Neuro Block 2 Flashcards
basal nuclei
striatum - caudate and putamen
lentiform nucleus - putamen and globus pallidus
substantia nigra
subthalamic nuclei
hyperkinetic
uncontrolled involuntary movement
Huntingtons
hypokinetic
rigidity, slowness, difficulty initiating movement
Parkinsons
inputs to basal nuclei
cortex to striatum - release Glu
SNc to putamen (nigrostriatal) - release Dopamine
outputs of basal nuclei
GPi to thalamus - motor of body (GABA)
SNr to thalamus - motor of head (GABA)
SNr and GPi to other - superior colliculus, pontomedullary reticular formation (GABA)
Basal nuclei direct pathway
promotes movement
cortex (Glu) to
striatum (GABA) to
SNr and GPi (GABA) to
Thalamus VA/VL (Glu)
Basal nuclei indirect path
inhibits movement
cortex (Glu) to
Striatum (GABA) to
GPe (GABA) to
STN (Glu) to
GPi and SNr (GABA) to
Thalamus VA/VL (Glu)
effects of dopamine
facilitate direct path
inhibit indirect path
so loss will lead to hypokinesia
effect of ACh
facilitate indirect path
increase leads to hypokinesia
sound transduction
- upward movement of basilar membrane pushes endolymph toward top of tectorial membrane
- shifting tectorial membrane deflects stereocilia of outer hair cels depolarizing them (activates prestin which contracts cells)
- enhanced deflection leads to increased endolymph flow and contact of tectorial membrane with iner hair cells
- depolarizaation of inner hair cells releases NTs to stimulate spiral ganglion neurons (cochlear nerve)
- opposite occurs when basilar membrane deflected downward
- efferent signals from superior olivary nucleus modulate effects of outer hair cells
macula
of saccule - cochrlear, connected to spiral organ of corti
of utricle - vestibular, connected to semicircular ducts
otoconia on top (move to stimulate vestibular nerve)
sitting on otolithic membrane
and embedded in otolithic membrane are hair cells
semicircular ducts
in the crista ampularis there are cupula which detect movement of endolymph (hair cells beneath cupula)
otic vesicle development
underneath the tubotympanic recess forms from first pharyngeal pouch
otic placode invaginates to become otic vesicle
vesicle forms endolymphatic sac and duct, utricle dorsally, saccule ventrally
sacule develops into saccule and cochlear duct
spiral organ development
cochlear duct from saccule development uses neuroepithelial cells to form outer hair cells
inside becomes tectoral membrane
inner ridge becomes spiral limbus
spaces form to create spiral tunnels, spiral sulcus
scala tympani and vestibuli development
forming around cochlear duct
originally cartilage which has vacuolization to create the 2 spaces
semicircular ducts development
utricle has outpocketings
vacuolization in middle of outpocketings create the circles
auditory ossicle development
start with mesenchymal condensation
osicles form and embed in loose mesenchyme
mesenchyme erodes leaving ligaments, tympanic cavity, and endodermal epithelium
parkinsons disease
loss of dopaminergic nuclei (substantia nigra and locus ceruleus)
neurons have Lewy bodies
slow movement, pill rolling tremor, loss of facial expression, shuffling gait
Huntington disease
increased CAG repeats (mutation in HTT gene called Huntingtin) - anticipation, less than 36 no disease, 36-39 may develop, over 39 will develop
atrophy/loss of neurons in caudate/putamen
chorea (dancelike mvmt), dementia, psychosis
autosomal dominant (onset late 40)
treat symptoms
multisystem atrophy.striatonigral degeneration
varied degenrations of varied nuclei
glial cytoplasmic inclusions in oligodendroglial cells (alpha synuclein)
-degeneration of substantia nigra and striatum, unresponsive to L-dopa
hemiballismus
wild flinging movements
subthalamic nucleus lesion
Wilsons disease
defeciency of ceruloplasmina nd build up of copper
degeneration of lenticular nucleus
kayser fleischer corneal rings
friederich ataxia (hereditary spinal ataxia)
starts 5-15 yrs
GAA repeats (normal is 7-34, abnormal is more than 90)
often autosomal dominant
loss of neurons in cerebellum, brainstem, spinal cord
ALS
loss upper and lower motor neurons
spastic and flacid paralysis
mutations in CU.Zn superoxide dismutase in familial forms
thalamogeniculate arteries
from posterolateral group
medial and lateral geniculate and pulvinar of thalamus
complete contralateral hemianesthesia, may resolve into thalamic pain
thalamoperforating arteries
from posteromedial group
subthalamic nucleus
