97
Q

What is an MUO?

A

Meningoencephalomyelitis of unknown origin

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98
Q

What are the 3 types of MUO?

A
  • GME= granulomatous meningoencephalomyeitis
  • NME= necrotising meningoencephalomyelitis
  • NLE= necrotising leucoencephalomyelitis
99
Q

Which kind of dogs are more affected by GME (granulomatous meningoencephalomyelitis)?

A

Young adults, toy and terrier breeds

100
Q

What are the 3 forms of GME (granulomatous meningoencephalomyelitis)?

A
  • Disseminated: multifocal signs involving forebrain, cerebellum, brainstem, spinal cord
  • Focal
  • Ocular: acute onset visual impairment, papillary changes, optic disc oedema
101
Q

Which dog breeds are prone to NE (necrotising meningoencephalitis and leucoencephalitis)?

A

Toy breeds eg pugs, maltese, chihuahua, pekinese

102
Q

How do you treat MUOs?

A

-Immunosuppression: corticosteroids, cytosine arabinoside, cyclosporin, lomustine

103
Q

Neurological signs associated with FIP are usually localised to which brain region?

A

Cerebellomedullary

104
Q

Give some neurological clinical signs that can be associated with FIP

A

Tetraparesis, ataxia, nystagmus, loss of balance, sometimes behavioural changes or seizures +/- iritis/anterior uveitis/chorioretinitis

105
Q

Which cranial nerves pass by the middle ear?

A
  • CNVII (facial)

- CNVIII (vestibulocochlear)

106
Q

Give some clinical signs of otitis media/interna

A
  • Pain opening the mouth
  • Horners syndrome
  • Facial paralysis
107
Q

Give some examples of ototoxic drugs

A
  • Antibiotics (aminoglycosides, tetracyclines)
  • Chemotherapy agents (vincristine, cisplatin)
  • Chlorhexidine -> perforated ear drum
108
Q

What is the only thing you should lavage the middle ear with?

A

Warm saline

109
Q

How can you investigate peripheral vestibular disease?

A
  • Examine ear canal
  • If tympanic membrane broken -> swabs, C&S
  • Myringotomy if indicated (small hole in tympanic membrane)
  • Lavage if indicated (warm saline)
  • MRI/CT
110
Q

How can you investigate central vestibular disease?

A
  • MRI
  • CSF analysis
  • Blood pressure/urine analysis/caogulation profile
  • Abdominal US/thoracic radiographs
  • Serology for infectious diseases
111
Q

What is the difference between sensorineural and conductive deafness?

A
  • Sensorineural: failure to conduct sound from cochlea to auditory cortex of brain
  • Conductive: failure to conduct sound from outer ear to inner ear
112
Q

Which dogs and cats are affected by sensorineural deafness?

A

Breeds with white pigmentation and blue eyes eg dalmation

113
Q

How can you assess hearing in dalmation puppies?

A
  • BAER test (brainstem auditory evoked response)

- Done at 8 weeks old

114
Q

Which cranial nerve does a BAER test assess?

A

Vestibulocochlear

115
Q

Which nerve plexus supplies the HLs?

116
Q

Which nerve plexus supplies the FLs?

117
Q

Which nerve plexus supplies the neck?

118
Q

What is discospondylitis?

A

Infection and inflammation of intervertebral disc and adjacent vertebrae

119
Q

Give the clinical signs of discospondylitis

A

Significant spinal pain, may have systemic signs of illness

120
Q

Discospondylitis is most likely to occur where along the spinal cord?

121
Q

Discospondylitis is most commonly caused by which infectious agent?

A

Staph intermedius

122
Q

How do you diagnose discospondylitis?

A
  • Imaging: radiographs, MRI or CT (narrowing of IVD space, roughening of endplates, proliferation of adjacent bone)
  • Bacteriology: blood, urine, CSF
123
Q

How do you treat discospondylitis?

A
  • Long-term antibiotics (based on sensitivity)

- NSAIDs initially when painful

124
Q

What is chiari-like malformation?

A
  • Malformation of the skull- cerebellum protrudes through foramen magnum
  • CKCS
125
Q

How do ischaemic myelopathies usually occur?

A
  • Fibrocartilage from nucleus pulposus embolises in spinal cardvasculature- fibrocartilagenous embolism
  • Hypertension in cats
126
Q

Which dog breed is more affected by ischaemic myelopathies?

A

Miniature schnauzer

127
Q

How do you diagnose an ischaemic myelopathy?

128
Q

How do you treat an ischaemic myelopathy?

