Lecture 9 - Cerebral Disorders 2 Flashcards
1
Q
Explain neuronal migration
A
- stem cells have to get to the periphery to form the cortex > they are guided by glial cells
- radial glial cells set out long projections > ‘railway system > neurons creep along the radial railways until they get to where they need to go
- when they get to periphery, they form connections with neighbours
2
Q
When can migration failure occur? What can this lead to?
A
- genetic predisposition
- maternal toxins, meds, smoking, drinking, flu, illness etc.
- often not effect on cog functioning, but can lead to seizures
- “double cortex syndrome”
- leads to “ectopic grey matter’ > poorly connected neurons; dysfunctional communities; not subject to same input as normal clinical cells (eg. pruning)
- low inhibitory potential therefore excitable and eliptigenic
3
Q
What is callosal dysgenesis?
A
- when the corpus callosum fails to develop
- children born with only partial CC or no CC at all
- some children develop normally, others not (depends on comorbidities)
- variable expression of neuropsych and behavioural features
- CC develops out of diencephalon (thalamus and hypothalamus) > develops out of subcortical structure
4
Q
What are the 2 types of brain plasticity?
A
- contralateral transfer
- ipsilateral re-organisation
5
Q
Explain contralateral transfer and when it can occur
A
- when the intact hemisphere takes on functions of the impaired hemisphere
- must occur EARLY in life for this to be able to happen
OCCURS IN
- early hemispherectomy (remove 1 hemi)
- neonatal infarction (very rare, stoke)
- major developmental abnormalities
6
Q
Explain ipsilateral re-organisation and when it can occur
A
- when functions of the lesioned area are taken on by the same hemisphere (usually the area around the lesion)
OCCURS IN
- focal developmental anomaly
- adult-onset stroke
7
Q
Explain the case eg of focal cortical dysplasia with intractiable seizures
A
- ipsilateral re-organisation occurred in the end
- she had a developmental lesion > cog asymptomatic but started having seizures
- thickening of cortex in one area (in this case, frontal lobes) > poorly connected neurons, low inhibitory potential therefore excitable and eliptigenic
- pre-op mapping: fMRI > showed activity in language tasks
- intera-op mapping: use electrical stimulation to disrupt activity > normal discourse, naming, sentence repetition, WM»_space;> RESECT!
- 2wks post-op > issues with speech (lots of activity in strange area, typical of troubled brain)
- 18mth post-op > ipsilateral re-organisation, area around the lesion
8
Q
What are the two types of compressive and infiltrating developmental lesions we discussed?
A
CAVERNOUS ANGIOMA
- cave-like ballooning out of artery > can leak blood into brain (toxic, eliptigenic)
- can be fully cog asymptomatic
DYSEMBRYOPLASTIC NEUROEPITHELIAL TUMOUR
- asymptomatic while in tact, but other areas affected with resection > symptoms
- seizures
- developmental origin (develop slowly over time)
PRE-SURGICAL DILEMMA
- left mesial TLE
- intact verbal memory
- typical left language lateralization
- normal T2 hippocampal signal
9
Q
Describe tumours and their onset
A
- lesions which are confined in space but occupy space
- insidious, asymptomatic onset
- infiltrative or compressive
- cog and behaviourally asymptomatic at start
- stuttering neuropsych features (may be interpreted as something else - anx, dep, delusion etc.)
- subtle persisting neuropsych features
10
Q
What are the 4 features of tumours?
A
- static v. progressive
- focal v. diffuse
11
Q
What are neurodegenerative conditions?
A
- insidious onset
- progressively and systematically symptomatic
- don’t sit in a particular space, but can ‘dissect out’ certain functions/systems across the brain
- system degenerations > affect distance parts of the NS that are linked to each other functionally via long-distance connections rather than topographical proximity
12
Q
Describe the 2 types of strokes we talked about
A
STRATEGIC
- bilateral thalamic lesions
- permanent amnesia! > tiny but destructive because so specific
REGIONAL
- occupy large areas
- non-progressive > hole in brain > cog impairment occurs immediately and then (usually) starts to get better
- CAN RECOVER (ipsilaterally)
- can lead to Broca’s aphasia; paralysis of one side etc.
- huge, but not nearly as big an effect as the tiny one
13
Q
Explain closed head injuries
A
- destructive, sudden onset > diffuse!
- resolve (to greater or lesser extent)
- brain rotates around brain stem > squeezes it out
- tearing blood vessels
- petechial bleeds > tiny bleeds all over the brain
14
Q
What are the 3 key characteristics to consider in lesions?
A
- impact on cognition is intimately related to the dynamics, nature and distro. of lesions
TEMPORAL: onset, course
NATURE: pathological features
DISTRIBUTION: focal, space-occupying, diffuse
15
Q
What are the 4 factors that interact to result in the effect of a lesion?
A
- anatomy
- pathology
- network effects
- functional consequences
