2016-04-04

DIT 1
Forebrain: Prosencephalon becomes the telencephalon and
diencephalon
Midbrain: Mesencephalon becomes the midbrain
Hindbrain: Rhombencephalon beceoms the metencephalon and
myelencephalon
Neural Tube Defects:
Neuropore fails to fuse
Connection between spinal canal and amniotic fluid persists
Main risk: low folic acid levels
Most multi vitmains have .4mg of folic acid
Prenatal vitamins have .8mg of folic acid
High risk should be taking 4mg per day
Check for neural tube defects:
You can use sonogram to check for it visually
You can examine using quadruple screen

Maternal AFP are elevated: anterior abdominal wall defect or

neural tube defect
Maternal AFP decreased: Down Syndrome
If there is an increase in AFP but you cant see and neural tube
defect or abdominal wall defect then you can do amniocentesis
Check AFP in amniotic fluid-> confirms defect
3 main types
Spina bifida
spinal canal
If you see a
Check to see
modalities

of neural tube defects

ocuclta: no herniation of spinal cord . failure of
to close on bony level (lumbo sacral area)
tuft of hair on a newborn at this lumbosacral area,
if bones have fused properly via appropriate imaging

Meningocele:Just meninges that herniate

Myelomeningocele: If both meninges and spinal cord herniate
Forebrain Anamolies:
Neural tube defects present at the lumbosacral region most of the
time, but they can present at the cranial end can occur: This is
called Anencephaly: nothing separating brain tissue from acidic
amniotic fluid which ultimately eats a way at the brain tissue
U/S: Polyhydramnios: Is when a fetus has excessive ammounts of
amniotic fluid because they have lost the swallowing part of the
brain. Amniotic fluid is made by fetal kidneys and is urinated
out and then the fetus swallows the amniotic fluid and reduces
the total amount.
Holoprosenecephaly: Hemispheres of the brain fail to separate
across the midline: 2 characteristic findings are cleft palate
and and cyclopia
This is seen in FAS(Fetal Alcohol Syndrome) and Trisomy 13(Patau
syndrome) and Sonic Hedgehog gene mutations

Posterior fossa abnormalities

Chiari Malformations:
Part of the cerebellum herniates downwards through foramen magnum
Type 1: Mild form, cerebellar tonsils herniate downwards: can
cause syringomyelia
Type 2: Lumbosacral myelomeningocele: significant herniation of
cerebellar tonsils, can cause stenosis of aqueduct which results
in hydrocephalus
Syringomyelia:
Syrinx= tube
SYringomyelia is a cavitory lesion in the spinal cord that fills
with CSF and creates this tube that is visible on MRI. Usually
occurs in cervical spine. It is associated with Chiari 1
As the syrinx dilates, it compresses the nerve fibres around it
resulting in neurological symptoms. Specifically it effects the
crossing fibres of the spinothalamic tract which deccusate at the
level of the spinal cord, resulting in a loss of pain,
temperature and course touch sensation. This will be bilateral.
Specifically if it is in the cervical region it will be loss in
the upper extremeties. Classically a cape like distribution. As
the extends you can have motor regions affected too
Syringomyelia can also be caused by spinal cord trauma developing
over months to years after.
Dandy-Walker Syndrome:
Enlarged posterior fossa results in the failure of the cerebellar
vermis to develop properly. This results in the dilation of the
4rth ventricle to fill up the space that is left.
Associated with hydrocephalus and spina bifida
Branchial Apparatus:

Pharyngeal Apparatus:
Branchial apparatus is composed of six lumps of tissue on each
side. We call these lumps the branchial arches. The grooves on
the lateral side of the lumps is known as branchial clefts while
the grooves on the medial side are known as the branchial
pouches.
Clefts=ectorderm. Therefore you know its lateral as they both
have C in them and ecto is always outwards
Arches are mesoderm, as mesoderm bridges the gap between endoderm
and ectorderm the arches bridghe between pouches and clefts
Branchial Clefts
Ectoderm portion of the branchial apparatus.
Adult structures that derive from the branchial clefts are the
following:
1st Cleft= external audiotary meatus
2nd, 3rd , 4rth- Temporal cervical sinuses that are
obliterated later. If some of these temporal cervical
sinuses persist then you can form a branchial cleft cyst.
Cyst can also form from thyroglossal duct which also
needs to be obliterated.
Two differentiate between the two cysts you can do the
following;
Branchial cysts are located on the lateral neck because
they form from temporal cervical sinuses that persist
which form from the branchial clefts which are ectorderm
and are lateral.
Thyroglossal duct cysts are formed in the midline because
think where is thyroid
Branchial cleft cysts do not move when you swallow
Thyroglossal duct cyst moves when you swallow because it
is pushed around by the thyroid cartilage

Branchial Pouch Derivatives (endoderm)