A
  • Supportive care, physio

- Usually takes 10 days to walk again (max. 3-4 months)

129
Q

What is SRMA?

A
  • Steroid-responsive meningitis-arteritis

- Immune-mediated inflammation of the blood vessels in the meninges lining the spine

130
Q

What are the clinical signs of SRMA?

A
  • Spinal pain, pyrexia, lethargy

- Occasionally neurological deficits

131
Q

Which dog breeds are more affected by SRMA?

A
  • Boxers, Beagles

- 6-18 months old

132
Q

How do you treat SRMA?

A

-Corticosteroids for 4-6 months +/- other immunosuppressive drugs (azathioprine)

133
Q

How do you diagnose SRMA?

A
  • Leucocytosis with neutrophilia
  • CSF analysis: increased neutrophils and protein
  • Increased IgA in CSF and serum
134
Q

Atlanto-axial (AA) instability occurs in which dog breeds?

Why?

A
  • Young dogs, toy breeds

- Failure of ligamentous support between the two vertebrae, usually asociated with aplasia/hypoplasia of the dens

135
Q

Give some clinical signs of atlanto-axial intability

A
  • Neck pain

- Ataxia or tetraplegia

136
Q

How do you treat atlanto-axial instability?

A
  • Conservative splint for 6-12 weeks

- Surgery

137
Q

Give some clinical signs of chiari-like malformation

A
  • Neck pain
  • Neck scratching
  • Torticollis/scoliosis
  • Thoracic limb weakness and atrophy
138
Q

How do you treat chiari-like malformation?

A
  • Medical: NSAIDs, furosemide, gabapentin, corticosteroids, amantadine
  • Surgery
139
Q

What is the difference between Hansens type I and II IVDD (intervertebral disc disease)?

A
  • Type I: herniation of nucleus pulposus through annular fibres and extrusion into the spinal canal (chondrodystrophic breeds)
  • Type II: annular protrusion but no extrusion of nuclear material (large breed dogs)
140
Q

Intervertebral disc disease typically affects which vertebrae?

141
Q

How would you diagnose IVDD?

A
  • Radiography: narrowed IVD space (spondylosis with type II)
  • Myelography
  • CT, MRI
142
Q

How would you treat IVDD?

A
  • Conservative: strict rest for 6-8 weeks for type I, 4-6 weeks for type II, NSAIDs
  • Surgical: if neurological deficits/ severe or recurrent pain
143
Q

Give some clinical signs of cervical spondylomyopathy (‘Wobbly dog’)

A
  • Large breeds and Basset hounds
  • Progressive ataxia, tetraparesis, sometimes pain
  • Signs worse in the pelvic limbs (paresis, ataxia)
  • Short stilted gait and muscle atrophy in thoracic limbs
144
Q

What might hyperviscosity of blood indicate?

A

Polycytaemia

145
Q

What might inclusion bodies indicate on a haematology?

A

Lysosomal storage disease

146
Q

What is the gold standard diagnostic tool for the acquired form of Myasthenia Gravis?

A

Acetylcholine receptor antibodies titres

147
Q

What is the gold standard diagnostic tool for masticatory muscle myositis?

A

Type 2M antibody titres

148
Q

Seizures occur due to a change in activity where?

149
Q

Give some deficits associated with a forebrain lesion

A

Seizures
Circling
Behaviour change
Head turn (to side of lesion)

150
Q

Give the 4 stages of a seizure

A
  1. Prodrome (any predicting events)
  2. Aura (initial manifestation of seizure)
  3. Ictal (seizure event- involuntary muscle tone or movement +/- abnormal sensations or behaviour)
  4. Post-ictal (can have unusual behaviour or neurological deficits for minutes to days after)
151
Q

How long does the ictal stage of a seizure normally last?

A

60-90 seconds

Occurs most commonly at sleep or rest

152
Q

What are the 2 major categories of seizure?

A

Generalised (involvement of both cerebral hemispheres simultaneously; consciousness is impaired)
Focal (activation of one part of one cerebral hemisphere)

153
Q

What are the phases of a generalised seizure?

A

Tonic-clonic (most common)
Tonic (conraction of all skeletal muscles, legs out, head back)
Clonic (rhythmic movements eg jerking, clamping jaw, paddling of legs)
Myoclonic (sudden jerking motions
Atonic (sudden and general loss of muscle tone -> collapse)

154
Q

What are the forms of a focal seizure?

A

Motor
Autonomic
Behavioural

155
Q

What are audiogenic reflex seizures?

A

Cats, late onset (15yrs)

Myoclonic seizures caused by high-pitched sounds (can progress to tonic-clonic)

156
Q

How do you control audiogenic reflex seizures?

