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523 Cards in this Set

  • Front
  • Back
Patient presents with decreased pain and temperature sensation over
the lateral aspects of both arms.a
Syringomyelia.
Penlight in patient’s right eyeiproduces bilateral pupillary
constriction. When moved to
the left eye, there is paradoxical
dilatation.
Atrophy of the left optic nerve.
Patient describes decreaed prick sensation on the lateral aspect of her leg and foot.
Dorsiflexion and eversion of foot
(common peroneal nerve).
 Elderly woman presents with
arthritis and tingling over the
lateral digits of her right hand.
Carpal tunnel syndrome,

median nerve compression.
20-year-old dancer reports decreased plantar flexion and sensation over the back of her thigh, calf,
and lateral half of her foot.n
Tibial (L4–S3). injury
Woman involved in a motor
vehicle accident cannot turn
her head to the left and has and
right shoulder droop.
Right CN XI (runs through
jugular foramen with CN IX
X), innervating sternocleidomastoid and
trapezius muscles.n
Man presents with one wild,
flailing arm.
lesion of Contralateral subthalamic nucleus
(hemiballismus).s
Patient with cortical lesion does not know that he has a disease.
lesion of Right parietal lobe.
Patient cannot protrude tongue
toward left side and has a
right-sided spastic paralysis
lesion in Left medulla, CN XII.
Teen falls while rollerblading
and hurts his elbow. He can’t feel the medial part of his palm.l
Ulnar nerve due to broken medial condyle.
Field hockey player presents to the ER after falling on her arm during practice. with midshaft humerous break. complications
Radial nerve and deep brachial artery, which run together.
patient can't blink on right side and can't seal lips
bells' palsy CN VII
patient complains of pain numbness and tingling and has wasting of thenar eminence
carpal tunnel syndrome; median nerve
stage of sleep with variable BP,penile tumescence, and variable EEG.
REM sleep.
Woman presents with headache,
visual disturbance, galactorrhea,
and amenorrhea.
Prolactinoma.
43-year-old man experiences
dizziness and tinnitus. CT
shows enlarged internal
acoustic meatus.z
Schwannoma.
25-year-old female presents
with sudden uniocular vision
loss and slightly slurred speech.
She has a history of weakness
and paresthesias that have resolved.
Multiple sclerosis.
10-year-old child “spaces out” in class (e.g., stops talking
midsentence and then continues
as if nothing had happened).
Absence seizures.
Man on several medications,
including antidepressants and his symptoms?
antihypertensives, has mydriasis
What is the cause
TCA.
Woman on MAO inhibitor
has hypertensive crisis after
a meal.
Tyramine (wine or cheese).
Astrocyte
marker:
GFAP.
Astrocytes
what they do
physical support, repair, K+ metabolism;
help maintain blood-brain barrier.
CNS/PNS Support Cells
role of
Ependymal cells
–inner lining of ventricles.
CNS/PNS Support Cells
role of Microglia
phagocytosis.
CNS/PNS Support Cells
role of Oligodendroglia
central myelin production
CNS/PNS Support Cells
role of Schwann cells–
peripheral myelin production.s
These cells are destroyed in
multiple sclerosis.
Oligodendroglia
Acoustic neuroma is an
example of
schwannoma.
Permeability barrier; must be rejoined in microsurgery for limb reattachment.
Perineurium–
Acoustic neuroma Location
commonly associated
with internal acoustic
meatus (CN VII, VIII).
Predominant type of glial cell in white matter.
Oligodendroglia
Mesodermal origin.

Not readily
discernible in Nissl stains.

Have small irregular
nuclei and relatively little cytoplasm.
Microglia
HIV-infected ????? fuse to
form multinucleated giant
cells in the CNS.
microglia
HIV-infected microglia fuse to
form ???
multinucleated giant
cells in the CNS.
Derivation of All CNS/PNS support cells
Microglia, like macrophages, originate from
mesoderm. All other CNS/PNS supportive
cells originate from ectoderm.
Sensory corpuscles
Meissner’s
where and what
small
in dermis of palms, soles, and digits of skin. glabrous (hairless) skin.

light discriminatory touch of
Sensory corpuscles
Pacinian
where and what
Large

found in deeper
layers of skin at ligaments, joint capsules, serous
membranes, mesenteries.

Involved in pressure,
coarse touch, vibration, and tension.
Sensory corpuscles
Merkel’s
where and what
Cup-shaped nerve endings (tactile disks) in dermis
of fingertips, hair follicles, hard palate.

Involved
in light, crude touch.
Small, encapsulated nerve endings found in
dermis of palms, soles, and digits of skin. Involved
in light discriminatory touch of glabrous (hairless)
skin.
Meissner’s
Large, encapsulated nerve endings found in deeper
layers of skin at ligaments, joint capsules, serous
membranes, mesenteries. Involved in pressure,
coarse touch, vibration, and tension.
Pacinian
Cup-shaped nerve endings (tactile disks) in dermis
of fingertips, hair follicles, hard palate. Involved
in light, crude touch.
Merkel’s
Inner ear
makeup of peri vs endo lymph
Peri––think outside of cell (Na+). ECF like

Endo––think inside of cell (K+). ICF like
Inner ear
location of of peri vs endo lymph
Peri––(bony labyrinth)


Endo––(membranous
labyrinth)
Hair cells are the sensory elements in
both vestibular
apparatus (spatial orientation) and cochlea
(hearing).
the sensory elements in both vestibular apparatus (spatial orientation) and cochlea
(hearing).
Hair cells
Semicircular canals contain
????? which detect
Ampullae

Angular acceleration.
Utricle and saccule contain
????? which detect .
maculae–

linear
acceleration.
?????? contain
maculae––detect linear
acceleration.
Utricle and saccule
???????? contain
Ampullae––detect Angular
acceleration.
Semicircular canals
cochlea
???????? picks up high-
frequency sound. ??????
picks up low-frequency sound.
Base of the cochlea

Apex of the cochlea
Hearing loss in the elderly––what pitch
high frequency → low
frequency.
what forms the BBB
. Tight junctions between nonfenestrated capillary endothelial cells

. Basement membrane

. Astrocyte processes
Other barriers include: not BBB
1. Blood-testis barrier

2. Maternal-fetal blood
barrier of placenta
BBB transport
wrt Glucose, proteins and lipids
Glucose and amino acids cross by carrier-mediated
transport mechanism.

Nonpolar/lipid-soluble substances cross more
readily than do
Parts of brain w/o BBB
(e.g., area postrema––vomiting after chemo) or
neurosecretory products to enter circulation

(e.g., neurohypophysis––ADH release).
e
infarction and BBB
Infarction destroys endothelial
cell tight junctions
→ vasogenic edema.
Hypothalamus
functions
The hypothalamus wears TAN
HATS.
Thirst
Adenohypophysis
Neruohypophysis
Hunger
Autonomic regulation
Temp regulation
Sexual urges
Hypothalamus
Location involved in
Thirst
Thirst and water balance (supraoptic nucleus).
Hypothalamus
Location involved in
Neurohypophysis
Neurohypophysis and median eminence release
hormones synthesized in hypothalamic nuclei.
Hypothalamus
Location involved in
Hunger ans satiety
Hunger (lateral ucleus; damage → anorexia/starvation

Satiety (ventromedial
nucleus; damage → hyperphagia and obesity).
Hypothalamus
Location involved in
Autonomic regulation
anterior hypothalamus
regulates parasympathetic;

posterior hypothalamus
regulates sympathetic

circadian rhythms
(suprachiasmatic nucleus).
Hypothalamus
Location involved in
Temperature regulation
(posterior hypothalamus
regulates heat conservation and production when cold;

Anterior hypothalamus coordinates Cooling when hot).
Hypothalamus
Location involved in
Sexual urges and emotions
(Septal nucleus––
destruction → rage).
Hypothalamus
mnemonic
Hunger
If you zap your ventromedial
nucleus, you grow ventrally
and medially.
Hypothalamus
mnemonic
Temp
If you zap your Posterior
hypothalamus, you become a
Poikilotherm (cold-blooded
snake).

