Neurology Embryo and Anatomy

eesohbel's version from 2015-08-01 20:54


Question Answer
nototchord inducesoverlying ectoderm to differentiate to neuroectoderm and form neural plate
neural plate gives rise toneural tube and neural crest cells
notochord eventually becomesnucleus pulposus of IV discs
alar plate (dorsal) becomessensory
basal plate (ventral) becomesmotor

Section NOT HY

Question Answer
walls of telencephaloncerebral hemispheres
cavities of telencephalonlateral ventricles
walls of diencephalonthalamus
cavity of diencephalonthird ventricle
wall of mesenchephalonmidbrain
cavity of mesenchephalonaqueduct
wall of metencephalonpons and cerebellum
wall of myelencephalonmedulla
cavity of myelenchephalonlower part of 4th ventricle
cavity of metencephalonupper part of 4th ventricle
forebraintelencephalon and diencephalon
hindbrainmetencephalon and myelencephalon


Question Answer
CNS neurons, ependymal cells, oligodendroglia, astrocytesneuroectoderm
PNS neurons, schwann cellsneural crest
when are neuropores supposed to fuse?4th week
when neuropores fail to fuse, there is a persistant connection betweenamniotic cavity and spinal canal
elevated levels of this in amniotic fluid and maternal serum in neural tube defectalpha-fetoprotein
helpful confirmatory amniotic fluid tests in neural tube defectselevated AChE (in CSF, transudates across defect)


Question Answer
defect in spina bifida occultafailure of bony spinal canal to close, but no structural herniation and dura intact
physical signs of spina bifida occultatuft of hair, skin dimple at level of bony defect
meningocele defectmeninges herniate through spinal canal defect
meningomyelocele defectmeninges and spinal cord herniate through spinal canal defect

Section NOT HY

Question Answer
defect in anencephalymalformation of anterior neural tube, no forebrain and open calvarium ("frog-like")
decrease risk of anencephaly by supplementing mom withfolate
clinical findings in anencephalyincreased AFP, polyhydramnios (no swallowing center in brain)
anencephaly associated with maternaltype I DM
holoprosencephaly defectfailure of left and right hemispheres to separate during week 5-6
holoprosencephaly related to this signaling pathwaysonic hedgehog
results of holoprosencephalymild form has cleft lip/palate, severe form cyclopia
holoprosencephaly seen inpatau and fetal alcohol syndrome


Question Answer
chiari II malformation defectcerebellar tonsillar and vermian herniation through foramen magnum, with aqueductalstenosis and hydrocephalus
clinical presentation of chiari IIthoraco-lumbar myelomeningocele, paralysis below defect
dandy-walker defectagenesis of cerebellar vermis with cystic enlargement of 4th ventricle (fills posterior fossa)
dandy-walker associated withhydrocephalus, spina bifida
absent cerebellumDandy Walker
Chiari Irelatively benign. May present in adult w headaches and cerebellar symptoms such as ataxia. Herniation of cerebellar tonsils may cause syrinogmyelia.


Question Answer
syringomyelia defectcystic enlargement of central canal of spinal cord
syringomyelia associated withchiari I malformation
most common location of syringomyeliaC8-T1
first fibers damaged by syringomyeliaspinothalamic tract (pain and temperature)
clinical symptoms of syringomyelia"cape-like" bilateral loss of pain and temperature in upper extremities, fine touch preserved


Question Answer
anterior 2/3 of tongue formed by1st and 2nd brachial arches
sensation in anterior 2/3 byCN V3
taste in anterior 2/3 byCN VII
posterior 1/3 of tongue formed by3rd and 4th branchial arches
sensation and taste to posterior 1/3 byCN IX, CN X in extreme posterior
motor innervation of tongue byCN X, XII
muscles of tongue derived fromoccipital myotomes
taste information goes tosolitary nucleus


Question Answer
Microglia CNS phagocytes, mesodermal origin, can't see in Nissl stains
Astrocytessupport/repair/K+ metabolism/remove excess NT/maintain BBB, marker is GFAP, reactive gliosis after injury
Neuroectoderm forms? CNS neurons, ependymal cells, astrocytes
Neural crest forms?schwann cells, PNS neurons
Mesoderm forms?microglia
Oligos vs schwann cellsOligodendroglia: wraps multiple CNS axons, look like fried eggs on H&E stain, predominant type of glial cell in white matter, destroyed in MS
Schwann cells: myelinates only 1 PNS axon, destroyed in Guillan barre
Slow adapting sensory receptorsfree nerve endings and merkels (light touch)
Meissner's corpusclesfine touch, rapid adapting, hairless skin
Pacinian corpusclesdeep pressure/vibration, in deep skin layers
Free nerve endingsin all skin/some viscera, pain/temp, C are slow unmyelinated, A are fast myelinated
Merkel's diskslarge myelinated for light touch, slow adapting
Which cells fuse to form multinucleated giant cells in the CNS in HIV?microglia