contralateral hemiballismus (sudden involuntary movement)
comatose
anterior choroidal arteries
from ICA
caudate tail, lateral geniculate, optic tract, posterior limb internal capsule
contralateral hemiplegia, possible contralateral hemianesthesia, homonomous hemianopia (lose half of visual field in both eyes)
lenticulostriate arteries
from anterolateral group
baody of caudate, globus pallidus, most of putamen, thalamus, post limb internal capsule
contralateral hemiplegia, contralateral hemianesthesia, possible aphasia, hyperkinesia
medial striate arteries
anterior putamen and caudate head, anterior limb internal capsule
auditory pathway
cochlear nerve to
dorsal cochlear nuclei or ventral cochlear nuclei (in rostral medulla partially on surface at pontomedullary junction)
ventral cochlear nucleus to ipsilater and contralateral (through trapezoid body) superior olivary nuclei (localization of sound) up the lateral lemniscus to inferior colliculus
dorsal cochlear nucleus form posterior acoustic stria to contralteral inferior colliculus and ascend lateral lemniscus to inferior colliculus
from inferior colliculus to medial geniculate (run in brachium of inferior colliculus) to primary auditory cortex via auditory radiation (inferior thalamic peduncle)
primary auditory cortex
transverse temporal gyri (#41 and 42) superior surface temporal lobe (floor of lateral fissure)
right under if (#22) auditory association cortex
auditory efferect path
functional inhibition of hair cells of dendrites
head/eye turning reflex (Corpora quadragemina)
auditory path to inferior colliculus to superior colliculus to CN III, IV, VI vio tectobulbar and tectospinal tract
middle ear reflex
dampens sounds by affecting ear ossicles
cochlear nuclei to superior olivary nucleus to motor nucleus of V to tensor tympani
cochlear nuclei to superior olivary nucleus to motor nucleus of VII to stapedius
parkinsons treatment
- first goal is to antagonize dopamine
-use dopamine precursor (levodopa)
-use dopamine agonist (pramipexole/ropinerole, bromocriptine, rotigotine, apomorphine)
-increase L-DOPA availability (carbidopa, entacapone/tolcapone)
-increase dopamine availability (amantadine)
-prevent dopamine breakdown (talcopone, seleggiline/rasagiline) - second goal is to reduce acetylcholine
-benztropine, trihexyphenidyl, orphenadrine
levodopa carbidopa
dyskinesia major limiting factor in treatment
contraindications with psychosis (drug interactions with antipsychotics)
drug induced parkinsons
phenothiazine antipsychotics (prochlorperazine, chlorpromazine, fluphenazine)
first generation antipsychotics (haloperidol)
2nd gen antipsychotics (risperidone, paliperidone)
dopamine blocking agents (metoclopramide)
cholinesterase inhibitors (donepezil, rivastigmine)
Huntingtons treatment
tetrabenazine (inhibit VMAT that releases dopamine)
may use antipsychotics
ALS treatment
riluzole
edaravone adjunct
spinocerebellar ataxia
usually begins after 25
autosomal dominant with one copy of affected gene
most CAG repeats (over 40 causes disease)
ataxia telangectasia
autosomal recessive defect in DNA repair
ATM gene mutated
spinal muscular atrophy
lower motor neurons decrease (degeneration anterior horn cells causing hypotonia and atrophy)
autosomal recessive
1. infantile - develop in first 6 months, problems swallowing and feeding
2. intermediate - by 1 year, most will never walk on own
3. juvenile - between 18 mo and 8 yrs, swaying gait
4. adult - adult onset but similar to 3
SMN1 (absent) and SMN2 (multiple) genes affected
leukodystrophy
pelizaeus merzbacher caused by defect in X linked PLP1 gene (multiple) leading to hypomyelination
fragile X
expansion of repeat in promoter of FMR1 gene
rett syndrome
X linked
MECP2 gene
intellectual disability in females
scoliosis often
alzheimers
early onset linked to epsilon 4 allele of apopliproprotein E
APP mutations
hyperopia
too little refraction to focus light from near points
myopia
too much refraction for far objects
absence seizure
sudden lapse of consciousless without loss of postural control, conscious returns as soon as it was lost
sometimes with rapid eye blinking or chewing movements
myoclonic seizure
sudden brief single or repetitive jerks of limbs without warning]
consciousness sometimes impaired
atonic
sudden loss of postural tone
consciousness briefly impaired
no postictal confusion
photoreceptor cells
outer segment - open ion channels to depolarize
inner segment - depolarization spreads