A/C = anterior cooling.
Posterior pituitary
aka
neurohypophysis
neurohypophysis
aka
Posterior pituitary
neurohypophysis
where axonal projections come from
Receives hypothalamic axonal projections from
-supraoptic (ADH)

-paraventricular (oxytocin)
nuclei.
Derivation of the word
Oxytocin
oxys = quick;
tocos = birth.
Major relay for ascending sensory information
that ultimately reaches the cortex.
Thalamus
Thalamus
Function of the
LGN
Lateral geniculate nucleus (LGN)––visual.

Lateral for Light.
Medial for Music.
Thalamus
Function of the
MGN
Medial geniculate nucleus (MGN)––auditory.

Lateral for Light.
Medial for Music.
Thalamus
Function of the
VPL
Ventral posterior nucleus, lateral part (VPL)

––body sensation (proprioception, pressure,pain, touch, vibration via dorsal columns, spinothalamic tract).
Thalamus
Function of the
VPM
Ventral posterior nucleus, medial part (VPM)

––facial sensation (via CN V).
Thalamus
Function of the
VA
Ventral anterior/lateral (VA/VL) nuclei
––motor.
Thalamus
Function of the
VL
Ventral anterior/lateral (VA/VL) nuclei
––motor.
Thalamus
which nucleus
Visual
Lateral geniculate nucleus (LGN)––visual.

Lateral for Light.
Medial for Music.
Thalamus
which nucleus
auditory.
Medial geniculate nucleus (MGN)––

Lateral for Light.
Medial for Music.
Thalamus
which nucleus
––body sensation (proprioception, pressure
pain, touch, vibration via dorsal columns,
spinothalamic tract).
Ventral posterior nucleus, lateral part (VPL)
Thalamus
which nucleus
facial sensation (via CN V).
Ventral posterior nucleus, medial part (VPM)
Thalamus
which nucleus
motor.
Ventral anterior/lateral (VA/VL) nuclei
Limbic system is
Responsible for
The famous 5 F’s.

Feeding, Fighting, Feeling, Flight, and sex (use your imagination).
Important in voluntary movements and making postural adjustments.
Basal ganglia
Parkinson’s disease symptoms due to ↓ input from the ??????(leading
to ↓ stimulation of the ?????and ↓ inhibition of the ???????
substantia nigra

direct pathway

indirect pathway).
Frontal lobe
functions
“Executive functions”––planning, inhibition, concentration, orientation, language,
abstraction, judgment, motor regulation, mood.
most notable in frontal lobe lesion.
Lack of social judgment
Anterior cerebral artery––supplies
medial surface of the brain, leg-foot area of motor and
sensory cortices.
Middle cerebral artery––supplies
lateral aspect of brain, trunk-arm-face area of motor
and sensory cortices, Broca’s and Wernicke’s speech areas.
most common site of circle of Willis aneurysm; lesion
may cause visual-field defects.
Anterior communicating artery––
supplies medial surface of the brain, leg-foot area of motor and
sensory cortices.
Anterior cerebral artery––
–supplies lateral aspect of brain, trunk-arm-face area of motor and sensory cortices, Broca’s and Wernicke’s speech areas.
Middle cerebral artery–
common area of aneurysm; causes CN III palsy.
Posterior communicating artery––
“arteries of stroke”; supply internal
capsule, caudate, putamen, globus pallidus.
Lateral striate––
divisions of middle cerebral artery
Lateral striate––
In general, stroke of anterior circle →
general sensory and motor dysfunction, aphasia;
stroke of posterior circle →
cranial nerve deficits (vertigo, visual deficits), coma,
cerebellar deficits (ataxia).
General location of a stroke that
leads to
general sensory and motor dysfunction, aphasia;
In general, stroke of anterior circle
General location of a stroke that
leads to
cranial nerve deficits (vertigo, visual deficits), coma,
cerebellar deficits (ataxia).
stroke of posterior circle
Venous sinuses run in the ?
dura mater where its meningeal and periosteal layers separate
Cerebral veins → ? → ?
venous sinuses → internal jugular vein.
Lateral ventricle → 3rd ventricle via
foramen of Monro.
3rd ventricle → 4th ventricle via
aqueduct of Sylvius.
4th ventricle → subarachnoid space via:
Foramina of Luschka = lateral.
Foramen of Magendie = medial.
Spinal nerves
number of each
There are 31 spinal nerves altogether: 8 cervical, 12
thoracic, 5 lumbar, 5 sacral, 1 coccygeal.

31, just like 31 flavors!
Vertebral disk herniation usually
occurs where
between L5 and S1.
lumbar puncture order of Structures pierced
1. Skin/superficial fascia
2. Ligaments (supraspinous, interspinous,
ligamentum flavum)
3. Epidural space
4. Dura mater
5. Subdural space
6. Arachnoid
7. Subarachnoid space––CSF
lumbar puncture
where does needle end up
Needle in
subarachnoid space
lumbar puncture
what is not pierced
Pia is not pierced.
lumbar puncture
where to go in
between L4 and L5 (at the level of iliac crests).
Spinal tract anatomy and functions
Tract and function

Dorsal column-medial
lemniscal pathway
(ascending pressure,
vibration, touch, and
proprioceptive
sensation)
Spinal tract anatomy and functions
Tract and function

Spinothalamic tract
(ascending pain and
temperature sensation)
Spinal tract anatomy and functions
Tract and function

Lateral corticospinal
tract
(descending
voluntary movement
of contralateral limbs)
Which Tract
(ascending pressure,
vibration, touch, and
proprioceptive
sensation)
Dorsal column-medial
lemniscal pathway
Which Tract
(ascending pain and
temperature sensation)
Spinothalamic tract
Which Tract
(descending
voluntary movement
of contralateral limbs)
Lateral corticospinal
tract
Dorsal column-medial
lemniscal pathway
1st-order neuron
Sensory nerve ending → dorsal root ganglion → enters spinal cord, ascends ipsilaterally in
dorsal column
Dorsal column-medial
lemniscal pathway
Synapse 1
Nucleus cuneatus or gracilis
(medulla)
Dorsal column-medial
lemniscal pathway
2nd-order neuron
Decussates in medulla → ascends contralaterally in medial lemniscus
Dorsal column-medial
lemniscal pathway
Synapse 2
VPL of
thalamus
Dorsal column-medial
lemniscal pathway
3rd-order neuron
Sensory cortex
Spinothalamic tract
1st-order neuron
Sensory nerve ending (A-delta and C fibers) → enters spinal cord
Spinothalamic tract
Synapse 1
Ipsilateral gray matter (spinal cord)
Spinothalamic tract
2nd-order neuron
Decussates at anterior white commissure → ascends contralaterally
Spinothalamic tract
Synapse 2
VPL of
thalamus
Spinothalamic tract
3rd-order neuron
Sensory cortex
Lateral corticospinal tract
1st-order neuron
Upper motor neuron:
1° motor cortex → descends ipsilaterally until decussating at caudal medulla
(pyramidal decussation)→ descends contralaterally
Lateral corticospinal tract
Synapse 1
Cell body of anterior horn
(spinal cord)
Lateral corticospinal tract
2nd-order neuron
Lower motor neuron:
Leaves spinal cord
Lateral corticospinal tract Synapse 2
Neuromuscular
junction
Lateral corticospinal tract 3rd-order neuron
None
Fasciculus gracilis =
Fasciculus cuneatus =
Legs


Arms
Dorsal column
organization

mnemonic
Fasciculus gracilis = legs.
Fasciculus cuneatus = arms.

