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Neurology Flashcards

1
Q

Give two examples of things that differ in neuro exam between central and peripheral vestibular disease

A
  • central: cranial nerves other than CN VII affected (ipsilateral to lesion) (peripheral can have affected CN 7 and horners syndrome)
  • central: loss of proprioception and motor function
  • central: mentation changes
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2
Q

What are the three parameters measured in modified glasgow coma score?

A

Motor activity, brainstem reflexes, level of consciousness

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3
Q

what are the levels/points in motor activity in the modified Glasgow coma scale?

A
  1. normal gait, normal spinal reflexes
  2. hemipares, tetrapares
  3. recumbent, intermittent extensor rigidity
  4. recumbent, constant extensor rigidity
  5. recumbent, constant extensor rigidity with opistotonus
  6. recumbent, hypotonia of muscles, depressed or absent spinal reflexes
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4
Q

what are the levels/points in brain stem reflexes in the modified Glasgow coma scale?

A
  1. normal PLR and oculocephalic reflexes
  2. slow PLR and normal to reduced oculocephalic reflexes
  3. bilateral unresponsive miosis with normal to reduced oculocephalic reflexes
  4. pinpoint pupils with reduced to absent oculocephalic reflexes
  5. unilateral, unresponsive mydriasis with reduced to absent oculocephalic reflexes
  6. bilateral, unresponsive mydriasis with reduced to absent oculocephalic reflexes
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5
Q

what are the levels/points in level of consciousness in the modified Glasgow coma scale?

A
  1. occasional periods of alertness and responsive to environment
  2. depression or delirium, capable of responding but response may be inappropriate
  3. semicomatose, responsive to visual stimuli
  4. semicomatose, responsive to auditory stimuli
  5. semicomatoes, responsive to repeated noxious stimuli
  6. comatose, unresponsive to repeated stimuli
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6
Q

What is the probability of survival in px with MGCS of 8 within the first 48h after initial TBI?

A

50%

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7
Q

Describe the gait in LMN and in UMN

A

LMN: Short and choppy gait.
UMN long, strided, spastic stiff gait. Often with general proprioceptive ataxia

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8
Q

Where can the neuro localisation be with a head turn?

A

Cerebral/thalamic lesion or forebrain lesion, rostral brainstem

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9
Q

Describe decerebrate and decerellebrate posture? How do these differ from Schiff Sherrington?

A

Decerebrate: extensor rigidity all four limbs and optisotonus, comatosed
Decerebellate: extensor rigidity front legs, hinds legs can be flexed at hips, opistotonus
Schiff Sherrington: extensor rigidity front legs with normal proprioception and voluntary movement. hind legs none ambulatory but normal spinal reflexes

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10
Q

Where is the lesion in the spine in a px with Schiff sherrigton

A

T3-L3

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11
Q

What does pleurosthotonus look like and where is the lesion localised?

A

Deviation of head and neck to one side. Brainstem or cerebral lesion.

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12
Q

What are the three types of ataxia

A

General proprioceptive, vestibular, cerebellar

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13
Q

What pathways can have been disturbed in general proprioceptive ataxia?

A

Peripheral nerve, dorsal root, spinal cord, brainstem.

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14
Q

Number and name the cranial nerves

A
  • N. Olfactorius (I)
  • N. Opticus (II)
  • N. Oculomotorius (III)
  • N. Trocklearis (IV)
  • N. Trigeminus (V
    o 3 delar: oftalmicus, maxillaris och mandibularis
  • N. Abducens (VI)
  • N. Facisalis (VII)
  • N. Vestibulocochlearis (VIII)
  • N. Glossofaryngeus (IX)
  • N. Vagus (X)
  • N. Accesorius (XI)
  • N. Hypoglossus (XII)
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15
Q

At what age does the menace response normally become present?

A

10-12 week of age

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16
Q

Where is the lesion in relation to the cutaneous trunci muscle reflex?

A

Reflex preserved for one to two vertebral bodies caudal to the level of the lesion (aka lesion is two vertebral bodies cranially)

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17
Q

Describe your clinical neuro findings in a spinal shock px

A

LMN (reduced or absent spinal reflexes and muscle tone) in pelvic limbs in a px with otherwise UMN localization (T3-L3 injury). Loss of flexion/withdrawal reflex seems most common, but loss of tendon reflexes also possible. Improvement noted in most px, ranging from h to weeks (12-24 m most common)

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18
Q

How do you different spinal shock and myelomalacia?

