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
2
Q
What are the three parameters measured in modified glasgow coma score?
A
Motor activity, brainstem reflexes, level of consciousness
3
Q
what are the levels/points in motor activity in the modified Glasgow coma scale?
A
- normal gait, normal spinal reflexes
- hemipares, tetrapares
- recumbent, intermittent extensor rigidity
- recumbent, constant extensor rigidity
- recumbent, constant extensor rigidity with opistotonus
- recumbent, hypotonia of muscles, depressed or absent spinal reflexes
4
Q
what are the levels/points in brain stem reflexes in the modified Glasgow coma scale?
A
- normal PLR and oculocephalic reflexes
- slow PLR and normal to reduced oculocephalic reflexes
- bilateral unresponsive miosis with normal to reduced oculocephalic reflexes
- pinpoint pupils with reduced to absent oculocephalic reflexes
- unilateral, unresponsive mydriasis with reduced to absent oculocephalic reflexes
- bilateral, unresponsive mydriasis with reduced to absent oculocephalic reflexes
5
Q
what are the levels/points in level of consciousness in the modified Glasgow coma scale?
A
- occasional periods of alertness and responsive to environment
- depression or delirium, capable of responding but response may be inappropriate
- semicomatose, responsive to visual stimuli
- semicomatose, responsive to auditory stimuli
- semicomatoes, responsive to repeated noxious stimuli
- comatose, unresponsive to repeated stimuli
6
Q
What is the probability of survival in px with MGCS of 8 within the first 48h after initial TBI?
A
50%
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
8
Q
Where can the neuro localisation be with a head turn?
A
Cerebral/thalamic lesion or forebrain lesion, rostral brainstem
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
10
Q
Where is the lesion in the spine in a px with Schiff sherrigton
A
T3-L3
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.
12
Q
What are the three types of ataxia
A
General proprioceptive, vestibular, cerebellar
13
Q
What pathways can have been disturbed in general proprioceptive ataxia?
A
Peripheral nerve, dorsal root, spinal cord, brainstem.
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)
15
Q
At what age does the menace response normally become present?
A
10-12 week of age
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)
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)
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
19
Q
What cells produce myelin in the CNS and the PNS?
A
Oligodendrocytes in cns, schwann cells in the pns
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)
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)
22
Q
Metronidazole intoxication and thiamine deficiency can cause neurological dysfunction, localised to where?
A
Central vestibular disease
23
Q
Hypothyroidism, aminoglycosides, chlorhexidine can cause neurological dysfunction, localised to where?
A
peripheral vestibular disease
24
Q
what pain fiber give a dull, aching pain and what give sharp pain?
A
Dull C fibers. Sharp A δ (a-delta)
25
What is the Monroe-kellie doctrine?
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.
26
What is the percentage of brain tissue, CSF and blood of the intracranial volume?
Brain tissue 80%, CSF 10%, blood 10%
27
Draw an intracranial pressure volume curve. What is on the x axel and the y axel?
X intracranial volume. Y intracranial pressure
_____/
28
In primary brain trauma, what are the three gradients of trauma and shortly describe their difference
Concussion, contusion, laceration
Concussion. No underlying histopathology changes
Contusion: parenchymal haemorrhage and oedema
Laceration: physical disruption of the brain barrier
29
What % of animals with severe head injury has extra-axial head injury?
80%
30
What % of animals with mild head injury has extra-axial hematoma?
10%
31
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
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)
32
What are the two types of brain odema
Vasogenic and cytotoxic
33
What is normal ICP
5-12 mmHg
34
What are the 4 protective haemostatic effects in increased intracranial pressure?
- Volume buffering (expansion of dura mater and displacement of csf and blood)
- Autoregulation of cerebral blood flow
- Cushings reflex
- Herniation of the brain parenchyma
35
What is the formula for cerebral perfusion pressure
CPP= MAP - ICP
36
What is normal cerebral perfusion pressure?