Dorsal column is organized as
you are, with hands at
sides––arms outside and legs
inside.
Clavicle fracture is relatively
common––brachial plexus is
protected from injury by
subclavius muscle.
Upper extremity nerve injury
Site of injury and motor deficit

Radial
Shaft of humerus

loss of triceps brachii (triceps reflex), brachioradialis (brachioradialis reflex),
and extensor carpi radialis longus (→ wrist drop).
Upper extremity nerve injury
Site of injury and motor deficit

Median
Supracondyle of humerus

no loss of power in
any of the arm muscles;

loss of forearm pronati
wrist flexion, finger flexion, and several thumb
movements; eventually, thenar atrophy.
Upper extremity nerve injury
Site of injury and motor deficit

Ulnar
Medial epicondyle––

impaired wrist flexion and
adduction, and impaired adduction of thumb
and the ulnar 2 fingers (→ claw hand).
Upper extremity nerve injury
Site of injury and motor deficit

Axillary
Surgical neck of humerus or anterior shoulder
dislocation

loss of deltoid action.
Upper extremity nerve injury
Site of injury and motor deficit

Musculocutaneous
Loss of function of coracobrachialis, biceps, and
brachialis muscles (biceps reflex).
Upper extremity nerve injury
Deficit in sensation/course

Radial
Posterior brachial cutaneous.
Upper extremity nerve injury
Deficit in sensation/course

Median
Posterior antebrachial
cutaneous. Passes through
supinator.
Upper extremity nerve injury
Deficit in sensation/course

Ulnar
Loss of sensation over the
lateral palm and thumb and
the radial 2 and 1/2 fingers.

Passes
through pronator teres.
Upper extremity nerve injury
Deficit in sensation/course

Axillary
Loss of sensation over the
medial palm and ulnar 11/2
fingers.

Passes through flexor
carpi ulnaris.
Upper extremity nerve injury
Deficit in sensation/course

Musculocutaneous
Passes through coracobrachialis.
Erb-Duchenne
palsy
cause
Traction or tear of the upper trunk of the brachial
plexus (C5 and C6 roots); follows blow to shoulder
or trauma during delivery.
Erb-Duchenne
palsy
findings
Findings: limb hangs by side (paralysis of abductors),
medially rotated (paralysis of lateral rotators),
forearm is pronated (loss of biceps).
Findings: limb hangs by side (paralysis of abductors),
medially rotated (paralysis of lateral rotators),
forearm is pronated (loss of biceps).
Erb-Duchenne
palsy
findings
“Waiter’s tip” owing to
appearance of arm.
Erb-Duchenne
palsy
Thoracic outlet syndrome
aka
Klumpke’s palsy
Klumpke’s palsy
aka
Thoracic outlet syndrome
Klumpke’s palsy
cause
An embryologic defect; can compress subclavian artery and inferior trunk of brachial
plexus (C8, T1), resulting in thoracic outlet syndrome:
Klumpke’s palsy
findings
1. Atrophy of the thenar and hypothenar eminences

2. Atrophy of the interosseous muscles

3. Sensory deficits on the medial side of the forearm and hand

4. Disappearance of the radial pulse upon moving the head toward the opposite side
1. Atrophy of the thenar and hypothenar eminences
2. Atrophy of the interosseous muscles
3. Sensory deficits on the medial side of the forearm and hand
4. Disappearance of the radial pulse upon moving the head toward the opposite side
Thoracic outlet syndrome
aka
(Klumpke’spalsy)
Lower extremity nerve injury
motor deficit

Common peroneal
Loss of dorsiflexion (→ foot drop).

Deep peroneal
nerve innervates anterior compartment;

superficial peroneal nerve innervates lateral
compartment.
Lower extremity nerve injury
motor deficit

Tibial
Loss of plantar flexion. Tibial nerve innervates
posterior compartment.
Lower extremity nerve injury
motor deficit

Femoral
Loss of knee extension/knee jerk.
Lower extremity nerve injury
motor deficit

Obturator
Loss of hip adduction.
foot nerve mnemonic
PED = Peroneal Everts and
Dorsiflexes; if injured, foot
dropPED.


TIP = Tibial Inverts and
Plantarflexes; if injured,
can’t stand on TIPtoes.
Which nerve is damaged and give spinal nerves
Loss of dorsiflexion (→ foot drop).
Common peroneal
(L4–S2)
Which nerve is damaged and give spinal nerves
Loss of plantar flexion.
Tibial nerve (L4-S3)
Which nerve is damaged and give spinal nerves
Loss of knee extension/knee jerk.
Femoral (L2–L4)
Which nerve is damaged and give spinal nerves
Loss of hip adduction.
Obturator (L2–L4)
Which nerve is damaged and give spinal nerves

loss of triceps brachii brachioradialis and extensor carpi radialis longus
Radial C5-T1
Which nerve is damaged and give spinal nerves
Supracondyle of humerus––no loss of forearm pronation
wrist flexion, finger flexion, and several thumb
movements
Median C6-T1
Which nerve is damaged and give spinal nerves

impaired wrist flexion and
adduction, and impaired adduction of thumb
and the ulnar 2 fingers
Ulnar C7-T1
Which nerve is damaged and give spinal nerves
loss of deltoid action.
Axillary C5-C6
Which nerve is damaged and give spinal nerves

Loss of function of coracobrachialis, biceps, and
brachialis muscles
Musculocutaneous C5-C7
Radial nerve
mnemonic
Radial nerve innervates the
BEST!

Known as the “great extensor nerve.” Provides
innervation of the Brachioradialis, Extensors of the
wrist and fingers, Supinator, and Triceps.
Known as the “great extensor nerve.” Provides
innervation of the Brachioradialis, Extensors of the
wrist and fingers, Supinator, and Triceps.
Radial nerve
Thenar-hypothenar
muscles
Thenar––Opponens pollicis, Abductor pollicis brevis, Flexor pollicis brevis.

Hypothenar––Opponens digiti minimi, Abductor digiti minimi, Flexor digiti minimi.
Clinically important
landmarks
Pudendal nerve block
––ischial spine.
Clinically important
landmarks
Appendix

Lumbar puncture––iliac crest.
––2/3 of the way from the umbilicus to the anterior superior iliac spine (McBurney’s point).
Clinically important
landmarks
Lumbar puncture
––iliac crest.
Landmark
dermatomes
cervical
C2 is the posterior half of a skull “cap.”
C3 is a high turtleneck shirt.
C4 is a low-collar shirt.
Landmark
dermatomes
Thoracic
T4 (at the Teat pore) at the nipple.

T7 is at the xiphoid process.

T10 (belly butTEN) is at the umbilicus (important for early
appendicitis pain referral).
Landmark
dermatomes
Lumbar and Sacral
L1 is at the IL inguinal ligament.

L4 (down on al 4's)includes the kneecaps.

S2, S3, S4 (keep the penis off the floor)erection and sensation of penile and
anal zones.
Landmark
dermatomes
wrt appendix
T10 (belly butTEN) is at the umbilicus (important for early
appendicitis pain referral).
Spindle muscle control
what they monitor

Muscle spindle
Muscle spindles monitor muscle
length (help you pick up a
heavy suitcase when you
didn’t know how heavy it
was).
Spindle muscle control
what they monitor

Golgi tendon
Golgi tendon organs
monitor muscle tension (make
you drop a heavy suitcase
you’ve been holding too long).
Muscle spindle
path
In parallel with muscle bers. Muscle stretch → intrafusal stretch → stimulates Ia afferent → stimulates α motor neuron → reflex muscle
(extrafusal) contraction.
Gamma loop
path
CNS stimulates γ motor neuron →contracts intrafusal fiber → increased sensitivity of reflex arc.
4 Primitive reflexes
1. Moro reflex––extension of limbs when startled

2. Rooting reflex––nipple seeking

3. Palmar reflex––grasps objects in palm

4. Babinski reflex––large toe dorsiflexes with
plantar stimulation
Primitive reflexes when do they go and when do they return
Normally disappear within 1st
year. May reemerge following
frontal lobe lesion.
Clinical reflexes
what nerve roots are tested
with the hammer
Biceps = C5 nerve root.
Triceps = C7 nerve root.
Patella = L4 nerve root.
Achilles = S1 nerve root.
Clinical reflexes
what does babinski test
Babinski––dorsiflexion of the big toe and fanning of other
toes; sign of UMN lesion, but normal reflex in 1st year
of life.
Cranial nerve function

I
Smell
Cranial nerve function

II
Sight
Cranial nerve function

III
Eye motion, Pupil constriction, accommodation, eyelid opening
Cranial nerve function

IV
Eye movement
Cranial nerve function

V
Mastication, facial sensation
Cranial nerve function

VI
Eye movement
Cranial nerve function

VII
Facial movement, taste from anterior 2/3 of tongue, lacrimation, salivation (submaxillary and sublingual glands), eyelid closing
Cranial nerve function

VIII
Hearing, balance
Cranial nerve function

IX
Taste from posterior 1/3 of tongue, swallowing, salivation (parotid gland), monitoring carotid body and sinus chemo- and baroreceptors
Cranial nerve function

X
Taste from epiglottic region, swallowing, palate elevation, talking, thoracoabdominal viscera, monitoring aortic arch chemo- and baroreceptors
Cranial nerve function

XI
Head turning, shoulder shrugging
Cranial nerve function

XII
Tongue movement
Cranial nerve
nuclei
in general where are they located
Located in tegmentum portion of brain stem (between dorsal and ventral portions).