1st Pouch: Middle ear cavity, Eustachian tubes, mastoid air
cells

Ear structures are first

2nd Pouch: Epithelial l ining of the tonsils
3rd Pouch: Inferior parathyroid glands and thymus
4th Pouch: Superior parathyroid glands
DiGeorge: immunodeficiency syndrome associated with abnormal
development of third and fourth pouches-> no parathyroid or
thymus. Without thymus you cant have mature t cells and without
parathyroid calcium levels will be low
Branchial Arches:
Mesoderm structures
1st Arch: gives rise to the M and T structures: Meckels
cartilage which gives rise to jaw structures like
Mandible,Mandibular ligament and malleus and incus. First arch is
forming the ossicles of the middle ear(malleus and incus)
ossicles are derived from neural crest which is ectorderm. Bone
and cartilage come from neural crest cells which migrate here.
Muscles: Jaaw (muscles of masticatiom, masseter, medial
pterygoid, temporalis) Mylohyoid, Tensor Tympani, Tensor veli
palatini , and Ant 2/3 of Tongue
Nerves: Mandibular and Maxillary branches of Trigeminal . If
neural cell crests fail you get Treacher-Collins Syndrome

2nd Arch: Gives to the S structures and L

-Cartilage: Stapes, styloid process and stylohyoid ligament
and lesser horn of the hyoid
-Muscles: muscles of facial expression, stapedius,
stylohyoid
CN Seven
Pharygneocutaneous fistula lateral cyst

3rd Arch: Pharyngeal word is quick association

Muscle:Stylopharyngeus
Nerve:Glossopharyngeal (CNIX)
4 and 6 arches ^: Cricoid and Larynx
Cricoid cartilage, and larynx cartilage.
Cricothyroid muscle
Laryngeal muscles
4+6=10 Vagus Nerve
Super laryngeal nerve does pharyngeal myscles
Rest of laryngeal msuscles for speech are due to recurrent
laryngeal nerve

End of session quiz

Chiari Malformation:
Type 1 and Type 2
Type 1 : Syringomyelia
Type 2: Myelomenengicele which can lead to hydrocephaly
Syringomyelia classical symptoms are:

1.)loss of spinothalamic tract= pain temp and course touch

loss on the bilaterally
2.) if bigg than also motor loss by affecting anterior horn
which can result in muscle weakness, atrophy,
3) Cervical area
AFP= anterior abdominal wall defects, neural tube defects,
liver cancer
Middle ear and Eustachian tube: 1st Pouch
Superior parathyroids = Fourth pouch
Inferior parathyroids= 3rd pouch
Epithelial palatine tonsil=2nd pouch
Thymus: 3rd Pouch

DIT 2 Neuro
WarmUP: Phenobarbital result in hypertrophy of the Smooth ER
Caloric restriction
Cells of Nervous System:
Different Types of Cells

Neurons: neurons are the cells that send and receive

signals. They are composed of cell bodies and dendrites which
receive signals and axons which are the way they send signals. At
the terminal end of an axon you have a terminal synapse which
releases neurotransmitters to send signal to the next cell.
Neurons have rough endoplasmic reticulum called Nissl
bodies. These Nissl bodies are found only in dendrites and not in
axons.
Non-neuronal Cells
Glial (support cells)
Astrocytes
Microglia
Oligodendroglia
Ependymal Cells
Schwann Cells
Astrocytes: provide physical support. They help in repair
processes, neurotransmitter excess removal, reactive gliosis
which is the formation of scar tissue, and make up one layer of
the Blood Brain Barrier. Reactive gliosis is similar to how
fibroblasts react to injury
One of the molecules found in astrocytes is GFAP(Glial
Fibrillary Acidic Protein). Astrocyte tumors have high lvels of
GFAP(+)
.gliblastoma: GFAP+
Microglia: CNS phagocytes: Macrophages are blood. Microglia
response to tissue damage and respomnsible for cleaning things
up. HIV-infected microglia fuse and form giant cells in the CNS.
Oligodendroglia: are the myelin cells of the CNS: white
matter white because of them. Myelin is essential for the
transmission of a signal down an axon. One oligodendrocyte can
myelinate many axons. These are the cells that are destroyed in
MS. Look like a fried egg on H and E stain. Large clear
cytoplasm.
Tumors of oligodendroglia are known as oligodendrogliomas

Schwann Cells: are the myelin cells of the PNS: one schwann
cell can only myelinate one axon. Peripheral axons are long.
Schwann cells also promote axonal regeneration. When you have an
injury to axons, schwann cells create the pathway to guide new
axonal growth. They maintain the integrity of the pathway. These
are the cells damaged in GB-Syndrome.
Acoustic Neuroma: schwannoma that occurs in the internal
auditory meatus. Neurofibromatosis Type 2: bilateral scwannoma
Lewis Note:
CNS Phagocyte: Microglia
Physical support: Astrocyte
Destroyed in MS: Oligodendrogcyte
Reactive Gliosis: Astrocyte
HIV nulit-nucleated giant cells: microglia
Fried-egg: oligodendroglia
Damaged in GB: schwannc cell
Cells of the Nervous System:
3 germ layers:
neuroectoderm:
1.neurons of CNS,
Make ependymal cells which line the ventricles and make
CSF through the choroid plexus.
Oligodendroyctes, astrocytes
Neural Crest Cells: migrate to make PNS neurons, schwann
cells and other stuffs.
Mesoderm:
Microglia

