neuropathology Flashcards
(106 cards)
1
Q
cerebrum
A
contains cortex and numerous subcortical structure eg. hippocampus
2
Q
basal ganglia
A
subcortical nuclei responsible primarily for motor control
3
Q
parietal lobe
A
integrates sensory information
4
Q
cerebellum
A
coordination of voluntary movements
5
Q
spinal cord
A
transmits messages between brain and periphery
6
Q
medulla oblongata
A
responsible for autonomic (involuntary) functions
7
Q
hippocampus
A
learning and memory
8
Q
amygdala
A
emotional information processing
9
Q
pituitary gland
A
hormone production
10
Q
hypothalamus
A
links nervous system to endocrine system
11
Q
thalamus
A
relay motor and sensory signals to the cerebral cortex
12
Q
frontal lobe
A
controls congitive skills/ logical thinking
13
Q
A
13
Q
corpus collosum
A
ensures both sides of the brain can communicate
14
Q
temporal lobe
A
sense perception, language and memory
15
Q
what happens in embryonic cleavage
A
- post fertilisation egg undergoes rapid cell divisions
16
Q
what is the last stage called of embryonic cleav.?
A
morula
17
Q
does embryo size change in Embry.Clv.?
A
- No overall change in embryo size
- but each divisions cell gets smaller
18
Q
what is gastrulation?
A
process of establishment of the 3 germ layers
19
Q
name the three cell mass areas before gastrulation
A
- OCM (outer cell mass)
- ICM: - hypoblast
- epiblast
( zygote now known as gastrula)
20
Q
when and how does the process happen
A
- 6 days post fertilisation
- epiblast cells migrate to primitive streak
- may move to lie between epiblast and hypoblast
- or displace cells of hypoblast
21
Q
three germ layers and what they do
A
ectoderm: epiblast cells that do not invaginate (stays on top surface of embryo)
mesoderm: cells that lie between epiblast and hypoblast
endoderm: cells that displace hypoblast (gut/digestive system)
22
Q
steps of neurulation
A
1) body axis formed as mid-line structure, notochord laid down
2) vertebrates this will form the spine
3) notochord induces neuroepithelium (ectoderm), which is the future CNS
4) Neural folds elevate, close and sink beliw the surface ectoderm = neurulation
23
Q
describe the neural tube structure
A
Forebrain:
telencephalon (c. cortex, hippocamp) & diencephalon (thalamus, hypothalmus)
midbrain:
mesencephalon
hindbrain:
metencephalon (Cerebellum)
myelencephalon (medulla oblongata)
& spinal cord
24
what happens after main shaping events of BRAIN development
- neuroblasts divide, differntiate die and forms connections
- support cells of N.S. (glia) will divide n diffnte
- - myelination occurs in late neural dev. in both PNS AND CNS
-
25
explain brain dev. in infants
- brain increases rapidly in size
- cerebellum and visual are early areas of enlargement
- lost of myelination going on
- connections used repeatedly, become stronger
26
brain increase from 3yo to 5yo?
from -75% to 95% adult size
27
what does synaptic pruning do
removes unnecessary synapses and neurons , which refines connections --
increases brain efficiency
28
why are adolescents more reactive, and take high risks
- rely more on amygdala for emotional response (As prefrontal cortex is still developing)
- and risk behv. as the reward centre (ventral striatum) is still not fully developed
29
what happens for 20-30yo brains?
more anamotically, physiologically and functionally mature
- neurogenesis continues in some brain regions
30
// what is spina bifida
- 'split spine'
- during devlopm. neural tube does not close correctly in region of spinal cord
- can cause anencephaly
31
Name the 3 NTDS (neural tube defects)
- open defects -> primary neural tube closure -> anencephaly (lacking brain/skulle parts)
- herniation defects (outpocketing/folding) -> primary mesodermal (bony) defects w neural tissue -> encephalocele (brain tissue outside of skull)
- closed defects -> tail bud (secdry. neurulation defects) -> spinal dysraphism
32
what can be used to prevent NTDS during pregnancies
Folid Acid (FA), at least 0.4mg daily
33
what are other factors linked to NTDs
- maternal insulin-dependent diabetes
- maternal prepregnant obesity
- maternal use of specific anticonvulsant drugs, including valproic acid
34
what environmental factor can be blamed?
- environmental teratogen: fungal product fumonisin (1990s, texas-mexico)
35
treatments of spina bifida
- early (or prenatal) surgery to repair defect
- nerve damage irreversible
- physiotherapy
- mobility aids
** some ppl dont event know they have it till later)
36
what is spina bifida OCCULTA
- mildest type of S.B.
