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232 Cards in this Set

  • Front
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A newborn should have:
**symmetric tone and movements.
complete head lag
Reflexic grasp-planter and palmar
alert to sounds, fixates on face and objects
By 2 months an infant should
**Regard object of face attentively
Lift head and shoulders off off bed
Follows past midline
Crying 3hrs/day
A baby should be able to regard objects or face attentively by?
2 months
By 4 months, a baby should
**Good head control in sitting
holds up head and puts weight on forearms
rolls to supine
bears weight on legs in stand
follows objects 180 degrees
coos responsively (vowels)
smiles responsively
A baby should have good head control in sitting by
4 months
A baby starts cooing at what age
4 months
A baby reaches with raking grasp-both hands by
6 months
By 6 months a baby can
***Reach with raking grasp-both hands
Transfer object hand to hand
Roll both directions
No head lag in pull to si
sits with support
Babbles (vowel-consonants
A child sits well alone by
9 months
By 9 months a child
**sits well alone
holds two objects at once
bangs two objects together
grasps pellet with radial-palmer grasp
finger feeds self
plays pat-a-cake
By 12 months a child can
neat pincer grasp of pellet
pulls to stand and cruises
takes a few steps alone
drinks from cup held by another
jargons
By 15 months a child can
drink from a cup
stoops and recovers (>80%)
walks well (>90)
scribbles with crayon (>50)
puts cube in cup
plays ball with examiner
gives and takes a toy
A child should be able to walk independently by
18 months
A child should be able to point to a desired object by
18 months
18 month landmarks include
**Walk well independently
**Point to desired objec
Run (>75%)
climb steps holding hands
throw or cast a ball
stacks 2 cubes (50%)
6 words in addition to mama/dada
feeds self with spoon
By 24 months a child should be able to
**combine 2 words
stack 4-6 cubes
kick a ball
jump with both feet off floor
throws a ball overhand (75%)
points to pictures in a book
remove clothes (>90)
wash and dry hands
put on a hat
use spoon/fork (>90)
A child should be able to combine 2 words by
24 months
By 36 months a child should be able to
**uses 3 word sentances
stack 8 cubes
imitate vertical stroke with crayon
broad jumps
stands on 1 foot for 1-2 seconds
pedal a tricycle
speech is 50% intelligible
uses 5-8 word sentances
knows simple adjectives
puts on tee-shirt and shorts
names a playmate
a child should be using 3 word sentences by
36 months
A child should be asking why, when, how questions by
4 years
By 4 years a child should be able to
**ask questions
name 4 colors
speech fully intelligible
pretend play
relate events
A child should be able to separate from parents for several hours at a time
by 5 years
By 5 years a child should be able to
**separate from parents for several hours a day
balance for 5-10 sec
copy a circle, square, triangle
draw a person
speak in full sentences with mostly correct grammer, lots of quesitons
play well with kids
take turns
follow directions
relate experiences
tell long stories
Are there more neurons or glial cells
More glial cells (10X more)
motor and sensory myelination
begins before birth, not completed until 1st birthday
critical period for vision
till 5 yrs
Gowers maneuver
indication of proximal weakness in children; muscular dystrophy
hypoperfusion from autonomic dystregulation in premature infants causing white matter lesion near ventricle
periventricular leukomalacia,
affects legs the most
hyperreflexia, clonus and spasticity of legs with normal upper body is a sign of what in premature infants?
periventricular leukomalacia
Hypotonic, head lage, no visual tracking, epilepsy, and cherry red spots in eyes are signs of?
Tay Sachs disease (lipid storage disease)
If CSF glucose is low without corresponding lactic acid buildup, diagnosis is
epileptic encephalopathy. Treat with ketogenic diet
multi-organ issues, brain issues, delay and seizures, maternal pattern of inheritance
mitochondrial disorders
Separation of telencephalon is called
Diverticulation
nerve cells migrate to cerebral cortex along
radial glial cells
Anencephaly
failure of brain to develop due to lack of closure of anterior neuropore
Encephalocele
Outpouching of epithelium enclosed by brain tissue through a cranial defect
Spina bifida oculta
failure of posterior neuropore to close
bony defect in vertebral column without dural component.