BBB:
3 layers
first layer: non-fenestrated capillary endothelial layer
that has tight junctions prevented things from readily passing
through
second layer: basement membrane
third layer: foot process of the astrocytes
Substances that cross the BBB
glc and amino acids can carry via a carrier-mediated transport
Lipid soluble, and nonpolar substances can cross the BBB
more easier. The more lipid soluble something is the more potent.
ADH and oxytocin via fenestrations through hypothalamus can
go through brain without having a BBB.
BBB can be damaged by trauma, infection or stroke leading to
edema.
Mannitol: is used to decrease ICP
Mannitol: is a weak diuretic. Osmotic. It pulls water in.
Neurotransmitters: are secreted from the terminal portion of an
axon
Different neurons make different neurotransmitters
Different neurotransmitters have different effects
Receptor determines the downstream effect

Dopamine:
Is both an excitatory(d1) and inhibitory(d2).
Dopamine is increased in schizophrenia
Dopamine Is decreased in depression
4 major dopaminergic pathways
Mesocortical Pathway: Ventral tegmental of the midbrain->
cortex: results of blocking of this pathway results in increasing
the negative symptoms associated with schizophrenia
Such as social withdrawal and depression
Mesolimbic pathway goes from the ventral tegmental of the
midbrain to the limbic system . blocking this system relieves the
positive symptoms of schizophrenia. This is the pathway you
target with neuroleptics which are dopamine antagonists.
Nigostriatal pathway: substrantia nigra pars compacta to
neostriatum. Which is related in Parkinsons disease. These are
part of the basal ganglia. Blocking these pathways result in
parkinsosn. Stimulating these pathways can resul
t in extra-pyramdidal sideeffects.
When you give neuroleptics you can cause Parkinson type
symptoms because they block mesolimbic pathway and nigrostriatal
pathway.
Blocking of the nigrostriatal pathway can result in
upregulation of dopamine receptors-> dyskinesia and dystonia
which are extra-pyramidal signs.
Tuberoinfundibular pathway:
Arcuate nucleus of hypothalamus-> pituitary: blocking this
pathway results in increase release of prolactin from anterior
pituarary. Elevated prolactin can cause hypogonadism ->
amenorhhea, decrease libido, gynecomastia, galactorrhea
Anti-dopamine agents can also cause prolactin increase. To
decrease prolacting you can give bromocriptine which is a
dopamine agonist.

Neuroepinephrine:
Secreted by certain neurons and also comes from adrenal medulla
NE: decreased in depression, increased in anxiety and mania
NE comes from locus ceruleus and made in the reticular formation
and solitary tract
Seratonin: 5-HT: decreased in anxiety,
Made in Raphe nucleus

decreased in depression.

Acetylcholine:
Decreased in alzeimers
Decreased in huntingtons
Increased in parkinsons
Degeneration of the basal nucleus of Meynert results in a
decrease of Acetylcholine
Neurotransmitters:
GABA:
Main inhibitory neurotransmitter of CNS
Less GABA increases more excitatory: seizures
Decreased in anxiety
Decreased in huntingtons

Location of synthesis is nucleus accumbens

Glycine: main inhib neurotransmitter of spinal cord
Glutamate: min excitatory neurotransmitter of the CNS
Reticular Activating System
Reticular Formation
Locus ceruleus: Norepeniphrine
Raphe nuclei: Seratonin
Reticular Activating System is responsible for
Consciousness, wakefulness, attentiveness, and stimulation
results in attentiveness
RAS lesion-> coma
Quizz:
Acetylcholine is produced in the basal nucleus of Meynart.
Degeneration of nucleus of Meynart results in Alzeimers.
Decreased ACH is also associated with Hungtingtons. And ACH is
increased in Parkinsons
Main inhib neuro of CNS= GABA
GABA is decreased in anxiety, huntingtons

BBB:
3 layers:
non-fenestrated capillary endothelium with tight junctions
basement membrane
astrocyte foot processes
DIT Cortex and Brain stem Lesions
Anxiety: Increased NE, , Decreased GABA.
Cerebral Cortex
Arcuate Fasciculus connects Broca with Wernicke
Homunculus:
Head and Face are lateral part of cortex
Hand and arm are and legs are medial
Blood Supply to Brain:
4 arteries that supply the brain
2 internal carotids and 2 vertebral arteries
Common carotid runs in carotid sheath. It divides into external
carotid which supplies the face, the scalp and the meninges. And
the internal carotid which supplies the brain. Specifically the
anterior compartment of the circle of willis.

