midterm Flashcards
diagnosis
what disease is it
etiology
what caused it
prognosis
long/short term outcomes
incidence
number of new cases of a disorder in a given time period
Prevalence
Number of people within a population who exhibit a disorder during a specified time period.
lifetime prevalence
percentage of people who have been diagnosed with a specific disorder at any time in their lives.
Cerebral cortex
high order processing, bumps; gyri, grooves; sulci.
central sulcus
separates frontal and parietal lobes.
lateral fissure
separates frontal and parietal lobes from temporal lobes.
reflexes
They are independent of brain’s involvement. The pain sensation does require the brain’s processing of sensory input, the actual motor response does not involve the brain.
2 types brain cells
neurons and glia
glia
support, not background, role in development of the NS.
3 types neuron
Sensory;
interneuron; connects sensory and motor neuron in SC.
Motor Neuron: cause muscle contraction
pain
it requires sensory afferents to the brain. Motor reflex does not.
neurons organization
layered; cortex, or Nucleus, where a distinct cluster of neural cell bodies form a group.
organization
cortical networks are organized, grid-like, sub-cortical networks aren’t, irregular organization.
grey matter
cell bodies and blood vessels, subcortical nuclei, groupings of similar cell bodies.
structures span more than one region
brainstem; consists of part of the forebrain, midbrain, hindbrain…
lateralization
Left; language, math, logic
Right; emotion, orientation facial recognition, art/music…
Association tract
Connect regions within the same hemisphere.
Precentral gyrus
frontal lobe; motor cortex,
postcentral gyrus
somatosensory cortex,
homunculus
how much real estate different body regions take up.
basal Ganglia
Caudate nucleus, Putamen = striatum
Globus Pallidus, internal and external.
cerebrum limbic system
emotional control, learning and memory, Cingulate cortex: emotional processing and memory.
Amygdala; fear, agression, emotional memories, decision-making.
Hippocampus; learning and memory,
brainstem 3 regions,
diencephalon, midbrain, hindbrain
diencephalon
thalamus; sensory relay station.
Hypothalamus: homeostasis, hormone release…
hindbrain
Pons; connects cerebellum to brainstem.
Medulla: controls breathing and heart rate.
Midbrain
Tegmentum: modulates sleep, attention, reward, clusters use same chemical messanger: dopamine.
Role: link auditory and visual systems, controls orienting movements.
colliculi
superior: vision
Inferior: hearing.
For midbrain.
Action potential
- stimulus, move to -55
- threshold has to be reached.
- NA channels open
- NA positive, cell to +30
- at +30 Na channel closes, K channel opens.
- K rushes out, cell gets more negative.
NT
1, amines: dopamine, norepinephrine, epinephrine, serotonin
- Amino acids: glutamate, GABA (gamma-aminobutyric acid)
- other: acetycholine.
NT transmission
NT are synthesized and stored in the presynaptic axon.
- AP stimulate release of NT
- NT bind to receptors, post syn..
- receptors are coupled w ion channels that open when bound to NT. EPSP IPSP.
NT change
Fast Ionotropic: trigger ion channel to open,
Slow Metabotropic: g-protein, second messenger.
4 way deactivate NT**
- diffusion:
- Degradation: enzyme break NT down
- Reuptake: recycle into pre-synaptic terminal
- Glial cells; take up stray NT.
hormones 5 points
- slow, gradual
- Change probability or intensity of behavior (not on/off)
- reciprocal relationship with behaviour.
- have multiple effects
- have specific temporal pattern.
dif.. neural v hormonal
local v distant
fast v slow
voluntary v involuntary
precise v imprecise
norepinephrine NT and hormone
CNS; arousal/alertness
PNS; released by adrenal glands in response to stress/anxiety.
adrenal gland
inner–medulla: secretes epinephrine
outer–cortex; cortisol.
cortisol
steroid hormone, binds to glucocorticoid receptor, has metabolic and immune effects,
cortisol
regulated by negative feedback.
chronic stress
changes HPA axis, increased CRH expression, hypertrophy of adrenal cortex, Fewer GR means less negative feedback can occur.
necrosis
cells rupture,
apoptosis
programmed cell death. dismantle in membrane bound vesicles.
TBI
two biggest risk factors are age and sex.
TBI mechanisms
- coup: where brain skull first make contact.
2. Contre-coup: rebound damage.
torque
the twisting of the brain inside the skull.
concussion generalized damage
grey matter and white matter, different density, different speed on impact.
ICP; intracranial pressure
swelling (edema), and bleeding (hematoma).
energy crisis: lack of oxygen (hypnoxia), lack of glucose (hypoglycemia).
DAI, diffuse axonal injury
twisting and sheering forces cause axon to tear from cell body.
Excitotoxicity
- necrosis leads to excess release of glutamate.