Lateral nuclei = sensory.
Medial nuclei = Motor.
Cranial nerve
nuclei
locations/levels of each
1. Midbrain––nuclei of CN III, IV.
2. Pons––nuclei of CN V, VI, VII, VIII.
3. Medulla––nuclei of CN IX, X, XI, XII.
Vagal nuclei
name them
Nucleus Solitarius
Nucleus aMbiguus
Dorsal motor nucleus
what does it do

Nucleus Solitarius
Visceral Sensory information (e.g., taste,
baroreceptors, gut distention).

VII, IX, X.
what does it do

Dorsal motor nucleus
Sends autonomic (parasympathetic) fibers to heart, lungs, and upper GI.
what does it do

Nucleus ambiguus
Nucleus aMbiguus IX, X, XI.

Motor innervation of pharynx, larynx, and upper
esophagus (e.g., swallowing, palate elevation).
Which nucleus

Visceral Sensory information (e.g., taste,
baroreceptors, gut distention).
Nucleus Solitarius
Which nucleus

Sends autonomic (parasympathetic) fibers to heart, lungs, and upper GI.
Dorsal motor nucleus
Which nucleus

Motor innervation of pharynx, larynx, and upper
esophagus (e.g., swallowing, palate elevation).
Nucleus ambiguus
What nerve/vessel passes through

Cribriform plate
CN I
What nerve/vessel passes through

Middle cranial fossa
(CN II–VI)––through sphenoid bone
What nerve/vessel passes through

Optic canal
CN II, ophthalmic artery, central
retinal vein)
What nerve/vessel passes through

Superior orbital fissure
(CN III, IV, V1, VI,
ophthalmic vein)
What nerve/vessel passes through

Foramen Rotundum
(CN V2)
What nerve/vessel passes through

Foramen Ovale
(CN V3)
What nerve/vessel passes through

Foramen spinosum
(middle meningeal
artery)
What nerve/vessel passes through

Posterior cranial fossa
(CN VII–XII)––through
temporal or occipital bone:
What nerve/vessel passes through

Internal auditory meatus
(CN VII, VIII)
What nerve/vessel passes through

Jugular foramen
(CN IX, X, XI, jugular vein)
What nerve/vessel passes through

Hypoglossal canal (CN XII)
(CN XII)
What nerve/vessel passes through

Foramen magnum
spinal roots of CN XI,
brain stem, vertebral arteries)
name the Middle cranial fossa and give the structures that pass through them
Middle cranial fossa (CN II–VI)––through sphenoid
bone:
1. Optic canal (CN II, ophthalmic artery, central
retinal vein)
2. Superior orbital fissure (CN III, IV, V1, VI,
ophthalmic vein)
3. Foramen Rotundum (CN V2)
4. Foramen Ovale (CN V3)
5. Foramen spinosum (middle meningeal
artery)
name the Posterior cranial fossa and give the structures that pass through them
Posterior cranial fossa (CN VII–XII)––through
temporal or occipital bone:
1. Internal auditory meatus (CN VII, VIII)
2. Jugular foramen (CN IX, X, XI, jugular vein)
3. Hypoglossal canal (CN XII)
4. Foramen magnum (spinal roots of CN XI,
brain stem, vertebral arteries)
Divisions of CN V exit owing
Divisions of CN V exit owing
to Standing Room Only.

Superior orbital fissure CN V1
Foramen Rotundum (CN V2)
Foramen Ovale (CN V )
Blood from eye and superficial cortex →
cavernous sinus → internal jugular vein.
CN ?????? and ????? fibers en route to ???? all pass
through the cavernous sinus. Only ?????? is
“free-floating.” Cavernous portion of ?????? is also here.
III, IV, V1, V2, and VI

postganglionic
sympathetic

the orbit

CN VI

internal
carotid artery
The nerves??????pass through the
cavernous sinus.
that control
extraocular muscles (plus V1
and V2)
Cavernous sinus syndrome
Cause and findings
due to mass effect

ophthalmoplegia, ophthalmic
and maxillary sensory loss.
due to mass effect

ophthalmoplegia, ophthalmic
and maxillary sensory loss.
Cavernous sinus syndrome
Mastication
muscles/nerves
and what each does
3 muscles close jaw: Masseter, teMporalis, Medial
pterygoid.
1 opens: lateral pterygoid.

All are
innervated by the trigeminal nerve (V3).
Mastication
muscles/nerves
mnemonic
M’s Munch.
Lateral Lowers (when speaking of pterygoids wrt jaw motion).
Muscles with
glossus innervation
All muscles with root glossus in their names (except
palatoglossus, innervated by vagus nerve) are
innervated by hypoglossal nerve.
Muscles with
glossus/palat
mnemonic
Glossus: hypoglossal nerve.

Palat: vagus nerve (except
TENSor, who was too
TENSE).
Muscles with palat innervation
All muscles with root palat in their names are innervated by vagus nerve.
(except tensor veli palatini, innervated by mandibular
branch of CN V)
Extraocular
muscles and nerves
CN VI innervates the Lateral
Rectus.
CN IV innervates the Superior
Oblique.(trochlear)
CN III innervates the Rest.

The “chemical formula”
LR6SO4R3.
actions of the The superior oblique
abducts,
introverts,
depresses.
Pupillary light reflex
pathway
CN II to pretectal nuclei in
midbrain that activate bilateral Edinger-Westphal nuclei; pupils contract bilaterally
(consensual reflex).
Internuclear ophthalmoplegia
aka
MLF syndrome
MLF syndrome
aka
Internuclear ophthalmoplegia
Internuclear ophthalmoplegia
mech and who gets
Lesion in the medial longitudinal fasciculus (MLF).
Results in medial rectus palsy on attempted lateral
gaze. Nystagmus in abducting eye.
Convergence is normal.

MLF =multiple sclerosis.
Internuclear ophthalmoplegia
mnemonic
MLF =MS.
Normal MLF function when looking left
When looking left, the left nucleus of CN VI fires, which contracts the left lateral rectus and stimulates the contralateral(right) nucleus of CN III via the right MLF to contract the right medial rectus.
Verbal CN testin
KLM sounds
Kuh-kuh-kuh tests palate elevation (CN X––vagus).

La-la-la tests tongue (CN XII––hypoglossal).

Mi-mi-mi tests lips (CN VII––facial).
Neural tube defects
cause and test
Associated with low folic acid intake during pregnancy.