usually a small bit of hair
meningocele
Dura herniates through bony defect
meningomyelocele
dura and tissue of spinal cord herniate through defect
Rachischisis
spinal cord directly open to air
Arnold Chiari
posterior fossa lesion. Formed by herniation of cerebellar tonsils into the foramen magnum
---psudeomicropolygyria
----hydrocephalus (occlusion of foramen magendi, lushka by cerebellar tonsils
----tonsilar gliosis
----flattening of pons
----breaking of tectum
----basicranial bone abnormalities
----lumbar meningomyelocele
Dandy-Walker
Posterior fossa leshion
vermal hypoplasia in cerebellum (usually inferior vermus)
outpouching of 4th ventricle ---> hydrocephalus
Arrhinencephaly
failure of olfactory development usually as a part of Kallman's syndrome
Holoncephaly
failure of midbrain fusion
1) Lobar (partial division of 2 hemispheres
Agenesis of corpus callosum
can cause mental retardation but is also assymptomatic in many patients
Lissencephaly
absence of gyri of the brain
Pachygyria
a disturbance of neuronal migration that occurs later, resulting in flattened and enlarged gyri, usually 4 instead of 6 layers
Micropolygyria
defect in neuronal migration later than pachygyria ---> 4 layers, small, mulitple gyri.
multicystic encepthalopathy
multi-ischemis insults during gestation ---> liquefactive necrosis
Hydrencephaly
complete occlusion of cartoid arteries, no brain tissue grows and you just get a sac of water
Ulegyria
perinatal vascular injury (thined out, glyotic gyri)...usually due to ischemic injury
Status Marmoratus
premature mylination in deep grey structures...marbled area in basal ganglia
Syringomyelia
Hole in spinal cord, can be developmental (arnold chiari) or post-traumatic.
WADA procedure
Assesses where dominant language side of the brain is located
Anomia
Difficulty recalling names of objects
Dysarthria
Cant speak bc muscles don't work
Pure word deafness
Sensory disconnection from language processing area
Left primary visual cortex plus splenium of corpus callosum lesion
alexia without agraphia
right homonymous hemianopia
conduction aphasia
lesion to arcuate fasciculous
myelitis
inflammation of spinal cord
Modes of entry of CNS infection
- Hematogenous (blood brain barrier, sometimes via circumventricular organs)
- Neural Route
- Continuous spread
- Direct inoculation
LP:
High pressure
high neutrophils
low glucose
high protein
Bacterial meningitis
Lp:
High pressure
high WBC (leukocytes)
normal protein and glucose
Viral meningitis
Increased intercranial pressure
focal deficits that progress
signs of systemic infection
suppuration surrounded by fibrous capsule
abscess
Histology of HSV encephalitis
perivascular lymphocytic cuffing
microglial profliferation
intranuclear inclusions
Perivascular lymphocytic cuffing
HSV encephalitis
Confusion and behavioral abnormalities along with fever point to
Encephalitis
When do you do a CT before an LP with suspected meningitis
Abnormal focal neurologic exam
elderly, h/o CNS disease, immunocompromised, seizures
What virus is found in all MS patients
EBV
Current MS hypothesis
T cells enter into CNS, Increase expression of adhesion molecules, matrix metalloproteinases, proinflammatory cytokines. This aids migration of immune cells, and you get an autoimmune response against myelin
Focal weakness, numbness, tingling, loss or blurry vision, spinal cord syndromes (bladder disfunciton, paraparesis
MS
What test do you use to evaluate MS
Gd-MRI
Acute Disseminated Encephalomyelitis
Neurologic symptoms develop over a few days, associated iwth a viral infection or vaccination.
Widespread CNS involvement
Headahc
Raccoon signs/Battles signs, CSF rhinorrhea/CSF Otorrhea area sign of
Basilar skull fracture
With diffuse axonal injury, CT may be? It is caused by?
normal or small hemorrhage;
shear force---> COMA
CPP=
MAP-ICP
(Cranial profusion pressure = mean arterial pressure - ICP)
According to the Monro-Kellie doctrine, additional brain volume causes
decreased blood, decreased CSF
As blood flow decreases, the brain does what?
extracts oxygen more efficiently until it fails
Secondary injury cascade causes what to happen to lactate, ATP, gluatmate, Adenosine
Decreased ATP due to Anaerobic glycolysis
Increased Glutamate --> increased calcium which leads to Free radicals, mitocondrial swelling, via mitochondrial transition pore
Increased Lactate
Vasculitis and hemhorrages in brain
Acute Pyogenic meningitis
Perivascular lymphocytic infiltrate,
Neuronophagia
microglial nodule
eosinophilic nuclear inclusion
acute lymphocytic meningitis
what causes chronic meningitis?
what is its gross presentation?
basilar exudate; tb, shyphilis,
Obliterative endarteritis with intimal hyperplasia and Giant cells
Chronic meningitis
White Brain, what else do you see?
Cryptococcal meningitis
bubbles of damage
pseudohyphae are found in what
Candida Albicans
hyphae
found in aspergillus, looks sea sponge
What is found in brain abscess having to do with blood vessles?
reticulin
Microglial stab cells
HIV (and tertiary sphyilis)
What are the four syndroms arising directly from HIVq
acute meningitis or encephalitis
subacute encephalistis
vacuolar myelopathy
peripheral neuropathy
multinucleated giant cell can be found with what virus
HIV
Taxoplasmosis
HIV, necrotizing cerebritis, Mulberry appearance of Toxo Cyst.
Crutzfelt-Jakob disease histology
white bubbles cause by protein accumulations
spongiform transformation is found in
Prion disease
histopathologic signs of MS
perivascular
oligodendrocytes are diminished
myelin loss
axons spared
macrophage formation with sudanophilic breakdown
concentric spread
Devic's Disease gross symptoms
plaques on spinal cord due to Aquoporin IV gene defect
Baro's Concentric Schlerosis
Concentric lesions.
ADEM
multi-focal perivenular demyelination that is reversible, after a vaccine or a virus
overcorrection of hyponatremia causes
central pontine myelinolysis
Progressive multifocal leukoencephalopathy is different from MS how? Histologically?
no sharp lines of demarcation of white matter degradation.
usually in immunocompromised people.
Histologically: bizarre astrocytes and decreased numbers of olgliodendrocytes
sulfer molecules in macrophages
metachromic leuokodystrophy
intra-axial vs extra-axial
Intra: origin in brain or spinal cord, small or no dural contact
extra: origin in meninges or skull, broad dural base.
Diffusion weighted MRI can tell you?
If it is an abscess bc pus has high viscosity so will appear brighter
Fever, back pain, radicular pain
spinal epidural abscess, rim enhancing epidural fluid.
multifocal lesions seen
MS (young patient), Metastasis or small vessel ischemic disease in older patients.
where do you see MS plaques?
Corpus Callosum
Middle Cerebellar Peduncle
Temporal and Occipital WM
Optic Neuritis
Cord demylination is usually found in the
cervical part of the cord
FLAIR shows?
Gd shows?
FLAIR = all plaques
Gd = acute plaques
The aging brain shows
Small Vessel ischemic WM disease
Atrophy of frontal lobes, thalamus, cerebellum
Decreased Cerebral Blood Flow/metabolism
Hypercellularity can be assessed through
MR spectroscopy (increased choline - myelin breakdaown - and increased NAA (neuronal and axonal marker)
Increased Lactate bc of necrosis
MR Perfusion image for brain tumers shows
increased cerebral blood flow at site of tumor
Capillary permeability of brain tumors can be seen on
contrast enhanced MRI
Glioblastoma multiforme spreads via
WM tracks
Metastases are usually found where
GM/WM junction
PET show what?
SPECT?
PET = glucose
SPECT = blood flow
most common cause of epilepsy
medial temporal schlerosis
neoplasm
medial temporal schlerosis
hippocampal neuronal loss and gliosis
risk factors: provoked generalized seizure, prolonged febrile seizure
Ictal seizure phase sees what glucose activity, blood flow
Increased.
decreased post-ictal
are high or low grade tumors a more likely cause of seizures
low grade
what is the name of the parasitic pork tapeworm?
Neurocysticercosis
Wernicke's encephalopathy has what gross findings
mammilary and hypothalamus lesions that look hemhorragic but really are just an increased proliferation of vessels
confabulations associated with Korakoffs is found where?
Dorsomedial thalamus
Loss of vermal tissue in cerebellum can result from?
This would be seen histologically as what?
EtOH
Phenytoin
Loss of purkinje cells and atrophy of the molecular layer
Hepatic encephalopathy results from?
What is the histological hallmark?
increased ammonia levels which cause WM swelling
Alzheimer type II astrocytes
VIT B12 deficiency causes what neurological condition?
degeneration of axons and demyelination of dorsolateral regions of spinal cord, usually sparing anterior columns
Spongy demyelination
Grade II astrocytoma: histological features
poorly defined
infiltrative
clumping of astrocytes to form satellites around neurons
Enlarged WM, does not enhance on MRI
Grade III astrocytoma: pathology
hypercellularity, more mitotic figures, pleomorphism
Glioblastoma Multiformi:
pathology
pseudopalisading necrosis
appears hemhorragic and cystic
HISTO: hyperchiamatic nuclei
endothelial proliferations (blood vessles)
Pseudopalisading necrosis is seen in
Glioblastoma multiformi
Rosenthal fibers are sign of?
pilocystic astrocytoma
Pilocytic astrocytoma has what kind of cells?
Rosenthal fibers (eosinophilic bodies formed in astrocyte processes)
and protoplasmic astrocystes (bipolar cells with hair like processes
characteristics of oligodendroglioma
well circumscribed, focally hemhorragic, calcification
HISTO: fried egg like cells
Ependymoma: pathology
4th ventricle, presents with hydrocephalus
spinal cord in middle age
solid or papillary masses
Perivascular pseudorosettes
Perivascular pseudorosettes
Ependymoma
Choroid plexus papilloma is found where?
children - lateral ventricles
adults - fourth ventricle
Medulloblastoma:
Location
pathology
Vermis of cerebellum
Disseminate through CSF
Microscopic: densely cellular
pleomorphic nuclei, Homer Wright Rosettes
Homer Wright Rosettes
Medulloblastoma
Meningioma:
Location
Pathology
From arachnoid cap cells
Location: Convexities, Falx Cerebri, Lesser wing of sphenoid, olfactory groove
HISTO: Psammoma bodies
Metastases:
Most are?
From where?
Carcinomas
Lung, breast, Skin, kidney, gastrointestinal
NEVER prostate
What is carcinomatous meningitis
irritation of meninges from tumor
A Na channel blocker extends or limits the refractory period
prolonges
Gingival hyperplasia is a sign of what toxicity
phenytoin
Absense seizures have medications that work on what type of receptor
Calcium
What disease do you need to rule out when treating ICH bc it has a different treatment
venous sinus thrombosis (use an anticoagulant)
Most common ICH locations
Putamen and internal capsule
thalamus
WM of temporal, parietal, frontal lobes
cerebellar hemisphere
pons
what is the most common cause of ICH in people over 60
Amyloid angiopathy
Most common cause of subarachnoid hemhorrage
Aneursyms
Complication of subarachnoid bleed
vasospasms, 3-13 days after incident
Low grade astrocytoma treatment
gross surgical resection, no radiation
Anaplastic astrocytoma treatment
GSR and post-op radiation
Glioblastoma multiformi treatment
GSR, radiation, chemo
chemo choice drug for brain tumors
temozolomide
Oligodedroglioma prognosis determined how
whether it has a 1p or 19q deletion, responds to chemo
most meningiomas are
typical and low grad
treatment of meningioma
total surgical resection and xrt or radiosurgery
little success with chemo after reoccurence
treatment for CNS lymphoma
high dose methaltrexate and leukovorin
treatment for cerebellar astrocytoma
surgical resection, no adjuvant therapy
Pontine glioma is
deadly childhood tumor, black pons
medulloblastoma
4th ventricle, seeds,
treatment is surgery, craniospinal XRT, and cheo
motor-oil like fluid
craniopharyngioma
occlusion of large arteries is what kind of stroke? what causes it
cardioembolic stroke, caused by atrial fibrillation, valvular heart disease
small vessel disease is caused by?
hypertension, we saw in corpus callosum
large vessel disease is caused by
cholesterol, occlusion of vessles
transient sensory aphasia is
Wernickes plus repetition
transient motor aphasia is
Brocas plus repetition
conduct aphasia results from a lesion is the
arcuate faciculus. cannot repeat
eyes deviate toward or away from lesion in a stroke
toward lesion
in spinal cord infarction, you usually have preserved
position and vibration sense
small vessel disease is caused by?
hypertension, we saw in corpus callosum
large vessel disease is caused by
cholesterol, occlusion of vessles
you can give tpa in 3-4.5 hour range if
no hypodensity greater than 1/3 MCA territory
no diabetes
no warfarin
not over 80
transient sensory aphasia is
Wernickes plus repetition
What is the best treatment for non-afib stroke?
anti-platlets such as aspirin
transient motor aphasia is
Brocas plus repetition
best choice for afib stroke
anticoagulants
conduct aphasia results from a lesion is the
arcuate faciculus. cannot repeat
eyes deviate toward or away from lesion in a stroke
toward lesion
in spinal cord infarction, you usually have preserved
position and vibration sense
you can give tpa in 3-4.5 hour range if
no hypodensity greater than 1/3 MCA territory
no diabetes
no warfarin
not over 80
What is the best treatment for non-afib stroke?
anti-platlets such as aspirin
best choice for afib stroke
anticoagulants
small vessel disease is caused by?
hypertension, we saw in corpus callosum
large vessel disease is caused by
cholesterol, occlusion of vessles
transient sensory aphasia is
Wernickes plus repetition
transient motor aphasia is
Brocas plus repetition
conduct aphasia results from a lesion is the
arcuate faciculus. cannot repeat
eyes deviate toward or away from lesion in a stroke
toward lesion
in spinal cord infarction, you usually have preserved
position and vibration sense
you can give tpa in 3-4.5 hour range if
no hypodensity greater than 1/3 MCA territory
no diabetes
no warfarin
not over 80
What is the best treatment for non-afib stroke?
anti-platlets such as aspirin
best choice for afib stroke
anticoagulants
carotid artery repair if
>70% occlusion on the same side of the stroke
What increases risk for alzheimers
ApoE4 allels.
pathological hallmarks of dementia
AD-amyloid plaques and tau neurfibillar tangels
DLS-Lewy bodies
VaD large or small vessle infarcts
FTD-tau tangles, pick bodies, intranuclear inclusions
vascular dementia hallmarks
step wise progression
executive dysfunction, apathy, depression
Lewy bodies are
Alpha synaclein in cortex
episodic memory in teh
medial temporal lobe, diencephalon
semantic memory in the
temporoparietal association cortex
procedural memory in the
basal ganglia
seratonin and sleep
promotes sleep
raphe neurons are active/inactive during REM
inactive during REM
nonadrenergic cells and sleep
promote arousal in the nucleus cerculleus.
Pontine lesions do what to sleep
REM without atonia and dream enhancement
synchronized means?
low frequency and high amplitude
cholinergic system and sleep
promotes REM
muscarinic antagonists - supress REM
synchronized when? unsynchronized when?
synchronized during NREM,
unsynchronized during REM, awake
what causes narcolepsy
hypocretin/orexin degeneration of cells
Encephalopathy clinical features
delirium
autonomic instability
abnormal movement (myoclonus, tremor, asterixis)
dysarthria
focal neurological signs and seizures
sodium imbalance
less than 127, greater than 150
glucose
greater than 450 or less than 40
BUN range
>60 is a problem
apathy, fatigue, inattention, irritability
B12 deficiency
degeneration of the lateral and dorsal columns
ataxia
mental deterioration
Localization of conciousness, place key for arousal
ascending reticular activating system
in paramedian mesopontine tegmentum
small reactive pupils
diencephalon
hyperventilation
midbrain
For coma to be present you need
bilateral cortical lesion
upper brainstem lesion
If you have a blown pupil
CN III; due to lateral uncal herniation
pinpoint pupils
pontine hemhorrage
Rubrospinal
arm flexion
two types of edema
vasogenic: damage from blood-brain barrier
cytotoxic: at cellular level
spongiform encephalopathy
prion disease
Hirano body
intranuclear inclusion of cytoskeleton breakdown product
Neurofibrillary tangles contain
Hyperphosphorylated Tau
senile plaques
extracellular accumulations of B-amyloid protein
Granulovascular degneration
pathonumonic for AD
trisomy 21 pathology
small brain with abnormal gyral pattern
decreased neuronal populations
abnormality of neuronal structure
what genes have been linked with early onset alzheimers
Precillin genes
in picks disease you see
pick bodies
balloon cells
where do you see lewy bodies
lewy body dementia
parkinsons disease
vertical gaze palsy,
resistant to parkinsons meds
instability
supranuclear palsey with neurofibrillary tangles in many subcortical structures...tangles instead of lewy bodies
In ALS you see
atrophy of anterior spinal roots
loss of lateral corticospainl tract degeneration
olivopontocerebellar atrophy
swollen purkinje cells - torpedos
loss of white matter in cerebellum
parkinsons symptoms
ataxia first in legs and then in arms/hands and bulbar musculature
whats the difference between freidreichs ataxia and vit b12 deficiency
no vaculated structures in friedreichs ataxia