Neuro Flashcards
Ectoderm differentiates into
neuroectoderm –> neural plate –> neural tube and neural crest cells
Notochord becomes
nucleus pulposus of intervertebral disc in adults
Alar plate
Dorsal
sensory
lateral nuclei
Basal plate
Ventral
motor
Medial nuclei
We begin with what three primary vesicles in embryonic development
Forebrain (prosencephalon) –> (telencephalon and diencephalon)
Midbrain (mesencephalon) –> Mesencephalon
Hindbrain (rhombencephalon) –> Metencephalon and myelencephalon
The three primary vesicles become these 5 secondary vesicles. What do the 5 secondary vesicles become
Telencephalon (1st) Diencephalon (2nd) (rest is alphabetical order) Mesencephalon Metencephalon Myelencephalon
The 5 secondary vesicles become adult derivatives of walls and cavities
Telencephalon becomes
Cerebral hemisphere and lateral ventricles
Diencephalon becomes
Thalamus, hypothalamus, third ventricle
Mesencephalon becomes
Midbrain and cerebral aqueduct
Metencephalon becomes
Pons, cerebellum, upper part of 4th ventricle
Myelencephalon becomes
Medulla and lower part of fourth ventricle
Neural crest forms
PNS neurons and schwann cells
Mesoderm forms
Microglia (like macrophages)
Neural tube defects
Neuropores fail to fuse (4th week) and persistent connection between amniotic cavity and spinal canal
What labs can you look at for neural tube defect detection
AFP elevated (except in spina bifida occulta) Increase in AChE as a confirmatory test
Failure of caudal neuropore to close but no herniation. Usually seen at lower vertebral levels and the dura is intact. Associated with tuft of hair or skin dimple at level of bony defect
Spina bifida occulta
Meninges (but no neural tissue) hernaites through bony defect and associated with spina bifida cystica
Meningocele
Meninges and neural tissue herniate through bony defect
Meningomyelocele
Also known as rachischisis. Exposed unfused neural tissue without skin/meningeal covering
Myeloschisis
Failure of rostral neuropore to close. No forebrain, open calvarium. Can see polyhydramnios (no swalling center in brain)
Anencephaly
Failure of the left and right hemispheres to separate. Moderate form shows cleft lip/palate, while more severe forms result in cyclopia. MRI can show a monoventricle and fusion of basal ganglia. What mutation and genetic defects is this related to?
Mutations in sonic hedgehog signaling pathway
Trisomy 13
Fetal alcohol syndrome
Ectopia/displacement of cerebellar tonsils
Chiari I malformation
congenital, usually asymptomatic in childhood and manifests in adulthood with headaches and cerebellar symtoms
Herniation of low lying cerebellar vermis and tonsils through foramen magnum with aqueductal stenosis causing hydrocephalus
Chiari II malformation
lumbosacral meningomyelocele is associated
Agenesis of cerebellar vermis leads to cystic enlargement of 4th ventricle that fills the enlarged posterior fossa
Dandy-walker syndrome
associated with noncommunicating hydrocephalus, spina bifida
Cystic cavity within central canal of signal cord. Patient presents with cape like, bilateral symmetrical loss of pain and temperature sensation in upper extremities. Fine touch sensation is preserved
Syringomyelia - a cyst forms within your spinal cord. As this fluid-filled cyst, or syrinx, expands and lengthens over time, it compresses and damages part of your spinal cord from its center outward
Fibers crossing in anterior white commissure (spinothalamic tract) are typically damaged first
associated with chiari malformation
most common at C8-T1
CN for taste
CN VII, IX, X (solitary nucleus)
CN for pain in tongue
CN V3,IX, X
CN for Motor in tongue
CN X, CN XII
CN XII is to the hyoglossus that retracts and depresses the tongue, genioglossus which protrudes tongue, and styloglossuswhich draws tongue upward to create a trough for swallowing
CN X to the palatoglossus which elevates posterior tongue during swallowing
What brachial arches form the anterior 2/3 of tongue
1st and 2nd
sensation CN V3
Taste CN VII
What brachial arches formt he posterior 1/3 of tongue
3rd and 4th
Sensation and taste from CN IX
Extreme posterior is CN X
What kind of stain do you use to see the cell bodies and dendrites of neurons
Nissl stain which stains the RER
doesnt stain the axon because the axon does not have any RER
Injury to axon causes degeneration of axon distal to site of injury and axonal retraction proximally
Wallerian degeneration
allows for potential regeneration of axon (if in PNS)
macrophages remove debris and myelin
Most common glial cell type in CNS.
