Neuro Flashcards
Describe the steps of the beginning of neural development. What does the neural plate give rise to? What does the notochord become? What are the alar and basal plates? When do the first steps occur?
Notochord induces overlying ectoderm to become neuroectoderm which forms the neural plate
The neural plate gives rise to the neural tube and neural crest cells
Notochord=nucleus pulposus
Alar=dorsal=sensory
basal=ventral=motor
Day 18-21
What are the three primary vesicles of the developing brain? What do they become/what are the five secondary vesicles? What do these structures become in adults? Where are the different ventricular cavities located?
Forebrain (prosencephalon), midbrain (mesencephalon), hindbrain (rhombencephalon
Forebrain leads to telencephalon (cerebral hemispheres)
Also to diencephalon (thalamus)
Midbrain leads to mesencephalon (midbrain)
Hindbrain leads to metencephalon (pons/cerebellum)
Also to myelencephalon (medulla)
lateral ventricles (1 and 2)=hemispheres third ventricle=thalamus cerebral aqueduct=midbrain upper part of fourth ventricle=pons Lower part=medulla
What neural cells originate as neuroectoderm? neural crest cells? Mesoderm?
NE=CNS, astrocytes, oligodendroglia, ependymal cells
NC=schwann cells, PNS neurons
Mesoderm=microglia (like macrophages)
What are neural tube defects? When do they occur? What increases their risk? Lab values? What is spina bifida occulta? Meningocele? Meningomyelocele?
Persistent connection between amniotic cavity and spinal canal (4th week=neural pores fail to close)
Low folic acid intake by mother
Incr. AFP
Incr. AChE in amniotic fluid
SBO=failure of bony spinal canal to close, but no herniation. Lower vertebral leves. Tuft of hair or skin dimple. Normal AFP
Meningocele=Meninges (no neural tissue) herniate through bony defect
Meningomyelo=meninges and neural tissue herniate
What is anencephaly? Lab values? Associations? What decrease risk?
Malformation of anterior neural tube leading to a lack of forebrain and calvarium
Incr. AFP, polyhydramnios (no swallowing center in brain)
Type 1 DM (maternal)
Incr. folate decr. risk
What is holoprosencephaly? Timing? Mutations? Moderate form symptoms? severe form? Associated syndromes?
Failure and left and right hemi to fuse (5-6 weeks)
Sonic hedgehog pathway
Cleft lip/palate —>cyclopia
patau and fetal alcohol
What is chiari II? What does it lead to? How does it present?
Herniation of cerebellar tonsils and vermis through foramen magnum
Aqueductal stenosis and hydrocephalus
Lumbosacral meningomyelocele and paralysis below defect
What is Dandy-Walker malformation? Associations?
Agenesis of cerebellar vermis with cystic enlargement of 4th ventricle (fills posterior fossa)
Hydrocephalus, spina bifida
What is syringomyelia? Hydromyelia? What is damage first? Presentation? Etiologies? Location?
cystic cavity in spinal cord (hydro=in central canal)
Crossing anterior commisural fibers
Cape like bilateral loss of pain and temperature sensation in upper extremities
Chiari malformations, trauma, tumors
What is chiari I malformation? Cause? Presentation?
cerebellar tonsillar ectopia > 3-5 mm
Congenital
Asymptomatic in childhood —>headaches and cerebellar symptoms
What does the anterior 2/3 of the tongue form from? Innervation? Posterior 1/3? Innervation? What are the muscles of the tongue? Function of each? Innervation of each? To what nucleus is taste transmitted?
ANT 2/3
1st and 2nd branchial arches
sens: CNV3
Taste: CNVII (to solitary nucleus)
POST 2/3
3rd and 4th branchial arches
Sens: mainly CNIX, very post. is CNX
Taste: Mainly CNIX, very post. is CNX
CNXII
Motor to hyoglossus (retracts/depresses)
Genioglossus (protrudes)
Styloglossus (draws sides of tongue upward to create trough for swallowing)
CNX
Motor to palatoglossus (elevates post. tongue while swallowing
With what stain can neurons be seen? Which parts? Describe wallerian degeneration. What are the functions of the astrocyte? Marker? What is the function of the microglia? When is it activated? What happens to them in HIV?