Elevated α-fetoprotein in amniotic
fluid and maternal serum.
Spina bifida occulta
mech and description
––failure of bony spinal canal to close, but no structural herniation.
Usually seen at lower vertebral levels.
Meningocele
––meninges herniate through spinal canal defect.
Meningomyelocele
–meninges and spinal cord herniate through spinal canal defect.
consequences of Brain lesions at

Broca’s area
Motor (nonfluent/expressive) aphasia with good
comprehension
consequences of Brain lesions at

Wernicke’s area
Sensory (fluent/receptive) aphasia with poor
comprehension
consequences of Brain lesions at

Arcuate fasciculus
Conduction aphasia; poor repetition with good
comprehension, fluent speech
consequences of Brain lesions at

Amygdala (bilateral)
Klüver-Bucy syndrome (hyperorality, hypersexuality,
disinhibited behavior)
consequences of Brain lesions at

Frontal lobe
Personality changes and deficits in concentration,
orientation, and judgment; may have reemergence of
primitive reflexes
consequences of Brain lesions at

Right parietal lobe
Spatial neglect syndrome (agnosia of the
contralateral side of the world)
consequences of Brain lesions at

Reticular activating
system
Coma
consequences of Brain lesions at

Mammillary bodies
(bilateral)
Wernicke-Korsakoff syndrome
consequences of Brain lesions at

Basal ganglia
May result in tremor at rest, chorea, or athetosis
consequences of Brain lesions at

Cerebellar
hemisphere
Intention tremor, limb ataxia
consequences of Brain lesions at

Cerebellar vermis
Truncal ataxia, dysarthria
consequences of Brain lesions at

Subthalamic nucleus
Contralateral hemiballismus
Where is the lesion with the following findings

Motor (nonfluent/expressive) aphasia with good
comprehension
Broca’s area
Where is the lesion with the following findings

Sensory (fluent/receptive) aphasia with poor
comprehension
Wernicke’s area
Where is the lesion with the following findings

Conduction aphasia; poor repetition with good
comprehension, fluent speech
Arcuate fasciculus
Where is the lesion with the following findings

hyperorality, hypersexuality,
disinhibited behavior
Amygdala (bilateral)
Where is the lesion with the following findings

Personality changes and deficits in concentration,
orientation, and judgment; may have reemergence of
primitive reflexes
Frontal lobe
Where is the lesion with the following findings

Spatial neglect syndrome (agnosia of the
contralateral side of the world)
Right parietal lobe
Where is the lesion with the following findings

Coma
Reticular activating
system
Where is the lesion with the following findings

Wernicke-Korsakoff syndrome
Mammillary bodies
(bilateral)
Where is the lesion with the following findings

tremor at rest, chorea, or athetosis
Basal ganglia
Where is the lesion with the following findings

Intention tremor, limb ataxia
Cerebellar
hemisphere
Where is the lesion with the following findings

Truncal ataxia, dysarthria
Cerebellar vermis
Where is the lesion with the following findings

Contralateral hemiballismus
Subthalamic nucleus
cerebellar lesion
mnemonic
Hemispheres are laterally located––affect lateral limbs.

Vermis is centrally located––affects central body.
Connects Wernicke’s to
Broca’s area.
Arcuate fasciculus
what does the Arcuate fasciculus do
Connects Wernicke’s to
Broca’s area.
mnemonic for speech problems and brain lesions
BROca’s is BROken speech.

Wernicke’s is Wordy but makes no sense.
word derivation

Chorea
dancing (Greek).
Think choral dancing or
choreography.
description

Chorea
Sudden, jerky, purposeless movements.
Chorea

what disease process
Characteristic of basal ganglia lesion (e.g.,
Huntington’s disease).
word derivation

Athetosis
Athetos = not fixed (Greek).
Think snakelike.
description

Athetosis
Slow, writhing movements, especially of fingers.
Athetosis

what disease process
Characteristic of basal ganglia lesion.
description

Hemiballismus
Sudden, wild flailing of 1 arm.
Hemiballismus

what disease process
Characteristic of contralateral subthalamic nucleu
lesion. Loss of inhibition of thalamus through
globus pallidus.
most common cause of
dementia in the elderly.
Alzheimer’s disease
Associated with senile
plaques (extracellular, β-amyloid core) and
neurofibrillary tangles (intracellular, abnormally
phosphorylated tau protein).
Alzheimer’s disease
Familial form (10%
associated with genes on chromosomes 1, 14, 19
(APOE4 allele), and 21 (p-App gene
Alzheimer’s disease
Alzheimer’s disease
what are the plaques and tangles made of and where are they
plaques (extracellular, β-amyloid core)

neurofibrillary tangles (intracellular, abnormally
phosphorylated tau protein).
Alzheimer’s disease
what genes/chromosomes are involved
Familial form (10%
associated with genes on chromosomes 1, 14, 19
(APOE4 allele), and 21 (p-App gene)
2nd most common cause of dementia in the elderly.
Multi-infarct dementia
Multi-infarct dementia
may cause
May cause amyloid angiopathy
→intracranial hemorrhage.
Pick’s disease
what and where
dementia, aphasia, arkinsonian
aspects;

and is specific for the
frontal and temporal lobes.
Pick bodies
(intracellular,
aggregated tau protein)
Name Degenerative diseases of the
Cerebral cortex
Alzheimer’s disease
Pick’s disease
Name Degenerative diseases of the
Basal ganglia and
brain stem
Huntington's
Parkinson's
Name Degenerative diseases of the
Spinocerebellar
Motor neuron
Olivopontocerebellar atrophy;

Friedreich’s ataxia.


Amyotrophic lateral sclerosis (ALS)

Werdnig-Hoffmann
Polio–
Huntington’s disease
who
mech
findings
autosomal-dominant

Atrophy of
caudate nucleus (loss of GABAergic neurons).

chorea, dementia.
Huntington’s disease
genetic location
with mnemonic
Chromosome 4––expansion of
CAG repeats.
CAG––Caudate
loses ACh and GABA.
Parkinson’s disease
major association
Lewy bodies and depigmentation of the substantia nigra pars
compacta (loss of dopaminergic neurons)
Parkinson’s disease
rare association
. Rare cases have been linked to exposure to MPTP, a
contaminant in illicit street drugs.
Parkinson’s disease
findings
TRAP =
Tremor (at rest),
cogwheel Rigidity,
Akinesia,
Postural instability (you
are TRAPped in your body).
Olivopontocerebellar atrophy
Friedreich’s ataxia.
Amyotrophic lateral sclerosis (ALS)–
findings and <cause/marker>
with both LMN and UMN signs; no sensory
deficit. Can be caused by defect in SOD1.
Can be caused by defect in SOD1.
Amyotrophic lateral sclerosis (ALS)–
Commonly known as Lou
Gehrig’s disease.
Amyotrophic lateral sclerosis (ALS)
Werdnig-Hoffmann disease
who
findings
mech
autosomal-recessive

presents at birth as a “floppy baby,” tongue fasciculations; median age of death 7
months.

Associated with degeneration of anterior
horns.
Poliomyelitis
clinical findings
Malaise, headache, fever, nausea, abdominal pain, sore throat.
Signs of LMN lesions––
muscle weakness and atrophy, fasciculations, fibrillation, and hyporeflexia.
Poliomyelitis
how acquired/virus steps
Caused by poliovirus, which is transmitted by the fecal-oral route. Replicates in the
oropharynx and small intestine before spreading through the bloodstream to the CNS,where it leads to the destruction of cells in the anterior horn of the spinal cord, leading in
turn to LMN destruction.
Poliomyelitis
lab findings
CSF with lymphocytic pleocytosis with slight elevation of protein. Virus recovered
from stool or throat.
Classic triad of MS
Classic triad of MS is a
SIN:
Scanning speech
Intention tremor
Nystagmus
MS
Epidemiology
Most often affects women in
their 20s and 30s; more
common in whites.

↑ prevalence with ↑ distance from the equator
MS
What are the plaques and subsequent lab values
plaques (areas of oligodendrocyte loss and
reactive gliosis) with preservation of axons; ↑
protein (IgG) in CSF.
MS
course
relapsing-remitting course
MS
clinical findings
optic neuritis (sudden loss of vision),

MLF syndrome (internuclear ophthalmoplegia),

hemiparesis,

hemisensory symptoms,

bladder/ bowel incontinence
PML
what is it
caused by
who gets it
Progressive multifocal leukoencephalopathy

associated with JC virus

2–4% of AIDS patients (reactivation of latent
viral infection).
name the Demyelinating and
dysmyelinating
diseases
MS

PML

Acute disseminated postinfectious) encephalomyelitis.