The vertebral arteries supply the posterior portions of the brain

The vertebral artery comes from the subclavian through the
transverse foramena . vertebral arteries give of the ASA and
pica. Then the vertebrals merge to form the basilar artery which
supplies the cerebellum and brain stem.
Circle of Willis:
Internal Carotid
ACA
MCA
PCA

Arterial Blood Supply to the Cortex

ACA reflect back along the corpus callosum (medial)
MCA( entire lateral part)
PCA: occipital lobe
Aphasias:
Expressive aphasia: difficulty generating language
Receptive aphasia: difficulty understanding
Broca: language production
Wernicke: language comprehension

Broca aphasia: Non-fluent aphasia, intact comprehrension

Broken Speech
Wernicke Aphasia: Fluent aphasia, impaired comprehension.
Conduction aphasia: intact comprehension, with fluent language,
but with poor repeititon results in lesion in arcuate fasiculus
which are fibres that connect Wernicke and broca
Global Aphasia: both broca and Wernicke effected
Dysprosody: rhythm and music of speech
The manner in wich things are said
Broca is usually on left hemisphere
Same area on right hemisphere results in dysprosody
Brain Lesions:
Gerstmann Syndrome:
Lesion to the dominant angular gyrus in parietal lobe (usually on
left)
Angular gyrus is associated with complex language functions

Lesion here will result in :

-agraphia (inability to write)
-acalculia (inability to calculate)
-Right-Left disorientation
-Finger agnosia
Hemispatial neglect:same lesion on non-dominant side:
Results in patients neglecting one side of the world,
contralateral side usually. Shave only one side. Eat only one
side of the plate. See arm but not recognize it
Frontal Cortex:
Judgement, decision making and supressing primitive urges of
limbic system are all functions of the frontal cortex.
-disinhibition
-poor judgjment
-return of primitive reflex
Frontal Eye Fields:
Eyes deviate towards side of lesion
PPRF:Paramedian Pontine Reticular Formation
Lesion here in the pons results eyes deviating the eyes in the
opposite way
Superior colliculus: Lesion results in paralysis of upwards gaze

Reticular Activating System

Responsible for alertness ,awakeness, arousal
Lesion results in stupor and cumor
Limbic System Lesions
Bilateral Hippocampus lesions:
Bilateral Results in anterograde amnesia
Mammilary body damage results in wernick-korsakoff syndrome:
Nystagmus, opthalmoplegia, ataxia, encephalopathy
Anterograde and reterograde amnesia resulting in confabulatin
Bilateral damage of amygydala = Kluver-Bucy syndrome
Basal Gangia Lesions
Hypokinesis=parkinsons
Hyperkinesis and chorea
Lesion in subthalamic nucleus results in hemiballismum
involuntary flaming of an isolated limb

Cerebellar lesions:
Lesions ipsilateral movemebt problems
Vermis is the midline lesion
Truncal ataxia
Lips and tongue damage
DIT 4 Cranial Nerves Part 1
Prequizz
Thromboxane: pro-thrombotic
A1-antitryptsin deficiency is the one where you have decrased
elastin, resulting in emphysema
Identifying Cranial Nerves in terms of where they come out
A)Pineal Body
B) Superior colliculus: lesions here prevent upward gaze
C)Optic Tract( comes from the CNII from the ventral side
D)Inferior Colliculus (receives a lot of auditory information and
relays it to the primary auditory cortex in the temporal lobe
E)Trochlear Nerve (CN IV)
F)Trigeminal Nerve
G)Vestibulochochlear Nerve (CNVIII)
H)Facial Nerve (CN VII)

I)
J)
K)
L)

Glossopharyngeal Nerve (CN IX)

Hypoglossal Nerve (CN XII)
Vagus Nerve
Accessory Nerve

Ventral View
M) olfactory tract
N)Optic Chiasm
O)Pituatary Stalk
P)Mammary bodies
Q) oculomotor nerve (CNIII)
R)Trochlear nerve (CNIV)
S) Trigememinal Nerve (CN V)
T)Abducens Nerve (CNVI)
U)Facial Nerve (CN VII)
V)Vestibulocochlear nerve (CN VIII)
W)Glossopharyngeal Nerve (CN IX)
X) Hypoglossal nerve
Y) Vaus
Z) Spinal Accessory nerve

Repeat The following anatomy above

Dorsal Part
A) Pineal Gland
B) Sup Colliculus
C) Optic Tract
D) Inf Colliciuls
E) Trochlear
F) Trigeminal Nerve
G) CN VIII Vestibulicochlear Nerve
H) Facial Nerve VII
I) Glossopharyngeal
J) Hypoglossal
K) Vagus
L) Accessory
Ventral View
M) Olfactory Tract
N) Optic Chiasm
O) Pituatary Stalk
P) Mammillary bodies