60-70 mmHg, ideal in TBI 50-90
37
Between which systemic systolic blood pressure can brain maintain normal CPP
50—150 mmHg
38
Name three herniation types (localisations)
Cerebellar, cirgulate, central, transcalvial, downward, upward
39
What does Biots respiration look like?
Apnea, alternating with periods of quick, shallow breathing
40
What does Cheyne-stokes respiration look like
Quick respiration in crescendo-decrescendo pattern followed by apnoea
41
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?
Good
Poor to grave (lesion is in pons, medulla)
Poor to grave
42
What are the indications for CT in TBI?
if moderate to severe neurological abnormalities on presentation,
lateralizing signs,
failure to improve significantly within the first few days,
acute deterioration in neuro status
43
give some neuroprotective strategies in TBI
- 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
44
name 3 advantages to hypertonic saline over mannitol in TBI
less likely to cause hypovolemia and decreased cerebral perfusion. Less likely to cause increased permeability of the blood brain barrier.
45
what is the initial effect of mannitol in TBI
rheological (increase in cerebral blood flow and cerebral oxygen delivery)
46
what percentage of dogs have seizures after TBI?
6.6%
47
Should you treat TBI dogs with prophylactic antiseizure medication?
No evidence that it help, but if have seizure treat aggressively and for at least 7 days
48
What are some poor prognostic indicators in TBI
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
49
Draw a cerebral perfusion pressure curve. What is on the x and y axel
X cerebral perfusion pressure
Y cerebral blood flow
___________________/
/
50
Explain the cerebral perfusion pressure curve?
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
51
What is the formula for cerebral metabolic rate of oxygen (CMRO2)?
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)
52
How can brain death be diagnosed
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
53
Reticular activating system (RAS), is important for which neurological function?
Level of consciousness/mentation
54
What parts of the CNS are involved in the oculocephalic reflex?
Brainstem pathway from the cranial cervical cord and medulla oblongata to CN III, IV, VI (oculomotor, trochlear, abducens)
55
What is spontaneous positional nystagmus in a head trauma patient indication of?
Vestibular dysfunction, common in increasing ICP
56
What is the most important factor for controlling cerebral volume and flow in intracranial hypertension?
PaCo2. Ideally 35-45 if mild to moderate, 30-35 if severe
57
Somebody suggest prophylactic hyperventilation in a px with ICH (intracranial hypertension), what do you say?
No. Not recommended by brain trauma foundation as can cause neuronal ischemia and exacerbation of ICH
58
When is corticosteroids recommended in intracranial hypertension?
Benefits unproven, only recommended if vasogenic oedema associated with primary inflammatory disease, tumour-associated oedema and acute ischemia
59
Why is it important to control pain, temperature and seizures in a px with intracranial hypertension?
Those things increase cerebral metabolic rate. Increased cerebral metabolic rate increases cerebral blood flow. Increased cerebral blood flow increases ICP
60
Give three immunomodulatory effects of hypertonic saline infusion
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
61
What receptor does glutamate bind to?
AMPA, NMDA
62
What receptor does GABA bind to?
GABAa (or GABAb)
63
Give 5 negative effect of hypertonic saline
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
64
Give 5 negative effects of mannitol
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
65
Give 6 precautions to take when administrating mannitol
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
66
Give three findings indicative of brain herniation in dogs presenting with neurological signs in admission (clinical exam and blood pressure measurement)
High SBP, greater difference between SBP and HR, combination of higher SBO and HR, low MGCS
67
Does Cushing’s response have a high or low specificity and sensitivity for brain herniation
Sensitivity 24%, specificity 100%. Her et al jvecc 2022
68
What is on the x and y axel of a ICP pressure waveform curve
X time.
