Neurology 1

evolv3's version from 2015-06-27 00:12

Neural Development

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

Regional specification of developing brain

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 & cerebellum
wall of myelencephalonmedulla
cavity of myelenchephalonlower part of 4th ventricle
cavity of metencephalonupper part of 4th ventricle

NTD: Background info

Question Answer
when are neuropores supposed to fuse?4th week
when neuropores fail to fuse, there is a persistent connection betweenamniotic cavity & spinal canal
elevated levels of this in amniotic fluid & maternal serum in neural tube defectα-fetoprotein (AFP)
helpful confirmatory amniotic fluid tests in neural tube defectselevated AChE (in CSF, transudates across defect)

NTD: Examples

Question Answer
defect in spina bifida occultafailure of bony spinal canal to close, but no structural herniation & 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 & spinal cord herniate through spinal canal defect

Forebrain anomalies

Question Answer
defect in anencephalymalformation of anterior neural tube, no forebrain & open calvarium ("frog-like")
↓ risk of anencephaly by supplementing mom withfolate
clinical findings in anencephalyincreased AFP, polyhydramnios (no swallowing center in brain)
anencephaly associated w/ maternaltype I DM
holoprosencephaly defectfailure of left & 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

Posterior Fossa Malformations

Question Answer
Chiari II malformation defectcerebellar tonsillar & vermian herniation through foramen magnum, with aqueductalstenosis & hydrocephalus
clinical presentation of Chiari IIthoraco-lumbar myelomeningocele, paralysis below defect
Dandy-Walker defectagenesis of cerebellar vermis w/ cystic enlargement of 4th ventricle (fills posterior fossa)
Dandy-Walker associated w/hydrocephalus, spina bifida


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
clinical symptoms of syringomyelia"cape-like" bilateral loss of main and temperature in upper extremities, fine touch preserved

Tongue Development

Question Answer
anterior 2/3 of tongue formed by1st branchial arch
sensation in anterior 2/3 byCN V3
taste in anterior 2/3 byCN VII
posterior 1/3 of tongue formed by3rd & 4th branchial arches
sensation & taste to posterior 1/3 byCN IX, CN X in extreme posterior
motor innervation of tongue byCN XII except palatoglossus (CN X)
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 & 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 & 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 & SNc (midbrain)
Location of 5-HT synthesisRaphe nucleus
Location of ACh synthesisBasal nucleus of Meynert
Location of GABA synthesisNucleus accumbens


Question Answer
Anxiety NTs?↑ NE, ↓ serotonin & GABA
Depression NTs?↓ NE, DA, serotonin
Parkinson's NTs?↓ DA, ↑ ACh & serotonin
Huntington's NTs?↑ DA, ↓ ACh & GABA
Alzheimer's Dementia NTs?↓ ACh
Schizophrenia↑ DA in mesolimbic pathway (positive symptoms); ↓ DA in mesocortical pathway (negative symptoms)


Question Answer
BBB formed by what?tight junctions b/t nonfenestrated capillary endothelial cells, basement membrane, astrocytes
Vasogenic edema?infarction that destroys endothelial cell tight junctions
Lateral hypothalamusfeeding; inhibited by leptin; destruction causes anorexia
Ventromedial hypothalamussatiety;stimulated by leptin; destruction causes obesity
Areas of hypothalamus projecting to posterior pituitary?supraoptic nucleus (ADH) & paraventricular nucleus (oxytocin)
Anterior hypothalamuscooling (destruction → HYPERthermia)
A/C cooling
posterior hypothalamusheating (destruction → HYPOthermia)
How glucose/AAs cross BBBSlowly by carrier-mediated transport
Suprachiasmatic nucleus (SCN)Circadian rhythm
Locations in brain with no BBBArea postrema - vomiting after chemo
OVLT - osmotic sensing
posterior pituitary (Neurohypophysis) - ADH release
Reward center, pleasure, addiction, fearNucleus accumbens & septal nucleus

Cerebellum/Thalamus/Limbic Anatomy

Question Answer
MCP of cerebellumcontralateral cortex input to cerebellum
ICP of cerebellumipsilateral proprioceptive info via ICP to cerebellum
Input nn. to cerebellum?climbing & mossy fibers
Output of cerebellum?deep purkinje fibers send info to deep nuclei of cerebellum and then go to contralat cortex via superior cerebellar peduncle
Deep nuclei of cerebellumlateral to medial- dentate, emboliform, globose, fastigial "don't eat greasy foods"
Lateral vs medial cerebellar nuclei functionslateral is for voluntary movement of extremities - injury causes fall towards injured side
medial is for balance, truncal coordination, ataxia


