Deck 9 Flashcards

1
Q

What is an alternative name for intracranial epidermoid cysts?

A

Cholesteotoma

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2
Q

What does each contain — epidermoid v dermoid cysts?

Significance of this?

A

Epidermoid — keratin
Dermoid — sweat, hair follicles, cholesterol

Dermoid cysts will often be pre-T1 hyperintense

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3
Q

Mai says that some areas of the brain are more susceptible to ischemia than others — what areas?

A
  • occipital lobes
  • parietal lobes
  • portions of hippocampus
  • cerebellum
  • caudate nucleus
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4
Q

When does vasogenic edema formation peak following an ischemic stroke?

A

3-4 days

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5
Q

Theoretically, the combination of what two imaging techniques can be used to determine the ischemic penumbra of a CVA?

A

DWI — shows the area of infarction
PWI — shows the area of ischemia

DWI — PWI = ischemic penumbra (tissue that could potentially get better)

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6
Q

Following an ischemic stroke, how do ADC values change with time?

A

ADC values drop for the first 24 hours (restricted diffusion) and stay low for the next 3-4 days. Then, they slowly normalize by days 4-10, and by day 10 onward they are elevated (unrestricted diffusion).

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7
Q

What are the distributions of the arterial blood supply to the brain?

A
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8
Q

What do each of these blood vessels supply?

A
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9
Q

How does methemoglobin become extracellular in the aging process of hemoglobin?

A

Lysis of the red blood cell it was in

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10
Q

True or false - diamagnetic substances increase the local magnetic field.

What does increasing the magnetic field do?

A

False — diagmagnetic substances (like oxyhemoglobin) decrease the magnetic field, while para and superparamagnetic substances (methemoglobin) increase it.

Increasing the local magnetic field results in shortening of both T1 and T2 relaxation times. If T1 relaxation times are shortened, then this leads to more signal on T1 weighted images, and thus explains why methemoglobin is T1 hyperintense).

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11
Q

What makes heme paramagnetic v diamagnetic?

A

The presence of un-paired electrons makes something paramagnetic.

Oxyhemoglobin possess iron in the ferrous (Fe 2+) state (paired electrons), making it diamagnetic. When the iron is oxized into ferric form (Fe3+), then the electrons are unpaired and it becomes paramagnetic. Deoxyhemoglobin is also paramagnetic because of the oxygen it lost.

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12
Q

Is the iron in hemosiderin / ferritin paramagnetic or diamagnetic? Why is it not T1 hyperintense?

A

It is paramagnetic (iron is in the ferric state), which normally shortens the T1 relaxation time. However, due to the molecular arrangement of hemosiderin / ferritin, they are shielded from the nearby environment and don’t get the spin-lattice relaxation that would be expected with T1 relaxation. Thus, hemosiderin / ferritin are T1 hypointense.

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13
Q

What stage of hemorrhage is this?

A

Late subacute — only time you will have both T1 and T2 hyperintensity

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14
Q

What MRI features can be used to help differentiate between a benign hemorrhagic lesion and a neoplastic hemorrhagic lesion?

A
  • strong contrast enhancement
  • multiple stages of hemorrhage
  • lack of T2 / T2* hypointense rib
  • areas of non-hemorrhagic tissue within the lesion
  • +/- more edema
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15
Q

True or false — extra-parenchymal intracranial hemorrhage has similar imaging characteristics as intra-parenchymal hemorrhage.

A

False — extra-parenchymal hemorrhage processes through the stages of hemoglobin degradation much more slowly than intra-parenchymal due to the presence of more oxygen outside the BBB.

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16
Q

What type of hemorrhage is “toxic” to the brain — epidural, subdural or subarachnoid?

A

Subarachnoid — direct contact of inflammatory mediators with the surface of the brain (compared to the others)

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17
Q

What type of hemorrhage is associated with shunt over-shunting?

What are two other reported causes of this type of hemorrhage?

A

Subdural

Trauma and secondary to brain atrophy in NCL.

