All Neuro Flashcards
(115 cards)
1
Q
What are two methods to test the cutaneous trunci reflex in cats?
A
(Pinching as you do in dogs or plucking their fur)
2
Q
How can you make a menace response test more accurate in cats?
A
(Coming from behind, cats typically do not find humans as menacing as dogs do some coming from the front can be difficult to make work)
3
Q
Feline hyperesthesia syndrome is a young/middle/old age disease (choose).
A
(Young)
4
Q
What is the typical treatment for feline hyperesthesia syndrome that works for most cats (~⅔ of patients)?
A
(Gabapentin)
5
Q
Is idiopathic epilepsy typical of cats less than or greater than seven years of age?
A
(Less than)
6
Q
When do idiopathic epilepsy episodes tend to occur in cats?
A
(When they are resting)
7
Q
What is a common presentation of idiopathic epilepsy episodes in cats?
A
(Rapid running)
8
Q
What are the two medications often used to treat idiopathic epilepsy in cats?
A
(Phenobarbital and levetiracetam/keppra)
9
Q
Of the commonly used medications to treat seizures, which two should never be used in cats due to adverse side effects?
A
(Potassium bromide → causes fatal eosinophilic pneumonitis and diazepam → causes liver failure)
10
Q
Idiopathic epilepsy in cats has a poorer prognosis as the age of diagnosis gets younger/older (choose).
A
(Older)
11
Q
What general pathology is indicated if a cat you put on phenobarbital has an elevated ALP on repeat bloodwork?
A
(They have underlying liver disease, unlike dogs, you should not expect cats’ ALP to rise once placed on phenobarbital unless they have existing liver disease)
12
Q
You are seeing a cat that has a history of seizures for unilateral swollen lymph nodes, what question do you need to ask this client?
A
(What medication are the seizures being controlled with, if it is phenobarbital, switch to keppra and see if it was pseudolymphoma or not)
13
Q
What species of cats is over represented in audiogenic reflex seizures?
A
(Birmans)
14
Q
What is the treatment of choice for audiogenic reflex seizures in cats?
A
(Keppra, has a better response rate than phenobarbital)
15
Q
How is hippocampal necrosis diagnosed in cats?
A
(MRI only, contrast enhancement at the site of the hippocampus)
16
Q
What two clinical signs are associated with hippocampal necrosis aka feline temporal lobe epilepsy?
A
(Focal facial seizures and episodic aggression)
17
Q
What two categories of medications are used for treatment of hippocampal necrosis in cats?
A
(Antiepileptics (phenobarbital, keppra, combo) and immunosuppressives (prednisolone) → bc there is some thought this dz is immune mediated since some of the cats develop autoantibodies to voltage-gated potassium channel-complexes)
18
Q
What is the most common cause of infectious brain and/or spinal disease in cats?
A
(Feline infectious peritonitis)
19
Q
Neurological signs typically result when a cat has the wet/dry (choose) form of feline infectious peritonitis.
A
(Dry → cat won’t have a lot of the other signs associated with FIP)
20
Q
What do you see on MRI of cats with FIP?
A
(Obstructive hydrocephalus (dilated ventricles) and post contrast periventricular enhancement → only other differential if you saw this on MRI could be lymphoma)
21
Q
Of the lesions caused by toxoplasmosis (there are three), which cause seizures, vestibular dz, cerebellar dz, and/or result in obtunded cats?
A
(Encephalitis or granuloma lesions in the brain)
22
Q
Of the lesions caused by toxoplasmosis (there are three), which causes proprioceptive ataxia, weakness, and incontinence?
A
(Segmental myelitis)
23
Q
What is the treatment protocol for a cat with toxoplasmosis?
A
(Clindamycin, add in trimethoprim sulphonamide plus folic acid if clinda alone not working)
24
Q
How is toxoplasmosis tested for?
A
(Serology and/or PCR)
25
How is cryptococcosis treated in cats?
(Fluconazole often tx for life and prednisolone, if refractory → amphotericin B (nephrotoxic) and flucytosine)
26
FIV is a neurotropic virus that can get into the brain and cause encephalitis (CNS changes are reported in a small percentage of cases), what are the common resultant histological findings?