A

Myelomalacia: often complete loss of reflexes and deep pain perception both hind limbs. Grave to poor prognosis
Spinal shock: reflex deficits often partial (ie absent flexion and withdrawal but tendon reflexes intact). Might lack deep pain perception but will have improvements of reflexes and tone to be more consistent with an UMN lesion

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19
Q

What cells produce myelin in the CNS and the PNS?

A

Oligodendrocytes in cns, schwann cells in the pns

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20
Q

What type of synaptic transmission does cardiac and smooth muscle cells have?

A

Electrical (ion flow directly between gap junctions if adjacent cells)
(the other option is chemical with gaba, glycine, glutamate, acetylcholine, occurs in cns, pns)

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21
Q

Where is the neuro localisation in paradoxical vestibular syndrome?

A

Cerebellum (has head tilt contralateral to lesion due to the lack of inhibitory effect from cerebellum causing excessive tone in ipsilateral extensor muscles)

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22
Q

Metronidazole intoxication and thiamine deficiency can cause neurological dysfunction, localised to where?

A

Central vestibular disease

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23
Q

Hypothyroidism, aminoglycosides, chlorhexidine can cause neurological dysfunction, localised to where?

A

peripheral vestibular disease

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24
Q

what pain fiber give a dull, aching pain and what give sharp pain?

A

Dull C fibers. Sharp A δ (a-delta)

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25
Q

What is the Monroe-kellie doctrine?

A

the sum of volumes of brain, CSF and intracranial blood is constant. An increase in one component must accompany a decrease in or both of the other components in order to maintain a stale and constant pressure.

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26
Q

What is the percentage of brain tissue, CSF and blood of the intracranial volume?

A

Brain tissue 80%, CSF 10%, blood 10%

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27
Q

Draw an intracranial pressure volume curve. What is on the x axel and the y axel?

A

X intracranial volume. Y intracranial pressure
_____/

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28
Q

In primary brain trauma, what are the three gradients of trauma and shortly describe their difference

A

Concussion, contusion, laceration
Concussion. No underlying histopathology changes
Contusion: parenchymal haemorrhage and oedema
Laceration: physical disruption of the brain barrier

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29
Q

What % of animals with severe head injury has extra-axial head injury?

A

80%

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30
Q

What % of animals with mild head injury has extra-axial hematoma?

A

10%

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31
Q

Give 5 examples of local changes that exacerbate neuronal cell death in the secondary phase of TBI/ most common factors leading to secondary brain injury

A

Glutamate accumulation (exitotoxicity)
Influx of Na and Ca intracellularly
Free radical production (ROS)
Inflammatory mediator release
Depletion ATP stores
NO accumulation
Cerebral lactic acidosis
ischemia
Loss of autoregulation
(systemic insults: hyperglycemia, hypoglycemia, acidbase disturbance, electrolyte disturbance, hyperthermia, hypoxemia, hypotension, hypercapnia, hypocapnia, systemic inflammation)

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32
Q

What are the two types of brain odema

A

Vasogenic and cytotoxic

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33
Q

What is normal ICP

A

5-12 mmHg

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34
Q

What are the 4 protective haemostatic effects in increased intracranial pressure?

A
  • Volume buffering (expansion of dura mater and displacement of csf and blood)
  • Autoregulation if cerebral blood flow
  • Cushings reflex
  • Herniation of the brain parenchyma
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35
Q

What is the formula for cerebral perfusion pressure

A

CPP= MAP - ICP

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36
Q

What is normal cerebral perfusion pressure?

A

60-70 mmHg, ideal in TBI 50-90

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37
Q

Between which systemic systolic blood pressure can brain maintain normal CPP

A

50—150 mmHg

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38
Q

Name three herniation types (localisations)

A

Cerebellar, cirgulate, central, transcalvial, downward, upward

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39
Q

What does Biots respiration look like?

A

Apnea, alternating with periods of quick, shallow breathing

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40
Q

What does Cheyne-stokes respiration look like

A

Quick respiration in crescendo-decrescendo pattern followed by apnoea

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41
Q

Interpretation of pupil size and PLR in head trauma. (Table 128.1 saccm)
If pupil size is midposition and PLR is normal, what is the prognosis?
If pupil size is midposition and there is no PLR, the prognosis is? And where is the localisation?
If pupil size is bilateral mydriasis and PLR is poor to none, what is the prognosis?

A

Good
Poor to grave (lesion is in pons, medulla)
Poor to grave

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42
Q

What are the indications for CT in TBI?