Astrocytes which are responsible for physical support, repair,extracellular K+ buffer, removal of excess NT, component of BBB, glycogen fuel reserve buffer
What are astrocytes derived from
neuroectoderm
Astrocyte marker
GFAP
Phagocytic scavenger cells of CNS that respond to tissue damage
HIV infected microglia fuse to form multiucleated giant cells in CNS
Glial cells with a ciliated simple columnar form that line the ventricles and central canal of spinal cord. Apical surfaces are covered in cilia (which circulate CSF) and microvilli (which help in CSF absorption)
ependymal cells
Function of myelin
Increase conduction velocity of signals transmitted down an axon
nodes of ranvier have high coentration of Na channels
What type of cells synthesize myelin the CNS (including CN I and II)
“COPS”
oligodendrocytes derived from neuroectoderm
1 oligodendrocyte per many CNS axons
What type of cells synthesize myelin in the PNS ( Including CN III-XII)
“COPS”
Schwann cells derived from neural crest
1 schwann cell per PNS axon
What type of cell is damaged in Guillian Barre syndrome
Schwann cells
What type of cell is damaged in MS, progressive multifocal leukoencephalopathy (PML), leukodystrophies
Oligodendrocytes
Free nerve endings
C- slow, unmyelinated fibers
Aδ- fast, myelinated fibers
skin, epidermis, some viscera
pain and temperature
Meissner corpuscles
Large myelinated fibers that adapt quickly
Gabrous (hairless)skin
dynamic, fine/light touch, position sense
Pacinian corpuscles
Large myelinated fibers that adapt quickly
Deep skin layers, ligaments, and joints
vibration and pressure
Merkel disc
Large myelinated fibers that adapt slowly
finger tips and superficial skin
pressure, deep static touch, position sense
Ruffini corpuscles
Dendritic ending with capsule; adapt slowly
finger tips, joints
pressure. slippage of objects along surface of skin, joint angle change
Peripheral nerve layers
Endoneurium (inner layer) - around single nerve fibers
Perineurium (around, blood nerve permeaility barrier) - surrounds each fasicle of nerve fibers
Epineurium (outer layer) - dense CT that surrounds entire nerve (fasicles and blood vessels)
inflammatory infiltrate in Guillain barre syndrome involves what layer of peripheral nerve
Endoneurium
Reaction of neuronal cell body to axonal injury that is concurrent with wallerian degeneration
Chromatolysis
changes reflect increased protein synthesis in an effort to repair the damaged axon
- Round cellular swelling
- Displacement of the nucelus to the periphery
- Dispersion of Nissl substance throughout the cytoplasm
Location of synthesis of ACh
Basal nucleus of Meynert
Location of synthesis of Dopamine
Ventral tegmentum, SNc
Location of synthesis of GABA
Nucleus accumbens
Location of synthesis of NE
Locus ceruleus
Location of synthesis of serotoning
Raphe nucleus
NT levels in anxiety
low GABA and serotonin
high NE
NT levels in Depression
low dopamine, NE, serotonin
NT levels in schizo
high dopamine
NT levels in alzheimers dz
low ACh
NT levels in huntington disease
low ACh and GABA
high Dopamine
NT levels in parkinson disease
low dopamine and serotonin
high ACh
Meninges layers
Dura mater (from mesoderm) Arachnoid mater (neural crest) Pia mater (neural crest)
Epidural
a potential space between the dura mater and skull containing fat and blood vessels
The blood brain barrier is formed by 3 structures
- tight junctions between nonfenestrated capillary endothelial cells
- basement membrane
- astrocyte foot processes
Can glucose and AA cross the BBB
yes they cross slowly by carrier mediated transport mechanisms
Can non polar/lipid soluble substances cross the BBB
yes rapidly via diffusion
effect of infarction or neoplasm on BBB
destroys endothelial cell tight junctions causing vasogenic edema
Hypothalamus
maintains homeostasis
TAN HATS
Thirst Adenohypophysis Neurohypothysis Hunger Autonomic NS Temperature Sexual urgers
What parts of the hypothalamus are not protected by the BBB
OVLT which senses changes in osmolarity
Area postrema found in medulla and responds to emetics
Lateral nucleus (Hypothalamus)
hunger
+ ghrelin
- leptin
injury: lateral injury makes you lean
Ventromedial nucleus (Hypothalamus)
Satiety
+ leptin
injury: VentroMedial injury makes you Very Massive
Anterior nucleus (Hypothalamus)
Cooling and parasympathetics
“ANTartica”
Posterior nucleus (Hypothalamus)
Heating and sympathetics
“Hot Pot”
Suprachiasmatic nucleus (SCN) of Hypothalamus
Circadian rhythm
“charismatic people need to sleep”
Supraoptic and paraventricular nuclei (Hypothalamus)
Synthesize ADH and oxytocin
which are carried by neurophysins down axons to the posterior pituitary
Preoptic nucleus (Hypothalamus)
thermoregulation and sexual behavior
releases GnRH
Kallman syndrome (Hypothalamus)
failure of GnRH producing neurons to migrate from olfactory pit
Vomiting is coordinated by what? where is it located? where does it receive information from?