Metachromatic leukodystrophy

Guillain-Barré syndrome
Metachromatic leukodystrophy
what type of disease is it
Demyelinating lysosomal storage disease
MS

Tx
β-interferon or
immunosuppressant therapy.
Guillain-Barré syndrome aka
acute idiopathic polyneuritis
acute idiopathic polyneuritis
aka
Guillain-Barré syndrome
Guillain-Barré
mech
Inflammation and demyelination of peripheral
nerves and motor fibers of ventral roots (sensory
effect less severe than motor), causing symmetric
ascending muscle weakness beginning in distal
lower extremities.
Guillain-Barré
clinical findings
rapid ascending paralysis

lower extremities. Facial diplegia in 50% of cas
Autonomic function may be severely affected
(e.g., cardiac irregularities, hypertension, or
hypotension).
Guillain-Barré
mortality and course
Almost all patients survive;

majority recover completely after weeks to months.
Guillain-Barré
associations
Associated with infections →
immune attack of peripheral
myelin (e.g., herpesvirus
or Campylobacter jejuni
infection), inoculations,
and stress, but no definitive
link to pathogens.
Guillain-Barré
Tx
Respiratory support is critical until recovery.

Additional treatment: plasmapheresis, IV immune globulins.
Guillain-Barré
lab findings
Findings: elevated CSF protein with normal cell count (“albuminocytologic dissociation”).

Elevated protein → papilledema.
Partial seizures
location and types
1 area of the brain.

1. Simple partial (consciousness intact)––
motor, sensory, autonomic, psychic

2. Complex partial (impaired consciousness)
Generalized seizures
location and types/descriptions
diffuse, more than one area.
1. Absence (petit mal)––blank stare
2. Myoclonic––quick, repetitive jerks
3. Tonic-clonic (grand mal)––alternating
stiffening and movement
4. Tonic––stiffening
5. Atonic––“drop” seizures
What is Epilepsy
Epilepsy is a disorder of
recurrent seizures (febrile
seizures are not epilepsy).
What can happen to partial seizures
can secondarily generalize
Causes of seizures by age:
Children––genetic, infection,
trauma, congenital, metabolic.

Adults––tumors, trauma, stroke, infection.

Elderly––stroke, tumor, trauma,
metabolic, infection.
CT shows “biconvex disk”
not crossing suture lines.
Epidural hematoma
Crescent-shaped hemorrhage
that crosses suture lines.
Subdural hematoma
Epidural hematoma
cause
Rupture of middle meningeal artery, 2° to
fracture of temporal bone.
Subdural hematoma
cause
Rupture of bridging veins.
Subdural hematoma
course
Venous bleeding (less
pressure) with delayed onset of symptoms.
Subdural hematoma
who
Seen
in elderly individuals, alcoholics, blunt trauma,
shaken baby
Subdural hematoma
predisposing factors
––brain atrophy
shaking, whiplash
Subarachnoid hemorrhage
cause
Rupture of an aneurysm (usually berry aneurysm) or an AVM. Bloody or xanthochromic spinal tap.
“worst headache
of my life.”
Subarachnoid hemorrhage
Subarachnoid hemorrhage
lab findings
Patients complain of Bloody or xanthochromic spinal tap.
Subarachnoid hemorrhage
clinical findings
“worst headache
of my life.”
Parenchymal hematoma
cause
hypertension,
amyloid angiopathy,
diabetes mellitus,
and tumor.
Berry aneurysms
where
Berry aneurysms occur at the bifurcations in the circle of Willis.
Most common site is
bifurcation of the anterior communicating artery.
Berry aneurysms
most common complication
Rupture
Berry aneurysms
Rupture leads to
hemorrhagic stroke/subarachnoid hemorrhage
Berry aneurysms
who specific conditions
adult polycystic
kidney disease,

Ehlers-Danlos syndrome,

Marfan’s syndrome. factors:
Berry aneurysms
risk factors (not APCKD, Marfan's,...)
advanced age,
hypertension,
smoking,
race (higher risk in blacks)
Brain tumor locations

The majority of adult 1° tumors are ?

the majority of childhood 1° tumors are ?
supratentorial,

infratentorial.
Adult Primary brain tumors

most common
GBM
Glioblastoma multiforme
(grade IV astrocytoma)
Adult Primary brain tumors

Prognosis grave; < 1-
year life expectancy. Found in cerebral hemispheres.
Can cross corpus callosum
GBM
Glioblastoma multiforme
(grade IV astrocytoma)
Adult Primary brain tumors

Stain astrocytes with GFAP.
GBM
Glioblastoma multiforme
(grade IV astrocytoma)
Adult Primary brain tumors

“Pseudopalisading” tumor
cells––border central areas
of necrosis and hemorrhage.
GBM
Glioblastoma multiforme
(grade IV astrocytoma)
Adult Primary brain tumors

2nd most common
Meningioma
Adult Primary brain tumors

Most often occurs
in convexities of hemispheres and parasagittal
region.
Meningioma
Adult Primary brain tumors

Arises from arachnoid cells external to
brain. Resectable.
Meningioma
Adult Primary brain tumors

Spindle cells concentrically
arranged in a whorled pattern;
Meningioma
Adult Primary brain tumors

often localized to 8th nerve →acoustic. Resectable.
C. Schwannoma
Adult Primary brain tumors

Bilateral schwannoma found in?
neurofibromatosis type 2.
Adult Primary brain tumors

Relatively rare, slow growing. Most often in
frontal lobes
Oligodendro- glioma
Adult Primary brain tumors

psammoma bodies (laminated calcifications).
Meningioma
Adult Primary brain tumors

Prolactin secreting is most common form.
Pituitary
adenoma
Adult Primary brain tumors

Bitemporal hemianopia and
hyper- or hypopituitarism are sequelae.
Pituitary
adenoma
Pituitary adenoma most common form
Prolactin secreting
Primary brain tumors Adult

Rathke's pouch
Pituitary adenoma
Primary brain tumors in adult

round nuclei with clear
cytoplasm.
Oligodendroglioma

“fried egg”
Primary brain tumors in Kids

Diffusely infiltrating glioma. most often found in posterior fossa. Benign; good prognosis.
Pilocytic astrocytoma
(low-grade)
Primary brain tumors in Kids

Highly malignant cerebellar tumor. A form of primitive neuroectodermal tumor (PNET).
Medulloblastoma
Primary brain tumors in Kids

compress 4th ventricle, causing hydrocephalus.
Medulloblastoma
or
Ependymoma
Primary brain tumors in Kids

Rosettes or perivascular
pseudorosette pattern of cells.
Medulloblastoma
Primary brain tumors in Kids

tumors most commonly found in
4th ventricle. Can cause hydrocephalus. Poor
prognosis.
Ependymoma
Primary brain tumors in Kids

Characteristic perivascular
pseudorosettes. Rod-shaped
blepharoplasts (basal ciliary
bodies) found near nucleus.
Ependymoma
Primary brain tumors in Kids

Most often cerebellar; associated with von Hippel-Lindau
Hemangioblastoma
Primary brain tumors in Kids

Can produce EPO →2°
polycythemia.
Hemangioblastoma
Primary brain tumors in Kids

Rosenthal fibers—eosinophilic,
corkscrew fibers.
Pilocytic astrocytoma
(low-grade)
Primary brain tumors in Kids

Foamy cells and high
vascularity are characteristic.
Hemangioblastoma
Primary brain tumors in Kids

Derived from remnants of
Rathke’s pouch.
Craniopharyngioma
Primary brain tumors in Kids

Calcification is common.
Craniopharyngioma
Primary brain tumors in Kids

Most common childhood supratentorial tumor.
Craniopharyngioma
Primary brain tumors in Kids

confused with pituitary
adenoma (can also cause bitemporal hemianopia).
Craniopharyngioma
Primary brain tumors in Kids
order of incidence
F. Pilocytic astrocytoma
(low-grade)

