final exam

neuropsychology

speciality field within clinical psychology that seeks to understand and treat patients with cognitive impairments resulting from aging, disease, injury

neuropsychologists

liscence doctoral level clinical psychologists with goal to develop informed treatment plan using standardized testing

neurocognitive disorders

patients experience decline in function in 1+ cognitive domains after known challenge to nervous system

tumors

independent growth of new tissue that lack purpose

primary tumors

og in brain and rare

secondary tumors

common and arise from glial/meninges/ependymal cells and move to brain

malignant tumor

cancerous tumor that can cause harm lacking distinct border and may move

benign tumor

noncancerous tumor that does no harm has distinct border and doesnt move

glimas

70% of tumors cancerous tumor of 1 types of the glial cells

meningiomas

20% of tumors when dividing goes wrong in meninges but encapsulated benign and surgically removable

tumors do not

arise from neurons bc not capable of dividing

tumor symptoms

pressure in skull headaches vomit double vision decreased heart rate/alterness seizures

tumor treatments

surgical removal brain radiation stereotaxic radio surgery chemo

stroke

sudden onset event that cause damage

infarct

dead brain tissues

penumbra

surrounds infarct dysfunctional but not dead may regain function

stroke causes

cerebral hemorrhage or cerebral ischemia

transient ischemic stroke

mini stroke no permanent damage but warning sign for larger stroke

cerebral hemorrhage

blood vessel ruptures

aneurysm

weakened point in blood vessel that makes a stroke more likely and could be cogetial

cerbral ischemia

disruption of blood supply from thrombosis, embolism, arteriosclerosis

thrombosis

plug forms

embolism

plug forms elsewhere then migrates to brain

arteriosclerosis

walls of blood vessel thicken usu from fat deposits

ischemia damage

doesnt develop immediately usually from excess GLU release from blood deprived neurons taking about 10 min

excess GLU causes

influx of Na and Ca → trigger more GLU → internal reactions → apoptosis

concussion

a disturbance of consciousness following blow to head with no structural damage

multiple concussions

may result in CTE chronic traumatic encephalopathy

brain infections

invasion of brain by microorganisms and resulting inflammation/encephalitis

bacterial brain infections

lead to cerebral absecesses/pockets of pus inflamming meninges

syphilis

bacterial infections and may produce insanity/dementia or general paresis

viral infections

some attack neural tissue

viral infection examples

rabies mumps herpses zika virus

zika virus

if pregnant women have this it can tranfer to their fetus and cause microcephaly

epilepsy

primary symptoms is seizures generated by brain dysfunction affecting 1% of pop and diverse/complex disorder

convulsions

motor seizures, tremors/clonus and rigidity/tonus → tensing and convulsions with loss of balance/consciouness

Function of Ach in the PNS

neuromuscular junctions in cardiac and skeletal muscles at preganglionic autonomic and postganglionic parasympathetic synapses function: movement, autonomic function, learning and memory

brain structure involved in emotion

limbic system especially amygdala

limbic system

hippocampus, amygdala, fornix, mammillary bodies, basal ganglia

hippocampus role in memory

holds short terms memories and transfer them to long term storage

CNS myelin

oligodendrocytes that can myelinate many areas on many axons

PNS myelin

schwann cells myelinates 1 part of 1 axon

info flow in neurons

dendrites → soma → axon hillock → axon (myelin and nodes of ranvier) → terminal buttons → synapse

retina structure

ganglion cell layer ← inner plexiform layer ← inner nuclear layer ← outer plexiform layer ← outer nuclear layer ← rods and cones ← pigmented epithelium

lobes

frontal, temporal, occipital, parietal

fissures

central calcarine lateral

gyri

precentral postcentral cingulate

cerebellum

important component of motor cortex located dorsal to the pons

glutamate

main excitatory NT function = excitatory and long term memory

GABA

major inhibitory NT function = mood seizure threshold

anterograde amnesia

unable to form new memories

hebbs rule

co-occurance is necessary for learning and memory

LTP

induction maintenance and expression

ltp induction

calcium flow into post synapse resulting in AMPA-R receptor trafficking and increased number at cell surface

ltp maintainance

cause more GLU to be released through diffusing nitric oxide/endocannabinoids into pre synaptic neuron as response to Ca influx

dendritic spine structural changes

CT

x ray of brain structure

PET

observe brain function by injecting glucose and see what neurons use it

MRI

spins atoms by shooting magnetic radiation and improved version of CT

fMRI

correlate brain activity with stimulus/emotional state/task performance based on O2 levels and blood flow

other types of seizures

subtle changes or thoughts moods behaviors

epilepsy causes

brain damage TBI and 70 known genes

epilepsy diagnosis

EEG shows seizures associated with high amplitude spikes

partial epilepsy

does not involve whole brain

simple partial seizures

symptoms are primary sensory/motor and spread as epileptic discharge spreads

complex partial seizures

restricted to temporal lobes and engage in compulsive/repetitive behaviors aka automatisms

generalized epilepsy

involves whole brain either grand mal or petit mal

grand mal

loss of consciousness/equilibrium and tonic-clonic convulsions resulting in hypoxia and possible brain damage

petit mal

disruption of consciousness associated with a cessation of ongoing behaviors without convulsions

epilepsy treatment

anticonvulsants like benzodiazepines

multiple sclerosis

a progressive autoimmune disease that attacks CNA myelin leaving scar tissue/sclerosis

MS symptoms

visual disturbances, muscle weakness, numbness, tremor, loss of motor coordination/ataxia

MS treatments

interferon (decrease frequency/severity of attacks) and glatiramer acetate (synthetic peptide)

alzheimers disease

most common cause of dementia develops with age and early stages characterized by confusion and selective decline in memory

alzheimer diagnosis

at autopsy look for neurofibrillary tangles and amyloid plaques

alzheimers causes

genes involved in amyloid synthesis and when phosphate ion attack to TAU protein strands

parkinsons disease

movement disorder of middle age + with tremors at rest