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Neurology Flashcards

1
Q

Signs of forebrain dysfunction

A
  1. Altered mental status
  2. Behavioural change
  3. Blindness (central) w/ decreased/absent menace reflex
  4. Loss of smell
  5. Abnormal movements and posture
  6. Altered postural reactions
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2
Q

Signs of brainstem dysfunction

A
  1. CN deficits
  2. Proprioceptive deficits
  3. Hemi/tetraparesis
  4. Stupor or coma w/ abnormal pupil size
  5. Abnormalities in resp. and CDV function
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3
Q

Signs of cerebellum dysfunction

A
  1. Unaltered (normal) mental status
  2. Intention tremors (head and eye) and hypermetria w/ preservation of strength
  3. Ataxia, wide base stance (ie. vestibular signs)
  4. Loss of menace response
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4
Q

4 segments of the spinal cord

A

C1-C5
C6-T2
T3-L3
L4-S3

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5
Q

List the order in which spinal functions (4) are lost

A
  1. CP
  2. Voluntary motor function
  3. Superficial pain sensation
  4. Deep pain sensation
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6
Q

What is the motor function of UMN lesions?

A

reduced

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7
Q

What is the motor function of LMN lesions?

A

reduced

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8
Q

What is the muscle tone of UMN lesions?

A

increased

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9
Q

What is the muscle tone of LMN lesions?

A

reduced

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10
Q

contrast the muscle atrophy of UMN and LMN lesions?

A

UMN: slow and mild
LMN: rapid and severe

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11
Q

increased reflexes are associated with UMN or LMN lesions?

A

UMN

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12
Q

why might a dog with forebrain disease have a decrease in appetite?

A

due to loss of smell

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13
Q

most common congenital cause of forebrain disease

A

hydrocephalus

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14
Q

ddx for acquired forebrain disease

A 
D
A: epilepsy
M: metabolic disorders (seizures)
N: brain tumours
I: inflammatory diseases (meningoencephalitis)
T: hydrocephalus
V: vascular accidents
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15
Q

why is congenital hydrocephalus usually asymptomatic?

A

because the CPP is normotensive

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16
Q

surgical management of hydrocephalus includes

A

insertion of a ventriculoperitoneal shunt

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17
Q

how do prednisolone/omeprazole help hydrocephalus cases?

A

they decrease CSF production

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18
Q

when are mannitol +/- frusemide indicated in hydrocephalus cases?

A

emergencies!

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19
Q

3 types of metastatic brain cancer

A
  • haemangiosarcoma
  • melanoma
  • mammary carcinoma
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20
Q

tumors arising from meninges or supportive structures

A
  • meningioma
  • gliomas
  • choroid plexus tumours
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21
Q

describe the palliative care plan of a dog with a brain tumour

A
  • dexamethasone then prednisolone = glucocorticoids reduce the peri-neoplastic inflam and oedema and can be surprisingly effective
  • manage seizures w/ anti-epileptic drugs
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22
Q

list 4 underlying disease states that could cause a ‘stroke’ in dogs

A
  • renal disease
  • hyperA
  • hypertension
  • hypercoagulable states
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23
Q

treatment of a ‘stroke’ in a dog

A

no specific treatment - episodes usually resolve over time (hrs to days)

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24
Q

the presence of an ‘aura’ indicates

A

that the cause of the seizure is intracranial

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25
Q

the most common type of seizure is

A

a generalised motor seizure - clonic-tonic muscle activity

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26
Q

describe the appearance of a partial/focal seizure

A

limited to a single region of motor activity - movement of a single limb/’fly catching’

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27
Q

describe the concept of kindling

A

The understanding that seizure frequency worsens over time and the seizure focus expands and enlarges to involve other regions of the brain. (like kindling a fire)
Thus best reason to be proactive in tx. of seizures

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28
Q

Generalisations of extracranial caused seizure presentation

A
  • sudden in onset, generalised/cont (status) as caused by sudden exposure to toxin/metabolic crisis
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29
Q

Generalisations of intracranial caused seizure presentation

A
  • tend to be isolated or clusters
  • worsen (freq + severity) over wks - months
  • focal or general
  • usu have all three phases
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30
Q

what are the 3 phases of seizures

A
  1. aura
  2. seizure
  3. post-ictal
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31
Q

DDx for intracranial causes of seizures

A

D: hydrocephalus
A: meningoencephalitis of unknown aetiology (necrotizing encephalitis, GME), idiopathic epilepsy
M
N: neoplasia
I: viral (CDV, FIP), parasite (neospora), fungal (cryptococcus)
T
V: cerebrovascular accidents (+ underlying disease)

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32
Q

when would you strongly advise seizure investigation?