(Perivascular cuffing and glial nodules)
27
(T/F) Cerebellar hypoplasia due to feline panleukopenia virus is non-progressive and is not associated with inflammatory changes within the brain.
(T, joaquin phoenix would turn a thumb up for these kitties aka don’t euthanize them)
28
Feline ischemic encephalopathy is thought to be a result of migration of what organism through the brain?
(Cuterebra)
29
What is the singular artery that supplies the brain in cats?
(Mandibular artery)
30
What results from impingement of the mandibular artery in cats for a length of time, such as in a dental procedure?
(Global cerebral ischemia)
31
What is the most common cause of cervical ventroflexion in cats?
(Hypokalemia, often secondary to CKD)
32
Thiamine or B1 is a water soluble vitamin needed for the metabolism of what primary nutrition?
(Carbohydrates, if you don’t have carbs you get weakness, this can be an early sign of thiamine deficiency and the prognosis can be good if caught early/prior to brain damage)
33
Why should you check a thoracic radiograph on a cat you suspect has myasthenia gravis?
(Myasthenia gravis is often linked with thymomas in cats, check for a mediastinal mass)
34
What neoplasia accounts for ~ 60% of primary brain tumors and 40% of all brain tumors in cats?
(Meningiomas)
35
What is the treatment for meningiomas in cats?
(Craniotomy, MST is 37 months, can be repeated)
36
What is the most common neoplasm affecting the spinal cord in cats?
(Lymphosarcoma)
37
Changes in sensation and behavior often proceed the ictus stage of seizures, what are the two stages that occur prior to ictus?
(Prodromal and aura)
38
How can you distinguish between narcolepsy and absent seizures?
(An EEG/encephalogram, will have epileptiform EEG with absent seizures whereas the EEG will show similar waves as REM sleep in narcoleptic patients)
39
What protein is either not available or not able to do its job in patients with narcolepsy?
(Orexin → can be a genetic mutation of a gene resulting in abnormal receptors or just a general deficiency in older animals)
40
What is the term for the collapsing events/paroxysms associated with narcoleptic patients?
(Cataplexy → sudden and complete atonia leading to collapse that can last several seconds to minutes)
41
How can you distinguish between narcolepsy and syncope?
(Slap an ECG on them, if its normal during an episode it's narcolepsy)
42
In what three ways can you distinguish between behavioral disorders (aggression or OCD, characterized by episodic stereotypies that may be confused for seizures) and seizures?
(No loss of consciousness, no change in muscle tone, there is usually an identifiable trigger)
43
A dog presents to you with a history of intermittent signs of a head tilt, veering off to one side when walking and you note nystagmus when the dog has an episode in-hospital. Blood work is normal, no signs of infection of either ear, but an elevated blood pressure. What are the episodes that dog is having?
(Transient vestibular/ischemic attacks → could be caused by systemic hypertension, hypothyroidism, otitis media/interna, and cerebellar malformations/degenerative dz, tx of underlying dz (if treatable) will resolve the attacks)
44
You are a shelter vet and are presented with a young little white dog with lots of long white hair so you can’t tell the breed, it has been reported that their back legs go stiff and their back arches when they are taken on their daily walks. What breed is this dog likely to be and what is the issue?
(Scottish terrier (though a similar syndrome is seen in cairn and norwich terriers and westies) and the issue is hypertonicity aka scottie cramp)
45
What is the term for involuntary, rhythmic oscillatory movements of a body part with symmetric velocity in both directions of movement?
(Tremors)
46
You are presented with a 2 year old Boston Terrier that the owner’s report has been having these episodes of nodding that last half an hour to an hour. The Boston starts nodding while she’s explaining and when she exclaims “Just like that!” the dog looks at her for a few seconds before going back to nodding. You let her know that it’s a tremor and she wants to know if there’s something she can do and if this could get worse, what do you tell her?
(No ma’am, there is no treatment but it’s okay, he’s not in pain or distress. Postural tremors are non-progressive so no, he will not get worse.)
47
You are examining Dawg when he suddenly collapses limply to the ground, something you weren’t expecting at all. He urinates and his thoracic limbs jerk a few times. Your tech came running over with midazolam and diazepam but you tell them to put them away because Dawg is already sitting back up and acting like nothing happened. What do you want to do next?