Nissl staining (stains RER, thus can only seen cell body and dendrites) Injury to axon leads to degeneration distal to injury and axonal retraction proximally; allows for potential regeneration of axon (in PNS)
Physical support, repair, K+ metabolism, removal of excess NT, blood brain barrier component, glycogen fuel reserve buffer, reactive gliosis in response to injury
GFAP
phagocytic svanger cells of CNS
Activated in response to tissue damage
HIV infected microglia fuse to form multinucleated giant cells in CNS
What is the function of myelin? What are the functions of schwann cells? Pattern? In what illness might they be injured? What is an acoustic neuroma? What is its association if bilateral? Function of oligodendroglia? Pattern? Histo appearance? In what illnesses are they injured?
Wraps and insulates axons
Incr. cond. veloc.—>saltatory conduction/nodes of ranvier (lots of Na)
Schwann cells myelinate only 1 PNS axon
Promote axonal regeneration
Guillain-Barre
Acoustic Neuroma: Schwannoma of CNVIII. Bilateral=NF2
Oligodendroglia can myelinate many CNS axons (30)
Fried egg appearance
MS, progessive multifocal leukoencephalopathy, leukodystrophies
Compare free nerve endings, meissner corpuscles, pacinian corp, merkel discs, and ruffini corpuscles concerning their description of fibers, adaptation, location, and senses.
FREE NERVE ENDINGS
C-slow, unmyelinated fibers
Adelta-fast, myelinated fibers
All skin, epidermis, some viscera
Pain, temp.
MEISSNER
Large myelinated
Adapt quickly
Hairless skin
Dynamic, fine/light touch, position sense
PACINIAN
Large myelinated
Adapt quick
Deep skin layers, ligaments, joints
Vibration, pressure
MERKEL
Large myelinated
Adapt slow
Finger tips, superficial skin
Pressure, deep static touch (shapes, edges), position sense
RUFFINI
Dendritic endings with capsule
Adapt slow
Finger tips, joints
Pressure, slippage of objects along surface of skin, joint angle change
What is the endoneurium? perineurium? Epineurium?
Endo-invests single nerve fiber
Peri-Surrounds a fascicle of nerve fibers
Epineurium-Dense connective tissue that surrounds entire nerve (fascicles and blood vessels within)
How is NE changed in certain diseases? Where is it synth? What nuclei are associated with the reward center, pleasure, addiction, and fear?
NE
Incr. anxiety
Decr. depression
Locus ceruleus (pons) (stress and panic)
DOPAMINE Incr. huntingtons decr. parkinsons decr. depression Ventral tegmentum and substantia nigra pars compacta (midbrain)
5-HT
Decr. anxiety
Decr. depression
Raphe nuclei (pons, medulla, midbrain)
ACH Incr. parkinsons decr. alzheimers Decr. huntingtons Basal nucleus of Meynert
GABA
Decr. anxiety
Decr. huntingtons
Nucleus accumbens
Nucleus accumbens and septal nucleus
What is the function of the BBB? What are the 3 structures that make it up? How do glucose and AAs cross? Nonpolar/lipid soluble molecules? What are a few areas with fenestrated capillaries in the brain and what are their functions? What can destory the tight cell junctions?
Prevents circ. blood substances from reaching the CSF/CNS
tight junctions b/w nonfenestrated capilary endo cells
basement membrane
astrocye foot processes
Glucose/AAs cross slowly by carrier mediated transport
Nonpolar cross rapidly via diffusion
Area postrema (emetic agents) OVLT (osmotic sensing) Neurohypophysis (secretes ADH into circ.)
Infarction/neoplasm can damage tight junctions (vasogenic edema)
What are the function of the hypothalamus in general? What are the two inputs not covered by the BBB?
TAN HATS
Thirst and water balance
Adenohypophysis control (regulates ant. pit)
Neurohypophysis releases ADH, oxy through post. pit
Hunger
Autonomic regulation
Temp. regulation
Sexual urges
OVLT (organum vasculosum of lamina terminalis, changes in osmolarity Area postrema (emetics)
What does the supraoptic nucleus do? Paraventricular nucleus? Lateral area? Ventromedial area? Anterior hypothalamus? Posterior hypothalamus? Suprachiasmatic nucleus?