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18
Q

In regards to extra-parenchymal intracranial hemorrhage, what type results classically from venous bleeding, and what type from arterial?

A

Venous — subdural
Arterial — epidural

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19
Q

What is the location of hemorrhage is this? How do you know?

A

Epidural — does not cross suture lines and has a biconvex shape

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20
Q

Describe the differences in appearance of the developing canine cerebrum over time?

A

1-4 weeks: white matter is more hyper-intense than grey matter, thin grey matter

~6 weeks: white and gray matter are isointense

8-36 weeks: relatively normal appearance

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21
Q

What part of the brain atrophies most in the aging canine brain?

A

Frontal lobes

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22
Q

What two locations do lacunar infarcts often occur in the aging canine brain?

A

Caudate nucleus and thalamus

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23
Q

What is one of the best MRI sequence types for visualizing cranial nerves?

A

3D balanced steady state free processions — tissues with a high T2/T1 ratio stand out

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24
Q

Identify these structures

A
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25
Identify these structures (paired in the photos)
26
What anatomic structure(s) composes the ‘duck’ of the inner ear on MRI?
The utricle and saccule (NOT the cochlea)
27
What cranial nerve is present at the level of the cochlea on a T2 Trv brain image?
Facial
28
The emergence of the trigeminal nerve from the pons is in the same transverse MRI slice as what prominent structure?
Caudal colliculi
29
True or false — in cats, the maxillary branch of the trigeminal nerve exits the skull via the round foramen, and then into the alar canal and rostral alar foramen.
False — cats do not have an alar canal
30
What is the normal height and width of the optic chiasm?
Height — 2.1 mm Width — 4.8 mm
31
What is the presumptive diagnosis?
Idiopathic oculomotor nerve palsy
32
At what level does the major petrosal nerve leave the rest of cranial nerve 7?
Within the facial canal, at the level of the geniculate ganglion
33
What is the diagnosis? What breed is over-represented for this disease?
Extra-ocular polymyositis Golden retriever
34
Describe the possible pathogeneses of acquired aural cholesteatomas. What is their alternative name? What do they fill up with?
Chronic otitis causes retraction of tympanic membrane (stratified squamous epithelium) into the middle ear cavity, or similar epithelium migrates through into the middle ear via a ruptured tympanic membrane. Epidermoid cysts Keratinaceous debris
35
Name these muscles
1 — temporalis 2 — masseter 3 — ptyergoids 4 — digastricus
36
In what breed of dog does a juvenile form of masticatory myositis occur in?
CKCS
37
What is a possible explanation for why lateralized disc herniations are more common in the neck?
The dorsal longitudinal ligament is thicker in the neck compared to the TL spinal column.
38
What percent of Dachshunds have abnormalities in their number / morphology of vertebrae?
10%
39
What are three pathophysiologic factors in DAWS?
- relative vertebral canal stenosis - more pronounced torsion in the caudal cervical vertebral column, leading to disc degeneration - protrusion of larger volume discs
40
When performing traction based cervical MRI, what percentage of BW should be applied as traction?
20%
41
What is approximate variation of the size of the caudal cervical vertebral canal between flexion and extension?
~30% (28.9 to be exact)
42
True or false — the size of the cervical intervertebral foramina increases when the patient is positioned in extension.
False — it decreases in extension and increases in flexion.
43
What is the diagnosis?
Sacral OCD
44
What medium/large breed dog has a known genetic anomaly for congenital vertebral malformations?
German short-haired pointer
45
Name / describe these malformations.
46
What is the diagnosis and what was this dog’s main clinical sign?
Diastematomyelia (although this looks more akin to diplomyelia) Lifelong urinary issues
47
What types of dermoid sinuses cause neurologic signs?
