neuro patho Flashcards
what are the time frames of fetal development
Pre-embryonic: fertilization to 2wks
Embryonic: 2-8wks
Fetal: >8wks
what stage do the majority of organs develop
embryonic
when is neuro development
2-20wks
what are blastomeres
cells from first mitotic division
what is a morula
The spherical embryonic mass of blastomeres formed before the blastula and resulting from cleavage of the fertilized ovum.
what is a blastocyte
when a cavity forms in the morula
which develops last (ectoderm, endoderm, mesoderm)
mesoderm
where are the ectoderm, endoderm, mesoderm formed
Ectoderm(Upper lip)
Endoderm (Lower lip)
mesoderm froms between them
what is the synchiotrophoblast
epithelial covering of the trophoblast that forms deep into the endometrial lining to establish nutrient circulation between the embryo and the mother
what is the cytotropoblast
inner layer of the tropoblast. deep to the synchiotrophoblast
what develops from the ectoderm
Sensory Organs
Epidermis
Nervous
System
what develops from the mesoderm
Dermis Muscles Skeleton Urogenital Systems Circulatory System
what develops from the endoderm
GI System
Liver
Pancreas
Respiratory System
what is neurulation
process of neural tube(spinal cord) formation
what is primary neurulation
infolding of neural plate
what is secondary neurulation
sacral and cocyxgeal formation
what portion of the neural plate is the last to close
inf region
what should occur by the 3rd week
dorsal midline ectoderm thickens to form neural plate
when should the ecoderm folds touch and close
touch at 21 days
close at 27 days
what do neural crest cells form
PNS, Posterior root ganglia Sensory: cranial nerves Autonomic ganglia Adrenal medulla Melanocytes Pancreatic Islets
what are radial glial cells
important for migrating neuroblasts and pivotal in CNS formation
what do the bumps on the ectoderm represent
each bump is a somite and represent dermatomal development of the dermis
what is colchicine and what is its SE
drug used for gout. cnat use in child bearing age women bc it blocks microtubules causing neurotube defects
what is the notochord
defines the long axis
orients vertebrae
nucleus pulposus
cell adhesive molecules
what is the alar plate
sensory
what is the basal plate
motor
what is polyneuronal development
migration of cells in the fetal stage
>50% die in the process of migration
Usually completed by 25th week
when does myelination occure (specifically Corticospinal tracts and Cortical association fibers)
Begins 4th month of gestation and finished by 3 years of age.
Corticospinal tracts myelinated by 2 years
Cortical association fibers by 3 years of age
what are association fibers
allow one cortex to make connections for fine motor skills
what are the causes and defects associated with closure 1
Folic acid deficiency
Metabolic teratogens
causing Spinal Bifida
what are the causes and defects associated with closure 2
Maternal hyperthermia
Folic acid deficiency
Metabolic teratogens
causing Anencephaly
what are the causes and defects associated with closure 3
Usually resistant
causing Mid-facial clefts
what are the causes and defects associated with closure 4
Maternal hyperthermia
causing Cephalocele
what are the causes and defects associated with closure 5
Valproic acid exposure
causing Sacral Meningocele
what is meningoencephalocele
meninges and brain tissue out of skull bc altered cranium closure
what is meningocele
meninges out of skull bc altered cranium closure
what is meningohydoencephalocele
meninges,ventricle, and brain tissue out of skull bc altered cranium closure
what are the characteristics of anencephaly
cerebral hemispheres replaced by vascular tissue making a frog like appearance
Protruding eyes:
Prominent nose
Long Arms
Most die in utero or within 1 week after birth
Rostral neuropore fails to close
Brainstem usually intact
what is spina bifida occulta
failure of dorsal vertebrae to close
10% of population(L5-S1)
usually asymtomatic
what is spina bifida-Meningocele
usually no deficits
what is spina bifida-meningomyelocele
part of cord gets outside
always defects
what is myeloschisis
spina bifida with no overlying skin
cord exposed on surface
what is arnold chiari
inf cerebellum and medulla protrude through foramen magnum
what are the manifestations of arnold chiari
asymptomatic CN defect (usually IX-XII) cerebellar defect hydrocephalus migraine
what is holoprosencephaly
Single large ventricle with fusion of midline structures, including thalami.
Affected fetuses and neonates typically have severe facial defects, such as cyclopia
what are possible causes of holoprosencephaly
Underlying chromosomal abnormalities, such as trisomy 13, or maternal diabetes mellitus are possible causes, but some cases are sporadic.
what are the somatic senses
Pain
Temperature
Crude touch/pressure
Discriminatory touch
what is stereognosis
the ability to perceive and recognize the form of an object
what is graphesthesia
ability to recognize writing on the skin purely by the sensation of touch
nociception
Recognition and signaling of a deleterious stimuli
pain
Conscious awareness of the nociceptive event
suffering
Emotional and behavioral sequelae
deafferentiation pain
pain due to loss of sensation of an afferent fiber
hyperalgesia
increased sensitivity to stimulation
what causes pain afferent nerve endings
“naked nerve endings” activated by thermal, mechanical, or chemicals increasing Na permeability= inc APs
what chemicals can activate afferent pain nerves
H+, bradykinin, histamine, prostaglandin, hypoxia
what are A-delta fibers (location, stimuli, type of pain, size, myelination, speed)
afferent pain neuron Location: body surface/skin Stimuli: mechanical, thermal, chemical Type of pain: sharp, prickly Large diameter Myelinated 5-30 m/sec
what are C-fibers (location, stimuli, type of pain, size, myelination, speed)
Location: deep skin/ tissue Stimuli: thermal, mechanical, chemical Type of pain: aching, burning Large diameter Unmyelinated .5-2 m/sec
what is Lissauers tract
Afferent pain fibers go a few segments up or below before crossing over
where would pain and temp loss in reguards to a spinal cord lesion
typically 2 segments down from lesion not at the lesion
where do I, II, and IV lamina send signals to
I and II- to brain
IV- reflex(not to brain)
why does chronic pain cause insomnia
the C-fibers signal the RAS on the way to the thalamus.