A

if moderate to severe neurological abnormalities on presentation,
lateralizing signs,
failure to improve significantly within the first few days,
acute deterioration in neuro status

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43
Q

give some neuroprotective strategies in TBI

A
  • hypoxemia, keep paO2 >80 mmHg
  • hypoventilation, keep arterial co2 30-35 mmHg, venous 40-45 mmHg
  • hypotension, keep MAP > 80 (if doppler >100)
  • elevate head 15-30 degrees
  • glycemic control > 10 mmol, avoid hypoglycemia
  • decrease cerebral metabolic demand with analgesia, neuromuscular blockers
    temperature control
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44
Q

name 3 advantages to hypertonic saline over mannitol in TBI

A

less likely to cause hypovolemia and decreased cerebral perfusion. Less likely to cause increased permeability of the blood brain barrier.

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45
Q

what is the initial effect of mannitol in TBI

A

rheological (increase in cerebral blood flow and cerebral oxygen delivery)

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46
Q

what percentage of dogs have seizures after TBI?

A

6.6%

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47
Q

Should you treat TBI dogs with prophylactic antiseizure medication?

A

No evidence that it help, but if have seizure treat aggressively and for at least 7 days

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48
Q

What are some poor prognostic indicators in TBI

A

Pupillary dilation, loss of PLR, deterioration of consciousness.
Small animal coma scale: retrospectively to correlate with 48-hour outcome in dogs with head trauma.
Hyperglycaemia at admission and persistent hyperglycaemia associated with worsened mortality and outcome in people, some evidence in vet med
Probability of survival is 50% in patients with an MGCS of 8 within the first 48h after initial head trauma and TBI

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49
Q

Draw a cerebral perfusion pressure curve. What is on the x and y axel

A

X cerebral perfusion pressure
Y cerebral blood flow
___________________/
/

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50
Q

Explain the cerebral perfusion pressure curve?

A

X cerebral perfusion pressure
Y cerebral blood flow
___________________/
/
Stable during autoregulation when CPP if 50-150 mmHg. Cerebral vascular tone responds to CPP. When autoregulation impaired (<50 and >150) the cerebral vascular tone passively follows systemic arterial blood pressure

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51
Q

What is the formula for cerebral metabolic rate of oxygen (CMRO2)?

A

Cerebral blood flow x (arterial blood oxygenation in % - venous blood oxygenation in %) x Ca (constant representing the amount of oxygen-carrying molecules per unit of blood)

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52
Q

How can brain death be diagnosed

A

Deep coma, absence of spontaneous respiration/apnea, loss of brainstem reflexes (fixed, dilated pupils)
EEG: prolonged inactivity or burst suppression in the absence of anaesthetic drugs. Dont depend on single reading, do several, wait 72 h after trauma, combine with BAER
BAER: early waveforms but no late

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53
Q

Reticular activating system (RAS), is important for which neurological function?

A

Level of consciousness/mentation

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54
Q

What parts of the CNS are involved in the oculocephalic reflex?

A

Brainstem pathway from the cranial cervical cord and medulla oblongata to CN III, IV, VI (oculomotor, trochlear, abducens)

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55
Q

What is spontaneous positional nystagmus in a head trauma patient indication of?

A

Vestibular dysfunction, common in increasing ICP

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56
Q

What is the most important factor for controlling cerebral volume and flow in intracranial hypertension?

A

PaCo2. Ideally 35-45 if mild to moderate, 30-35 if severe

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57
Q

Somebody suggest prophylactic hyperventilation in a px with ICH (intracranial hypertension), what do you say?

A

No. Not recommended by brain trauma foundation as can cause neuronal ischemia and exacerbation of ICH

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58
Q

When is corticosteroids recommended in intracranial hypertension?

A

Benefits unproven, only recommended if vasogenic oedema associated with primary inflammatory disease, tumour-associated oedema and acute ischemia

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59
Q

Why is it important to control pain, temperature and seizures in a px with intracranial hypertension?

A

Those things increase cerebral metabolic rate. Increased cerebral metabolic rate increases cerebral blood flow. Increased cerebral blood flow increases ICP

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60
Q

Give three immunomodulatory effects of hypertonic saline infusion

A

Decreased neutrophil activation and adherence, stimulate lymphocyte proliferation, inhibit proinflammatory cytokines (TNFa) by macrophages. Increase IL10, may reestablish Na/glutamate pump activity following TBI and reduce excitoxicity

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61
Q

What receptor does glutamate bind to?