synaptic terminal - Ca cahnnels open and release glutamate
light hyperpolarizes rods and cones
light causes Na/Ca channels to close
ion channels are cyclic nucleotide gated ion channels (CNG channels)
binding cGMP increases opening
photopigment rhodopsin - light causes shape change in retinal (photoisomerization) which changes shape of opsin triggering G protein transducin
alpha GTP of transducin activates phosphodiesterase which hydrolyse cGMP to GMP (decreasing cGMP to bind)
the dark current
in dark conditions ion cahnnels open
mechanisms promoting increase of cGMP
- rhodopsin kinase stops mechanism by phosphorylating rhodopsin making it unable to activate transducin
- cGMP continuously produced from GTP by guanylate cyclase
- G alpha has slow GTP>GDP hydrolysis which deactivates and allows alpha to hook back with G beta gamma. which stops activating PDE’s
adaptation to dark
in the dark Ca increases which blocks production cGMP, decreases cation channel affinity for cGMP, and blocks rhodopsin kinase so transduction mechanism stays on longer
optic pathway
optic nerves to
optic chiasm (crossing) to
optic tracts to
lateral geniculate to
optic radiations (inferior visual field up to parietal lobe, superior visual field to meyers loop in temporal lobe) to
primary visual cortex (parietal lobe to upper bank or cuneus, temporal lobe to lower bank or lingula)
visual processing paths
ventral - midget cells to LGN parvocellular to occipitotemporal association cortex (analyze form and color)
dorsal - parasol cells to LGN magnocellular to parietooccipital association cortex (analyze motion and spatial relations)
pupillary light reflex
optic nerve/tracts to pretectal nuclei (superior colliculus) to both edinger westphal nuclei to both oculomotor nuclei to both ciliary ganglion to constrictor pupillae
accomodation and vergence
optic nerve and tract to lateral geniculate nucleus to visual cortex to supraocular motor area to oculomotor and edinger westphal nuc (both sides) to medial rectus and constricot pupillae
argyll robertson pupil
react to accomodation but not light
potentially damage to posterior commissure
horizontal saccades
frontal eye field to superior colliculus to contralateral PPRF to contralateral abducens nucleus to lateral rectus or to ipsilateral oculomotor nucleus via medial longitudinal fasciculus to medial rectus
smooth pursuit
move eyes to follow moving object
info to dorsolateral pons to flocculus to vestibular nuclei to abducens, trochlear, oculomotr nuclei
optokinetic reflex
movement of eyes for whole visual field movement (visual slip)
info to accessory optic system to nucleus reticularis tegmenti pontis and inferior olive to flocculus to vestibular nuclei to abducens trochlear and oculomotor nuclei
vestibulo oculomotr reflex
head turns left
left lateral semicircular duct increases firing to medial vestibular nucleus
neurons decusate to contralat abducens nucleus
one neuron to contralat (right) lateral rectus
one neuron to left oculomotor nucleus (via right medial longitudinal fasciculus) to activate medial rectus
lesion to vestibulocochlear nerve
same side stumbling
opposite side nystagmus
saccule
measures position and acceleration in sagital plane
utricle
measures horizontal position and acceleration
medial vestibulospinal tract
head accelerates forward
hair cells in superior semicircular ducts detect
axons activate neurons in medial vestibular nucleus
this sends neurons to lower motor neurons to activate extensors of head and neck
lateral vestibulospinal tract
lateral movement detected by utricle
neurons send impulses to lateral and inferior vestibular nuclei
which send axons to lower motor neurons to actival ipsilateral extensor muscles
cavernous sinus
CN III, IV, V1 and V2
ophthalmic artery
optic nerve
superior hypophyseal artery (anteromedial arteries)
optic chiasm
anterior choroidal artery
optic tract
posterior choroidal artery
lateral geniculate nucleus
middle cerebral/lenticulostriate artery
temporal optic radiations
posterior cerebral artery
occipital cortex
SSRIs
fluoxetine
paroxetine
sertraline
fluvoxamine
citalopram
escitalopram
-sexual dysfunction, CYP450 interactions
inhibit serotonin and norepinephrine transporters
TCAs - imipramine, amitriptyline, clomipramine, trimipramine, doxepin, amoxapin, pprotriptyline, desipramine, nortryptyline
-orthostatic hypotension, QT prolongation, cardiovascular effects