- called "hidden" s.b.
- small gap in spine, but no opening/sac on back
- spinal cord and nerves normal
- not discovered until adulthood usually and does not cause disabilities
37
what is ASD and what is it characterised by
Autism spectrum disorder,
characterised by : communication, social and behavioural challenges.
- great variation in symptoms and their SEVERITY
38
what happens, with autism in the brain?
- no particular brain regions that explains
- no cellular change either
- hypotheses exist
39
40
name the 4 theories for ASD
1) early and postnatal overgrowth
2) signalling imbalance theory
3) excess serotonin theory
4) connectivity theory
41
explain fors and against for the early brain overgrowth theory
FOR:
- larger brain size in early childhood (Esp white matter)
- meta-analysis suggests 2-5% increase in vol
AGAINST:
- data for late childhood/adulthood is less convincing
42
explain the signalling imbalance theory for ASD
- autistic brain is hyper-excitable
- balance of excitatory and inhibitory signals enables neurons to be active in some circumstances, while muted in others
- 80% of neurons in cerebral cortex transmit EXCITATORY neurons, by releasing neurotransmitter GLUMATE
- 20% neurons are inhibitory, operate via GABA (gamma-aminobutyric acid)
43
for and againsts for signalling imbal. theory
for:
- many autistic people have epilepsy
- many autistic people have unusually frequent spikes of activ. during sleep
- mouse models show signal imbal. with deficit in inhibt. neurons
against:
- one study found high number of inhibitory neurons
- 1 research showed larger proportion of GABAergic signalling in neurons in autistic boys
44
explain how the sertonin excess theory works
- serotonin trasnporter moves serotonin from gut to blood
- in brain, serotonin levels at synapse level, regulated by serotonin trsprter, which pumps serotonin back into neurons and recycles it for later use --- may be altered in ppl with autism
- leaves less serotonin availb. to relay msgs across synapses
45
against... serotonin excess theory
- 3 in 4 ppl w autism's serotonin lvls are unremarkable
- brain and blood levels do not necessarily correlate
46
what is the connectivity theory? for asd
- communication is de-synchronised between brain regions
- **UNDERCONNECTVITY** between DISTANT brain regions
-** OVERCONNECTIVITY **between CLOSE brain regions
47
for and against connectivity
for:
- strong evidence in brain scans of changes in connectivity
against:
- some find no difference between autistic and typical brain
48
// what causes ageing in the brain
- for women decrease of oestrogen post menopause
- brain mass shrinks esp in front lobe +hippocamp
- cortical density, cortex thins
- white matter, shrinks
49
current consesus on WHY we age?
- by-product of bio reactions can damage cells
- body has defence mechnsms to protect against this
- over time damage cellular component accuml.
50
what is the most damaging by-product and how can we avoid it
- oxidants, carry extra electron which can damage dna & proteins
- must eat food rich in anti-oxidants (dark choc, blueberries, strawbs)
51
describe ageing and physical changes in the brain
- 5% decreased vol. every decade (From 40 yrs)
- decreased grey matter vol (due to neuronal death)
- decreased in white matter vol (myelin sheath begin to deterioate) + white matter lesions increase w age
52
other causes for ageing?
- head-heart link: blood vessels become weaker as we age, collagen hardens (artherosclerosis)
- microbleeds
- plaque build up
53
name psychologing changes in ageing
- processing speed:
cognitive activites
motor respose
- memory:
reduced ability to ignore irrelv. info
encoding new info and retrieval info declines w age
- language:
remains intact
- attention:
selective attention declines w age
54
how can we ensure healthy brain ageing?
- lifestyle, no drinking smoking
- healthy diet and regular exrc
- good sleep
- support elderly with social networks, to avoid loneliness
55
parkinson's symptoms
- mask-like facial expression
- reduction in spont. blink rate
- soft monotonous voice
- festination (posture/gait)
- bradykinetic & hypokinetic movements
- cogwheel phenomenon (rigid limbs)
56
explain cell loss for P.D.
- there is a loss of dopaminergic neurons of the midbrain
- most loss in substantia nigra pas compacta
58
59
What does the substantia nigra do
- neurons that die make dopamine
- makes dopamine for the striatum
- dopamines role is to regulate movement by inhibiting striatal neurons
60
what happens in the absence of dopamine, and striatum
- parkison's syptoms can arise
- striatum is also known as reward system region, which can result in behavl. changes e.g. gambling
61
what are lewy bodies and what do they do?