A

Levetiracetam

157
Q

What are the criteria for a diagnosis of idiopathic epilepsy?

A

2 or more seizures (24 hours apart)
Age of onset 6m to 6y
Unremarkable inter-ictal examination (period between seizures)
No clinically significant abnormalities on minimum database (haem/biochem/fasting bile acids/urinalysis)
Unremarkable MRI and CSF analysis

158
Q

When should you start treatment for epilepsy?

A

Structural/metabolic epilepsy
Status elipticus or cluster seizures
6 months or less between seizures
Post-ictal signs are severe or last longer than 24 hours
Seizure frequency and/or duration is increasing
1st seizure is within 1 month of a traumatic event

159
Q

Are any seizure medications licensed in cats?

160
Q

Which are the 3 licensed seizure medications?

A

Phenobarbitone
Bromide (Potassium or sodium bromide salts)
Imepitoin

161
Q

What is the mechanism of action of phenobarbitone?

A

Enhances GABA (inhibitory neurotransmitter of CNS)

162
Q

What are the initial doses for phenobarbitone in cats and dogs?

A

Dogs: 3mg/kg BID
Cats: 2mg/kg BID

163
Q

Give some side effects of phenobarbitone

A

Sedation, ataxia
PUPD, polyphagia
Hepatotoxicity
Haematological abnormalities (anaemia, neutropenia, thrombocytopenia)

164
Q

When is phenobarbitone contra-indicated?

A

Dogs with hepatic dysfunction

165
Q

What is the mechanism of action of bromide (anti-seizure medication)?

A

Raises the seizure threshold by inhibiting transport of Na+

166
Q

What are the initial doses for bromide in cats and dogs?

A

Dogs: 30mg/kg SID

DON’T USE IN CATS

167
Q

Give some side effects of bromide

A

Sedation

Ataxia and HL weakness

168
Q

What is the dose for imepitoin in dogs?

A

10-30mg/kg BID

169
Q

What is status elipticus?

A

Seizure lasting >5 mins, or >2 seizures without full recovery
Emergency

170
Q

What are cluster seizures?

A

2 or more seizures within 24 hours

Emergency

171
Q

Give some causes of status elipticus seizures in dogs

A 
Neoplasia
CNS inflammatory disease
Trauma
Metabolic disorders
Toxicities
Idiopathic epilepsy
172
Q

Why are status elipticus and cluster seizures an emergency?

A

Stage 1: increased autonomic activity (tachycardia, hypertension, hyperglycaemia)
Stage 2: irreversible neuronal damage (after 30 mins; hypotension, hypoglycaemia, hyperthermia, hypoxia, brain damage)

173
Q

How do you stop a seizure?

A

Diazepam 1mg/kg per rectum

174
Q

What is meant by ‘breakthrough seizures’?

A

When an epileptic dog is medicated and still has seizures, we call them “breakthrough seizures”

175
Q

How would you begin medicating a dog that is experiencing cluster seizures/status elipticus?

A

Place iv catheter
Phenobarbital 3mg/kg BID
If seizures don’t stop/there are further seizures over the next 1-3 hours: phenobarbital iv loading (boluses)
If further seizures: levetiracetam loading

176
Q

Give a side effect of using potassium bromide as an anti-seizure medication in cats

A

Eosinophilic bronchitis

177
Q

Give a side effect of using diazepam as an anti-seizure medication in cats

A

Hepatic necrosis (oral administration)

178
Q

Give some differentials for acute onset non-ambulatory tetraparesis

A

Neuropathy: polyradiculoneuritis
Junctionopathy: myasthenia gravis, botulism, organophosphate toxicity
Myopathy: severe polymyositis, electrolyte abnormalities eg Addisons

179
Q

Which markers do we use for acquired myasthenia gravis?

A

Acetylcholine receptor antibodies

180
Q

Which markers do we use for masticatory myositis?

A

2M antibodies

181
Q

What is polyradiculoneuritis?

A

Inflammation of nerve and roots

Fairly common

182
Q

Give some causes of polyradiculoneuritis

A

Idiopathic/rabies vaccine, immune-mediated?
Breed predisposition in Bengal cats
Demyelination

183
Q

Give some clinical signs of polyradiculoneuritis

A

Acute onset, rapidly progressive (days)
Tetra/paraparesis -> non-ambulatory tetraparesis/plegia
Flaccid, reduced motor fuction (inc absent reflexes)
Can affect respiratory muscles

184
Q

How do you diagnose polyradiculoneuritis?