SON=ADH synth
PVN=Oxytocin synth
Lateral area=Hunger. Inhibited by leptin (Lose weight)
Damage leads to anorexia, failure to thrive
Zap your lateral nucleus, lateral shrinking
Ventromedial area=satiety. Stimulated by leptin (Lose)
Damage (craniopharyngioma) leads to hyperphagia
Zap VM area leads to ventral and medial growth
Anterior hypothalamus=cooling, parasymp
A/C: anterior cooling, cool off (cooling, parasymp=settles)
Posterior hypothalamus=heating, sympathetic
Get fired up (heating, symp)
Suprachiasmatic=circadian rhythm
You need sleep to be charismatic
What is the sleep cycle regulated by? What hormones does this regulation control? Explain the mechanism? What is its input?
Circadian rhythm (suprachiasmatic nucleus)
ACTH, prolactin, melatonin, NE
SCN leads to NE release leads to pineal gland act. leading to melatonin
SCN regulated by environment (light)
What are the two stages of sleep? What causes extraocular movements during REM sleep? How often does REM sleep occur? How does it change through the night? What drugs are associated with decr. REM sleep and delta wave sleep? Just decr. REM sleep? How should bed wetting be treated? How should night terrors and sleepwalking be treated?
REM (rapid eye movement) and non REM
PPRF (paramedian pontine retic. formation)
Every 90 min., incr. in duration throughout the night
Alcohol, benzos, and barbituates
NE
Bedwetting: oral desmopressin
Night terrors: Benzos
What are the stages of sleep like? What percentage of sleep are we in each one? Which waveforms are associated with each? What are the waveforms like?
Awake (eyes open)=beta waves (highest freq, lowest ampli)
Awake (eyes closed)=alpha waves
NREM Stage N1 (5%): light sleep-theta Stage N2 (45%): deeper sleep, bruxism=sleep spindles and K complexes Stage N3 (25%): Deepest NREM sleep (slow wave sleep): sleepwalking, night terrors and bedwetting=delta (lowest frequency, highest ampl)
REM (25%): Loss of motor tone, incr. brain O2 use, incr. variable pulse and BP; dreaming and penile tumescence occur; memory processing function=beta
at night, BATS Drink Blood
Beta, alpha, theta, sleep spindles/k complexes, delta, beta
What is the major function of the thalamus? What is the input for the VPL? What info is received their? Destination? Same questions for VPM, LGN, MGN, and VL
VPL
Input: spinothalamic and dorsal columns/medial lemniscus
Info: pain, temp; pressure, touch, vibration, proprio
Destination: primary somatosensory cortex
VPM
Input: trigeminal and gustatory pathway
Info: face sensation, taste
Destination: primary somatosensory cortex
LGN
Input: CNII
Info: Vision
Destination: Calcarine sulcus
MGN
Input: superior olive and inf. colliculus of tectum
Info: Hearing
Destination: auditory cortex of temporal lobe
VL
Input: basal ganglia, cerebellum
Info: motor
Destination: motor cortex
What are the functions of the limbic systems? What structures are involved? What are the 5 F’s?
neural structures involved in emotion, long term memory, olfaction, behavior modulation, and ANS function
Hippocampus Amygdala Fornix mammilary bodies cingulate gyrus
Feeding, fleeing, fighting, feeling, and fornicating
What are the symptoms of osmotic demyelination syndrome? Pathophys? What usually causes it? What related syndrome causes cerebral edema?
Acute paralysis, dysarthria, dysphagia, diplopia, and loss of consciousness
Massive axonal demyeination in white pontine matter
secondary to osmotic changes
Correcting hyponatremia too fast (add sodium, water rushes out of axons)
From low to high, your pons will die (osm. demy syn)
From high to low, your brain will blow (edema/herniat)
What is the overall function of the cerebellum? What are its inputs? What is its output? By which pathway? What are its deep nuclei? What do lateral lesions result in? Medial lesions?
Modulates movement; aids in coordination and balance
Input:
Contralateral cortex via middle cerebellar peduncle
Ipsilateral proprioceptive info via inf. cereb. ped. from spinal cord
Output: To contralateral cortex to modulate movement via purkinje nerves (purkinje to deep nuclei to contralateral cortex via cerebellar peduncle
Deep:
Dentate, emboliform, globose, fastigial (Don’t Eat Greasy Foods)
Lateral: voluntary movment of extremities; when injured propensity to fall toward injured side
Medial lesins: Midline structures and/or flocclonodular lobe=truncal ataxia (wide based cerebellar gait), nystagmus, head tilting. Bilateral lesions affecting axial and proximal limb muscles
What is the main function of the BG? Input/output? What are the 4 components of the basal ganglia? What is the indirect pathway? Direct pathway? Describe the pathway of dopamine in the basal ganglia and how it affects these pathways.