Q)
R)
S)
T)
U)
V)
W)
X)
Y)
Z)

Oculomotor
Trochlear
Trigeminal
Abducens
Facial
Facial
Glossopharyngeal
Hypoglossal
Vagus
Accessory

Cranial Nerve Nuclei:

4 Cranial Nerve Nuclei in Pons
4 Cranial Nerve Nuclei in Medulla
4 Cranial Nerve Nuclei Above Pons
1,2(forebrain),3,4(midbrain)
5,6,7,8,(pons)
9,10,11,12 (medulla)
Spinal ACcesory Nerve Nuclei found in spinal cord

1)
2)
3)
4)
5)
6)
7)
8)
9)
10)
11)
12)

O,O,O,T,T,A,F,V,G,V,A,H
Olfactory
Optic
Oculomotor
Trochlear
Trigeminal
Abducens
Facial
Vestibulochoclear
Glossopharyngeal
Vagus
Acceosry
Hypoglossal

1) Olfactory: smell
Cranial Nerve 1 exits the skull at the cribiform plate sending
branches into the nasal cavity. Fracture here will sever these
branches
2) Optic Nerve: sight
Cranial Nerve 2 exits through optical canal.
Test using VA,Pupillary Reflexes and VF

Visual Fields:
Nasal and Temporal side
Lense projects a mirror image on to retina, so the objects on
temporal side are perceived on the nasal side of the retina. As
you follow the optic signal down the optic nerve towards the
brain you reach optic chiasm(crossing). Objects on Right are
perceived by the left side of the brain. Information from the
temporal side of the left eye and the nasal side of the right eye
are perceived by the right side of the brain
5 Basic VF Defects
Lesion at Optic Nerve: Vision Loss in affected eye
Lesion at Optic Chiasm: Bitemporal Hemianopsia
Lesion at optic tract: ie say Right Tract: Then you would have
loss of the nasal side of right eye , and loss of temporal side
on left eye, You will therefore lose vision on left VF. This is
known as homonymous hemianopsia
Loss of vision in only center. Macular degeneration
Homonymous Hemianopsia with macular sparing is PCA Infarction.
Macular receives collateral blood supply from MCA.
CNIII: Oculomotor Nerve
It provides motor innervation to most muscles associated with the
eye
It provides motor innervation to the levator palpebrae muscle
which raises the eye lid
It also sends parasympathetic fibres to the ciliary muscle to
the pupillary sphincter so CNIII can impair accomdation and
result in pupil dilation
Trochlear Nerve: Supplies the superior oblique muscles
CNVI: innervates lateral rectus
All of the above exit the skull through the superior orbital
fissure.
Extraocular Muscles and Nerves

Lateral Rectus: Abducts eye. Moves eye laterally

Medial Rectus: adducts eye: moves eye medially
Sup Oblique: reverse: opposite. Sup oblique moves eye down when
adducted.
Inf Oblique: reverse: opposite moves up. Almost perpindicular
Sup Rectus: elevates eye when eye is abducted
Inf Rectus: depressses eye when eye is abducted.
Test Sup and INf rectuse by asking patient looking out and then
up or down
SO4LR6
Lateral Rectus: Lesion in CNVI. Unable to move eye
laterally/abduct
Medical Rectus: CNIII: Unable to move eye medially
Superior Rectus: elevates eye when eye is abducted
Inferior Rectus: depresses eye when eye is abducted
Pupillary Control
Mydriasis: pupillary dilation
Parasympathetic constriction myoisis.
Ambient Light
What happens when you shine light into the left eye to examine
the pupillary light reflex

The afferent signa is carried from the eye to the brain by the
optic nerve to the optic chiasm and then down both optic tracts.
Some of these neurons synapse at the lateral geniculate nucleus
which is part of the thalamus which relays visual information to
the primary visual cortex. Some of the optic tract neurones are
bypassing the lateral geniculate projecting to the pretectal
nucleus. The pretectal nuclei project to the Edinger-Westphal
Nucleus bilaterally. The Edinger-Westphal Nucleus are located in
the midbrain and contribute the parasympathetic neurons to
cranial nerve 3. So when the pretectal nuclei get a signal that
theres an increase in light entering the eye, they stimulate the
edinge-westphal nucleus, sending a signal back up the through the
ocular motor nerve to the ciliary ganglia.. From there the sugnal
goes up to the pupillary constrictor muscles of the iris and the
pupils constrict.
There are 2 main ways you can mess up this pupillary light
reflex.
1.)
impair the afferent signal, therefore you are blocking
the incoming message that light is coming into the eye. APD
2.)
impaur effecrent signal , the parasympathetic signal
that causes pupillary constriction. Efferent defect.
Optic Nerve damage= APD
Shine light in one eye and neither eye constricts, it tells
you that you have an APD. Marcus-Gunn pupil
Damage to oculomotor nerve results in one pupil unable to
constrict
Parasympathetic fibres on cranial nerve III are located on the
outer part of the nerve while the motor innervation is in the
inner part. Mass lesion on CNIII is most likely to affect
parasympathetic. As they are on the periphery. But since the
fibres of the EOMuscles are mmore deep, they are more
susceptible to ischemic damage, therefore diabetes are more
susceptible to pupil sparing eye cranial nerve palsies.
DIT 5 Neuro 5
1.)intrinsic apoptosis=mitochonidra
A)ACA
B)ACOM
C)MiddleCA
D)INTERNAL CAROTID
E)PCOM