SNRIs - duloxetine, venlafaxin, desvenlafaxin, levomilnacipran
-ssri effects plus nausea and dry mouth
serotonin antagonists and reuptake inhibitors
trazodone and nefazodone
vilazodone and vortioxetine
atypicals
mirtazapine 5HT and NE
bupropion DA and NE
-lowered seizure threshold, weight loss
monoamine oxidase inhibitors
phenelzine
tranylcypromine
isocarboxazid
selegiline
-many drug and food interactions
-last line for depression
mood stabilizers
lithium - reduce hyperexcitability of neurons, renal disease contraindication
valproic acid/valproate - also anticonvulsant, first line for mania, CYP450 inhibitor, hepatic disease contraindication - blocks NA channels/block GABA transaminase/block Ca channels (hepatotoxicity, teratogenicity, pancreatitis)
carbamazapine - also anticonvulsant, second line for mania, CYP450 inducer
lamotrigine - also anticonvulsant, second line BP (more helpful for depression but may help mania), blocks Na channels, skin rashes
anticonvulsants
CYP450 inducers - phenytoin, carbamazepinek phenobarbital
CYP450 inhibitors - valproic acid
adverse effects - skin reactions, CNS depression, suicidal ideation, bone disease, teratogenic potential
phenytoin - block sodium channels, 90% protein bound (hypotension and cardiac arythmias)
carbamazepine - bllock sodium channels (skin rash, hyponatremia)
phenobarbital - prolong opening of Cl channels (sedation)
status epilepticus
use lorazepam, diazepam, or midazolam first followed by fosphenytoin, valproic acid, or levertiracetam/phenobarbital
absence seizures
ethosuximide - blocks T type Ca channels (nausea, vomiting, diarrhea)
levetiracetam
block synaptic vessicle proteins 2A
1st line for focal and generalized tonic clonic
2nd line for status epilepticus
also for myoclonis
can cause neuropsychiatric behavior
preferred in pregnancy
renally excreted
gabapentin
inhibit Ca
focal seizures and neuropathic pain
sedation and dizziness, edema
100% renally eliminated
topiramate
blocks Na channels, augment GABA action, antagonize glutamate receptors
for migrain prophylaxis and focal/generalized tonic clonic seizures
cause paresthesia, weight loss
benzodiazepines
increase Cl entering, inhance GABA effects
can cause sedation
vigabatrin
infantine spasms
inhibit GABA metabolism
can cause vision loss
typical antipsychotics
more EPS potential
block D2 receptors
treats positive symptoms
chlorpromazine, thioridazine, fluphenazine, prochlorperazine, haloperidol, thiotixene
atypical antipsychotics
block 5HT receptors and D2 receptors
higher risk metabolic effects
treats negative symptoms
clozapine, olanzapine, risperidone, quetiapine, ariprazole, ziprasidone, paliperidone, lurasidone
EPS symptoms
acute dystonia (spasms of tongue, neck, face)
akathisia (motor restlessness)
parkinsonism (bradykinesia, rigidity, tremor)
tardive dyskinesia (oral fascial dyskinesia, choeathetosis, dystonis)
neurolefptic malignant syndrome
from blockade of dopamine receptors
fever, rigidity, altered mental status, autonomic instability
olfactory neurons
G proteins that depolarize cell when stimulus attaches
olfactory pathway
olfactory epithelium to
olfactory bulb (cortical zone) as olfactory neurons
olfactory bulb to olfactory stalk as mitral cells to create olfactory tract
tufted cells also in cortical zone
centrifugal fibers go back to olfactory neurons to regulate
from olfactory stalk lateral striae continue ipsilateral
mitral cells synapse granule cells which synapse medial stria cross after having cell bodies in anterior olfactory nucleus (anterior commisure)
taste pathway
CN VII from geniculate nucleus to nucleus solitarius to superior salvitory nucleus to VPM
CN IX from petrosal nucleus to nucleus solitarius to inferior salvitory nucleus to VPM
CN X from nodose nucleus to nucleus solitarious to dorsal nucleus of vagus to VPM
then all to cortical areas of taste via central tegmental tract
declarative memory (hiipocampal formation)
entorhinal cortex to CA3 pyramidal cells, synapse and use another neuron (mossy fibers)
info from CA3 to CA1 via schaffer collaterals (some info from CA3 leaves in fornix)
info from CA1 to subiculum then back to entorhinal cortex via mossy fibers
papez circuit
hippocampal formation to body of fornix to postcommissural fornix to mammillary body to mammilothalamic tract to anterior nucleus of thalamus to cingulate gyrus
amygdala
fear response
orbital and medial prefrontal cortex
inhibit predatory attack and defensive rage