A

Electrophysiology (f waves will be lost/delayed) and CSF analysis (lumbar)

185
Q

How do you treat polyradiculoneuritis?

A

Supportive: nursing, physio, ventilatory support if necessary
Fair prognosis

186
Q

What is myasthenia gravis?

A

Muscle weakness due to reduced neuromuscular transmission

187
Q

What causes the 2 forms of myasthenia gravis?

A

Acquired: immune-mediated; Ab-mediated destruction of acetylcholine receptors
Congenital: deficiency of acetylcholine receptors

188
Q

> 80% of dogs with myasthenia gravis also have what?

A

Megaoesophagus (only 15% in cats)

189
Q

Which cat breed is predisposed to myasthenia gravis?

A

Abysinnian

190
Q

25% of cats with myasthenia gravis also have what?

191
Q

How do you treat myasthenia gravis?

A

Anti-cholinesterase (pyridostigmine po)
Immunosuppression?
Postural feeding if mega-oesophagus

192
Q

What is meant by the ‘fulminant’ form of myasthenia gravis?

A

Sudden onset of megaesophagus and frequent regurgitation of large volumes of fluid

193
Q

How does botulism affect nerves?

A

Toxins prevent acetylchline release at nerve junctions

194
Q

Give some clinical signs of botulism

A

Acute onset rapidly-progressing tetraparesis
Cranial nerves may be affected: facial paralysis, megaoesophagus, altered jaw tone
Respiratory muscles may be affected
Urinary dysfunction, GI dysmotility, mydriasis, reduced tear production

195
Q

How do you treat botulism?

A

Supportive care

Physiotherapy

196
Q

Give some clinical signs of immune-mediated polymyositis

A

Exercise intolerance, generalised weakness, muscle atrophy

Pyrexia, stiffness, non-ambulatory tetraparesis, reluctance to move, lowered head carriage, myalgia (muscle pain)

197
Q

How do you diagnose immune-mediated polymyositis?

A

Inflammatory leucogram, elevated CK/AST

Muscle biopsies

198
Q

How do you treat immune-mediated polymyositis?

A

Prednisolome +/- other immunosuppressives

199
Q

Are cats or dogs affeced by masticatory myositis?

200
Q

Why does masticatory myositis occur?

A

Antibodies to 2M myosin -> myositis

201
Q

Give some clinical signs of acute and chroninc masticatory myositis

A

Acute: swollen/painful masticatory muscles, exophthalmos
Chronic: trismus (pain/fibrosis), mastictory muscle atrophy

202
Q

How do you diagnose mastictory myositis?

A

Imaging
CK (may be slightly elevated)
2M antibodies

203
Q

How do you treat masticatory myositis?

A

Prednisolone +/- other immunosuppressive drugs

Physio

204
Q

What is the most likely cause of an infectious myositis?

A

Protozoa eg Toxoplasma, Neospora

205
Q

Give some clinical signs of Neosporosis in puppies

A

Radiculoneuritis and polymyositis
Pelvic limb hyperextension
Ascending paralysis of pelvic limbs with muscle contracture and arthrogryposis

206
Q

How do you diagnose Neosporosis in puppies?

A

Clinical signs, biopsy, CK/AST. serology

207
Q

How do you treat Neosporosis in puppies?

A

Clindamycin/TMPS and pyrimethamine

208
Q

What is neuropraxia?

A

Temporary nerve damage but no disruption of the nerve or myelin sheath
Good prognosis, will return to normal function in a few days

209
Q

What is axonotmesis?

A

Disruption of the axon but intact myelin sheath

Good prognosis but slow recovery

210
Q

What is neurotmesis?

A

Partial/complete transection of the nerve

Partial recovery is possible

211
Q

Give some clinical signs of brachial plexus avulsion

A

Monoparesis, cutaneous trunci absent ipsilaterally, Horner’s syndrome

212
Q

Give some clinical signs of a brachial plexus tumour?

A

Malignant peripheral nerve sheath tumour
Chronic progressive thoracic limb lameness, pain, muscle atrophy
Neurological deficits

213
Q

How do you diagnose a brachial plexus tumour?

A

Electrodiagnostics

Imaging (MRI best)

214
Q

How do you treat a brachial plexus tumour?

215
Q

How do you differentiate central from peripheral vestibular disease?