G. Medulloblastoma

H. Ependymoma

I. Hemangioblastoma

J. Craniopharyngioma
Primary brain tumors in Adults
order of incidence
A. Glioblastoma multiforme
(grade IV astrocytoma)

B. Meningioma

C. Schwannoma

D. Oligodendroglioma

E. Pituitary adenoma
Given the Spinal cord lesion
give the Conditions and the clinical findings

lower motor neuron lesions only, due to destruction of
anterior horns
Poliomyelitis and Werdnig-
Hoffmann disease:

flaccid
paralysis
Given the Spinal cord lesion
give the Conditions and the clinical findings

mostly white matter of cervical region; random and
asymmetric lesions, due to demyelination;
Multiple sclerosis:

scanning
speech, intention tremor,
nystagmus
Given the Spinal cord lesion
give the Conditions and the clinical findings

degeneration of dorsal roots
and dorsal columns;
Tabes dorsalis (3° syphilis):
Impaired proprioception,
ocomotor ataxia
Given the Spinal cord lesion
give the Conditions and the clinical findings

fibers of spinothalamic
tract damaged
Syringomyelia:

bilateral
loss of pain and
temperature sensation
Given the Spinal cord lesion
give the Conditions and the clinical findings


demyelination of dorsal
columns, lateral corticospinal
tracts, and spinocerebellar
tracts;
Vitamin B12 neuropathy and
Friedreich´s ataxia:

ataxic gait,
hyperreflexia, impaired
position and vibration sense
Given the Spinal cord lesion
give the Conditions and the clinical findings

spares dorsal columns and
tract of Lissauer
Complete occlusion of
ventral artery;
Given the Spinal cord lesion
give the Conditions and the clinical findings

combined upper
and lower motor neuron
deficits with no sensory
deficit; both upper and
lower motor neuron signs
ALS:
What is Syringomyelia
what is damaged
and how does it present
Enlargement of the central canal of spinal cord.
Crossing fibers of spinothalamic tract are damaged.
Bilateral loss of pain and temperature sensation in
upper extremities with preservation of touch
sensation. tion
derivation of
Syringomyelia
Syrinx (Greek) = tube, as in
syringe.
Syringomyelia
association
Often presents in patients with
Arnold-Chiari malformation.
Syringomyelia
location
Most common at C8–T1.
What is Tabes dorsales and what are the clinical findings
Degeneration of dorsal columns and dorsal roots due to 3° syphilis, resulting in impaired
proprioception and locomotor ataxia.
Tabes dorsalis
what other symptoms are associated with it
Charcot’s joints,

shooting Lightning) pain,

Argyll Robertson pupils (accommodation but not reactive to light),

absence of DTRs.
Charcot’s joints
progressive degeneration of a weight-bearing joint leading to deformity
Hemisection of spinal cord.
aka
Brown-Séquard syndrome
Brown-Séquard syndrome
aka
Hemisection of spinal cord.
Brown-Séquard syndrome
findings
1. Ipsilateral UMN signs (corticospinal tract) below
lesion––not shown
2. Ipsilateral loss of tactile, vibration, proprioception
sense (dorsal column) below lesion
3. Contralateral pain and temperature loss
(spinothalamic tract) below lesion
4. Ipsilateral loss of all sensation at level of lesion
5. LMN signs at level of lesion
Brown-Séquard syndrome above T1
If lesion occurs above T1, presents with Horner’s syndrome.
Horner’s syndrome aka
Sympathectomy of face
Sympathectomy of face
aka
Horner’s syndrome
Horner’s syndrome
clinical findings
1. Ptosis (slight drooping of eyelid)

2. Anhidrosis (absence of sweating) and flushing (rubor) of affected side of face

3. Miosis (pupil constriction)
Horner’s syndrome
assiciations
Associated with lesion of spinal cord above T1

(e.g., Pancoast’s tumor, hemisection, late-stage syringomyelia).
The 3-neuron oculosympathetic pathway projects from
the hypothalamus to the
intermediolateral column of the spinal cord, then to the superior cervical (sympathetic)
ganglion, and finally to the pupil, the smooth muscle of the eyelids, and the sweat
glands of the forehead and face.
findings of CN and cerebellar lesions

CN XII lesion (LMN)
tongue deviates toward side of lesion (lick your wounds).
findings of CN and cerebellar lesions

CN V motor lesion
jaw deviates toward side of lesion.
findings of CN and cerebellar lesions

Unilateral lesion of cerebellum
patient tends to fall toward side of lesion.
findings of CN and cerebellar lesions

CN X lesion
uvula deviates away from side of lesion.
findings of CN and cerebellar lesions

CN XI lesion
weakness turning head to contralateral side of (away from)lesion.

Shoulder droop on side of lesion.
CN VII lesions
associations
BLASTeD
Bell's palsy seen in
-Lyme
-AIDS
-Sarcoid
-Tumors
-Diabetes
CN VII lesions

UMN
vs
LMN
Contralateral paralysis of lower face only.

Ipsilateral paralysis of upper and lower face.
Brain herniation syndromes

name them and what they herniate through
1. Cingulate herniation
under falx cerebri

2. Downward transtentorial
(central) herniation

3. Uncal herniation

4. Cerebellar tonsillar
herniation into the
foramen magnum
Brain herniation syndromes

complications
Can compress anterior cerebral artery.

Coma and death result when these herniations compress the brain stem.
What is the Uncus
medial temporal lobe.
in Uncal herniation
what causes

Ipsilateral dilated pupil/ptosis
Stretching of CN III
in Uncal herniation
what causes

Contralateral homonymous hemianopia
Compression of ipsilateral posterior cerebral artery
in Uncal herniation
what causes

Ipsilateral paresis
Compression of contralateral crus cerebri (Kernohan’s notch)
in Uncal herniation
what causes

Duret hemorrhages/ paramedian artery rupture
Caudal displacement of brain stem
In Uncal Herniation what does

Stretching of CN III lead to?
Ipsilateral dilated
pupil/ptosis
In Uncal Herniation what does

Compression of ipsilateral posterior cerebral artery lead to?
Contralateral homonymous
hemianopia
In Uncal Herniation what does

Compression of contralateral crus cerebri (Kernohan’s notch) lead to?
Ipsilateral paresis
In Uncal Herniation what does

Caudal displacement of brain stem lead to?
Duret hemorrhages––
paramedian artery
rupture
Parkinson’s disease drugs
name 4 strategies
-Agonize dopamine
receptors

-Increase dopamine

-Prevent dopamine
breakdown

-Curb excess
cholinergic activity
Parkinson’s disease drugs
Name the ones that
Agonize dopamine
receptors
And give mechanisms
Bromocriptine (ergot alkaloid and partial dopamine agonist), pramipexole, ropinirole
Parkinson’s disease drugs
Name the ones that
Increase dopamine
And give mechanisms
Amantadine (may ↑ dopamine release)

L-dopa/carbidopa (converted to dopamine in
CNS)
Parkinson’s disease drugs
Name the ones that
Prevent dopamine
breakdown
And give mechanisms
Selegiline (selective MAO type B inhibitor)
; entacapone, tolcapone (COMT inhibitors)
Parkinson’s disease drugs
Name the ones that
Curb excess
cholinergic activity
And give mechanisms
Benztropine (Antimuscarinic; improves tremor
and rigidity but has little effect on
bradykinesia)
Parkinson’s disease
drugs

improves tremor
and rigidity but has little effect on
bradykinesia
Benztropine
Parkinson’s disease
drugs
mnemonic
BALSA:
Bromocriptine
Amantadine
Levodopa (with carbidopa)
Selegiline (and COMT
inhibitors)
Antimuscarinics
Parkinsonism is due to loss ?????
loss of dopaminergic neurons and excess cholinergic activity.
L-dopa (levodopa)

Mechanism
↑ level of dopamine in brain. Unlike dopamine, L-dopa can cross blood-brain barrier
and is converted by dopa decarboxylase in the CNS to dopamine.
L-dopa (levodopa)

Clinical use
Parkinsonism.
L-dopa (levodopa)

