Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neuro > Tarc: Neuro Imaging And Diagnostics > Flashcards

Tarc: Neuro Imaging And Diagnostics Flashcards

1
Q

Clinical signs nd pathogenesis of hydrocephalus

A
  • congential (more common dogs) or acquired
  • domed head shape
  • open fontanel
  • diverging strabismus
  • blindness with absent menace OU
  • ataxia and v postural reactions
    > on imaging
  • thin cortex w/ greatly distended lateral ventricles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Best diagnostic modalities for diagnosing hydrocephalus?

A
  • MRI
  • CT
    0 Ultrasound
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Tx hydrocephalus?

A 
> medical 
- low dose GCs
- acetazolamide
- omeprazole
- mannitol (emergency) 
> surgical
- ventriculoperitoneal shunt placement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What breeds hav ^ risk of hydrocephalus?

A
  • toy breeds with brachycephalic skulls
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How long after ventriculoperitoneal shunt sx are clinical signs likely to improve?

A

4 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

WHat proportion of animals are likely to develop shun complications following surgery for hydrocephalus?

A

25%~

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What radiographic abnormalities indicate IVDD?

A
  • ^ opactiy over intervertebral foramen
  • mineralisation of intervertebral disks
  • narrowed intervertebral disk space
  • spondylosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the intervertebral disk made up of?

A
  • annulus fibrosus

- nucleus pulposus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the SC surrounded by?

A

Epidural fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What 3 planes can CT/MRI be taken in?

A
  • transverse
  • median/sagittal
  • dorsal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How can a cervical vertebrae e identified on MRI?

A

Only vertbrae to contain BVs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the 2 types of IVDD?

A 
> type 1 (Hansen) EXTRUSION
- chondroid degeneration 
- extrusion of degenerate nucleus 
- acute -> spinal cord trauma (contusion and/or compression)
> type 2 (Hansen) PROTRUSION 
- fibroid degeneration 
- protrusion of hypertrophied annulus > chronic compression of SC
- may still present acutely
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Tx IVDD?

A

> thoracolumbar spine: Hemilaminectomy
- removal of half the lamina, articular facet joint and pedicle allowing access to vertebral canal from a lateral approach
cervical spine: Ventral slot
- slot burred though the centre of the disk and adjecent vertebral endplates to gain access to vertebral canal from ventral aproach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Can radiographs dx disk disease?

A

No, but can indicate disk diseas

- myelography needed for dx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Where is the most common space for IVDD?

A

T13- L1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is present above the disk hat -> asymetrical signs of IVDD?

A

longitudinal ligament along dorsal aspect of annulus fibrosus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

WHERE IS CONTRAST INJECTED FOR A MYELOGRAM?

A

SUBARACHNOID SPACE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is decision to go to surgery for IVDD based upon?

A
  1. pain
  2. progression
  3. deep pain/neuro deficits severity
19
Q

Ddx for a chronic progressive asymmetrical painful forebrain dz. What about if ^ cellularity (mononuclear cells) found on CSF tap

A

> Neoplastic
- supretentorial tumours cause pain d/t ^ICP
infectious/inflam
with CSF findings > GME (magnitude and type of pleiocytosis will vary in this condition)

20
Q

Histo findings associated with GME

A
  • mononuclear inflammatory cells
  • located perivascularly (around the BVs)
    > macroscopically brownish lesions seen in the white matter (enlarged sie of brain w/ oedema and inflammatory focus)
21
Q

What is SRMA?

A
  • steroid responsive meningitis arteritis
    (acute, progressive, symmetircal, painful)
  • inflamamtory cells (mainly neutrophils) within meninges and around BVs and nerve roots
  • young dogs commonly
  • may be febrile
  • usually neurologically normal
  • cervical hyperaesthesia (+- spine)
  • risk of haemorrhage into vertebral canal
22
Q

What is GME?

A
  • granulomatous meningioencephalitis

- a type of MUA (meningitis of unknown origin)

23
Q

What would a population of small, mature lymphocytes on CSF tap indicate?