A

AMPA, NMDA

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62
Q

What receptor does GABA bind to?

A

GABAa (or GABAb)

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63
Q

Give 5 negative effect of hypertonic saline

A

Hypernatremia
Hyperosmolality
Hyperchloremic metabolic acidosis
Irritant if given im or sc
Bradycardia
Brochospams
If conc >10% can cause increased brain blood barrier permeability
Contraindications: if severe electrolyte disturbances, uncontrolled haemorrhage, lung oedema, hypertonic dehydration, hypertonic fluid overload

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64
Q

Give 5 negative effects of mannitol

A

Increased permeability blood brain barrier if ICP
Acute renal failure/nephrotoxicity if serum osmolality exceed 320 mOSM/L
Rebound intracranial hypertension
Fluid and electrolyte imbalance (Na, Cl, P). Intravascular volume depletion. Reduced serum Na reabsorption + hypo na due to osmotic effects
May influence measurement urine SG
May increase osmolar gap and increased osmolality
seizures
Cant give if overhydrated or anuria as requires large amounts

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65
Q

Give 6 precautions to take when administrating mannitol

A

Maintain euvolemia. Correct hypovolemia first but don’t overhydrate. U cath to monitor outs
Use a fluid filter or dissolve visible crystals first
Administer slow bolus over 20 min
If possible, monitor and maintain serum osmolality at or below 320 mOsm/L, particularly if concern for renal failure
Avoid prophylactic administration and multiple repeat dosages (typically <3 doses/day)
Monitor serum electrolytes and maintain normal range
Monitor urine output. If urine production is not evident within 15 min of admin, give furosemide to induce diuresis
Do not use when ongoing intracranial haemorrhage is suspected

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66
Q

Give three findings indicative of brain herniation in dogs presenting with neurological signs in admission (clinical exam and blood pressure measurement)

A

High SBP, greater difference between SBP and HR, combination of higher SBO and HR, low MGCS

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67
Q

Does Cushing’s response have a high or low specificity and sensitivity for brain herniation

A

Sensitivity 24%, specificity 100%. Her et al jvecc 2022

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68
Q

What is on the x and y axel of a ICP pressure waveform curve

A

X time.
Y intracranial pressure (mmHg)

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69
Q

What does a P2 increase in a ICP pressure waveform mean

A

Raised ICP and reduced intracranial compliance, is a proxy for intracranial compliance

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70
Q

What physiological systems affect the ICP pressure waveform W1 and W2 fluctations

A

W1 fluctuations due to systemic arterial cycle
W2 fluctuations in response to respiratory cycle

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71
Q

What is the gold standard way of measuring intracranial pressure

A

Intraventricular catheter

72
Q

Give 3 examples of invasive intracranial pressure monitoring systems and 2 non invasive

A

Invasive:
Ventriculostomy catheter in external transducer
Microsensor (catheter-tipped) devises
Fluid filled catheter
Telemetric ICP monitoring system
Non invasive:
Optic nerve sheet diameter
Transcranial doppler ultrasonography

73
Q

What is the definition of a cluster seizure

A

two or more self limiting seizures within a 24 h period

74
Q

what is the definition of status epilepticus

A

continuous seizure, or two or more discrete seizures between which there is incomplete recovery of consciousness, lasting at least 5 min.

75
Q

Name 5 toxins that can cause seizures

A

Alphacloralose, arsenic, algae, doxopram, cannabis, ethylene glycol, lead, metaldehyde, netronidazole, paracetamol, onrganophosphate, pyrethrin, SSRI, strychnine, theophylline, rodenticides

76
Q

What drugs are first, second, third and fourth line in tx of SE in dogs in hospital? From saccm??

What drugs are first, second, third and fourth line in tx of SE in dogs in hospital according to ACVIM SE consensus

A

saccm:
First: diazepam/midazolam
Second: ?
Third: propofol
Fourth: pentobarbital

ACVIM:
First: diazepam/midazolam
Second: phenobarbital, levetiracetam
Third: ketamine, dexmedetomidine, propofol, barbiturates, inhalants
Fourth: iv magnesium, allopregnalone, non-pharmacological interventions, mild hypothermia

77
Q

What is the side effect of the propylene glycol in diazepam

A

Phlebitis, hypotension, metabolic acidosis (one of the DUEL), especially in cats

78
Q

Is intranasal midazolam or rectal diazepam to be preferred at home in tx SE?

A

Intranasal in dogs. In cats same level of recommendation (low level)

79
Q

What happens postsynaptically after gaba is released

A

Binds to GABAa channels. CL in increased and increases the neg (hyperpolarization) membrane potential, making it harder for Na to depolarise. GABA removed from synaptic cleft via GAT1 channel and re-absorbed on presynaptic membrane

80
Q

Are diazepam and midazolam water or lipid soluble

A

Midazolam water-soluble, diazepam lipid soluble

81
Q

What is the mechanism of action of potassium bromide

A

Potentiated GABA by moving neg bromide ions via GABA activated Cl channels

82
Q

Why is potassium bromide not recommended in cats

A

Lobar airway /pneumonitis. Seen in 35-42%

83
Q

What are the signs of bromide toxicity

A

Subacute and progressive signs: altered mentation, mydriasis, reduced PLR, anisocoria, bilateral blindness, abnormal behaviour, head pressing, ataxia, paresis, reduced spinal reflexes, dysphagia, megaesophagus, muscle pain. Tx reduce dose and NaCl 0.9%

84
Q

What is the response rate to levetiracetam in cats refractory to phenobarbital monotherapy?

A

70%

85
Q

What are the side effect of levetiracetam

A

Sedation, ataxia (dog), vomiting, hypersalivation (cats on oral suspension), behavioural changes, PU/PD if pulse therapy

86
Q

What is the mechanism of action of imepitoin

A

Partial agonist to GABAa

87
Q

What are side effects of imepitoin

A

Well tolerated. Polyphagia, PU/PD, sedation, ataxia, hypersalivation, vomiting, diarrhea. Third eye protrusion, decreased sight, sensitivity to sound, behavioural changes. Cats: emesis, lethargy, decreased appetite. No significant biochemical or haematological changes

88
Q

What is the mechanism of action of zonasamide

A

Na and Ca channel blocker on the presynaptic neuron. Inhibition of T type Ca channels, modulation of dopaminergic activity, enhancement of GABA activity in CNS, inhibition of carbonic anhydrase activity

89
Q

Side effects of zonasamide

A

Mild. Sedation, ataxia, vomiting, inappetence, KCS, decreased Total thyroxine concentration. Severe idiosyncratic hepatopathy

90
Q

Mechanism of action of propofol

A

GABAa agonist

91
Q

What are the mechanisms of action of dexmedetomidine in seizures

A

a2 agonist. Decreased excitatory neurotransmitters via suppression of the sympathetic nervous stimulation and noradrenaline release, mainly in the region of the amygdala, hippocampus, cerebral cortex .
Neuroprotective properties by decreasing cerebral metabolic and oxygen demands, decreasing brain oedema via vasoconstriction and contributing to maintain normal mean arterial pressure

92
Q

What is magnesium mechanism of action in seizure treatment

A

Inhibits NMDA and Ca channels

93
Q

What is excitotoxicity

A

nerve cells suffer damage or death when levels of neurotransmitters like glutamate becomes pathological high and cause excess stimulation of receptors. Ex excess glutamate leads to excess Ca ion entering cells -> activating enzymes like phospholipase, endonucleases and proteases -> damages cell structures and DNA

94
Q

what is the definition of status epilepticus according to ILAE and AES

A

continuous seizure activity (>5 min), or >1 sequential seizure without full recovery of consciousness in between, with a duration of > 30 min

95
Q

what is the underlying pathophysiology of SE and what are the names of the 4 stages according to the ACVIM consensus

A

stage 1 impending. 5-10 min. Neurotransmitter release/imbalance. Ion channels opening/closing

stage 2 established. 10-30 min. GABAa receptor decrease. Internalization of GABAa receptor subunits. NMDA and AMPA receptors upregulation

stage 3 refractory. >30 min. Excitatory and inhibitory neuropeptides release/imbalance. +/- blood brain barrier transporters upregulation

stage 4 (super) refractory >24 h. Gene expression alterations

96
Q

what drugs are have high evidence for SE tx in dogs according to the ACVIM SE consensus

A

midazolam iv bolus and CRI, intranasal
diazepam iv bolus
propofol iv bolus and cri
ketamine iv bolus and cri
phenobarbital iv

97
Q

what drugs are have high evidence for SE tx in cats according to the ACVIM SE consensus

A

none. Highest level is moderate.
midazolam iv and CRI, intranasal
diazepam iv bolus
levetiracetam iv
phenobarbital iv
inhalant anaesthetics

98
Q

in the parasympaticus system what is the name of the neurotransmitter and what receptor does it bind to in the ganglion and what receptor in the target organ?