- nucleus tractus solitarius (NTS) in the medulla
- receives info from the chemoreceptor trigger zone (CTZ within area postrema in 4th ventricle), GI tract via vagus, vestibular system, CNS
The 5 major receptors in the CTZ
muscarinic (M1), dopamine (D2), histamine (H1),serotonin (5HT3), and neurokinin (NK-1)
____,____,____ antagonists used to treat chemotherapy induced vomiting
5HT3
D2
NK-1
____ and ____ antagonists used to treat motion sickness and hyperemesis gravidarum
M1 and H1
Circadian rhythm controls nocturnal release of ___, ____, ____, ____
ACTH
Prolactin
Melatonin
NE
SCN –> NE release—> pineal gland –> melatonin
SCN is regulated by the environment
Effect of alcohol, benzos, and barbiturates on sleep cycle
decrease REM sleep and delta wave sleep
Sleep cycle stages
Awake eyes open –> Beta (high f, low amp)
Awake eyes closed –> Alpha
Non-REM sleep
-Stage N1 (light sleep) –> theta
-Stage N2 (deeper sleep) –> sleep spindles and K complexes
-Stage N3 (deepest non-REM sleep, slow wave) –> Delta
-REM sleep –> Beta waves
What stage of sleep does bruxism occur
Stage N2 of non REM sleep
sleep spindles and K complexes
What stage of sleep does sleep walking, night terrors, and bedwetting occur
Stage N3 of non REM sleep
Delta wave
Stage of sleep where there is a loss of motor tone, increased brain O2 use, increased and variable pulse and blood pressure, increase ACh
REM sleep
occurs every 90 minutes and duration increases through the night
What stage of sleep do you experience dreaming, nightmares, penile/clitoral tumescence, and may serve a memory processing function
REM sleep
extraoccular movements are due to activity of
PPRF or paramedian pontine reticular formation or conjugate gaze center
Ventralposterolateral nucleus (thalamus)
Input: spinothalamic and dorsal columns/medial lemniscus
Senses: vibration, pain, pressure,proprioception, light touch, temperature
Destination: primary somatosensory cortex
Ventralposteromedial nucleus ((thalamus)
Input:Trigeminal and gustatory pathway
Senses: Face sensation, taste
Destination: primary somatosensory cortex
Lateral geniculate nucleus ((thalamus))
Input:CN II, optic chiasm, optic tract
Senses: vision
Destination: Calcarine sulcus
lateral …think “light”
Medial geniculate nucleus ((thalamus))
Input:superior olive and inferior colliculus of tectum
Senses: Hearing
Destination: auditory cortex of temporal lobe
medial…think “music”
Ventral lateral nucleus (thalamus)
Input: Basal ganglia
Senses: Motor
Destination: Motor cortex
Limbic system is responsible for
emotion, long term memory, olfaction, behavior modulation, ANS function
5 F: Feeding, Fleeing, Fighting, Feeling, (Fucking)Sex
Structures of the limbic system
hippocampus, amygdala, mammillary bodies, anterior thalamic nuclei, cingulate gyrus, entorhinal cortex
Mesocortical (Dopaminergic pathways)
decreased activity causes negative symptoms
Mesolimbic (Dopaminergic pathways)
inceased activity causes positive symptoms
primary target of antipsychotic drugs which decrease positive symptoms
Nigrostriatal (Dopaminergic pathways)
decreased activity causes extrapyramidal symptoms
significantly affected by mvoement disorders and antipsychotic drugs
Tuberoinfundibular(Dopaminergic pathways)
decreased activity causes increase in proalctin and decreased libido, sexual dysfunction, galactorrhea, gynecomastia
Input into cerebellum
contralateral cortex via middle cerebellar peduncle
ipsilateral proprioceptive info via inferior cerebellar peduncle from spinal cord
Output into cerebellum
The only output of cerebellar cortex is the purkinje cells which are always inhibitory –> deep nuclei of cerebellum –> contralateral cortex via superior cerebellar peduncle
Deep nuclei from lateral to medial
Dentate, Emboliform, Globose, Fastigial
Lateral lesion to cerebellum
Affects LATERAL structure
voluntary movement of extremities
fall toward injured side (ipsilateral)
Medial lesion to cerebellum
affects MEDIAL structures
truncal ataxia (wide based cerebellar gait) , nystagmus, head tilting.