Voluntary movements and making structural adjustments
Receives cortical input (negative feedback to cortex to modulate movement)
substantia nigra pars compacta
globus pallidus (internus and externus)
subthalamic nucleus
striatum (putamen + caudate)
INdirect=INhibitory (less direct pathway-more steps)
Direct=facilitaes movement
Direct: Striatum inhibits the GPi from inhibiting the thalamus. Then, the thalamus facilitates movement
Indirect: Striatum inhibits the GPe from inhibiting the STN. The STN then stimulates the GPi so it greatly inhibits the thalamus from stimulating movement.
The pars compacta releases dopamine. The direct pathway has a D1 receptor and the independent pathway has a D2 receptor. D1 receptor is stimulatory and D2 is inhibitory. Therefore, dopamine stimulates movement through both pathways.
D1Receptor=D1Rect
substantia pars reticula functions much like the GPi.
What is the presentation of athetosis? Characteristic lesion? Chorea? What is the presentation of dystonia? 2 examples? Presentation of hemiballismus? Lesion? Myoclonus? Example? Associations?
Ath: slow writhing movements, especially in fingers (BG/Caudate/Hunting)
Chorea: Sudden jerky purposeless movements (BG/Caudate/Hunting)
Dystonia: sustained involuntary muscle contractions (writers cramp and sustained eyelid twitch)
Hemiballismus: sudden, wild flailing of 1 arm and may ipsilateral leg (Contralateral Subthalamic nucleus)
Myoclonus: sudden, brief, uncontrolled muscle contraction (jerks, hiccups=metabolic abnormalities such as renal and liver failure)
What is an essential tremor like? When is it worsened? Cause? Treatments? Self treatment? What is an intention tremor like? Lesion? What is a resting tremor like? What alleviates it? Lesion? Another name?
High frequency tremor with sustained posture (outstretched arms)
Worse with movement or when anxious
Familial
Self medicate with EtOH (decr. amplitude of tremor)
Beta blockers and primidone
Slow, zigzag motion when pointing/extending toward a target
Cerebellar dysfunction
Uncontrolled movement of distal appendages at rest
Alleviated by intentional movement
parkinsons
Pill rolling tremor.
What is the histo of parkinsons? pathophys? Symptoms?
Degenerative disorder of CNS Loss of dopaminergic neurons (depigmentation) of substantia nigra pars compacta Lewy bodies (intracellular eosinophillic inclusions-alpha synuclein)
TRAPS
Tremor Rigidity (cogwheel) Akinesia Postural instabililty Shuffling gait
What are the genetics of huntingtons? Symptoms? Labs? Pathophys? MRI?
Auto dom. CAG repeat on chromosome 4.
Onset b/w 20 and 50
Choreiform movements, aggression, depression, dementia
Incr. Dopamine, decr. GABA, Decr. ACh
Neuronal death via NMDA-R binding and glutamate toxicity
Atrophy of caudate nuclei disrupts BG pathways leading to unwanted movement.
Atrophy of caudate w/ ex vacuo dilatation of frontal horns.
What is aphasia? Dysarthria? What are symptoms of Broca aphasia? Location of lesion? Wernicke aphasia? Location? Conduction? Global? Transcortical motor? Transcortical sensory? Mixed transcortical?
Aphasia=higher order inability to speak (language deficit)
dyarthria=motor inability to speak
Broca=nonfluent aphasia with intact comprehension and impaired repetition
(brocas area in inferior frontal gyrus of frontal lobe=language production)
Wernicke=fluent aphasia w/ impaired comprehension and repetition
(Wernickes area is superior temporal gyrus of temporal lobe=language interpretation/analysis)
Conduction=Poor repetition, but fluent speech, intact comprehension (Arcuate fasciculus)
Global=nonfluent aphasia w/o comprehension, poor repetition (arcuate, wernickes, broca)
Transcortical motor=nonfluent aphasia with good comprehension and intact repetition (area around broca)
Transcort. sensory=poor comprehension w/ fluent speech and intact repetition (area around wernickes)
Mixed transcorticals=poor comprehension and influent speech but intact repetition (areas around wernickes and areas around brocas)
What are the symptoms of Kluver Bucy syndrome? Lesion? Association?