- they are cellular level bags of protein, build up in cells
- they attempt to prevent cell death/may be toxic
62
name drug treatments and non-drug for P.D.
DRUG:
- levodopa, building block of dopamine
- COMT inhibitors, block levodopa breakdown
- dopamine agonists - mimic dopamine (skin patches, more consitent)
NON-DRUG:
- nursing
- physio
63
onset symptoms for p.d.
- tremor, stiffness, clumsiness
- difficulty walking
- dysathria (difficulty spking due to weak muscles)
64
alzheimer early symptoms
- memory loss
- everyday problems: handling money, planning, introducing people
65
mid alzheimer's symptoms
- forgetting events or personal history
- moody/withdrawn
- altered sleep patterns
- behaviour chg: susppiciousness, delusions
66
late alzheimers symptoms
- personal care around the clock
- loss awareness of recent experiences
- vulnerable to infections, pneumonia
67
causes for alzheimer's
- primary cellular changes:
extracellular plaques
intracellular tangles
inflammation
- loss of volume esp. in cortex/hippoc.
68
explain plaques and tangles
plaques = accumulation of amyloid beta 1-42
tangles = accumulation of hyper-phosphorylated tau
69
how do plaques and tangles cause AD
- dont rlly know
- amyloid inside neurons could be more toxic so plaques could be a false target for drug design
70
current pharmacological treatm. for A.D.
- acetylcholine esterase inhibitors and memantine (regulates glumate) for memory loss
- drugs for behav. changes
- sleep meds
71
care for A.D.
- social care
- physio/speech
- music activates in regions of brain with lowest plaques and tangles
( future stem cell therapies/drugs)
72
what do the ventral and dorsal horns do?
orientate us within the spinal cord and contain sensory synapses and motor-neurons respectively
72
describe the spinal cord
- long structure running from base of brain to base of spine
- info high way from brain to body
- regions named after spinal regions
cervical, thoracic, lumbar and sacral
73
what do ventral root and dorsal root emerge to
dorsal root -> directly from spinal cord -> dorsal root ganglion
ventral -> ventral spinal cord -> fibres form spinal nerve
74
what are the central canal and median fissure structures
central canal - carries cerebrospinal fluid (CSF)
median fissure - is the midline struct of the SC
75
what does the spinal ganglion (dorsal root) do
collection of cell bodies whoch transmit sensory info from PHS TO CNS
76
what does the grey matter do
process info to make it ready to send to send to body or brain
- made of soma (cell bodies of neurons) and dendrites (short range connections)
- axons (long range connections)
77
what do dorsal and ventral HORNS do
- neurons of dorsal horns = receive sensory info that enters spinal cord via dorsal roots
- ventral horns = contain cell bodies of motor neuropns that send axons via ventral roots of spinal nerves to terminate striated muscles
78
explain DRGs (dorsal root ganglions)
- collection of neurons lying outside the CNS
- transmit messages from thermorecptors, nocireceptors, propriorecptors
- easy access , unlike cranial ganglia
79
reflex response
- not all info received goes up to brain
- some motors reflexes controlled by spinal cord independently of the brain
80
EXPLAIN STEPS OF PATELLAR REFLEX (knee bone)
1) STIMULUS
2) **Sensory receptor activation**: tap stretches the patellar tendon, stimulating muscle spindles within quadriceps muscle
3) **sensory neuron activation**: muscle spindle fibres detect streching of muscle + genr action potentials
4) **transmission of nerve impulses** : sensory neurons carry these action potentiald from muscle spindles to spinal cord via femoral nerve
5) ** spinal cord processing** sensory neurons synapse w motor neurons in spinal cord grey matter
6) ** motor neuron activation ** synapsed motor neurons part of reflex arc, receving signals quickly transmit action potential to quadr. msc.
7) ** muscle contraction**
action potentials arrving at quadri. muscle, causing involuntary contraction
-- feedback loop: leg extends -- tension on patellar tendon decrs. --- reduces stimult. of muscle spindles -- dampening reflex response , preventing excsv contrctn.