Bilateral motor defects affecting axial and proximal limb musculature
Basal ganglia
voluntary movements and making postural adjustments
Basal ganglia’s striatum =
putamen (motor) + caudate (cognitive)
Basal ganglia’s Lentiform =
putamen + globus pallidus
Basal ganglia’s D1 receptor
direct pathway
Dopamine binds to D1 to stimulate the excitatory pathway
Basal ganglia’s D2 receptor
Indirect
Inhibitory pathway
Dopamine binds to D2 to inhibit the inhibitory pathway and increase motion
Direct (excitatory) pathway
Substantia nigra input stimulates the striatum causing GABA release
The release of GABA inhibits GABA release from the GPi (globus pallidus)
This causes DISINHIBITION of thalamus and therefore increased movement
Indirect (inhibitory) pathway
Substantia nigra input stimulates the striatum which releases GABA that DISINHIBITS the subthalamic nucleus via GPe inhibition
Subthalamic nucleus stimulates the GPi (globus pallidus) to inhibit the thalamus and therefore decreases movement
What is cerebral perfusion primarily driven by
PCO2
hypoxemia increases CPP only if PO2 <50 mmHg
CPP is directly proportional to PCO2 until PCO2>90 mmhg
Cerebral perfusion pressure equation
MAP-ICP
if CCP=0 then braindeath
How does therapeutic hyperventilation affect the CCP (cerebral perfusion pressure)
It causes a drop in PCO2 which results in vasoconstriction and ultimately decreased cerebral blood flow and drop in intracranial pressure (ICP)
Anterior cerebral artery supplies
anteromedial surface
Middle cerebral artery supplies
lateral surface
Posterior cerebral artery supplies
posterior and inferior surfaces
Watershed zones in the brain
between anterior cerebral/middle cerebral (cortical border zone)
between posterior cerebral/middle cerebral (cortical border zone)
Superficial and deep vascular territories of the middle cerebral artery (internal border zone)
circle of willis pathway
The vertebral arteries join to form the basilar artery
the basilar artery bifurcates into the posterior cerebral artery
the posterior cerebral artery communicates with the middle cerebral artery with the posterior communicating branch
The middle cerebral artery joins the anterior cerebral artery to form the internal carotids
Dural venous sinuses drain into
internal jugular vein
Dural venous sinus drainage pathway
Superior sagittal sinus, straight sinus, and occipital sinus. join to form the confluence of sinuses
Then proceeds to drain into the left and right transverse sinuses. –> sigmoid –> jugular foramen –> internal jugular vein
Venous sinus thrombosis
Patient presents with the signs and symptoms of increased ICP
can lead to venous hemorrhage
Ventricles
The lateral ventricles drain into the third ventricle via the right and left interventricular foramina of monro
The third ventricle (chicken head) then drains into the 4th ventricle via cerebral aqueduct of sylvius
The 4th ventricle drains into the subarachnoid space via the foramina of luschka (lateral) and the foramina of Magendie (medial)
CSF made by
ependymal cells of choroid plexus
then reabsorbed by arachnoid granulations and then drains into dural venous sinuses
CNs and where they exit from
4 exit above the pons - 1,2,3,4
4 exit the pons-5,6,7,8
4 are in the medulla - 9,10,11,12
4 nuclei are medial - 3,4,6,12 (factors of 12)
Pineal gland
melatonin secretion and circadian rhythms
Superior colliculi
direct eye movements to stimuli or objects of interest
Inferior colliculi
auditory
note: superior is eyes and inferior is ears. The eyes are above the ears