Question Answer
LGNvision Lateral=Light
input: CN2
output: calcarine sulcus
MGNhearing (Medial=Music)
input: superior olive & inferior colliculus of tectum
output: auditory cortex of temporal lobe
VPMFace sensation & taste (Makeup goes on face)
input: CN5
output: 1° somatosensory cortex
VPLbody pain/temp, pressure, touch, vibration, proprioception
input: spinothalamic & dorsal columns/medial lemniscus
output: 1° somatosensory cortex
input: basal ganglia
output: motor cortex


Question Answer
Limbic system functions5Fs- feeding, fighting, fleeing, feeling, f-ing
Structures of limbic systemhippocampus
mammillary bodies
cingulate gyrus

Basal ganglia & Parkinson's

Question Answer
Function of BGvoluntary movements & making postural adjustments
Direct pathway (D1)facilitates movement
cortex(+)→striatum→GABA -----l GPi/SNr → (disinhibits) thalamus
Indirect pathway (D2)inhibits movement
cortex(+)→ striatum ----l GPe → (disinhibits) STN → + to GPi/SNr -----l thalamus
DA & D1 pathwayNormal: stimulation of excitatory pathway (↑ motion)
Losing DA in Parkinson's inhibits this pathway (↓ motion)
DA & D2 pathwayNormal: inhibition of inhibitory pathway (↑ motion)
Losing DA in Parkinson's reactivates inhibitory pathway (↓ motion)
Loss of DA in Parkinson's & overall result?Degeneration of DA-containing neurons in SN → ↓ activity of D1 + ↑ activity of D2 → net inhibition of thalamus → ↓ movement (due to loss of DA)
Parkinson's sxsTRAP sxs- tremor (at rest - pill-rolling), cogwheel Rigidity, Akinesia, Postural instability
Parkinson's pathdegenerative disorder of CNS with Lewy bodies (made of α-synuclein- intracellular inclusions) & depigmentation of SNc (lose DA)
rare cases linked to MPTP (contaminant in illicit street drugs)
Striatumputamen (motor) + caudate (cognitive)
Lentiformputamen + globus pallidus


Question Answer
Huntington's pathologyCAG repeat disorder, autosomal dominant; age of onset usually 20-50
neuronal death via NMDA-R binding & glutamate toxicity
Caudate loses ACh & GABA
Striatal (caudate/putamen) atrophy: (main inhibitors of movement)→ loss of D2 neurons first → removal of inhibition from GPe allowing it to inhibit STN → lessens inhibition of thalamus= ↑ movement
Huntington's sxschorea, aggression, depression, progressive dementia
sometimes initially mistaken for substance abuse
Choreasudden jerky purposeless movements
due to BG lesion (HD)
Athetosiswrithing, esp. fingers
BG lesion (HD)

Movement Disorders

Question Answer
Hemiballismussudden involuntary, wild flailing of arm/leg on side contralateral to lesion
contralateral subthalamic nucleus lesion (lacunar stroke in HTN pt)
Mechanism: Lacunar infarct of subthalamic nucleus → loss of excitatory subthalamic nucleus projection to globus pallidus internal → lessens inhibition of thalamus= ↑ movement
Myoclonussudden brief uncontrolled muscle contraction
Hiccups - common in metabolic abnormalities like renal/liver failure
Dystoniasustained involuntary muscle contractions
Essential tremoraction tremor, genetic predisposition
self-medication with alcohol can ↓ tremor amplitude
tx: β-blockers & primidone
Resting tremormost noticeable distally (hands)
stops w/ intentional movement
seen in parkinson's
intention tremorslow zigzag when pointing toward target
cerebellar dysfunction

Common Brain Lesions

Question Answer
Frontal lobe functionsdamage → disinhibition, planning, language, judgment, mood, social judgement
deficits in concentration & possible reemergence of primitive reflexes
Lesion of amygdalaKluver-Bucy syndrome- hyperorality, hypersexuality, disinhibited behavior
Lesion right parietal lobespatial neglect syndrome, agnosia of contralateral world
Lesion RAS in midbrainreduced arousal & wakefulness
Lesion mamillary bodiesWernicke-korsakoff- confusion/ophthalmoplegia/ataxia AND memory loss/confabulation/personality change, seen in alcoholics (thiamine def)
Lesion BGmay result in resting tremor, chorea, or athetosis
Lesion cerebellar hemisphereintention tremor, limb ataxia
damage results in ipsilateral deficit → fall towards side of lesion
Lesion cerebellar vermistruncal ataxia, dysarthria
Lesion subthalamic nucleushemiballismus (contralateral)
Lesion hippocampusanterograde amnesia (cant make new memories)
Lesion PPRFeyes look away from side of lesion
Lesion Frontal eye fieldeyes look toward lesion