A

Acetylcholine to N2 in ganglion and ach to muscarine in target organ

99
Q

in the somatic system what is the name of the neurotransmitter and what receptor does it bind to in the ganglion and in the target organ?

A

Acetylcholine to N1 in target organ. There is no ganglion “stop”

100
Q

What type of bacteria is clostridium botulinum

A

Gram positive, nonencapsulated, anaerobic spore-forming

101
Q

What botulinum toxin is most common in dogs

A

Type C

102
Q

Describe how botulinum gets to the blood stream

A

Most often ingestion pf preformed toxin in rancid food or carrion. In the alkaline environment of the GI tract, the inactive progenitor toxin is activated. Toxin absorbed from GI tract by endocytosis, enters lymphatic system and blood stream.

103
Q

What is the botulinum toxins mechanism of action in the presynaptic nerve terminals

A

Modifies SNARE proteins required for exocytosis of acethylcholine. Most common toxin C cleaves SNAP 25 and syntaxin (A cleaves SNAP 25. B, D, F, G cleaves synaptobrevin)

104
Q

How is congenital myasthenia gravis syndrome classified

A

Presynaptic (defect in synthesis of AcH), synaptic (deficiency of acetylcholinesterase or postsynaptic (defect of ACH receptors)

105
Q

Name 3 breeds that get congenital myasthenia syndrome

A

Old Danish pointing dogs, labradors, jack russel terriers

106
Q

How do you diagnose congenital myasthenia syndrome

A

Combination of skeletal muscle weakness and fatigability + onset from birth or a few weeks or months of age – decremental response upon repetitive nerve stimulation + affected relatives + absence of skeletal muscle or nerve pathology + negative NMJ autoantibody testing for ach receptors
Definitive diagnosis identification of the mutation and clinical signs

107
Q

what acquired syndrome has autoantibodies against nicotinic acetylcholine receptors

A

acquired myasthenia gravis

108
Q

with what medication is acquired myasthenia gravis associated with

A

thiourylene

109
Q

thiourylene treatment in cats can cause what acquired syndrome

A

myasthenia gravis

110
Q

what percentage if myasthenia gravis patients test negative for acetylcholine receptor antibodies testing by radioimmunoassay

A

25% (said 80-90% positive in other source)

111
Q

Name 1 breed overrepresented in acquired myasthenia gravis

A

German Shepard, labrador, akita

112
Q

What are the 3 clinical pictures seen in acquired myasthenia gravis

A

Focal, generalised, acute fulminate

113
Q

What is the definition of focal myasthenia gravies

A

Weakness in >1 focal skeletal muscle group that does not involve the appendicular skeletal muscle -> facial, esophageal, pharyngeal, laryngeal skeletal muscle

114
Q

What is the classification if acquired myasthenia gravis in dogs and cats according to Mignan et al

A

Focal
- Nonthymoa associated
- Thymoma associated
Generalized
- Nonthymoma associated
- Thymoma associated
- Thiourylene medication associated
- seronegative
Acute fulminate
- nonthymoma associated
- thymoma associated

115
Q

what is the gold standard testing for acquired myasthenia gravis

A

radioimmunoassay

116
Q

what are the symptoms in acute fulminate myasthenia gravis

A

weakness, recumbency, frequent regurgitation, facial, pharyngeal, laryngeal dysfunction. No improvement with rest.

117
Q

What is the treatment for acquired myasthenia gravis

A

Pyridostigmine bromide po – inactivates acetylcholinesterase. If dysphagia and regurgitation or fulminant MG, neostigmine bromide im

118
Q

What is the one year mortality in all subgroups in myasthenia gravis

A

40-60% in dogs, 15% in cats

119
Q

What bacteria causes tetanus

A

Clostridium tetani, gram positive, anaerobic, non encapsulated, spore forming

120
Q

Name two toxins the tetanus bacillus secrete

A

Tetanolysin, tetanospasmin

121
Q

What snare protein does tetanus interfere with

A

Synaptobrevin

122
Q

What percentage of dogs progress to recumbency with several muscle spasm in tetanus