Y intracranial pressure (mmHg)
69
What does a P2 increase in a ICP pressure waveform mean
Raised ICP and reduced intracranial compliance, is a proxy for intracranial compliance
70
What physiological systems affect the ICP pressure waveform W1 and W2 fluctations
W1 fluctuations due to systemic arterial cycle
W2 fluctuations in response to respiratory cycle
71
What is the gold standard way of measuring intracranial pressure
Intraventricular catheter
72
Give 3 examples of invasive intracranial pressure monitoring systems and 2 non invasive
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
What is the definition of a cluster seizure
two or more self limiting seizures within a 24 h period
74
what is the definition of status epilepticus
continuous seizure, or two or more discrete seizures between which there is incomplete recovery of consciousness, lasting at least 5 min.
75
Name 5 toxins that can cause seizures
Alphacloralose, arsenic, algae, doxopram, cannabis, ethylene glycol, lead, metaldehyde, netronidazole, paracetamol, onrganophosphate, pyrethrin, SSRI, strychnine, theophylline, rodenticides
76
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
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
What is the side effect of the propylene glycol in diazepam
Phlebitis, hypotension, metabolic acidosis (one of the DUEL), especially in cats
78
Is intranasal midazolam or rectal diazepam to be preferred at home in tx SE?
Intranasal in dogs. In cats same level of recommendation (low level)
79
What happens postsynaptically after gaba is released
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
Are diazepam and midazolam water or lipid soluble
Midazolam water-soluble, diazepam lipid soluble
81
What is the mechanism of action of potassium bromide
Potentiated GABA by moving neg bromide ions via GABA activated Cl channels
82
Why is potassium bromide not recommended in cats
Lobar airway /pneumonitis. Seen in 35-42%
83
What are the signs of bromide toxicity
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
What is the response rate to levetiracetam in cats refractory to phenobarbital monotherapy?
70%
85
What are the side effect of levetiracetam
Sedation, ataxia (dog), vomiting, hypersalivation (cats on oral suspension), behavioural changes, PU/PD if pulse therapy
86
What is the mechanism of action of imepitoin
Partial agonist to GABAa
87
What are side effects of imepitoin
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
What is the mechanism of action of zonasamide
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
Side effects of zonasamide
Mild. Sedation, ataxia, vomiting, inappetence, KCS, decreased Total thyroxine concentration. Severe idiosyncratic hepatopathy
90
Mechanism of action of propofol
GABAa agonist
91
What are the mechanisms of action of dexmedetomidine in seizures
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
What is magnesium mechanism of action in seizure treatment
Inhibits NMDA and Ca channels
93
What is excitotoxicity
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
what is the definition of status epilepticus according to ILAE and AES
continuous seizure activity (>5 min), or >1 sequential seizure without full recovery of consciousness in between, with a duration of > 30 min
95
what is the underlying pathophysiology of SE and what are the names of the 4 stages according to the ACVIM consensus
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
what drugs are have high evidence for SE tx in dogs according to the ACVIM SE consensus
midazolam iv bolus and CRI, intranasal
diazepam iv bolus
propofol iv bolus and cri
ketamine iv bolus and cri
phenobarbital iv
97
what drugs are have high evidence for SE tx in cats according to the ACVIM SE consensus
none. Highest level is moderate.
midazolam iv and CRI, intranasal
diazepam iv bolus
levetiracetam iv
phenobarbital iv
inhalant anaesthetics
98
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?
Acetylcholine to N2 in ganglion and ach to muscarine in target organ
99
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?