A

If >1 seizure/cluster/status or residual neurological abnormalities between seizures

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33
Q

what infectious diseases do you want to rule out early in seizure investigations?

A

Toxoplasma
Neospora (dogs)
Cryptococcus
FIP (cats)

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34
Q

Rough cost of CSF tap and analysis

A

1k

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35
Q

CT scan estimated cost

A

1.5-2k

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36
Q

MRI cost

A

> 2k

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37
Q

idiopathic epilepsy is unusual in cats (T/F?)

A

true - more likely to have primary disease

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38
Q

age of onset of idiopathic epilepsy

A

1-5yrs

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39
Q

two initial choices of AED

A
  1. Phenobarbitone

2. Imepitoin

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40
Q

add potassium bromide to initial treatment of idiopathic epilepsy if:

A
  1. Young GSD

2. Dogs w/ particularly severe seizures

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41
Q

Phenobarbitol dose

A

2-4mg/kg q12h PO

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42
Q

main side effects of phenobarbitol

A

drowsiness, ataxia – once tolerance develops this usu. wears off

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43
Q

less common side effect of phenobarbitol

A

PU/PD, polyphagia, biochemical hepatopathy

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44
Q

what is your aim phenobarbitol serum concentration?

A

15-30ug/ml

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45
Q

MOA of imepitoin

A

partial GABA agonist

46
Q

Imepitoin dose

A

10mg/kg q12h PO

can increase by 10mg weekly to maximum dose 30mg/kg q12 PO if seizures not controlled

47
Q

Potassium bromide dose w/ pheno

A

20-30mg/kg/day (single or divided) PO w/ phenobarbitol

48
Q

Potassium bromide dose alone

A

40-50mg/kg/day (max 80mg/kg)

49
Q

how long should you be seizure free before considering to stop AED?

A

at least 12months –> still risk of recurrence

50
Q

reasons for refractory epilepsy

A
  1. Disease related: undiagnosed underlying disease/cause
  2. Drug related: not efficacious - inadequate dose/serum levels
  3. Patient/client related: poor compliance
51
Q

List 4 AED you can add to PB

A
  1. Imepitoin
  2. Levetiracetam (Keppra)
  3. Gabapentine (Neurontin)
  4. Zonisamide
52
Q

Levetiracetam dose

A

20mg/kg q8h IV/PO

53
Q

Gabapentin dose

A

20mg/kg q8h IV/PO

54
Q

Common extracranial causes of seizures

A

Hypoglycaemia

Hypocalcaemia

55
Q

Less common extracranial causes of seizures

A
  1. Toxins (most cause SE - some recurrent)
  2. Electrolyte derangement (esp. Sodium)
  3. Hyperlipidaemia
  4. Thiamine deficiency
  5. Polycythemia
  6. Hypoxaemia (advanced resp. or cardiac disease) differentiate from syncope
56
Q

List 6 toxins that cause seizures

A
  1. OPs and carbamates: snail baits/ sprays
  2. Metaldehyde
  3. Rodenticides (1080, strychnine)
  4. Mouldy food (penetrem mycotoxin)
  5. Lead (paint, fishing sinkers)
  6. Bufo toxins (toads
  7. Pyrethrins (cats)
  8. Naphthalene (cats)
57
Q

What drug + dose can you use to stop SE?

A
  1. diazepam 0.5-1mg/kg IV bolus
  2. Midazolam 0.2mg/kg IV bolus
    Rpt up to two more times
58
Q

If seizures do not stop after 2 boluses of diazepam at 1mg/kg IV what drug can you use next?

A
  1. Phenobarbitol 2-4mg/kg IV to effect
  2. Levetiracetam IV
  3. Propofol 1-3.5mg/kg IV bolus OR 6-12mg/kg/h CRI
59
Q

what are two relatively common complications of prolonged seizure activity?

A
  1. Cerebral oedema

2. Hyperthermia

60
Q

Abnormalities of eye position can be caused by dysfunction in which CNs?