(This is supposed to be syncope, put a holter on and go to a rave)
48
(T/F) Seizures are the most common paroxysmal event associated with autonomic signs (salivation, urination, defection).
(T)
49
Seizures are uncommonly/frequently/always (choose) associated with an impairment of consciousness.
(Frequently)
50
If a patient is obtunded, where can the lesion in the brain be located?
(Either the forebrain or the brainstem)
51
If a patient is stuporous or comatose, where is the lesion in the brain located?
(Kinda a trick question, could be forebrain or brainstem but the key is that the forebrain lesion is bad enough that is is causing issues with the brainstem and that is truly what is leading to the stuporous or comatose presentation, if it were forebrain only then the patient would be obtunded)
52
What is something you need to keep in mind when treating a patient with exposure to a neurological toxin with intravenous lipids?
(If the patient were to start having seizures, the anti-seizure medications given will bind to the lipids and be ineffective)
53
Using mean arterial pressure and intracranial pressure, how can you calculate cerebral perfusion pressure?
(Subtraction ICP from MAP, give you CPP → CPP should be around 60-140mmHg to maintain the optimal cerebral blood flow of 50ml/100g/min)
54
If you have an increase in intracranial pressure, what do you need to do in a general sense (not specific treatments but more the result of those treatments)?
(Either increase MAP or decrease ICP, both will increase CPP)
55
What is the main purpose of the Cushing’s reflex?
(To increase MAP and therefore increase CPP but that increase in MAP can trigger reflex bradycardia)
56
As ICP increases, how will the pupils change?
(In early increases in ICP, you will see miotic pupils but as the increased ICP gets worse, they will become mydriatic)
57
A severe enough increase in ICP results in a decerebellate/decerebrate (choose) posture. Describe the posture you chose.
(Decerebrate → extensor rigidity in all limbs and opisthotonus (for review: decerebellate would be extensor rigidity in forelimbs, flexion of hindlimbs, and opisthotonus))
58
You are presented with a HBC patient that is stuporous with miotic pupils and bradycardic, what should you assess prior to administering either mannitol or hypertonic saline to decrease ICP?
(Hydration, you do not want to give mannitol to a dehydrated patient; (for review: mannitol dose is 1g/kg over 20 minutes, 7.2% hypertonic saline dose is 4ml/kg over 15 minutes, mannitol thought to last longer but both are short duration treatments for increased ICP))
59
What are two long term management options for maintaining a decreased intracranial pressure after emergency treatments were successful?
(Corticosteroids at an anti-inflammatory dose or diuretics (specifically mentioned carbonic anhydrase inhibitors))
60
What is status epilepticus? Two answers.
(Any seizure lasting longer than 5 minutes and/or when a patient has 2 or more seizures without return to normal consciousness between)
61
Status epilepticus can lead to brain damage via the release of glutamate which stimulates NMDA receptors in the brain, that stimulation leads to an influx in what two electrolytes?
(Calcium and sodium (for review: sodium influx → cytotoxic edema leading to cell death; calcium influx → additional calcium release from endoplasmic reticulum leading to mitochondrial damage and cell death)
62
How does status epilepticus lead to hypertension, tachycardia, hyperglycemia and eventually arrhythmias?
(Activation of the SNS, hyperglycemia will also exacerbate neuronal damage)
63
You were presented with a patient who had been seizing for an unknown amount of time prior to presentation but at least 5 minutes, you administered intranasal midazolam (at 0.25mg/kg) as soon as you got your hands on them in addition to starting active cooling and oxygen support. You have since given 2 additional doses of midazolam intranasally but there has been no improvement. What medication should you reach for next?
(Propofol (for review: propofol dose is 4-6 mg/kg given to effect))
64
If an animal is exposed to Clostridium tetani, in what timeline after exposure will they present with signs? Answer is a range.
(5-10 days)
65
If any animal is exposed to Clostridium botulinum, in what timeline after exposure will they present with signs?
(Within 12 hours of exposure)
66
(T/F) The diaphragm is resistant to botulinum toxin.
(T)
67
What is the treatment for botulism?
(Supportive care while you wait for the toxin to work its way out of the body)
68
The inability of what molecule to do its normal job leads to seizures associated with hypoglycemia?