- glutamate binds and activates post-synaptic receptors, this leads to influx of Na and Ca…
- Too much Ca is bad. ends up mitochondria, disrupts production of ATP.
ATP
- required to make glucose and use it.
2. ATP production requires glucose, but the energy crisis has made glucose in short supply.
excitotoxicity
leads to overproduction of lactic acid, acidosis, and this damages the BBB.
cytokines
hormones for immune signalling.
Vagus Nerve
- innervate heart and digestive tract.
- 90% of afferent connections between bodily organs and CNS.
- special cells called paraganglia located along nerve that release NT when cytokines bind.
immune **
because brain interacts with the immune system, it means that it is not immune privileged.
ROS; reactive oxygen species
reactive, in excess under stress, leads to oxidative stress an imbalance between ROS and antiOX. need more antiOX…..
CTE; chronic traumatic encephalopathy.
degenerative disease, from concussions.
Circle of Willis
arteries form circle base of brain.
ischemia
lack of blood flow to tissue.
2 type stroke
ischemic: blockage in blood vessel. (large and small vessel thrombosis).
Hemmorhagic: rupture in….
sham animal
trial condition, they are like placebo but they still have surgery just to make sure it isn’t an intervening variable.
TIA; transient ischemic attacks
mini strokes, may precede a severe stroke,
but the brain can adapt if changes take place slow,
2 damage regions after a stroke
Core; dead cells, fed by occluded vessel
Penumbra: outside lesion, some chance to heal.
stroke weakened BBB
when blood flow reactivates, peripheral immune cells can leak through and exacerbate the immune response and….Leukocytes (white blood…) infiltrate via damaged BBB and release even more inflammatory molecules, this impedes recovery.
why is increase Ca bad for neurons?
- triggers release of Glu, (excitotoxic cascade)
- Excess Ca = more ROS.
- ***Mitochondria can’t deal, release signals to induce apoptosis.
mitochondria
release a variety of signal molecules (CASPASES) these are protease enzymes playing roles in programmed cell death and inflammation.
Collateral circulation
blood flow through secondary pathways after the obstruction to the principle path occurs.
anosognosia
unaware of the illness. Inability to recognize impairment. lack of self-awareness.
genes
are like recipes for proteins,
chromatin
DNA + histone
alleles
variants of genes. cause diversity.
** proteins
- cell structure,
- catalyze reactions, aid in cell metabolism
- hormone receptors, cytokines, membrane proteins…
epigenetics
changes in gene expression related to experience.
acetylation
loose, = gene expression
methylation tight = no gene expression
huntington
neurodegenerative genetic disorder, autosomal-dominant pattern of inheritance.
bradykinesia
rigidity, prob with voluntary movement.
huntington MSN; medium-spiny neuron…
*caudate, and putamen at risk, MSN are GABA and makeup 95% STR neurons.
basal ganglia 2 pathways…
direct; excitation of motor neurons, movement.
indirect; inhibition of motor neurons, …
htt protein
accumulate nucleus, correlate to CAG repeats.
huntinton
directionality and progression are not yet known.
huntington excito
glutamate, NMDA receptors are glutamate receptor, and agonists mimic certain HD like symptoms…. thus Glu receptor stimulation may contribute to symptoms.
ALS up low MN
upper motor N originate in the brain, signal to lower motor N.
LMN; info to muscles,
Upper Motor N (cant leave CNS)
- tell LMN to carry start signals to muscles.
2. Tell LMN when to stop sending signals to contract.
lower motor neuron
synapse on muscles, can pass through spinal and cranial nerves,
spasticity
feature of UMN injury,
Flaccidity
with LMN injury LMN is unable to tell muscle to start contracting, thus not muscle contraction and loss of muscle tone.
UMN injury
hyperreflexia, increase muscle stretch reflexes,
also** extensor plantar response (Babinski sign)
LMN injury
hyporeflexia; decrease in muscles stretch reflex, (limp baby),
*also hypotonia, muscle atrophy, as well as fasciculations (twitching).
idiopathic
no known cause.
ALS
affects only voluntary muscles,
necroptosis
programmed necrosis, membrane breakdown,
in vitro
petri dish…
dementia
refers to a set of symptoms that are caused by disorders that affect the brain.
normal memory loss, dysfunctional neurons, not dying N.
mild cognitive impairment
memory problems greater than expected for age.
alzeymers
sporadic 95% cases, can only be definitively diagnosed after death.
alzymer 2 pathological feature
beta-amyloid plaques: outside cell.
Neurofibrillary tangles, inside cell.
amyloid angiopathy
beta-amyloid plaques can elicit an immune response by glial cells and can deposit near blood vessels
calcium stroke
AP stimulates calcium and calcium is responsible for bringing vesicles to membrane thus more flutamate and more firing.