A

CN III, IV and VI

61
Q

How can you test CN VII?

A
  • menace reflex

- palpebral reflex

62
Q

what nerves does the menace reflex test?

A

CN II and VII

63
Q

what nerves does the palpebral reflex test?

A

CN V and VII

64
Q

DDx of CN VII paralysis?

A 
D: myasthenia gravis
A: idiopathic
M: hypoT (debated)
N: neoplasia of CN VII or assoc. structures
I: otitis media/interna
T: trauma (to side of head)
V
65
Q

causes of temporal muscle atrophy

A
  • Trigeminal nerve disease
  • MMM
  • corticosteroid use
  • old age
66
Q

what are the two functions of the CN V?

A

Trigeminal nerve

  • sensory nerve of the face
  • motor nerve (LMN) to muscles of mastication
67
Q

Treatment for idiopathic trigeminal neuritis

A

there is none

- assist eating/nutrition - tube/hold mouth closed

68
Q

DDx for unilateral CN V disease

A

nerve sheath tumour

69
Q

Dx of MMM

A

CS and serum [anti-2M fibre antibodies]

70
Q

damage to the oculomotor nerve (CN III) results in

A

lateral strabismus

71
Q

damage to the trochlear nerve (CN V) results in

A

rotated strabismus?

72
Q

damage to the abducens nerve (CN VI) results in

A

medial strabismus

73
Q

4 signs of horner’s syndrome

A
  • miosis
  • enopthalmus
  • prolapse of third eyelid
  • ptosis
74
Q

what are the three neural components that when damaged result in horner’s?

A
  1. UMN midbrain to T1-3
  2. LMN vagosympathetic trunk to cranial cervical ganglion
  3. LMN cranial cervical ganglion to eye
75
Q

DDx for horner’s syndrome

A

50% idiopathic vs other.
T: brachial plexus nerve root injury/avulsion, neck injuries (choker chains, needle stick, bite wounds), otitis externa/media, skull fractures and retrobulbar lesions, cervical spinal injury, anterior mediastinal lesions, brainstem injury

76
Q

define syncope

A

sudden, transient loss of consciousness and postural tone - a secondary neuro event to an extracranial disease

77
Q

3 causes of ataxia

A
  1. vestibular disease
  2. cerebellar disease
  3. sensory (proprioceptive) deficit (dt disruption of sensory pathways) - loss of sence of limb/body position. Any lesion of sensory pathways in peripheral nerves or central in spine (most common) or brain.
78
Q

4 neuro signs of vestibular disease

A
  • ataxia
  • head tilt
  • nystagmus
  • falling/circling
79
Q

the disease process of central vestibular system occurs in..

A

the vestibular nuclei in brainstem

80
Q

the disease process of peripheral vestibular system occurs in..

A
  • the inner ear (semicircular canals)

- cranial nerve VII

81
Q

differentiate peripheral and central vestibular disease based on CS

A

P: often has Horner’s and CN VII/V signs
C: often has nystagmus changes direction, vertical nystagmus, CP and postural deficits and paresis, but RARELY horners/CN V/VII signs

82
Q

Causes of peripheral vestibular disease

A
  • otitis externa (externa/media)
  • ototoxic drugs
  • trauma to lateral skull
  • tumours of middle ear
  • idiopathic (geriatric)
83
Q

causes of central vestibular syndrome

A
  • brain tumours (meningiomas, choroid plexus papillomas)
  • GME
  • meningoencephalitis - cryptococcus, toxoplasma, neospora, viral CDV
  • metronidazole toxicity
  • head trauma
  • cerebrovascular accidents
84
Q

management of idiopathic peripheral vestibular syndrome

A
  • remove from owners 24-48hrs
  • keep in quiet/dark
  • maropitant 1-2mg/kg q24h SC (motion sickness) OR ACP judicious dose
  • should improve over 24-48hs and gradually recover over 1-4wks
85
Q

congenital and acquired cerebellar disease results in severe ataxia with preservation….