NTs and hypothalamus

Question Answer
Which layer of nerve has blood vessels/fascicles?epineurium (surrounds whole nerve)
Location of NE synthesisLocus ceruleus
Location of DA synthesisVentral tegmentum and SNc (midbrain)
Location of 5-HT synthesisRaphe nucleus (pons)
Location of ACh synthesisBasal nucleus of Meynert
Location of GABA synthesisNucleus accumbens
Increased in anxietyNE
Parkinson's NTs?decreased DA and increased acetylcholine
Alzheimer's NTs?decreased Ach
Huntington's NTs?decreased ACh and GABA
Excitatory neurotransmittersglutamate
Inhibitory neurotransmittersglycine and GABA
BBB formed by what?tight junctions between nonfenestrated capillary endothelial cells, basement membrane, astrocytes
Vasogenic edema?infarction that destroys endothelial cell tight junctions
Lateral hypothalamushunger. feeding, destruction causes anorexia, inhibited by leptin
Ventromedial hypothalamussatiety, destruction causes obesity, stimulated by leptin
Areas of hypothalamus projecting to posterior pituitary?supraoptic nucleus (ADH) and paraventricular nucleus (oxytocin)
Anterior hypothalamuscooling (destruction leads to hyperthermia)
A/C cooling
posterior hypothalamusheating (destruction leads to hypothermia)
How glucose/AAs cross BBBSlowly by carrier-mediated transport
Suprachiasmatic nucleusCircadian rhythm
Locations in brain with no BBBArea postrema - vomiting after chemo
OVLT - osmotic sensing
Neurohypophysis - ADH release
Reward center, pleasure, addiction, fearNucleus accumbens and septal nucleus
vasogenic edemaBBB failure. increased water in extracellular space. mostly affects white matter. seen in tumors, brain abscesses, trauma, HTN. Treat with steroids
cytotoxic edemaBBB remains intact. Does not respond to steroids or diuretics
paraventricularCRH, TRH, oxytocin


Question Answer
lateral lesionsvoluntary movement of extremities. when injured falls toward ispilateral side.
medial lesionsbilateral motor defects
cerebellar vermisataxia

Basal ganglia and Parkinson's

Question Answer
Fn of basal gangliavoluntary movements and making postural adjustments
Direct pathwayfacilitates movement
D1 (+)-->striatum -----l GPi/SNr → (disinhibits) the thalamus
Indirect pathwayinhibits movement
D2 (-) ---> striatum ----l GPe → (disinhibits) subthalamus → + to GPi -----l thalamus
DA and D1 pathwayNormal: stimulation of excitatory pathway (increased motion)
Losing DA in Parkinson's inhibits this pathway (decreased motion)
DA and D2 pathwayNormal: inhibition of the inhibitory pathway (increased motion)
Losing DA in Parkinson's reactivates the inhibitory pathway (decreased motion)
Loss of DA in Parkinson's and overall result?in both direct and indirect pathway, loss of DA results in decreased motion
Parkinson's sxsTRAP sxs- tremor (at rest - pill-rolling), cogwheel Rigidity, Akinesia, Postural instability
Parkinson's pathologydegenerative disorder of CNS with lewy bodies (made of alpha-synuclein- intracellular inclusions) and depigmentation of SN (lose DA)
rare cases linked to MPTP a contaminant in illicit street drugs
Striatumputamen (motor) + caudate (cognitive)
Lentiformputamen + globus pallidus
lesions of substania nigracauses hypokinesis
lesions of subthalamic nucleuscauses hemiballismus. always contralateral to lesion

Sleep Quick Review

Question Answer
awake (eyes open)beta
awake (eyes closed)alpha
stage N1theta
stage N2sleep spindles and K complexes
stage N3delta
REM sleepbeta
alcohol, benzos, barbs associated withdecreased REM

Huntington's & Movement disorders

Question Answer
Huntington's pathologyCAG repeat disorder, AD
neuronal death via NMDA-R binding and glutamate toxicity
age of onset usually 20-50
caudate loses ACH and GABA, increases dopamine
Striatal (caudate/putamen) atrophy
hypoacetylated histones bind tightly to DNA
Huntington's sxschorea, aggression, depression, progressive dementia
sometimes initially mistaken for substance abuse
Hemiballismussudden wild flailing of arm/leg
contralateral subthalamic nucleus lesion (lacunar stroke in HTN pt)
lose inhibition of thalamus thru globus pallidus
Choreasudden jerky purposeless movements
due to BG lesion (huntingtons)
Athetosiswrithing, especially of fingers
BG lesion (huntingtons)
Myoclonussudden brief m. contraction
Hiccups - common in metabolic abnormalities like renal/liver failure
Dystoniasustained involuntary m. contractions
Essential tremoraction tremor, AD
self-medication with alcohol can reduce
beta blockers & primidone can help
Resting tremormost noticeable distally (hands)
stops with intentional movement
seen in parkinson's
intention termorslow zigzag when pointing toward target
cerebellar dysfunction