A

Central: may have paresis and prorioceptive deficits, nystagmus may be vertical, horizontal or rotatory
Peripheral: may have Horner’s syndrome, nystagmus may be horizontal or rotatory

216
Q

Give some causes of acute onset vestibular disease

A

Idiopathic vestibular dz
Cerebrovascular dz
Head trauma
Trauma to middle/inner ear

217
Q

Give some causes of chronic onset vestibular disease

A 
Otitis media/interna
Brain and middle ear tumours 
Thiamine deficiency 
Lysosomal storage dz
MUO, FIP
Degenerative dz
Brain malformation
Congenital vestibular dz
218
Q

Give some causes of vestibular disease that can be acute or chronic onset

A

Metronidazole toxicity
Ototoxic drugs
Hypothyroidism

219
Q

How do you diagnose MUOs?

220
Q

How do you diagnose FIP in cats?

A

Clinical signs
Lymphopenia, neutrophilia, non-regenerative anaemia
Increased serum alpha-1-acid glycoprotein
High serum titres of feline coronavirus Ab
MRI: ventricular dilation

221
Q

Give some signs of metronidazole toxicity

When does it occur?

A

Seizures, tremors, rigidity, hypermetria

Usually when doses are >60mg/kg/day

222
Q

How do you treat metronidazole toxicity?

A

Discontinue drug

Give diazepam

223
Q

Give some clinical signs of a thiamine deficiency

A

Bilateral central vestibular signs, seizures

224
Q

Give some clinical signs of bilateral vestibular disease

A

Crouching low to the ground
May fall to both sides
Wide lateral excursions of the head

225
Q

What age of dogs are affected by idiopathic vestibular disease?

A

Adult to geriatric

226
Q

How do you treat idiopathic vestibular disease?

A

No tx needed-will resolve spontaneously

227
Q

How do you diagnose idiopathic vestibular disease in dogs?

A

Diagnosis of exclusion

228
Q

What are the 2 forms of feline idiopathic vestibular disease?

A

Acute onset, non-progressive, improves over 2-4 weeks
Atypical form: acute onset but clinical signs progress over 3 weeks; recover after 3 months but milk residual head tilt may remain

229
Q

How do ischaemic myelopathies occur?

A

Fibrocartilage from nucleus pulposus embolises in the spinal cord vasculature -> fibrocartilagenous embolism -> blocks off blood supply to part of spinal cord

230
Q

When do clinical signs of ischaemic myelopathies occur?

What signs do you see?

A

Exercise

Vary from mild weakness or incoordination, to inability to walk

231
Q

What is chiari-like malformation?

A

Mismatch between caudal fossa volume and its contents, with caudal displacement of the cerebellum through foramen magnum
Can develop syringomyelia (fluid-filled ‘cyst’ in spinal cord)

232
Q

How do you diagnose cervical spondylomyelopathy?

A

Myelography +/- CT, MRI

233
Q

How do you treat cervical spondylomyelopathy?

A

Anti-inflammatories, rest

Surgery

234
Q

What is ‘cauda equina’ syndrome?

A

Degenerative lumbosacral stenosis
Arthritis of the joint between the last lumbar vertebra and the sacrum -> narrowing of spinal canal -> pressure on nerves coming off spinal cord

235
Q

Give some clinical signs of ‘cauda equina’ syndrome?

A

Reluctance to exercise, rise, jump into car, do stairs
Proprioceptive deficits, reduced withdrawal reflex, muscle atrophy
Lameness
Lumbosacral/hip pain
Mono/paraparesis
Urinary and/or faecal incontinence

236
Q

How do you treat cauda equina syndrome?

A

Conservative: rest and NSAIDs
Surgery: dorsal laminectomy/ dorsal fusion-fixation/ foraminotomy

237
Q

Give some clinical signs of degenerative myelopathy

A

Insidious, progressive ataxia and paresis of pelvic limbs -> paralysis
Not painful
Age of onset: 5-9y

238
Q

Are there any treatment options for degenerative myelopathy?

A

No therapeutical options

Physio

239
Q

How do you perform a hemilaminectomy?

A

Remove one half of the vertebral arch (lamina, articular process and pedicle) and expose spinal cord -> remove ruptured disc material
Used to correct slipped or herniated discs in the thoracolumbar spine

240
Q

How do you perform a dorsal laminectomy?

A

Remove dorsal spinous process and laminae -> access to spinal cord

241
Q

Which drug can you give to dogs with canine cognitive dysfunction?

A

Selegiline

242
Q

Give some clinical signs of canine cognitive dysfunction?

A

Disturbances in sleeping; pacing/vocalising at night
Getting stuck in corners, staring into space
Loss of house-training ability
New behavioural problems

243
Q

What is myelography?

A

Injection of positive contrast into subarachnoid space

244
Q

Where should you inject when doing a myelography?

A 
Cistern puncture (easier)
Lumbar puncture (safer, more difficult)

Year 4 (51 decks)

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