A

50% over a median of 4 days

123
Q

What are the classes of tetanus

A
  • class I: only facial signs
  • class II: generalised rigidity or dysphagia with or without class I signs
  • class III: class I or II and recumbent or seizures
  • class IV: class I, II or III and autonomic dysfunction (normal HR, RR or BP)
124
Q

what is the difference between an anaphylaxis and an anaphylactoid reaction

A

anaphylaxis require previous exposure. IgE mediated
anaphylactoid is not immune mediated, doesn’t require previous exposure. Direct mast cell degranulation

125
Q

what is the mechanism of action of magnesium in tetanus and what is an early sign of Mg toxicity

A

Thought to inhibit Ca channels and decrease Ca entry into presynaptic terminals and thereby decrease acetylcholine release + decrease sensitivity of postsynaptic motor endplate to Ach and thereby reduce muscle contraction
Loss of patella reflex (other signs lethargy, nausea, respiratory depression, bradycardia, hypotension)

126
Q
A
127
Q

What is the mortality in tetanus in dogs

A

18-50%

128
Q

What are poor prognostic indicators in tetanus

A

Prescence of autonomic signs, young age

129
Q

What % of class I or class II survive tetanus according to (unsure of source)

A

100%

130
Q

What % of class III or IV survive tetanus?

A

58%

131
Q

Full recovery may not be possible in at least x % of those that survive tetanus

A

15%

132
Q

What % develops sleep disorders after tetanus? What % has spontaneous resolution within 6 months?

A

Approx 50%. 40% recover

133
Q

Diseases of the motor unit is normally divided into 3 types

A

Neuropathy, neuromuscular junction (junctionopathies), muscle (myopathy)

134
Q

What receptor does acetylcholine bind to on the postsynaptic membrane in the neuromuscular junction

A

Nicotine receptor

135
Q

Give one example of electrophysiology testing in motor unit disease

A

Electromyography or evoked response testing

136
Q

Give 3 diff dx for cant close mouth, difficulty eating and drinking, severe ptyaslim,

A

Trigeminal neurtis, rabies, round cell neoplasia, polyneuritis

137
Q

What tumor most commonly affects the trigeminal nerve

A

Nerve sheat tumour

138
Q

Name one breed predisposed to idiopathic facial nerve paralysis

A

Cocker spaniel, beagles

139
Q

What nerves are normally affected in laryngeal paralysis

A

Recurrent laryngeal nerves or vagus. Causes impaired arytenoid cartilage abduction by dorsal cricoarytenoid muscles during inspiration

140
Q

Give 3 causes of laryngeal paralysis

A

Trauma, degeneration (hypothyroid, polyneuropathie, myasthenia gravis), toxic (lead, organophosphates), idiopathic, neoplastic. Genetic (congenital)

141
Q

Give one breed predisposed to congenital laryngeal paralysis

A

Siberian husky, bouviers de flanders, damalation, rottweiler, bull terrier, german shepard, pyrenean mountain dog

142
Q

What % of px get aspiration pneumonia after arytenoid lateralisation for laryngeal paralysis

A

8-33%

143
Q

What are the three categories of traumatic neuropathies and describe them

A

Neuropraxia: no structural change
Axontemesis: axonal damage without loss of supporting structures
Neurotemesis: complete severance of the nerve

144
Q

Give 3 metabolic causes of acute polyneuropathy

A

Hypoadrenocorticism, diabetes meelitus, hypothyroid, hypoglycemia (insulinoma)

145
Q

What is the most common acute polyneuropathy in dogs

A

Acute polyradiculoneuritis

146
Q

What is the suspected pathophysiology in acute polyradiculoenuritis

A

Immunmediated attack on proteins in the ventral nerve root and motor nerves

147
Q

Give one example of intoxications that can cause acute polyneuropathies

A

Vincristine, thallium, organophosphate

148
Q

What muscles can be affected in masticatory myositis

A

Pterygoid, temporalis, masseter

149
Q

How do you diagnose masticatory myositis

A

Muscle biopsy or antibodies against type 2M muscle fibers

150
Q

What is the name of the toxin in tick paralysis

A

Holocyclotoxin

151
Q

What is the mechanism of action in tick paralysis

A

Holocyclotoxin in the tick block Ca influx presynaptically and thereby stops release of acetylcholine

152
Q

What is the mortality of tick paralysis in Australia

A

5%

153
Q

In tick paralysis, after how long does clinical signs appear after tick attached and when to the resolve after removal of tick

A

3-5 days to appear. Resolve after 24-72 h

154
Q

What time of neurological dysfunction can aminoglycoside intoxication cause

A

Acute LMN disorder

155
Q

What symptoms does envenomation from elapid snakes and Mojave rattlesnakes cause and where are the snakes found