A

of strength and normal mentation (unless multifocal cause)

86
Q

DDx for generalised LMN disease

A

D: Drugs (vincristine, cisplatin), myasthenia gravis
A:
M: hyperglycaemia (cats w/ diabetic neuropathy), hypoglycaemia, lytes (Na, K, Ca), hypothyroidism
N: paraneoplastic syndromes, lymphoma
I: polyradiculoneuritis, toxoplasma or neospora polyneuritis
T: envenomation (Ixodes holocyclus/cornuatus, snakes), poisons (tetrodotoxin, botulism)
V: hypoxaemia/ischaemia (FATE)

87
Q

diseases of the NMJ

A
  • tick paralysis
  • botulism
  • myasthenia gravis
88
Q

What is idiopathic polyradiculoneuritis?

A

aka Coonhound paralysis –> immune-mediated inflm of the spinal nerves causing ascending tetraparesis/plegia for 2-4d

89
Q

recovery period of idiopathic polyradiculoneuritis?

A

weeks to months

90
Q

management actions of prolonged recumbency

A
  1. Good nursing care + proactive rehab
  2. Hydration via IVFT
  3. Nutrition: hand feeding/tube
  4. Freq. turning
  5. Physio
  6. Cushions/padded support
  7. Bladder/bowel care - U-cath, shave hair + barrier creams, mild laxatives, nappies?
91
Q

Complications of recumbency

A
  1. Progressive muscle atrophy
  2. Pressure sores and necrosis
  3. UTI
  4. Pneumonia
92
Q

what AB for toxoplasmosis/neospora?

A

clindamycin

93
Q

Most common causes of meningoencephalitis

A
  1. Granulomatous meningoencephalitis (GME)

2. Aseptic meningitis-arteritis (‘steroid-responsive meningitis arteritis’ SRMA)

94
Q

Causes of infectious meningoencephalitis

A
  1. Fungal -cryptococcosis and aspergillus (in GSD)
  2. Protozoal – neosporosis and toxoplasmosis
  3. Bacterial – very low incidence. Any bacteria (Brucella canis overseas)
  4. Viral – very low incidence in dogs AUS. Distemper and rabies overseas. FIP in cats.
95
Q

GME diagnosis requires

A

CSF collection –> Mononuclear pleocytosis (lymphocytes and macrophages), increased protein (but normal CSF has also been recorded occasionally)

96
Q

GME tx

A
  1. Immunosuppressive medication:
    - Pred 2-4mg/kg/day divided
    - Cytarabine 50mg/m2 q12h for 4 doses rpt q3wks for 4 cycles
97
Q

survival time for GME

A

1-2.5yrs

98
Q

what type of dog usu. gets GME?

A

small/minis, geriatric

99
Q

Prognosis of SRMA

A

good prognosis, tx/ w prd for 6-12months

100
Q

Detrusor muscle is innervated by

A

the pelvic nerve (parasymp) (S1-S3) and hypogastric nerve (L1-L4) (symp)

101
Q

Internal urethral sphincter (smooth m.) is innervated by

A

the hypogastric n (L1-L4)

102
Q

Anal sphincter and external urethral sphincter are innervated by

A

pudendal nerve (S1-S3)

103
Q

UMN bladder signs

A

Increased tone to external urethral sphincter: urethral obstruction, full bladder that is difficult to express

104
Q

what segment of the spinal cord results in UMN bladder signs

A

cranial to segment L7 ( = L5 vertebrae)

105
Q

LMN bladder signs

A

Decreased tone to external urethral sphincter: incontinence, bladder that is easy to express

106
Q

Define neurapraxia

A

Mildest form of nerve injury from blunt trauma or compression. Transient conduction block w/out nerve degeneration  recovery in weeks to months

107
Q

Define axonotmesis

A

Disruption of nerve cell axon, w/ Wallerian degeneration occuring below and slightly proximal to the site of injury. Axons and their myelin sheath are damaged, but Schwann cells, the endoneurium, perineurium and epineurium remain intact –> loss of conduction but recovery is possible at ~1mm/day.

108
Q

Define neurotmesis

A

Both nerve and nerve sheath disrupted (eg. Severance) –> regeneration will not occur, no recovery

109
Q

Immune-mediated polymyositis can often see very elevated CK - what values?

A

2,000-20,000+

110
Q

tx of immune-mediated polymyositis

A

corticosteroids + other immunsuppresives

  1. Prednisolone +
  2. Azathioprine OR cyclosporine OR mycophenolate
111
Q

if immune-mediated polymyositis is not treated what happens?

A

fibrosis and stiffness of muslces

pc vet (16 decks)

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