Acetylcholine to N1 in target organ. There is no ganglion “stop”
100
What type of bacteria is clostridium botulinum
Gram positive, nonencapsulated, anaerobic spore-forming
101
What botulinum toxin is most common in dogs
Type C
102
Describe how botulinum gets to the blood stream
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
What is the botulinum toxins mechanism of action in the presynaptic nerve terminals
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
How is congenital myasthenia gravis syndrome classified
Presynaptic (defect in synthesis of AcH), synaptic (deficiency of acetylcholinesterase or postsynaptic (defect of ACH receptors)
105
Name 3 breeds that get congenital myasthenia syndrome
Old Danish pointing dogs, labradors, jack russel terriers
106
How do you diagnose congenital myasthenia syndrome
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
what acquired syndrome has autoantibodies against nicotinic acetylcholine receptors
acquired myasthenia gravis
108
with what medication is acquired myasthenia gravis associated with
thiourylene
109
thiourylene treatment in cats can cause what acquired syndrome
myasthenia gravis
110
what percentage if myasthenia gravis patients test negative for acetylcholine receptor antibodies testing by radioimmunoassay
25% (said 80-90% positive in other source)
111
Name 1 breed overrepresented in acquired myasthenia gravis
German Shepard, labrador, akita
112
What are the 3 clinical pictures seen in acquired myasthenia gravis
Focal, generalised, acute fulminate
113
What is the definition of focal myasthenia gravies
Weakness in >1 focal skeletal muscle group that does not involve the appendicular skeletal muscle -> facial, esophageal, pharyngeal, laryngeal skeletal muscle
114
What is the classification if acquired myasthenia gravis in dogs and cats according to Mignan et al
Focal
- Nonthymoa associated
- Thymoma associated
Generalized
- Nonthymoma associated
- Thymoma associated
- Thiourylene medication associated
- seronegative
Acute fulminate
- nonthymoma associated
- thymoma associated
115
what is the gold standard testing for acquired myasthenia gravis
radioimmunoassay
116
what are the symptoms in acute fulminate myasthenia gravis
weakness, recumbency, frequent regurgitation, facial, pharyngeal, laryngeal dysfunction. No improvement with rest.
117
What is the treatment for acquired myasthenia gravis
Pyridostigmine bromide po – inactivates acetylcholinesterase. If dysphagia and regurgitation or fulminant MG, neostigmine bromide im
118
What is the one year mortality in all subgroups in myasthenia gravis
40-60% in dogs, 15% in cats
119
What bacteria causes tetanus
Clostridium tetani, gram positive, anaerobic, non encapsulated, spore forming
120
Name two toxins the tetanus bacillus secrete
Tetanolysin, tetanospasmin
121
What snare protein does tetanus interfere with
Synaptobrevin
122
What percentage of dogs progress to recumbency with several muscle spasm in tetanus
50% over a median of 4 days
123
What are the classes of tetanus
- 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
what is the difference between an anaphylaxis and an anaphylactoid reaction
anaphylaxis require previous exposure. IgE mediated
anaphylactoid is not immune mediated, doesn’t require previous exposure. Direct mast cell degranulation
125
what is the mechanism of action of magnesium in tetanus and what is an early sign of Mg toxicity
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
127
What is the mortality in tetanus in dogs
18-50%
128
What are poor prognostic indicators in tetanus
Prescence of autonomic signs, young age
129
What % of class I or class II survive tetanus according to (unsure of source)
100%
130
What % of class III or IV survive tetanus?
58%
131
Full recovery may not be possible in at least x % of those that survive tetanus
15%
132
What % develops sleep disorders after tetanus? What % has spontaneous resolution within 6 months?