A

Neurotoxin snakes. Cause CNS depression, muscle paralysis, vasomotor instability, mild reaction at bite site. Due to postsynaptic neuromuscular blockade
Elapid- coral snakes of north America. Mojave southwest USA and Mexico

156
Q

If you take a CSF and suspect infection and it comes back as mononuclear pleocytosis, what type of infection should be suspected

A

Viral

157
Q

What % of MRI are normal in dogs with inflammatory CSF

A

25%

158
Q

What can the IgG index of CSF tell you

A

If >0.272 suggest true increase of IgG as opposed to passive transfer secondary to compromised blood brain barrier

159
Q

What needs to be taken into consideration when prescribing antimicrobials for the cns

A

Effective against organism, penetrate blood brain barrier, avoid efflux pumps

160
Q

What antimicrobial is recommended in tetanus

A

Metronidazole

161
Q

Why is broad-spectrum antimicrobials recommended in bacterial meningitis whilst pending culture

A

Coinfection are as common as single infection

162
Q

What fungal infection is most commonly associated with meningoencephalitis in dogs and cats

A

Cryptococcus neoformans

163
Q

Which breed is overrepresented in aspergillus meningoencephalitis

A

German Shepard

164
Q

With coccidiomycosis and meningoencephalitis, what is the most common clinical presentation

A

Generalized tonic clonic seizure

165
Q

What concurrent extra neural involvement is common in fungal meningoencephalitis

A

Respiratory and ocular

166
Q

Give 3 examples of neurotropic viruses in the dog

A

Canine distemper, pseudorabies, canine herpes, west nile virus. (Direct viral replication)

167
Q

What are the three neurological forms of canine distemper

A

Acute encephalitis in young dogs, chronic encephalomyelitis in mature dogs, old dog encephalitis

168
Q

What % of cats with toxoplasma has overt neurological signs

A

10% (but cns involvement is common, just dont have the signs)

169
Q

Give three negative prognostic factors in MUO

A

Prescence of decreased mentation at the time of presentation, seizures, increased neutrophilic percentage in the CSF. MRI findings consistent with multiple brain lesions, mass effect, herniation, sulci effacement

170
Q

Give two dogs breed common in srma

A

Beagles, Bernese mountain dog, boxer, German shorthaired pointers

171
Q

What is a classic finding in CSF in SRMA

A

marked neutrophilic pleocytosis

172
Q

How does the csf flow through the CNS

A

caudally from the lateral ventricles through intraventricular foramina to the third ventricle, then via mesencephalic aqueducts to the fourth ventricle. Then circulated both cranially to brain and caudally to spinal cord and subarachnoid space

173
Q

What do you do if the px develops apnoea during collecting csf

A

Immediate tx with hypertonic therapy, mechanical ventilation, possibly steroids.

174
Q

What are the clinical signs of herniation of brain after rapid reduction of intracranial hypertension during csf sampling

A

Apnea, mentation decline, mydriatic unresponsive pupils. Immediate tx for intracranial hypertension

175
Q

Describe how to take a csf

A
  • preparation
    o propofol infusion with midazolam +/- fentanyl or dexmedetomidine and an opioid
    o sterile gloves
    o disposable spinal needles with stylets
     22 G, if cisternal any size, and lumbar small dogs and cats
     22 G longer needle if giant dogs cisterna, and lumbar if >10 kg
     25 G if small cats and toy breeds
    o Glass blood collection tubes without additives
  • Collection site and techniques
    o Cisterna magna, lumbar cisterna, rarely lateral ventricle
    o Collect caudal to the lesion
    o If multifocal, do both cisternal and lumbar cistern
    o Cisternal puncture
     Right lateral, parallel to table, prep from occipital protuberance and C3. flex neck 90-100 degrees at atlantooccipital joint.
     Landmarks: external occipital protuberance, spinous process of C2, dorsal arch of C1 (slip rostrally off C2), atlas wings
     Or triangle between occiput and the wings of the atlas
     Go through: skin, sc tissue, muscle, epidural space, dura, arachnoid space (suddural space), arachnoid, subarachnoid space
     Stop in subarchanoid space
     Cats and small dogs: 1-2 ml
     Larger dogs: 6 ml
     Free flow, don’t aspirate
     If flows at high velocity, or if initially very good flow and then suddenly – terminate. Don’t want to drop intracranial pressure too quick in increased ICP. Pop-off valve effect

x (25 decks)

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