(NA/K pump, lack of glucose equates to a lack of phosphorus which is needed to run the pump, if the pump cannot work there is an accumulation of sodium in neurons and of potassium outside of neurons, leads to an inability the neuron to relax and return to a resting membrane potential)
69
How does hypocalcemia lead to seizures, behavior/mentation changes, and/or cortical blindness?
(Calcium is important for preventing sodium from influxing into neurons, if calcium is not present sodium will readily flow into neurons causing the neuron to be unable to relax and return to a resting membrane potential)
70
Excess ammonia causes hepatic encephalopathy by converting what excitatory neurotransmitter into its non-functional counterpart?
(Glutamate into glutamine, glutamine causes astrocyte swelling and brain edema via an osmotic shift which leads to neuronal dysfunction (this is what I found on PubMed when I wanted more than what was explained in lecture))
71
How can you tell the difference between a withdrawal response and conscious perception of deep pain?
(When you do your test such as a pinch, the animal attempts to turn and look at the source of the pain, not just pulling their limb back (that’s just withdrawal))
72
How is instability of a vertebral injury assessed?
(Vertebrae are divided into 3 compartments, dorsal, middle, and ventral, and if ⅔ of the compartments are disrupted in the injury, the injury is unstable)
73
What does a modified frankel score of 5 mean?
(Paraplegia with absent deep pain perception)
74
What does a modified frankel score of 3 mean?
(Non-ambulatory paraparesis)
75
What does a modified frankel score of 1 mean?
(Pain only)
76
When should radiographs be repeated for conservative management of spinal injuries?
(4 weeks, if using coaptation for an unstable injury that was not a surgical candidate, coaptation can be removed when radiographic healing is evident)
77
What are the four clinical signs associated with horner’s syndrome?
(Miosis, ptosis, enophthalmos, and 3rd eyelid protrusion)
78
What are the central vestibular anatomical structures and what parts of the brain are they located in?
(Vestibular nucleus in the medulla oblongata and the flocculonodular lobe in the cerebellum)
79
How can consciousness be used to distinguish between peripheral and central vestibular disease?
(Peripheral vestibular disease should not impact consciousness at all whereas central vestibular disease can)
80
Is peripheral or central vestibular dz associated with weakness?
(Central, peripheral has vestibular ataxia but should have good strength whereas central can be associated with tetra or hemiparesis)
81
How can postural reactions be used to distinguish between peripheral and central vestibular dz?
(Peripheral vestibular dz should have no postural deficits whereas central vestibular dz will have ipsilateral postural deficits)
82
What is the typical strabismus position associated with vestibular disease (though this is not always the case especially when nystagmus is present)?
(Ventrolateral)
83
(T/F) The fast phase of pathologic nystagmus associated with vestibular dz is towards the lesion.
(F, fast phase/jerk is away from the lesion in peripheral or in any direction for central but usually away)
84
Idiopathic vestibular disease can crop up seasonally in cats, around July/August, it is thought to be related to what other pathology due to this seasonality?
(Aberrant cuterebra larval mirgans)
85
Central vestibular disease can result from metronidazole toxicity which occurs when doses exceed what value?
(60 mg/kg/day)
86
What is the treatment for metronidazole toxicity induced central vestibular disease?
(Diazepam, reverses the signs)
87
You’re presented with a cat that is of normal mentation, has nystagmus that changes direction as you change their position, and vestibular ataxia. The cat has postural deficits on the right side of their body and their head tilts to the left. Where is the lesion likely located in their brain?
(This is paradoxical vestibular disease; the right half of the cerebellum involving at least flocculonodular lobe)
88
You’re presented with a dog that is of normal mentation, has nystagmus that changes direction as you change their position, and right sided facial paralysis. The dog has postural deficits on the right side of their body and their head tilts to the right. Where is the lesion likely located in their brain?
(This is central vestibular disease; the right, either the flocculonodular cerebellum (with no other issues with the cerebellum) or the right vestibular nucleus)
89
What is abiotrophy?
(When something is normal at birth but degenerates overtime after birth, this can occur to the cerebellar cortex)
90
Cerebellar cortical abiotrophy is most commonly found in what breed?