81
types of spinal cord injury
complete: complete loss of sensation and motor function below level of injury
incomplete:
- some function is retained below point of injury
- retain function : unilteral/ bilateral
82
symptoms of s.c. injury
loss of movement
paralysis :
tetraplegia - all 4 limbs, trunk pelvic organs affected
paraplegia - all part of trunk, legs, organs affected
loss of bowel/bladder control
83
acute treatment for s.c. injury
- immobilise
- maintaining breathing and minimise shock
- used to be methylprednisolone (IV) but not anymore due to blood clots/pnuemonia
84
ongoing care for s.c. inj.
medical: drugs for muscle spasms
rehabitliat: physio, psych
tech. support: wheelchairs etc.
85
why and how do scientists boost energy supply to spinal cord
- to encourage axons to regrow
- many mitochondira within axon
- when axons cut off, neurons lose their power supply
86
how is energy supply transmitted to neurons
- anchored by a protien called *syntaphilin*
- when knocked out of mtioc. energy prod. incrsd
- energy released when ATP -> ADP (removal of phosphate group)
- high energy bonds when broken , release energy (dephosphorylation)
87
in future what is important to regrow axons to connect to targets
cells of the CNS system **microglia**
88
how do microglia behave after SCI
- form a protective barrier
- they need a protein called Plexin-B2, if removed regrowth is less and injury 'spills over'
89
how can stem cells help in sci
the relative simplicty of spinal cord compared to brain means stem cell therapies are attractive .... can be drive to replace neurons.
90
how exactly would stem cells support spinal cord
- neurotrophind and cytokines support neuron survival
- angiogenesis dev of blood supply
- gliosis = inflammation
- cavitation = fluid enlarges the central canal
91
results from stem cell trials....
- human embryonic stem cell derived from oligodendrocyte (makes myelin) progenitor cells
- primary outc: no significant adverse events
- secondary outcome: functional improvement: inprogress
- safety concerns: ESCs could form tumours
92
what do the cerebellar nuclei do
output structures that connect with other parts of the body
- encased by highly convoluted by cerebellar cortex
93
explain the cerebellar cortex layout
outer layer: molecular layer compromising axons from the other 2 layer
middle: purkinje cell layer of large neurons w dramatic dendritic tree
inner: granule cell layer, small densely packed neurons
94
explain how info is gathered by GRANULE CELLS in cerebl. cortex
- granule cells receive input from mossy fibres (excitatry projct. from other neuronal regions)
- granule cells project their output via an axon that goes to molecular layer
-
- splits in 2 and processes run parallel to fold of cereball. cortex
- parallel fibres make excit. synapses w dendrites from purkinje cells
95
explain Purkinje cells
- arranged perpendic. to parallel fibres
- each Pkj. cell receive excit. input from parallel fibres
- also receive input from INFERIOR OLIVE (medulla part involv w motor control)
- known as climbing fibres
96
more about purkinje cells and climb fibre
- each pkj cell receive powerful exc. input from single climbing fibre
- each fib contacts up to 10 Pkj cells
- climbers wrap their axons around pkj cell
- pkj cells only source of output from cerebell.
97
how do pkj cells perform output from cerebell.
- make inhibitory connections w cells of deep cerebell NUCLEI
- mossy fibre -> granule cell -> parallel fibre -> pjk cell - > crb nuclei
98
what are cerebell. 3 MAIN functions
1) working w cerebral cortex and other areas -- visually guided movements
2) receives proprioceotive info/ regulates body movements
3) working w vestibular system -- balance, ocular reflexes
99
what is cerebellar ataxia
- neurodegenrative disease, "ataxia", " a taxis" = greek = without order or incoordination
- can be either hereditary or acquired
100
ataxia symptoms
- eye movement abnormalities, links w vestibular system
- heart problems
101
explain the inherited ataxia, autosomal
autosomal dominant/recessive
- if parent carries dominant autosomal gene 1/2 children will be affected
- recessive, unaffected both parents only CARRYING , 1/4 children affected
102
inherited X-linked genes for ataxia (gene for ataxia only on X genes)
- X-linked mother (unaffected carrier) ,can affect 1/2 of boys and only give carrier gene to XX progeny
- X-linked father: can only carry to female (XX progeny)
103
explain acquired ataxia
- prelude to other disorder e.g. spinal muscular atrophies
- pure cerebellar: linked to degen of cerebell. structurs.
- cerebell. plus: linked to additional symptoms e.g. neuropathy, dementia...,
104
causes for ataxia...
- vitamin deficiencies
- various cancers
- exposure to toxic substances
- infections (agriculture)
105
treatments for ataxia
- lost neurons cannot be reinstated
- treatment is to improve quality of life
- symptomatic relief: depressive symptoms, diziness,fatigue