Central pontine myelinolysis (CPM)

Question Answer
CPM sxsacute paralysis, dysarthria (motor inability to speak, a movement deficit), dysphagia, diplopia & loss of consciousness
CPM pathcaused by very rapid correction of hyponatremia
Massive axonal demyelination in pontine white matter tracks
Abnormal ↑ signal in pons in T2 MRI


Question Answer
Broca's (motor) aphasianonfluent, good comprehension, poor repetition, "Broken Boca", location=INFERIOR FRONTAL GYRUS (frontal lobe)
Wernicke's (sensory) aphasiafluent, poor comprehension, poor repetition, location= SUPERIOR TEMPORAL GYRUS (temporal lobe)
Conduction aphasialesion arcuate fasciculus (connecting broca/wernicke)
fluent, good comprehension, poor repetition


Question Answer
Anterior spinal a.Lateral corticospinal tract - contralateral hemiparesis of lower limbs
ML - no contra proprioception
Caudal medulla - ipsilateral paralysis of hypoglossal n. - tongue deviates ipsi
PICA occlusionLateral medulla
Vestibular nuclei - vomiting, vertigo, nystagmus
lateral spinothalamic tract, spinal trigeminal nucleus - ↓ pain/temp in limbs/face
nucleus ambiguus - dysphagia, hoarseness ↓ gag reflex
Sympathetics - ispilateral Horner's
ICP - ataxia, dysmetria
"Don't PICA horse that can't eat"
AICA occlusionLateral pons:
CN nuclei - vomiting, vertigo, nystagmus, paralysis of face, ↓ lacrimation/salivation, ↓ taste from anterior 2/3rds of tongue, ↓ corneal reflex
Ipsi ↓ pain/temp/hearing, horner's
MCP/ICP - ataxia, dysmetria
"Facial droop means AICA's pooped"
PCA occlusionOccipital cortex, visual cortex:
contra homonymous hemianopia w/ macular sparing
ACA occlusionContra lower limb paralysis & loss of sensation
MCA occlusioncontra face/arm paralysis & sensory loss
aphasia (if lesion on left side)
left sided neglect (if lesion on right side)
Anterior communicating a.most common site of saccular (berry) aneurysm in Willis
visual field defects
Posterior communicating a. occlusionSaccular (berry aneurysm)
CN3 palsy - eye is "down & out" w pupil dilation
Lateral striate (lenticulostriate) aa. occlusiondivisions of MCA, supply internal capsule, striatum (caudate/putamen)
contralateral hemiparesis/hemiplegia
lacunar infarcts (2° to unmanaged hypertension)
Watershed zonesbt ACA/MCA, & PCA/MCA
damage in severe hypotension→upper leg/upper arm weakness, defects in high-order visual processing
Basilar a. infarctlocked in syndrome, only CN3 works
Stroke of anterior circlegeneral sensory/motor dysfunction, aphasia
Stroke of posterior circledeficit in CNs, coma, cerebellar deficits, dominant hemisphere (ataxia), nondominant (neglect)
Cerebral perfusion regulated byPCO2, except in severe hypoxia (severe COPD) - then PO2 takes over
Medial medullary syndromeparamedian branches of ASA & vertebral arteries
Contra LL hemiparesis
↓ contra proprioception
Tongue deviation toward lesion
Lateral medullary (Wallenberg's) syndromePICA (lateral medulla)
CN deficits
Dysphagia, hoarseness, ↓ gag reflex
Ipsi Horner's
Most common site of Berry aneurysmbifurcation of anterior communicating a.
sx of berry aneurysm rupture"worst headache of my life" d/t subarachnoid hemorrhage
Bitemporal hemianopia via compression of optic chiasm
Associated with berry aneurysmADPKD
Ehler's Danlos syndrome
Marfan's syndrome
Advanced age, HTN, smoking, AAs
Charcot-Bouchard microaneurysmChronic HTN
Small vessels - basal ganglia, thalamus