IV and VI — only ones to actually connect with neural tissue
48
What is the insertion of the ligament of the dens? The paired alar ligaments?
Apical — basioccipital Alar — occipital condyles
49
What are the strongest stabilizers of the AA joint in dogs?
Paired alar ligaments
50
What are the success rates of rectal diazepam v intranasal midazolam for control of status epilepticus?
PR diazepam — 20% IN midazolam — 70%
51
What is the diagnosis? What can this potentially predispose to?
Incomplete ossification of the atlas AA instability
52
Describe the ossification centers of the axis. Which one does it ‘steal’ from the atlas? What is the one that is ‘missing’ from this naming scheme, and where is it actually?
There are 7 ossification centers of the axis (see photo). The centrum of the proatlas is technically a part of the atlas that ends up fusing with the dens. Intercentrum 1 is ‘missing’, but forms the ventral arch of the atlas.
53
What breed of dog is over-represented for enlargement of their internal ventral vertebral venous plexus? Did this enlargement cause clinical signs of myelopathy?
Greyhounds Yes
54
What is the most common location for vertebral osteomyelitis? Why?
L2-4 — this is where the crura of the diaphragm insert, and migrating foreign bodies can follow them
55
What CNS fungal infection can mimic meningiomas? How can you distinguish between them?
Coccidiodomycosis Meningiomas typically have sharp boundaries following contrast administration, while cocci granulomas are less sharply marginated.
56
Primitive neuroectodermal tumors arise from what cell type?
Neural crest cells
57
What common tumor type can frequently be pre-T1W hyperintense?
Meningiomas
58
What are the four possible theories as to how FCEM occur?
- penetration into spinal vessels - penetration into sinusoidal vessels of the adjacent vertebral body bone marrow - penetration into new vessels forming in degenerative disc - penetration into embryonic remains of NP vessels
59
True or false — animals with FCEM can occasionally have a normal MRI
True
60
When is contrast enhancement most common in FCEM?
Around 5-7 days
61
What is the presumed location of this hemorrhage?
Subdural
62
What was the main finding of this paper?
An area of HASTE attenuation > 7.4 was predictive of the development of PMM
63
Where does the dural sheath blend with the epineurium?
At the level of the intervertebral foramina
64
What percent of dogs with SADs have spinal hyperesthesia?
Almost 1/4 (18-24%)
65
Describe the signal changes of muscles secondary to neurogenic atrophy.
Increased T2W signal — edema / fibrosis Increased T1W signal — fatty infiltration Increased contrast enhancement
66
On MRI, what are the signal characteristics of spondylosis and DISH?
Spondylosis — T1 and T2W hypointensity (relatively sclerotic bone) DISH — T1 and T2W iso/hyperintensity (trabecular bone, w/ fat in narrow cavity)
67
True or false — a Schwann cell can provide up to 60 internodes of myelin to nearby axons.
False — oligodendrocytes can do this, but one Schwann cell only produces on internode of myelin.
68
What are pseudo-Negri bodies? Where are they found commonly, and in what species?
Eosinophilic inclusion bodies of unknown / no clinical significance, often found in the lateral geniculate nucleus and hippocampus of cats.
69
What is this an example of? In sheep with copper deficiency, where does this occur? What cranial nerve nuclei have a similar appearance normally?
Central chromatolysis Ventral horns of spinal cord CN V and VII — but the nuclei are not marginated
70
Global ischemia results in acidophilic neuronal necrosis in what specific sites?
Cerebral cortex Hippocampus Purkinje cells
71
Preservation of silver-staining components with loss of luxol fast blue staining components indicates what type of disease process?
Primary demyelination (aka leukodystrophy) The LFB stains for myelin and the silver stains for axons.
72
There are two types of reactive astrocytes — what are they?
- gemistocytes (right photo)— present in acute pathologies, very eosinophilic, enlarged cytoplasm with short/fat cell processes - fibrillary (left photo) — present in chronic pathologies, more spindly than gemistocytes with lots of cell processes
73
Where are the majority of gitter cells derived from?