F)PCA
G)SCerbellarartery
H) BAsilar
I) AICA
J)Vertebral arteries
K)PICA
L)ASA

AFP is a component of quadruple screen with b-HCG, estriol

and inhibin-a
Acetylcholinesterase
Cranial Nerves Part 2
Trigeminal Nerve
CNV is the trigeminal nerve with three divisions:
1) the opthalmic
2) the Maxillary
3) the mandibular
First two branches are purely sensory while the mandibular
branch has both sensory and motor
Opthalmic branch exits the skull from the superior orbital
fissue

The maxillary branch exits at the foramen rotundum

The mandibular branch exits at the foramen ovale
In terms of function:
The ophthalmic branch provides sensation to the forehead and
down the bridge of the nose
The maxillary branch provides sensation basically from eyes
down to the upper lips as well as sides of nose and nasal
mucosa, palate and upper teeth
The mandibular branch provides sensation to the jaw and
extends in front of the ears all the way to the temples.
Provides touch sensation to the anterior 2/3 of the tongue,
but not taste sensation which is provided by the facial nerve
and the glossopharyngeal nerve
Mandibular nerve also provides motor function to the muscles
of mastication.
Trigeminal nerve sensation can be examined by pinprick or
light touch on all three regions of the face, and you can rest
corneal reflex(ophthalmic branch of CN V and temporal branch
of CN VII supplies motor innervation.
Lacrimation reflex.
Compression of trigeminal nerve will cause trigeminal
neuralgia.
Mandibular branch supplies motor innervation for the muscles
of mastication, Masseter muscle, Medial pterygoid muscle,
Temporalis
Origins and Insertions of
Mastication
NFL (N=Nasocilliary, F=frontal, L=lacrimal.)
Lateral pterygoid muscle: opens the jaw
Temporalis, Masseter and the medial pterygoid are responsible
for closing the jaw. Open the jaw against resistance. Clench
the teeth

Cavernous Sinus: First and Second divisions of trigeminal

nerve run right through this cavernous sinus. Other nerves
that run through it are the oculomotor nerve, the trochlear
nerve and the abducens nerve. Internal carotid, pituary gland
and sphenoidal sinuses, and optic chiasm
Danger Triangle: area in cavernous sinus thrombosis which
cranial nerve palsy.
Facial Nerve: Cranial Nerve VII
Facial Nerve exits the skull through the internal acoustic
meatus along with cranial nerve VIII. When we looked at the
cranial nerves off the brainstem they both came off the
posterior pons together
Five Branches of the Facial Nerve:
Temporal Branch
Zygamoatic
Buccal
Marginal Mandibular
Cervical
Ten Zebras Bit My Chin.
The big function of the facial nerve is the motoer innervation
of the muscles of facial expression, stylohyoid muscle,
stapedius muscle, posterior belly of disgastric muscle,
stapedius. All of these structures are derived from the second
brachial arch. S= Cranial Nerve Seven, S for Stylohyoud,
S=Stapedius, S for Second brachial arch
Facial nerve in addition to motor innervation, it supplies
parasympathetic innervation to the lacrimal glands to cause
tearing, it inntervates the submandibular glands and subingual
glands make saliva. Facial Nerve passes through parotid
glands. Submandibular glands make more saliva than parotid.
Facial Nerve also provides taste sensation anterior 2/3 of
tongue.
To test facial nerve you can do wrinkle forhead, puff out
cheaks raise eyebrows or close eyes tightly.

Unilateral Facial Weakness. Bells Palsy. Right sided facial

droop with assymtery. Right side of face weak.
Bells palsy is idiopathic facial nerve palsy
Conditions that can cause facial nerve:
Lovely Bella had an STD:
Lyme Disease
Bells Palsy
Herpese Simplex/Zoster
AIDS
Sarcoid
Tumors
Diabetes
Number 1 cause is HSV
Unilateral facial weakness worry about stroke
How do they symptoms of a facial nerve ( or a facial nerve
nucleus) lesion differ from the symptoms of a facial motor
cortex lesion(such as stroke)
Facial Nerve/Nucleus lesion-paralysis of ipsilateral side of
entire face