what is the pathway of the neospinothalmic tract
RAS
Thalamus(VPL)
Somatosensory cortex
Pain localization and intensity
what is the pathway of the paleospinothalmic tract
RAS (more than neospinothalmic) Thalamus(VPL Limbic (emotion, inc aggression with chron pain) Somatosensory Cortex Emotional response to pain
what is the Periaqueductal gray
in the midbrain
activated by Mu-R
release Enkephalin and neurotension at the Raphe Nucleus in the medulla
what does the raphe nucleus do
activated from periaqueductal gray
releases 5-HT and Enkephalin at terminal afferent neuron to block release of substance P and block pain
what does 5-HT do
causes more enkephalin release
what does enkephalin do
endogenous opiod that blocks substance P release to block pain
what does Fentinil do
used in epidurals to bind opiod Mu-R and prevent substance P release= block pain
why do they give tricyclic antidepressents for chr pain
block seratonin, dopamine, NE reuptake to alleviate pain
Keeps seratonin around so Enkephalin can block substance P
what is the danger of epidurals and intrathecal(sub arachnoid) opiod administration
can diffuse upward and stop breathing
how do local anesthetic agents work
block Na channels
what is lidocaines and Marcaines(bupivicaine) MSD
Lido=5-7mg/Kg
Marcaine= 2-3 mg/kg
(can use the higher doses if epi is used bc keeps it local)
what is the toxicity from Lidocaine
CNS before cardiac
CNS: twitch, tinnitus, Sz
Cardiac:heart block
what is the toxicity from Marcaine
Cardiac before CNS (need to be on cardiac monitor. watch for vfib)
what is 1% lido
1g/100ml or 10mg/mL
how do NSAIDs dec pain
block prosteglandin production
how does a cordotomy help pain
lateral spinothalmic tractotomy= loss of pain on one contralateral side one to 2 segments down
Temporary relief
What is a Rhizotomy
cut dorsal root to prevent pain but also blocks other sensory
what does a lesion of intralaminar nuclei do
decreases suffering type of pain and leaves the acute pain
what does a VPL lesion cause
Lesion is in thalamus causing contralateral loss of all sensory
what does a VPM lesion cause
lesion is in the thalamus causing contralateral loss of facial sensory
what is radicular pain vs local pain
radicular pain is along a dermatome
what is thalamic syndrome
Posteriolateral branch of posterior cerebral artery (anterior thalamus OK)
Loss of sensation opposite side of body bc VPL and VPM blocked
Ataxia
Usually damage to internal capsule
After insult there is hemianesthesia followed by burning pain after several weeks
how does the cerebellum and thalamus maintain balance
cerebellum compares intended action to actual act and makes adjustments. Adjustments are sent through thalamus to upper motor cortex.
what is the pain component of complex regional pain syndrome(reflex sympathetic dystrophy)
Out of proportion to injury
Burning, numbness, tingling, itching
May be confined to dermatomal or diffuse (less diffuse and of a vascular distribution)
Usually distal
Superficial nonnoxious stimuli: ie air accentuates pain
Behavioral changes: seclusion/withdrawn
what is the circuit of continuing pain in complex regional pain syndrome
Pain= inc SNS= dec circulation=hypoxia/inc H+=inc Pain
what is CRPS I
triggerd by tissue inj with no identified nerve inj
AKA reflex sympathetic dystrophy(RSD)
what is CRPS II
Associated with nerve inj
AKA causalgia
what is the 2nd component of complex regional pain syndrome
unspecified abnormalities of sensation, motor function and blood flow Soft puffy edema Skin color changes Cold or warm Joint limitations
what is the 3rd component of complex regional pain syndrome
Sweating and trophic changes in the skin and soft tissue Excessive moisture or dryness Increased hair or nail growth Osteoporosis(dec circulation) Muscle atrophy(dec circulation)
what are the three types of pain from complex regional pain syndrome
1Algodystrophy: pain and all features of dystrophy
2Dystrophy without pain
3Sympathetically maintained pain, not exhibiting dystrophic changes
what is the 1st stage of complex regional pain syndrome
pain is in the limb.
distribution is not compatible with single nerver, trunk, or root lesion
vasomotor disturbance
radiology normal
what is the 2nd stage of complex regional pain syndrome
progressive soft tissue edema, thickening of skin, mm wasting
is the 3rd stage of complex regional pain syndrome
limitation of movement, contractures, bone demineralization
what is the Tx of complex regional pain syndrome
Medications -Phenoxybenzamine hydrochloride (alpha blocker) -Clonidine (alpha 2 agonist) -GABA analogs Nerve blocks -Inject into dorsal root ganglion