Approx 50%. 40% recover
133
Diseases of the motor unit is normally divided into 3 types
Neuropathy, neuromuscular junction (junctionopathies), muscle (myopathy)
134
What receptor does acetylcholine bind to on the postsynaptic membrane in the neuromuscular junction
Nicotine receptor
135
Give one example of electrophysiology testing in motor unit disease
Electromyography or evoked response testing
136
Give 3 diff dx for cant close mouth, difficulty eating and drinking, severe ptyaslim,
Trigeminal neurtis, rabies, round cell neoplasia, polyneuritis
137
What tumor most commonly affects the trigeminal nerve
Nerve sheat tumour
138
Name one breed predisposed to idiopathic facial nerve paralysis
Cocker spaniel, beagles
139
What nerves are normally affected in laryngeal paralysis
Recurrent laryngeal nerves or vagus. Causes impaired arytenoid cartilage abduction by dorsal cricoarytenoid muscles during inspiration
140
Give 3 causes of laryngeal paralysis
Trauma, degeneration (hypothyroid, polyneuropathie, myasthenia gravis), toxic (lead, organophosphates), idiopathic, neoplastic. Genetic (congenital)
141
Give one breed predisposed to congenital laryngeal paralysis
Siberian husky, bouviers de flanders, damalation, rottweiler, bull terrier, german shepard, pyrenean mountain dog
142
What % of px get aspiration pneumonia after arytenoid lateralisation for laryngeal paralysis
8-33%
143
What are the three categories of traumatic neuropathies and describe them
Neuropraxia: no structural change
Axontemesis: axonal damage without loss of supporting structures
Neurotemesis: complete severance of the nerve
144
Give 3 metabolic causes of acute polyneuropathy
Hypoadrenocorticism, diabetes meelitus, hypothyroid, hypoglycemia (insulinoma)
145
What is the most common acute polyneuropathy in dogs
Acute polyradiculoneuritis
146
What is the suspected pathophysiology in acute polyradiculoenuritis
Immunmediated attack on proteins in the ventral nerve root and motor nerves
147
Give one example of intoxications that can cause acute polyneuropathies
Vincristine, thallium, organophosphate
148
What muscles can be affected in masticatory myositis
Pterygoid, temporalis, masseter
149
How do you diagnose masticatory myositis
Muscle biopsy or antibodies against type 2M muscle fibers
150
What is the name of the toxin in tick paralysis
Holocyclotoxin
151
What is the mechanism of action in tick paralysis
Holocyclotoxin in the tick block Ca influx presynaptically and thereby stops release of acetylcholine
152
What is the mortality of tick paralysis in Australia
5%
153
In tick paralysis, after how long does clinical signs appear after tick attached and when to the resolve after removal of tick
3-5 days to appear. Resolve after 24-72 h
154
What time of neurological dysfunction can aminoglycoside intoxication cause
Acute LMN disorder
155
What symptoms does envenomation from elapid snakes and Mojave rattlesnakes cause and where are the snakes found
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
If you take a CSF and suspect infection and it comes back as mononuclear pleocytosis, what type of infection should be suspected
Viral
157
What % of MRI are normal in dogs with inflammatory CSF
25%
158
What can the IgG index of CSF tell you
If >0.272 suggest true increase of IgG as opposed to passive transfer secondary to compromised blood brain barrier
159
What needs to be taken into consideration when prescribing antimicrobials for the cns
Effective against organism, penetrate blood brain barrier, avoid efflux pumps
160
What antimicrobial is recommended in tetanus
Metronidazole
161
Why is broad-spectrum antimicrobials recommended in bacterial meningitis whilst pending culture
Coinfection are as common as single infection
162
What fungal infection is most commonly associated with meningoencephalitis in dogs and cats
Cryptococcus neoformans
163
Which breed is overrepresented in aspergillus meningoencephalitis
German Shepard
164
With coccidiomycosis and meningoencephalitis, what is the most common clinical presentation
Generalized tonic clonic seizure
165
What concurrent extra neural involvement is common in fungal meningoencephalitis
Respiratory and ocular
166
Give 3 examples of neurotropic viruses in the dog
Canine distemper, pseudorabies, canine herpes, west nile virus. (Direct viral replication)
167
What are the three neurological forms of canine distemper
Acute encephalitis in young dogs, chronic encephalomyelitis in mature dogs, old dog encephalitis
168
What % of cats with toxoplasma has overt neurological signs
10% (but cns involvement is common, just dont have the signs)
169
Give three negative prognostic factors in MUO
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
Give two dogs breed common in srma
Beagles, Bernese mountain dog, boxer, German shorthaired pointers
171
What is a classic finding in CSF in SRMA
marked neutrophilic pleocytosis
172
How does the csf flow through the CNS
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
What do you do if the px develops apnoea during collecting csf
Immediate tx with hypertonic therapy, mechanical ventilation, possibly steroids.
174
What are the clinical signs of herniation of brain after rapid reduction of intracranial hypertension during csf sampling
Apnea, mentation decline, mydriatic unresponsive pupils. Immediate tx for intracranial hypertension
175
Describe how to take a csf
- 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