Facial Motor Cortex Lesion- Paralysis of contralateral side of

lower face. Right side of face is controlled by left motor
cortex.
Facial motor nucleus receives fibres for the lower face from
the contralateral motor cortex, but receives motor fibres for
upper face from both motor cortex.
If Forehead and lower face is paralyzed then Bells Palsy
Stroke is only going to affect lower face. If a patient can
move his eyebrows then serious chance of stroke being the
cause
Vestibulocochlear
CN VIII. It exits the skull through the internal acoustic
meatus with facial nerve.
It is responsible for equilibrium and hearing and can test it
by looking for nystagmus, balance problems and hearing.
Glossopharyngeal Nerve.
CN IX
Jugular Foramen
Supplies motor innervation to stylopharygneaus muscle
Parasympathetic innervation to parotid gland
Sends branches to the carotid sinus to measure blood pressure
Sends branches to the carotid bodies to measure blood
chemistry
Sensory pharynx and back of tongue
Taste Sensation to posterior one third of tongue
Test it by checking gag reflex

Vagus Nerve
Jugular Foramen
Motor innervation of pharyngeal muscles and larynx
Swallowing and speaking
Parasympathetic to heart and GI
Sensory to pharynx, trachea and esophagus so irritiation to it
can cause coughing
Taste to very back of tongue
Testing involves elevating the palate by saying AAH
Check Gag relex and look at voice quality
If the right vagus nerve of nucleus is damaged, to which side
will the uvula deviate. The oposite side. The levator valei
pallatinie is the main muscle that lifts the palate.
A patients uvula deviate to the right when she says Ah. Wjat
meurologic structures may be involved?
Rightward deviation of the uvula means that that the muscles
of the right are working but the left are not. This can be
cause by damage to left vagus, to left nucleus ambigious as
the vagus nerves originate from the nucleus ambigious.
Nucleus AMbigius is associated with speak, and swallowing. It
receives input from
-Right corticobulbar tract
-Right motor and cortex
but it receives input from both sides of the cortex. A lesion
above wont cause it to deviate.
Accesory Nerve
Sternoclaidomastoid and Trapezius

Test by shrugging shoulders and turn head

Hypoglossal Nerve
Hypoglossal Canal
Glossal=tongue
Motor innervation to intrinsic tongue. Stick out tongue
Right injury, licks the lesion
Gag reflex is associated with vagus nerve and glossopharyngeal
346 go through cavernous sinus= opthalmoplesgua
CNIII= down and out
CNVI= unable to abduct, in
Presents with diplopia
CNV= facial pain and numbness on upper face
Stroke will cause only contralateral lower facial droop.
Bells palsy will cause both lower and upper facial droop.
Right Brain Bonus:

Tongue:
What nerves innervate the tongue for motor and taste
Taste: anterior 2/3 = facial, posterior= glossopharyngeal,
vagus
Motor= hypoglossal
DIT 7 Brain Lesions
Hall mark sign of a brainstem lesion.
Alternating syndromes: long tract symptoms on one
side(hemiparalysis) and cranial nerve symptoms on the other
side.
The Rule of 4s:
Medial brainstem and lateral brainstem receive blood from
different arteries
Pons: Medial Structures receive blood from Basilar artery
(paramedian branches of basilar artery)
Cranial Nerve Nuclei are arranged sequentially
The Rule of 4s
1.)
There are 4 medial structures that begin with M
2.)
There are 4 lateral structures that begin with S
3.)
There are 4 Cn that originate below pons, and 4 that
originate in the pons and 4 that originate above pons
4.)
4 Motor Nuclei are midline are the ones that divide
into 12 equally except for CN1 and CNII.

5.)
The nuclei that do not divide equally into 12 are
sensory and lateral
There are four medial structures beginning with M
a) Motor pathway(corticospinal tract): medial pons and pyramids
of medulla: motor deficits, ie weakness of contralateral arm
and leg
b) Medial Lemniscus: continuation of dorsal column. Loss of
vibration, proprioception and fine touch in contralateral arm
and leg
c) Medial Longitudinal Fasciculus: Controls vertical gaze.
Intranuclear opthalmooplegia ipsilateral
d) Motor Cranial Nerve Nuclei: 3,4,6,12. Ipsilateral loss
e)
There are four Side lateral structures beginning with S
(sensory)
Spinocereballar: runs in the inferior cerebellar peduncle.
Lesion will cause ipsilateral leg and arm ataxia
Spinothalamic Tract: loss of pain and temperature on the
contralateral side
Sensory Nucleus of CN V:
Sympathetic pathway: ipsilateral horner syndrome
OOOTTAFVGVAH
Case 1:
Horase voice and difficulty swallowing tells me that CN10 and
glossopharyngeal (CN9)
Loss of pain and temp in right arm tells me it is
spinothalamic and that lesion is on left
Ataxia on left arm indicates spinocerebellar is affected and
lesion is lateral
Uvula deviates to the right: CN12 left