(American staffordshire terriers) → this is because they do not show signs of dz until later in life and if they are breeding stock, they will have already been bred by that time and passed on their genes)
91
What is seen on histopathology of a cerebellum affected by cerebellar cortical abiotrophy?
(Loss of purkinje neurons and thinning of all layers)
92
What is the main insult/issue associated with Chiari-like malformation?
(The syrinx that results from disrupted CSF flow, CSF disruption from herniation of cerebellum through foramen magnum and kinking of the medulla → that is what truly leads to the variable clinical signs seen with this dz)
93
What are the variable clinical signs associated with Chiari-like malformation? Four answers.
(Random episodes of pain, phantom scratching, ataxia, and weakness)
94
What are the treatment options for Chiari-like malformation?
(Gabapentin/pregabalin for pain, prednisone for inflammation/decreasing fluid backup, and/or foramen magnum decompression)
95
Feline cerebellar hypoplasia results from perinatal infection of the dam with what virus?
(Panleukopenia virus)
96
What layer of the cerebellum is particularly affected by panleukopenia virus?
(The granular layer, in babies it is on the outside of the cerebellum and migrates inward, panleuk prevents that and the granular cells degenerate)
97
(T/F) Cerebellar infarctions are thought to be the most common location for intracranial infarctions.
(T)
98
If a lesion is described as hyperintense on an MRI, what color do you expect it to be?
(White, isointense = grey and hypointense = black)
99
On a T1-weighted MRI, fluid will be hypo/iso/hyperintense when compared to grey matter.
(Hypointense → black; muscle will be isointense, fat will be hyperintense, white matter will be hyperintense)
100
Tissues that uptake contrast will be hypo/iso/hyperintense on a T1-weighted contrast MRI sequence.
(Hyperintense)
101
On a T2-weighted MRI, fluid will be hypo/iso/hyperintense when compared to grey matter.
(Hyperintense → white; muscle will be isointense, fat will be hyperintense, white matter will be hypointense)
102
Why are T2-weighted MRIs good for identifying pathologies such as edema, inflammation, bleeding?
(Because most pathologies appear hyperintense on T2-weighted MRIs so they will be nice and bright compared to everything else)
103
What is the purpose of a T2-weighted FLAIR MRI sequence?
(To identify pathological fluid in the brain → pure fluids (CSF) will be black while pathological fluid will be white)
104
On a gradient echo or T2* MRI sequence, what pathology are you looking for and how will it appear?
(Pathology is hemorrhage and it will appear black → don’t forget air and bone also always appear black on any MRI sequence)
105
As the timeline increases for paradoxical vestibular disease from acute to chronic, how does that change the top differentials?
(Acute → traumatic, vascular, or anomalous; chronic → neoplastic, degenerative, or anomalous)
106
(T/F) Meningiomas and choroid plexus tumors are extra-axial versus gliomas which are intra-axial.
(T)
107
What type of meningioma can present similarly to a glioma on post contrast MRIs (ring enhancement)?
(Microcystic meningiomas)
108
If vacuolization is present on histopathology of the brain, what pathology is indicated?
(Edema)
109
What is wallerian degeneration?
(Anterograde degeneration of an axon distal to an injury)
110
The presence of the Babinski reflex is an upper/lower (choose) motor neuron sign and is indicative of an acute/chronic (choose) injury/lesion.
(Upper motor neuron sign and chronic injury/lesion)
111
How do you distinguish between ANNPE (acute non-compressive nucleus pulposus extrusion) and FCE (fibrocartilaginous emboli) on MRI?
(ANNPE will show hyperintensity right above a degenerative disc whereas FCE will show hyperintensity not related to a disc at all, usually site is larger)
112
Why will the grey matter undergo necrosis prior to the white matter in cases of FCE?
(Bc grey matter is more metabolically active, has a higher need for blood flow)
113
What is a secondary pathology that can occur after a disc herniation that owners must be warned about?
(Ascending/descending myelomalacia → fatal; can occur for up to two weeks post an injury, rare in other dzs besides disc herniation)
114
What is the term for protein elevation in the CSF with no signs of inflammation?
(Albuminocytologic dissociation)
115
What is pleocytosis?
(Increased WBCs/cell count in general in CSF, indicates inflammation, can be single cell type or mixed)