Disinhibited behavior (hyperphagia, hypersexuality, hyperorality)
Amygdala (bilateral)
HSV-1
What lesion will result in disinhibition and deficits in concentration, orientation, judgment; reemergence of primitive reflexes?
Frontal lobe
what lesion will result in hemispatial neglect syndrome (agnosia of contralat. side of world)
Non dominant parietal temporal cortex
what lesion will result in Gerstmann syndrome? Symptoms?
agraphia, acalculia, finger agnosia, and left-right disorientation
Dominant parietal temporal cortex
What lesion will result in reduced levels of arousal and wakefullness (coma)?
Reticular activating system (midbrain)
What are the symptoms of wernicke korsakoff? Associations? Lesion?
confusion, opthalmoplegia, ataxia
Memory loss, confabulation, personality changes
Thiamine deficiency and EtOH use
Mammilary bodies (bilateral)
What lesion will result in anterograde amnesia? What does this mean?
Bilateral hippocampus
No new memories
What lesion will cause the eyes to look away from side of lesion?
Paramedian pontine reticular formation (PPRF)
What lesion will cause eyes to look toward lesion?
Frontal eye fields
Where are the water shed zones? When are they damaged? What are the results?
Between ACA/MCA and MCA/PCA.
Severe hypotension
Upper leg/upper arm weakness (ACA/MCA)
Defects in higher order visual processing (MCA/PCA)
Describe the vasculature of the brain.
Vertebral arteries come off the subclavian.
They both give of Posterior inferior cerebellar arteries
They both give off anterior spinal arteries which join together and head down the spinal cord.
They join together to form the basilar artery (at pons)
Just as they join together, they give off ant. inf. cerebellar arteries
The basilar artery travels along the pons giving off pontine branches
At the end of the pons, it gives off Superior Cerebellar arteries
It then splits into two posterior cerebral arteries
The PCAs give off posterior communicating arteries
The interal carotids break off from the common carotid
They give off arteries which anastomose with PComs
They give off anterior cerebral arteries
The ACAs have an anterior communicating artery.
The ICAs give off an anterior choroidal artery
It then becomes the middle cerebral artery
The middle cerebral artery gives off lenticulostriate arteries
Where is the leg located in the homunculus? Arm? Face?
Leg=medial
Arm=less medial
Face=most lateral
What modulates cerebral perfusion? When does this change? What can be done to help in cases of acute cerebral edema? How do panic attacks cause fainting?
PCO2 (incr. PCO2 leads to incr. cerebral blood flow)
In extreme hypoxia (<50mmHg), decr. PO2 will cause perfusion to increase
In acute cerebral edema, hyperventilation can lead to Decr. PCO2 leading to decr. cerebral blood flow
In panic attacks, decr. PCO2 can lead to decr. blood flow leading to fainting
What does CPP equal? What happens if its zero?
Cerebral perfusion pressure=MAP (blood pressure) - ICP (intracranial pressure)
If BP is decr. or ICP is incr., it can reach zero which will result in brain death (no perfusion)
contralateral paralysis-upper limb and face
Contralateral loss of sensation-upper limb and face
Aphasia if in dominant
Hemineglect if in non dominant
Where is the lesion and what stroke caused it?
motor cortex-lateral
sensory cortex-lateral
Temporal lobe
MCA
CL paralysis-LL
CL loss of sens-lower limb
Where is the lesion and what stroke caused it?
Motor cortex-medial
Sensory cortex-medial
ACA
contralateral hemiplegia/hemiparesis
Where is the lesion and what stroke caused it? Cause of stroke?
Striatum, internal capsule
Lenticulostriate
Lacunar infarcts (2nd to unmanaged hypertension)
Contralateral hemiparesis-upper and lower limb
Decr. contralateral proprioception
Ipsilateral hypoglossal dysfunction
Where is the lesion and what stroke caused it? Which side does it often affect? What syndrome does it cause?
Lateral corticospinal tract
Medial lemniscus
Caudal medulla-hypoglossal nerve
ASA
Often bilateral
Medial medullary syndrome: infarct of paramedian branches of ASA and vertebral arteries.
Vomiting, vertigo, nystagmus; decr. pain and temp sensatin from ipsilateral face and CL body; dysphagia/hoarseness; decr. gag reflex; ipsilateral horner syndrome; ataxia, dysmetria
Where is the lesion and what stroke caused it? What syndrome does it cause? Which symptoms are unique to it?