Wallenberg Syndrome:
KNOW: lateral medullary syndrome:
CNV has a nucleis so big it stretches down
Nucleus ambiguous is effected: speech and swallowing.
Vestibular nucleus is affected: Vertigo,nystagmus, and
vomiting
Inferior cerebellar peduncle: ipsilateral cerebellar defects
such as ataxia and past pointing
Spinothalamic, left
Motor left
Medial left
Tongue deviate to the left indicates that it is left lesion
Left facial droop: ipsilateral facial nerve damage if it
affects both upper and lower it is nuclei
Cn VII
Spinothalamic on left
Lateral Pons inferior
If you cant abduct or adduct right eye. Oculomotor. Above pons
midbrain
Nystagmus in left eye when looking left
Left arm and leg weakness tells me lesion is on right

Motor
Medoal
INO:
Intranuclear opthalmoplegia
Is a lesion in the MLF
MLF=helps eyes tracks side to side, it allows lateral rectus on
one eye to co-ordinate movements with the medial rectus on the
other eye so your eyes can point in the same direction.
Multiple Sclerosis and Medial Pontine Syndrome:
Locked-in syndrome
Occurs due to a basilar artery stroke that affects both sides of
the pons. Can also occur if you rapidly correct hyponatremiaCentral Pontine Myelonosis. MRI: increased intensity signal
Weber Syndrome:
Midbrain syndrome: PCA Stroke
Infarction of the cerebral peduncles; corticobulbar and cortical
tracts are effected.
Infarction of the corticobulbar tract will cause problems with
swallowing, speaking and moving tongue. Oculamotor nerve
ipsilateral can also occcure. Down and OUT.
Right sided CN VI: medial and its ons
Therefore medial pons and most likely Basilar
O,O,O,T,T,A,F,V,G,V,A,H

Vertigo, nystagmus= Vestibulochochlear= CN VIII PONS

Lateral Right sided
Gag reflex= Vagus and Glossopharyngeal
Uvula to left= right
Pain and temperature on the right = trigeminal nerve
Spinothalamic on right
Lateral Pon and Medulla
Pons= AICA
Medulla=PICA
Wallenberg:
10 right sided weakness.. right side medulla medial. ASA
and out = oculomotor CN III = PCA
DIT 8
Neural crest cells eventually become
Autonomic CNS
Celiac Ganglia
Chromaffin cells
Dorsal root ganglia

down

Schwann Cells
Pia and arachnoicd
Cornea
Sclera
Iris
Thyroid cartilage
Mealnocytes
Parafollicular cells of thyroid
Serine, Threonine, Asparagine
Basement mebrnae
Foot processes of astrocytes
Non-fenestrated capillary endothelial cells
Cerebrum:
Limbic and Hypothalamus
Limbic system controls emotional behaviour and emotional drive
Limbic System is responsible for the 5 Fs:
Fighting
Fleeing

Feeding
Feeling
Fornication
Limbic system is like the caveman brain
Animal portion of the brain
Limbic system is also involved in learning and memory
Limbic system is closely tied to the pleasure systems of the
brain
Closely tied to the prefrontal cortex which is involved in
executive functions and problem solving and personality
Prefrontal cortex also inhibits limbic system
Limbic system consists of the singulate gyrus, the fornix, the
hippocampus, the septal nucleus, the mammillary bodies, the
amygdala
Amygdala is a group of nuclei that receive inputs from many
places.
It is responsible for summation of signals. Including limbic
cortex, parietal cortex, temporal cortex, the occipital lobes,
the visual and auditory association areas.
Its an area of summation of signals and then it transmits back
signals from areas which it has received signals from.
What happens when you stimulate amygdal?
- Increase or decrease arterial BP and HR
- Effects GI motility and secretion
- Urination
- Effects anterior pituitary hormones
- Movements related to eating

- Negative emotions(fear,rage and aggressive behaviour)

- Awareness of invasion of personal space
- Complex sexual responses
Amygdala is a paired structure
KLUVER BUCY SYNDROME IS BILATERAL AMYGDALA DAMAGE
-disinhibition
-docile
-extreme curiosity
-hyperorality
-inappapproiate sexual behaviour
-mounting inanimate objects
Hypothalamus:
Part of the brain that provides law and order. It regulates
body temperature, hunger and thirst, sleep and circadian
rythms, and endocrine system through regulation of the
pituitary gland.
Anterior Hypothalamus Nuclues:
Anterior Nucleus: thermoregulation
Suprachiasmatic: circadian rhythm
Preoptic area: secretes GnRH
Supraoptic area: secretes Water balance ADH
Paraventricular: Secretes oxytocin, CRH,TRH, regulates
anterior pituitary
Middle of hypothalamus is sometimes called the tuberal
hypothalamus.
Arcuate nucleus: secretes GHRH, dopamine, pulsatile GnRH,
regulates apetite
Lateral: hunger regulation, inhibited by leptin
Venteromedial: regulates satiety, stimulated by leptin
Dorosmedial: regulates hunger
Posteror Nucleus: thermoregulation (warms the body) via
piloerection
Mammilary: memory