Blood borne monocytes (fewer come from the resident microglial cells)
74
What type of cells in the CNS are ciliated? What can cause them to lose cilia?
Ependymal cells Increased pressure from hydrocephalus
75
What is the most common autolytic change affecting the CNS? What autolytic changes can often be seen in the cerebellum?
Vacuolation Purkinje cell vacuolation and loss of granular cell layer
76
What is the arrow pointing to?
The subcommisural organ within the third ventricle (just ventral to the caudal commissure)
77
What is the arrow pointing to? Is this significant?
Lipofuscin pigment accumulation in a neuron; common finding in normal, older animals.
78
What is the main histopathologic finding in cats with hypertensive encephalopathy?
Hyalinosis / thickening of CN arteries / arterioles is the main finding. Vasogenic edema and hemorrhages can be associated findings.
79
What are common stains for identifying disc material?
Giemsa, toluidine blue or alcian blue
80
True or false — the CNS is able to mount strong innate and adaptive immune responses.
False — it is able to mount an innate immune response bc microglial cells and astrocytes possess PRRs, but it has no real resident lymphocyte population to facilitate an adaptive immune response.
81
What cytokine is released in SRMA to draw WBCs into the CSF?
IL-8
82
What are the typical path findings in patients with neurotropic viral diseases?
- non-suppurative polioencephalitis/myelitis - neuronal destruction via neurophagia - glial nodules - perivascular mononuclear cuffing
83
In horses, where are the main pathologic findings of rabies located?
Spinal cord
84
What type of virus causes pseudorabies?
Herpesvirus, specifically an alpha type
85
West Nile virus typically affects the _________, while the equine encephalitides typically affect the ________. Broadly speaking, these diseases cause _______ because they are _______. What type of viruses are these?
WNV — brainstem and spinal cord Encephalitides — cerebral cortex They cause polioencephalomyelitis because they are neuronotropic viruses, of the arbovirus category.
86
What type of pathology does vaccine induced CDV cause?
Non-suppurative polioencephalitis
87
CAE causes what type of inflammation?
Granulomatous meningoencephalomyelitis with massive perivascular cuffs
88
What feline virus can rarely cause a myelopathy?
FeLV
89
What is hairy shaker disease in sheep?
It is caused by border disease virus, resulting in hypomyelinogenesis and an abnormally curly hair coat. Apparently it is related to viral infection of the pituitary gland.
90
The presence of what structure is implicated in the development of sella turcica abscesses?
Rete mirable — convoluted blood vessels easily trap bacteria
91
What is the diagnosis?
Listeriosis causing a rhombencephalitis, with microabscess formation
92
What is the diagnosis?
Pithing from poor CSF collection technique
93
What type of virus causes dysmyelinogenesis? What are three examples?
Pestivirus - border disease in lambs - bovine viral diarrhea virus in cows - classical swine fever in pigs
94
What are the three criteria to diagnose Dandy Walker syndrome?
- vermal agenesis - cystic dilation of 4th ventricle - enlarged caudal fossa
95
Which form of polioencephalomalacia is accompanied by an eosinophilic infiltrate? What species?
Water intoxication (following water deprivation) Pigs
96
Does selenium poisoning or deficiency cause poliomyelomalacia in pigs?
Poisoning
97
What is the way that Fumonisin B induces leukoencephalomalacia?
Selective vascular damage to the white matter
98
Deficiency of what micronutrient causes swayback? Species? What is another way to develop swayback? What are the histologic features?
Copper deficiency = swayback in lambs Excessive molybdenum exposure Leukoencephalomalacia with edema / rarefaction of white matter
99
What is focal symmetrical encephalomalacia?
This a type of enterotoxemia that is also called overeating disease, and occurs in ruminants fed large amounts of carbohydrates. This results in overgrowth of clostridium perfringens D. The toxin it secretes then causes symmetrical areas of malacia throughout the brain.
100
How does edema disease result in neurologic signs?
Pigs have intestinal ecoli that produce a verotoxin, which causes widespread damage to small arteries and arterioles, leading to edema formation in the CNS.