A

inflmmation - MUA

24
Q

How si GME dx confirmed?

A

PME

25
Q

Tx MUA?

A

Cytarabine

26
Q

What would a CSF tap of marked pleiocytosis, predominanty neutrophils give as Ddx?

A
  • SRMA (no and type of pleiocytosis may vary in this condition)
  • infectious
  • neoplasia (eg. meningiomia)
  • IVDD (can -> neutrophilic pleiocytosis)
27
Q

How do nerves respond to damage?

A

SWELL!

28
Q

Ddx for spinal ataxia in the horse

A
  • CVM/S
  • EHV1
  • EDM
  • trauma
  • migrating parasites
  • EPM (foreign imports)
  • ryegrass staggers
29
Q

Clinical signs of EHV1 infection?

A
  • ascending paresis/ataxia
  • systemic signs: pyrexia, depression
  • bladder incontinence, tail paresis
  • urine scalding
  • occasionally cranial nerve signs
30
Q

Pathogenesis of EHV1?

A

> transmission
- inhalation: aerosolised infective droplets
- fomites: hands, water, eeed
viral replication in nasal epitheliem and shedding in nasal secretions
- within 2hrs
- usually for 7d, up to 14d in immunologically naive horses

31
Q

Which part of the SC does EHV1 mostly affect?

A
  • grey matter (vasculitis and thrombosis -> sharply demarcated haemorrhage)
32
Q

What causes the clinical signs of EHV?

A

result of vascular compromise (extent of neuro deficit correlates to haemorrhage)

33
Q

How can EHV1 be diganosed?

A

> IHC

  • vial antigen in endothelial cells and myocytes surrounding BVs
  • first detected @6-8d post infection
34
Q

Pathogenesis of EHV1

A
  • endotheliotopic
  • dissemination to uterus, lung or CNS, then to endothelium
  • vasculitis and thrombo-ischaemia (peripheral vasculitis (limb oedema), SC vasculitis, immune complex deposition)
  • some strains more liekly to be associated with neuro form of dz
35
Q

What codes of practice hsould be consulted for appropriate measures around EHV1 disease?

A

HBLB

36
Q

Tx EHV1

A

Look up

37
Q

Management of an EHV1 outbreak?

A

Look up

38
Q

How can good quality standing radiographs of the cervical spine be judged?

A

Ventrolateral processes should be perectly aligned

39
Q

What boney changes are ofen seen in older horses? Are these pathological?

A
  • articular face changes @ C5-C7 common in adult healthy horses
  • NOT neurological
40
Q

What radiographic signs may indicate Opathology of the spine?

A

> subjective
- spinal canal aligment
- OA of articular processes
- caudal epiphyseal flare (ski ramping)
objective
= intRAvertebral ratios (more senstiive and specific in young horses)
- measure minimum canal diameter (perpendicular to canal floor) and maximum vertebral physis diameter (perpendicula to canal floor)
- calculate ratio (canal/physis) to adjust for distance of radiograph from xray machine and size of horse
- if

41
Q

If ratio of

A

No not necessarily

42
Q

Pathogenesis of CVM/S. What are the 2 types?

A

> neuro signs d/t progressive SC compression
2 main types of osseus malformation/stenosis
- type 1: dynamic (flexion C3-C5, extension C5-C7, young animals)
- type 2: absolute (osseus changes in vertebrae -> SC compression, older horses @ C5-7, O changes in articular process joints (facets) d/t congenital OCD?)

43
Q

How may the location of the lesion be determined at PME with CVMS?

A

> Wallerian degeneration

  • ascending tracts cranial to the lesions and descedning tracts caudal to the lesion degenerate
  • white and grey matter changes at site of lesion
44
Q

Outline the flow of CSF

A
  • produced choroid plexus of lateral ventricles
  • flows into 3rd ventricle then 4th
  • exits via arachnoid villi to the lymphatics

Neuro (30 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions