Download History of the Nervous System Cells of the Nervous System

History of the Nervous System
Cells of the Nervous System

2 Types:
o Neurons
 Cannot divide; however, they have the capacity to undifferentiated
and then divide, becoming tumors.
Classification of Neurons
Multipolar
Many processes
Common for motor
neurons
Unipolar
Common for sensory
neurons of PNS
Bipolar
Found in sense
organs
One process from
axon to soma
Axon and dendrite
make up two
processes
o Glia (means glue)
 Can divide!
 May also become tumors as well
 6 Types of Glia:
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Ependymal Cells:
 Line the ventricles
 Have cilia
Anaxonic
Can’t tell axon and
dendrites apart
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Microglia:
 Specialized immune cell… will proliferate if pathogen is
present
 Have phagocytic properties
Astrocytes:
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Most common in CNS
Mediator b/w blood and
the neuron… decides
what the neuron gets
from the blood
This helps form the
Blood Brain Barrier!
Also, repair damaged tissue
o Can lead to gliosis = scar formation from massive
proliferation of astrocytes
o
white area in brain
Two types:
o Fibrous  associated w/ axons
o
fibrous astrocytes
o Protoplasmic  associated w/ soma
protoplasmic
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Oligiodendrocytes
 Myelinate segments of several axons
 In CNS
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Schwann Cell
 In PNS
 Myelinate segment of one axon
 Assist in axon repair by acting like a tunnel for it to grow
back through
Satellite Cell
 In ganglia b/c associated w/ cell bodies
 Regulate environ and provide nutrients to soma
o Glia Limitans
 Purpose is to regulate movement of molecules into and out of the
brain
 External:
 Outermost layer of neural tissue (b/w pia and brain)
 Formed by the feet of the astrocytes
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Internal:
 Also formed by astrocyte foot processes
 B/w brain and ventricular CSF
o Ependymal cells associated w/ it
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o Myelin
 A lipoprotein made up of either schwann or oligiodendrocyte
membrane
 Increases the speed of the AP
o Neuropil
 Synaptically dense region containing dendrites, glia and
unmyelinated axons
Neuron Histology

Soma (cell body):
o Contains same organelles as normal cells…
 Nucleus (nucleolus = all the dark spots in pic. below)
 RER (Nissl bodies)
 They give off the gray color in gray matter
 Golgi, mitochondria, lysosomes
 Storage vesicles
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May contain lipofuscin, which is brown/yellow pigment
of fatty residues left over from lysosomal digestion
 Result of aging
Axon Hillock (AH)
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clear area (b/c no RER) that signifies we are going into
an axon
This is where membrane potentials are summated
before entering the axon
Dendrites
o Increase neuron surface area and allow for more synapses
o Shape is formed by actin filament
o
o Dendritic spines (DS) are dynamic protrusions at the synapse.
 They form as you gain new experiences… trippy…
 B/c of this learning is associated w/ formation of DS.
 Alcohol reverses this problem and thus Fetal Alcohol
Syndrome causes problems
Axon
o One axon per one neuron!
o Purpose is to transmit action potential to an effector cell (every cell
except a neuron) or a neuron.
o
o The cytoskeleton in axons create the Axoplasmic Flow:
Anterograde Axoplasmic Transport
Retrograde Axoplasmic
Transport
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Cell body  axon  synaptic terminal
Synaptic terminal  axon  cell body
Kinesin
Dynein
Brings Neurotransmitters to synapse
How rabies gets into CNS… picks up
the toxin and carries it to the cell
body then to the CNS. This is why
there is a short window of time in
order to deal w/ it.
Axon Terminal (Synaptic Boutons)
o Site of Neurotransmitter (NT) release
o Has synaptic vesicles (w/ NT) and mitochondria
o
o Chemical Synapse:
 Presynaptic membrane, synaptic cleft, and postsynaptic
membrane
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o Electrical Synapse:
 Ions flow through gap junctions
o Types of Synapses
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o
PNS – Ganglia
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CT of PNS goes epineurium  perineurium  endoneurium
OVERALL
 Afferent = peripheral  central
o sensory
 Efferent = central  peripheral (exits the CNS)
o motor
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Gray matter = region of cell bodies, unmyelinated axons and dendrites
o Gray due to Nissl bodies (RER)
White matter = region of axons, myelinated and unmyelinated axons
o White b/c of the phospholipids from the cell membranes of glia
(myelin sheath)
In brain  white matter is deep and gray is superficial
In spinal cord  white matter is superficial and gray is deep
Oligiodendrocytes = CNS
Schwann = PNS
Myelinated neurons = very large diameter, faster impulse
Unmyelinated neurons = very small diameter, slower impulse
Group of Axons
Group of Cell Bodies
Neural Tube Defects
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CNS
PNS
Tract
Nucleus
Nerve
Ganglion
CNS Malformations
Occur when a part of the neural tube fails to close OR a part of the tube can
reopen after it has fully closed
Inadequate folate during initial weeks of gestation is a huge risk factor for
these defects!
Diagnosis base on ultrasound and maternal blood screening of elevated
alpha-fetoprotein
Spina Bifida
Occulta
Asymptomatic bony
defect
Meningocele
-Meninges and CSF
protrude out through
spina bifida defect
Note: occult spinal
dysraphism (OSD) is
hair/birthmark over
the spina bifida
occulta defect and
sometimes can also
have protrusion of
meninges/spinal
cord
Neural Tube Defects
Myelomeningocele
Encephalocele
-Spinal cord, meninges,
and CSF protrude out
through spina bifida
defect
-Most common form
and usually happens in
the lumbosacral region
-Present w/ problems
w/ lower extremity
motor skills and
bowel/bladder control
-Malformation of cranium
causing brain to protrude
-Usually in the posterior fossa
or through the cribiform plate
in the anterior fossa (may be
mistaken for a nasal glioma)
Anencephaly
-Malformation of anterior end of
neural tube
-Absence of brain and calvarium
-The forebrain does not develop at day
28.
-All that is there is the area
cerebrovasculosa (flattened remnant
of disorganized brain tissue)
Note: Spina bifida (aka split spine) is a broad category that encompasses spina bifida occult, occult spinal dysraphism,
meningocele, and myelomeningocele.
Forebrain Anomalies

Abnormalities in generation and migration of neurons = forebrain malformations
o Either effects part of the forebrain or the whole thing
Megalencephaly Microencephaly
-Brain is abnormally
large
-Brain is abnormally
small
-More common than
megalencephaly
-Can be caused by
chromosome
abnormalities, fetal
alcohol syndrome,
or HIV-1 infection
Lissencephaly
-Few or no gyri (agyria)
Two Patterns:
Smooth surface
 Mutations w/
signaling for
migration and
cytoskeleton
motor proteins
 Results in
inability of
neuroblasts to
migrate
Rough/cobblestoned
surface
 Mutations that
disrupt the stop
signal for
migration
Forebrain Anomalies
Polymicrogyria
-Small, numerous gyri
-Entrapment of
meningeal tissue in the
4 layers of gray matter
leads to an irregular
cortical surface
Neuronal
Heterotopias
Holoprosencephaly
Agenesis of
corpus callosum
-Migrational
disorders
associated w/
epilepsy
-Collections of
neurons in the
wrong places
along
migrational
pathways
-Commonly
found along the
ventricular
surface
-Periventricular
heterotopias =
mut. in filamin A
(responsible for
creating
meshwork of
filaments)
-Incomplete separation of
cerebral hemispheres
-Result in midline facial
abnormalities (cyclopia)
-Arrhin-encephaly = absence
of CN 1
-Associated w/ trisomy 13
-Common
-absence of corpus
callosum
-Batwing deformity =
misshapen lateral
ventricles
-May be either
asymptomatic or lead
to mental retardation
Posterior Fossa Anomalies
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Malformations that affect the brainstem and the cerebellum
Dandy-Walker Malformation
-Enlarged posterior fossa
-Cerebellar vermis is absent (associated
w/ posture and locomotion)
-Large midline cyst lined w/ ependymal
and contiguous w/ leptomeninges
represents the 4th ventricle and replaces
the cerebellar vermis
Posterior Fossa Abnormalities
Chiari Type II (Arnold-Chiari)
-Small posterior fossa, misshapen midline cerebellum,
and downward extension of vermis through foramen
magnum
-Usually also has hydrocephalus and lumbar
myelomeningocele
Chiari Type I
-Low cerebellar tonsils extend into
vertebral canal
Syringomyelia
Hydromyelia
-Cystic cavities that occur around the central canal that is NOT lined w/
ependymal cells
-Associated w/ Chiari I, intraspinal tumors, or traumatic injury
-Dilation of the central canal of the spinal cord that is lined w/ ependymal
cells
-Sometimes this dilation can connect w/ the fourth ventricle
-Called syringobulbia if cavity extends to the brainstem
Note: both of these cause a syrinx (fluid filled cavity in spinal cord) and result in the same symptoms  isolated loss of pain
and temperature sensation in the upper extremities b/c anterolateral spinal tract can’t cross the ventral commissure in the
cervical area
Ataxia Telangectasia
Sturge-Weber Syndrome
-Autosomal recessive
-Beginning in early childhood, loss of full control
of body movements (ataxia) and subsequent
development of dilation of capillaries
(telangiectasia) in the conjunctiva and eye. Also,
immunodeficient.
-Mutated ATM gene on chromosome 11q22-q23
 kinase responsible for cellular response to
dsDNA breaks… they continue to replicate
damaged DNA
-Abnormalities in cerebellum (loss of Purkinje
and granule cells)
-Degeneration of dorsal columns,
spinocerebellar tracts, anterior horn cells, and
peripheral neuropathy
Clinical:
-Very progressive, early death
-Initial recurrent sinopulmonary infections and
unsteady walking
-Rare congenital disorder
-Venous angiomatous masses in cortical
leptomeninges w/ ipsilateral facial port wine
nevi
 Basically, malformation of the veins that
drain the brain
-Associated w/ mental retardation, seizures,
hemiplegia
Tuberous Sclerosis
-Autosomal dominant  1/6000 births
-Hamartomas (benign neoplasm that represents
tissue of origin)
 Take form of cortical tubers (abnormal
development of brain)
o Cause epilepsy
 And subependymal nodules
o Subependymal giant cell
astrocytomas
-Associated w/ benign neoplasms in other
organs of the body (liver, kidney, pancreas, lung,
heart)
-TSC1  encodes hamartin
-TSC2  encodes tuberin
-Hamartin and tuberin bind  inhibit mTOR
kinase (key regulator in protein synthesis)
-Later  difficulty talking and moving eyes
-Usually develop T-cell leukemias
Metabolic Diseases of the Nervous System
Neuronal Storage Diseases
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Autosomal recessive  deficiency of a specific enzyme for  catabolism of sphingolipids, mucopolysaccharides, or
mucolipids  causes accumulation of the substrate for deficient enzyme in lysosomes of neurons  neuronal death
If occurs in cortical neurons  loss of cognitive function and possibly seizures
Neuronal Storage Diseases
Neuronal Ceroid Lipofuscinoses
Tay-Sachs Disease
Accumulation of lipofuscin
Accumulation of Gm2 gangliosides
Neuronal dysfunction  blindness, mental and motor deterioration, and
seizures
Def. in hexosaminidase A
Characterized by age of onset or pattern of inclusion on electron
microscopy
Infantile  INCL
Late Infantile  LINCL
Juvenile  JNCL
Adult  ANCL  Kuf dz
Leukodystrophies
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Autosomal recessive  Myelin abnormalities  w/ synthesis or turnover  causes progressive degeneration of white
matter
o Adrenoleukodystrophy is x-linked!!
Do NOT have neuronal storage defects
If problem in white matter  deterioration in motor skills, spasticity, hypotonia, or ataxia
Krabbe Disease
Leukodystrophies
Metachromatic Leukodystrophy
Adrenoleukodystrophy
Autosomal recessive
Autosomal recessive
X-linked
Definiciency of galactocerebroside betagalactosidase (galactosylceramidase)  does
catabolism of galactocerebroside to  ceramide
and galactose
Deficiency of arysulfatase A… a lysosomal
enzyme  accumulation of sulfatide
(cerebroside sulfate)
Progressive dz w/ symptoms of myelin loss from
the CNS and PNS and adrenal insufficiency
(atrophy of adrenal cortex)
Distal end of chromosome 22q
ALD gene on chromosome X (g28)  ATPbinding cassette transporter ABCD1
Chromosome 14q31
Excess galactocerebroside  becomes
galactosylsphingosine  cytotoxic compound
that causes oligodendrocyte injury
Clinical
Motor stiffness and weakness
Gradual feeding difficulties
Rapidly progressive  survival beyond 2 y.o.
uncommon
Clinical
Late infantile form  most common
Juvenile form
 Both child forms present w/
progressive motor symptoms  death
in 5-10 years
Adult form
 Psychiatric/cognitive symptoms then
motor symptoms
Inability to catabolize very long chain fatty acids
in peroxisomes  elevated VLCFA in blood
Clinical
Earlier onset  more rapid course
 Child w/ neurological symptoms and
adrenal insufficiency  rapidly
progressive and fatal
Later onset  more protracted
 Peripheral n. involvement  slowly
progressive
Mitochondrial Encephalomyopathies
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Problem w/ oxidative phosphorylation  can’t produce ATP  mutations in mitochondrial DNA  involves gray
matter (CNS) and skeletal muscle
Usually presents as muscles diseases
Mitochondrial Encephalomyopathy,
Lactic Acidosis, and Strokelike
Episodes (MELAS)
Mitochondrial Encephalomyopathies
Myoclonic Epilepsy and Ragged Red
Fibers (MERRF)
Most common type!
Maternally transmitted
Mutation in tRNAs
Mutation in tRNAs  diff. from MELAS
Recurrent episodes of everything it says in the
name + muscle weakness
Myoclonus  seizure disorder w/ myopathy
Areas of infarction w/ vascular proliferation and
focal calcification
Leigh Syndrome (Subacute
Necrotizing Encephalopathy)
Early childhood dz of  Lactic academia, lack of
psychomotor development, feeding problems,
seuizures, extra-ocular palsies, and weakness w/
hypotonia
Death w/in 1 to 2 years
Ataxia  w/ neuronal loss from cerebellum
system (inferior olive, cerebellar cortex, and
deep nuclei)
Mutations mitochondrial genome 
components for oxidative phosphorylation and
tRNAs
Acquired Metabolic Diseases
Thiamine (Vit. B1) Disorder
Beriberi  cardiac failure
Wernicke encephalopathy 
Psychotic symptoms or
ophthalmoplegia w/ sudden onset
Korsakoff syndrome  memory
disturbances
Vitamin B12 Deficiency
Anemia  can be the cause of
neurological symptoms 
numbness, tingling, ataxia in lower
extremities  can progress to
spastic weakness and complete
paraplegia
Hypoglycemia
Low blood glucose  not good b/c
glucose is the fuel for the brain
Pyramidal neurons, hippocampus,
and purkinje cells are especially
sensitive to this
Hyperglycemia
Most commonly found in
inadequately controlled diabetes
mellitus
Associated w/ ketoacidosis or
hyperosmolar coma
Paraplegia usually the only thing
that cannot be recovered
Wernicke-Korsakoff syndrome 
usually used b/c the two
syndromes are closely linked
-Result of chronic alcoholism
Toxic Disorders
Carbon Monoxide
Methanol
Hypoxia from altered oxygen-carrying capacity
of hemoglobin
Usually affects the retina  degeneration of
retinal ganglion cells  blindness
Injury to neurons of layers 3 and 5 of the
cerebral cortex  Sommer sector of
hippocampus and purkinje cells
Severe  bilateral putamenal necrosis and focal
white-matter necrosis
Bilateral necrosis of the globus pallidus
Ethanol
Chronic alcohol abuse  Cerebellar dysfunction
 truncal ataxia, unsteady gait, nystagmus
Lysosomal Storage Diseases
 Lysosomal enzymes (acid hydrolases)  synthesized in ER  transported to golgi  post-translation modifications 
attachment of mannose-6-phosphate  lysosomal enzymes w/ mannose-6-P pinch of golgi in a vesicle
 Lysosomal enzymes break down things from autophagy (metabolic turnover of intracellular organelles) of heterophagy
(stuff acquired from outside the cells by phagocytosis)
 Lysosomal storage diseases are a deficiency in a lysosomal enzyme  leads to build up of insoluble metabolite w/in
lysosome  lysosome enlarges w/ this stuff
Tay Sachs Dz
Hexosaminidase A (alpha subunit)
Gm2 gangliosidoses
Morphology
-hexosaminidase A is absent in all
tissue  Gm2 gangliosidoses
accumulations every where  mostly
in neurons of CNS and ANS and retina
Lysosomal Storage Diseases
Neimann-Pick Dz types A
Gaucher Dz
and B
Inherited def. in sphingomyelinase
 accum. of lysosomal
sphingomyelin (usually in
mononuclear phagocyte system)
Chromosome 11p15.4
Type A
-Severe infantile form
-Extensive neurologic involvement
-Visceral accumulations of
sphingomyelin
-Progressive wasting and early
death w/in 3 years of life
-Missense mut.  almost complete
deficiency of sphingomyelinase
-Infants w/ big belly 
hepatosplenomegaly
-Progressive deterioration of
psychomotor function
Autosomal recessive  mut. in
glucocerebrosidase (cleaves
glucose from ceramide)  accum.
of glucocerebroside in phagocytes
and CNS
Pathology from accumulations and
activation of MO’s  secretion of
IL-1, IL-6 and TNF
3 Subtypes
-Type 1, Chronic nonneuronopathic form
 Most common
 Glucocerebrosides only in
mononuclear phagocytes
 Splenic and skeletal
involements… NO brain
 Detectable enzyme
 Jews
Mucopolysachharidoses
Autosomal recessive  def. in
lysosomal enzymes that degrade
mucopolysaccharides
(glycosaminoglycans)
 Hunter syndrome is an Xlinked recessive trait
Glycosaminoglycans include:
 Dermatan sulfate,
heparan sulfate, keratan
sulface, and chondroitin
sulfate
Mucopolysaccharides are a part of
proteoglycans  abundant in
ground substance of connective
tissue
Accumulations of
mucopolysaccharides are found in
Type B
-Organomegaly but NO CNS
involvement
Morphology
-“Foam cells”
-Found in spleen (massive
enlargement), liver, lymph nodes,
bone marrow, tonsils, GI tract, and
lung
-In brain  gyri shrunken and sulci
widened  diffuse neuronal
involvement
-Retinal cherry-red spot seen here
too
Clinical
-Symptoms at 6 months old
-Relentless motor and mental
deterioration
-Cherry-red spot in macula of eye
-Death at 2-3 y.o.
Other Gm2 gangliosidosis
-Sandhoff dz  beta subunit defect
-Gm2 activator deficiency
-Same clinical manisfestations as TaySachs
-Type 2, Acute neuronopathic
 Infantile acute cerebral
pattern
 No detectable enzyme
 Splenomegaly but mostly
CNS involvement
 No Jews
-Type 3
 Intermediate b/w type 1
and 2
 Systemic involvement like
type 1, but progressive
CNS like type 2
Morphology
-Spleen, liver, bone marrow, lymph
nodes, tonsils, thymus and Peyer’s
patch
mononuclear phagocytic cells,
endothelial cells, smooth muscle
cells and fibroblasts.
 Usually in the spleen,
liver, bone marrow,
lymph nodes, blood
vessels, and heart
Clinical
-Hepatosplenomegaly
-Skeletal deformities
-Valvular lesions
-Subendothelial arterial deposits
 myocardial ischemia 
myocardial infarction and cardiac
decompensation  death
MPS 1  Hurler syndrome
 Def. in alpha-1iduronidase
 Very severe, affects
children
MPS 2  Hunter syndrome
 X-linked
 Absence of corneal
clouding and milder
clinical course
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Tay Sachs and Niemann-Pick dz are both common among Ashkenazi Jews
Peripheral Nerve Tumors
Tumors of the peripheral nerves can arise from Schwann cells, perineurial cells, and fibroblasts
Schwannoma
Benign tumor that arises in Schwann cells that
arise from the neural crest
 Well encapsulated  easily separated
from the nerve
Peripheral Nerve Tumors
Neurofibroma
Benign nerve sheath tumors
Neoplastic schwann cells mixed w/ perineuriallike cells, fibroblasts, mast cells and CD34+
spindle cells
Malignant Peripheral Nerve Sheath
Tumor
½ arise in NF1 PT’s probably from malignant
transformation of a plexiform neurofibroma
Usually in larger peripheral nerves of chest,
abdomen, pelvis, neck or limb-girdle
Common component of neurofibromatosis 2
 Inactivating mutations in the NF2 gene
on chromosome 22
Loss of expression of merlin
 Normally restricts the cell-surface
expression of growth factor receptors
(EGFR)
 W/o it cells hyperproliferate in
response to GF’s
Morphology
-Antoni A  moderate to high cellularity
-Verocay bodies  nuclear free zones
-Antoni B  less densely cellular
May either be sporadic or NF1-associated
Exhibit complex chromosomal aberrations
Distinguished by growth pattern:
 Superficial cutaneous neurofibromas
Unencapsulated nodular lesions
Neurofibromatosis Type 1
-Common autosomal dominant  LOF mut. in
NF1 gene  no neurofibromin  RAS is on
-Systemic dz w/ nonneoplastic manifestations
-Mental retardation, seizures, skeletal defects
- Pigmented nodules of the iris (Lisch nodules)
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Diffuse neurofibromas
Plaque on skin
Plexiform neurofibromas
-Grow in nerve fascicles  entrapping
axons
-“Bag of worms”  expanded, ropy
thickening of multiple nerve fascicles
-Collagen looks like “shredded carrot”
-Not possible to separate tumor from
nerve
-Loss of NF1 function  no
neurofibromin (tumor suppressor that
-Cutaneous hyperpigmented macules (café au
lait spots)
-Elephant man
Neurofibromatosis Type 2
inhibits RAS)
Presence of multiple neurofibromas or plexiform
neurofibromas  neurofibromatosis type 1
Clinical
-Usually at the cerebellopontine angle  attach
to vestibular branch of CN 8  tinnitus and
hearing loss  aka acoustic neuroma
-Autosomal dominant
-Bilateral CN 8 schwannomas and multiple
meningiomas
-W/in dura  sensory nerves, CN 5, and dorsal
roots
-Extradural  where motor and sensory nerve
fibers mixed
Skull Fractures
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CNS Trauma
Fall while awake  usually occipital bone fracture
Fall w/ loss of consciousness  usually frontal bone fracture
Diastatic fracture  fracture that crosses sutures
Displaced (depressed)
Bone displaced into cranial cavity
by a distance greater than the
thickness of the bone
Ex: PT struck by hard object… like a
hammer
Skull Fractures
Linear/curvilinear
Basilar (basal)
Can have branching fractures off of
the main fracture
Usually skull fractures are linear
fractures of the calvarium
Ex: PT fallen and hit their head on a
hard surface… like concrete
Fracture of the base of the skull
Suspicion of this if symptoms from
cranial nerves in the
cervicomedullary region and orbital
or mastoid hematomas
Ring
Occurs at base of skull where
fracture encircles the foramen
magnum
When head forcibly pushed
inferiorly or vertebral column
forcibly pushed superiorly
Ex: someone jumping from a great
height and lands on feet
Ex: impact to occiput or sides of
head
CSF discharge from nose or ear and
meningitis may follow
Parenchymal Injuries
Concussion
Types of Parenchymal Injuries
Direct Parenchymal Injury
Altered consciousness after a head injury
Laceration  tearing of brain tissue
Symptoms
-Instantaneous onset of transient neurologic
dysfx
-Loss of consciousness
-Temporary respiratory arrest
-Loss of reflexes
Contusion  bruising of brain tissue
-Blow to surface of the brain transmitted
through the skull
-Crests of gyri most susceptible
Diffuse Axonal Injury
Damage in the form of extensive lesions in white
matter tracts occurs over a widespread area
 Damage to axon at the node of Ranvier
that alters axoplasmic flow
Can be caused by angular acceleration in the
absence of impact
50% of coma PT have this
Common sites  frontal lobes along the orbital
ridges and temporal lobes
Uncommon sites  occipital lobes, brainstem,
cerebellum
 Fracture contusions may occur here
though
Types of Contusions
 Coup injury  develops a contusion at
the point of contact
 Countrecoup injury  develops a
contusion opposite to point of contact
Traumatic Vascular Injuries

Epidural Hematoma  temporal skull fracture  middle meningeal a. ruptured  neurosurgical emergency

o
Subdural Hematoma  lateral aspects of cerebral hemispheres  tear in bridging veins at point where they penetrate
the dura  slowly progressive neurologic deterioration

o
Subarachnoid and intraparenchymal compartment hemorrhages usually happen at the same time if there has been
brain trauma
Gunshot Wounds
 Something weird /(funny…?) to wake you up to keep studying
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Penetrating  into but not through the head
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Perforating  through the head
Entrance Wounds  round to ovoid w/ marginal abrasion
Exit Wounds  create tears in skin and irregular margins
Contact Gunshot Wound  Muzzle stamp or soot deposition
Close-range  Soot and searing of skin
Medium range  Some soot around the entrance wound
Distance range  no gunpowder
Child Abuse
 Scalp contusions, subdural hematoma, perioptic nerve hemorrhages, retinal hemorrhages (shaken baby syndrome)
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Sequelae of Brain Trauma
 Post-traumatic hydrocephalus  obstruction of CSF resorption from hemorrhage into subarachnoid spaces
 Post-traumatic dementia and punch drunk syndrome  repeated head trauma
 Post-traumatic epilepsy, tumor, infectious dz, psychiatric disorders
Spinal Cord Trauma
 Thoracic vertebrae or below  paraplegia
 Cervical lesions  quadriplegia
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Above C4  respiratory compromise from paralysis of diaphragm
Principal cause of neurological deficits is from damaging the tracts in the spinal cord and disconnecting them from its
cortical connections in the cerebrum and brain stem
Cerebral Edema, Hydrocephalus, Raised Intracranial Pressure (ICP), and Herniation
Cerebral Edema
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Brain edema, increased CSF, and focally expanding mass lesions can cause ICP
Generalized  both vasogenic and cytotoxic edema  Gyri flattened. Sulci narrowed. Ventricals compressed.  can
result in herniation if too much ICP
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Interstitial edema (hydrocephalic edema)  around lateral ventricles  from increase in intravascular pressure that
causes intraventricular CSF to cross the ependymal lining into the white matter
Types of Cerebral Edema
Vasogenic
Cytotoxic
BBB disruption and increased vascular permeability  intercellular
spaces of the brain  edema is b/w the cells
Increase in intracellular fluid secondary to neuronal, glial, or endothelial
cell membrane injury  edema is in the cells themselves
Fluid accumulated in the intercellular spaces b/c brain has limited
lymphatics, therefore lack of resorption
Can result from hypoxic/ischemic insult or metabolic damage that
prevents maintenance of the membrane ionic gradient
Can be either localized (inflammation/neoplasms) or generalized
Hydrocephalus
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Excess CSP in the ventricles usually from impaired flow/resorption or rarely overproduction (tumors of the choroid
plexus)
CSF Circulation:
Choroid plexus  ventricles  foramina of luschka
(lateral aperture) and magendie (median aperture)
 cisterna magna  subarachnoid space 
arachnoid granulations  venous blood  back to
bodies circulation
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Infancy  enlargement of head  increase in head circumference b/c sutures aren’t closed.
Adult  enlargement of ventricles w/ ICP  w/o change in head circumference.
Non-communicating Hydrocephalus
Only a portion of ventricles enlarged
Possibly from mass in 3rd ventricle
Types of Hydrocephalus
Communicating Hydrocephalus
All of the ventricles are enlarged
Hydrocephalus ex vacuo
Dilation of ventricles w/ incease in CSF volume 
due to a loss of brain parenchyma
Raised Intracranial Pressure and Herniation
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Occurs if CSF and Venous drainage cannot compensate for all of the extra fluid
Diffuse  like generalized brain edema
Focal  tumors, abscesses, or hemorrhages
ICP can cause restriction of vessels  exacerbated cerebral edema b/c can’t drain the fluid out if vessel closed off
The dural folds of the brain (flax cerebri, tentorium cerebelli, and falx cerebelli) can cause herniation of the
cerebrum/cerebellum  if bad enough then you can get herniation syndrome
Types of Herniation Syndromes
Subfalcine (Cingulate) Herniation
Transtentorial (Uncinate, Mesial
Tonsillar Herniation
Temporal) Hernation
Unilateral or asymmetric expansion of a cerebral
hemisphere displaces the cingulate gyrus under
the falx cerebri
Can cause compression of the anterior cerebral
a.
Medial aspect of the temporal lobe is
compressed against the tentorium cerebelli
Displacement of the cerebellar tonsils through
the foramen magnum
Can cause problems w/ CN 3  pupillary
dilation and inability to move eye on the same
side as the lesion
Life-threatening  due to brainstem
compression of respiratory and cardiac centers
in the medulla
Can cause compression of the posterior cerebral
a.  hypoperfusion to primary visual cortex
Kemohan’s notch  Contralateral cerebral
peduncle may be compressed  hemiparesis on
same side of the herniation
Secondary brainstem (duret) hemorrhages 
hemorrhagic lesions in the midbrain and pons
due to the herniation