Lateral medulla: vestibular nucl, lateral spinothalamic, spinal trigeminal nucl, nucl ambiguus, sympathetic fibers, inferior cerebellar peduncle
PICA
Lateral medullary (wallenberg) syndrome Nucleus ambiguus effects (dysphagia/hoarseness) are unique to PICA
Don’t PickA horse that can’t eat
vomiting, vertigo, nystagmus.
Paralysis of face
Decr. lacrimation, salivation, taste from anterior 2/3 of tongue
Ipsi decr. pain and temp of face
CL decr. pain and temp of body
Where is the lesion and what stroke caused it? What syndrome does it cause?
Lateral pons: CN nuclei (vestibular nuclei, facial nucleus, spinal trigeminal nucl, cochlear nuclei), symp. fibers
Middle and inferior cerebellar peduncles
AICA
Lateral pontine syndrome
Facial nucleus effects unique to AICA
Contralateral hemianopia with macular sparing
Where is the lesion and what stroke caused it?
Occipital cortex, visual cortex
PCA
Preserved consciousness and blinking, quadriplegia, loss of voluntary facial, mouth, and tongue movements
Locked in syndrome
Where is the lesion and what stroke caused it?
Pons, medulla, lower midbrain, corticospinal and corticobulbar tracts, ocular CN nuclei, PPRF
Basilar
Visual field defects
Where is the lesion and what stroke caused it? Type of lesion?
Aneurysm (saccular) impinges CNs
ACom
CNIII palsy=symptoms?
Where is the lesion and what stroke caused it? Lesion?
Saccular aneurysm
Eye is down and out with ptosis and mydriasis
PCom
What is an aneurysm? What is a berry aneurysm? Where does it usually occur? What are its complications? ASsociations? Risk factors? What is a charcot bouchard microaneurysm? Association? Location?
Abnormal dilation of artery due to weakening of vessel wall
Bifurcations in the circle of willis (ACA and ACom)
Rupture–>SAH or hemorrhagic stroke
Bitemporal hemianopia via compression of optic chiasm
ADPKD, Ehler Danlos
Advanced age, hypertension, smoking, blackness
CHARCOT
Chronic hypertension Small Vessels (BG and thalamus)
What is central post stroke pain syndrome? Pathophys? How common is it?
Neuropathic pain due to thalamic lesions. Initial paresthesias followed in weeks to months by allodynia and dysesthesia.
10% of stroke pts
What causes an epidural hematoma? Presentation/symptoms? Time course? CT scan?
Rupture of middle meningeal artery after fracture of temporal bone.
Lucid interval. Rapid expansion on systemic pressure leading to transtentorial herniation and CNIII palsy
biconvex, hyperdense blood collecction
does not cross suture lines
Cross falx, tentorium
What cuases at subdural hematoma? Time course? What is the bleeding like? Epid? CT?
Rupture of bridging veins
Slow venous bleeding (develops over time)
Elderly, alcoholics, blunt trauma, shaken baby
Crescent shaped hemorrhage
Crosses suture lines
Midline shift
Doe not cross falx, tentorium
What causes a subarachnoid hemorrhage? Time Course? Presentation? Lab findings? Compications?
rupture of an aneurysm or AV malformation
Rapid time course
WHOML
Bloody or yellow spinal tap
Risk of vasospasm due to blood breakdown (not visible on CT=nimodipine)
risk of rebleed (visible on CT)
2-3 days later
What is the usual cause of an intraparenchymal hemorrhage? Other causes? typical location?
systemic hypertension
Amyloid angiopathy, vasculitis, neoplasm
BG and internal capsule
Can be lobar
What is ischemic brain disease/stroke? Time time for damage? Most vulnerable areas? Timetable for imaging? Why is imaging necessary? time table for histology?
Irreversible damage after 5 min. of hypoxia
Hippocampus, neocortex, cerebellum, watershed areas
Noncontrast CT to exclude hemorrhage (before tPA given)
CT detection after 6-24 hrs
Diffusion weighted MRI within 3-30 min.
12-48 hours=red neuron 24-72 hrs=necrosis + neutro 3-5 days=microglia 1-2 weeks=reactive gliosis + vasc. prolif >2 weeks= glial scar
What is hemorrhagic stroke? Causes? Most common site?
Intracerebral bleeding
Hypertension, angicoag, cancer, ischemic stroke followed by reperfusion
BG