Toxicity
Arrhythmias from peripheral conversion to dopamine. Carbidopa minimizes this
L-dopa (levodopa)

wrt long term use
Long-term use can →
dyskinesia following administration, akinesia between doses.
Carbidopa

mech and uses
a peripheral
decarboxylase inhibitor, is given with L-dopa in order to ↑ the bioavailability of
L-dopa in the brain and to limit peripheral side effects.
Selegiline

mech
Selectively inhibits MAO-B, thereby ↑ the availability of dopamine.
Selegiline

Clinical use
Adjunctive agent to L-dopa in treatment of Parkinson’s disease.
Selegiline

Toxicity
May enhance adverse effects of L-dopa.
Sumatriptan

Mechanism
5-HT agonist. Causes vasoconstriction. Half-life < 2 hours.
Sumatriptan

Clinical use
Acute migraine,
cluster headache attacks.
Sumatriptan

Toxicity
Coronary vasospasm, mild tingling

(contraindicated in patients with CAD or Prinzmetal’s angina).
contraindicated in patients with CAD or Prinzmetal’s angina)

Coronary vasospasm, mild tingling
Sumatriptan
Which epilepsy drugs can be used for partial seziures
All except

-Ethosuximide

-Benzodiazepines
(diazepam or
lorazepam)
Epilepsy drugs
1st line for

Tonic-Clonic
Phenytoin

Carbamazapine

Valproic acid
Epilepsy drugs
1st line for

trigeminal
neuralgia
Carbamazepine
Epilepsy drugs
1st line for

Absence
Ethosuximide
Epilepsy drugs
1st line for

prophylaxis of Status
Phenytoin
Epilepsy drugs
1st line for

acute Status
Benzodiazapines (diazapam or lorazapam)
Epilepsy drugs
1st line for

Pregnant women or children
Phenobarbital
Epilepsy drugs
which one is

Also used for peripheral neuropathy
Gabapentin
Epilepsy drugs
which one is

Also used for acute seizures of
eclampsia
Benzodiazepines (diazepam or
lorazepam)
Epilepsy drugs
which one is

Also used for myoclonic
seizures
Valproic acid
Epilepsy drugs
1st line for

prevent seizures of eclampsia
MgSO4
Epilepsy drugs mech

Phenytoin
↑ Na+ channel inactivation
Epilepsy drugs mech

Carbamazepine
↑ Na+ channel inactivation
Epilepsy drugs mech

Lamotrigine
Blocks voltage-gated Na+
channels
Epilepsy drugs mech

Gabapentin
↑ GABA release
Epilepsy drugs mech

Topiramate
BlocksNa+ channels,
↑ GABA action
Epilepsy drugs mech

Phenobarbital
↑ GABAA action
Epilepsy drugs mech

Valproic acid
↑ Na+ channel inactivation,
↑ GABA concentration
Epilepsy drugs mech

Ethosuximide
Blocks thalamic T-type Ca2+
channels
Epilepsy drugs mech

Benzodiazepines
(diazepam or
lorazepam)
↑ GABAA action
Epilepsy drug toxicities

Benzodiazepines
Sedation, tolerance, dependence.
Epilepsy drug toxicities

Carbamazepine
dyscrasias (agranulocytosis, aplastic anemia),
liver toxicity,
teratogenesis,
induction of cytochrome P-450.
Epilepsy drug toxicities

Ethosuximide
GI distress,
urticaria,
Stevens-Johnson syndrome.
Epilepsy drug toxicities

Phenobarbital
Sedation, tolerance, dependence, induction of cytochrome P-450.
Epilepsy drug toxicities

Phenytoin
Nystagmus, diplopia, ataxia, sedation, gingival hyperplasia, hirsutism, megaloblastic
anemia, teratogenesis, SLE-like syndrome, induction of cytochrome P-450.
Epilepsy drug toxicities

Valproic acid
GI distress,
rare but fatal hepatotoxicity (measure LFTs),
neural tube defects
in fetus (spina bifida), tremor, weight gain.
Epilepsy drug toxicities

Lamotrigine
Stevens-Johnson syndrome.
Epilepsy drug toxicities

Gabapentin
Sedation, ataxia.
Epilepsy drug toxicities

Topiramate
Sedation, mental dulling, kidney stones, weight loss.
How to treat an overdose of

Barbiturates
Treat overdose with symptom management (assist
respiration, ↑ BP).
How to treat an overdose of

Benzodiazepines
Treat overdose with flumazenil (competitive antagonist
at GABA receptor).
Epilepsy drug toxicities

Contraindicated in porphyria.
Barbiturates
Clinical use for

Phenytoin
Tonic-clonic seizures. Also a class IB antiarrhythmic
Clinical use for

Barbiturates
Sedative for anxiety, seizures, insomnia, induction
of anesthesia (thiopental).
Clinical use for

Benzodiazepines
Anxiety, spasticity, status epilepticus (lorazepam and
diazepam), detoxification (especially alcohol
withdrawal–DTs), night terrors, sleepwalking.
short acting Benzo's
Short acting = TOM Thumb =
Triazolam, Oxazepam,
Midazolam.
Benzodiazepines
Mechanism
Mnemonic
FREnzodiazepines (increased
FREquency).


Facilitate GABAA action by ↑ frequency of Cl− channel opening.
Barbiturates
Mechanism
mnemonic
BarbiDURATe (increased
DURATion).

Facilitate GABAA action by ↑ duration of Cl− channel opening, thus ↓ neuron firing.
Anesthetics—
general principles
blood and lipid soubility
Drugs with ↓ solubility in blood = rapid induction and recovery times.

Drugs with ↑ solubility in lipids =↑ potency =1/MAC
Anesthetics—
general principles
required characteristic
CNS drugs must be lipid soluble (cross the blood-brain barrier) or be actively transported.
Anesthetics—
general principles

N2O vs Halothane
N2O has low blood and lipid solubility, and thus fast induction and low
potency.

Halothane, in contrast, has ↑ lipid and blood solubility, and thus high potency and slow induction.
Name the
Inhaled anesthetics
Halothane, enflurane, isoflurane, sevoflurane, methoxyflurane,

nitrous oxide.
Mech of

Inhaled anesthetics
unknown.
effects of

Inhaled anesthetics
Myocardial depression, respiratory depression, nausea/emesis, ↑ cerebral blood flow
(↓ cerebral metabolic demand).
toxicity of

Inhaled anesthetics
Hepatotoxicity (halothane), nephrotoxicity (methoxyflurane), proconvulsant (enflurane),
malignant hyperthermia (rare).
Name the
Intravenous anesthetics
B. B. King on OPIATES
PROPOses FOOLishly.

Barbiturates
Benzodiazepines
Arylcyclohexamines
(Ketamine)
Opiates
Propofol
Intravenous anesthetics
Barbiturates
which one, potency and uses
Thiopental––high potency, high lipid solubility, rapid
entry into brain. Used for induction of anesthesia
and short surgical procedures.
Intravenous anesthetics
Barbiturates
how terminated
Effect terminated by
redistribution from brain. ↓ cerebral blood flow.
Intravenous anesthetics
Benzodiazepines
which one, uses
Midazolam most common drug used for endoscopy; used adjunctively with gaseous anesthetics and
narcotics.
Intravenous anesthetics
Benzodiazepines
adverse reactions and Tx
May cause severe postoperative
respiratory depression, ↓ BP (treat with flumazenil),
and amnesia.
Intravenous anesthetics
Arylcyclohexamines
name, use, adverse reactions
(Ketamine)

PCP analogs that act as dissociative anesthetics.
Cardiovascular stimulants. Cause disorientation,
hallucination, and bad dreams. ↑ cerebral blood flow.
Intravenous anesthetics
Opiates
Morphine, fentanyl used with other CNS depressants
during general anesthesia.
Intravenous anesthetics
Propofol
Used for rapid anesthesia induction and short
procedures.
Intravenous anesthetics
nausea and propofol
Less postoperative nausea than
thiopental.
Local anesthetics which are
Esters vs Amides
Esters––procaine, cocaine, tetracaine;

amides––lIdocaIne, mepIvacaIne, bupIvacaIne
(amIdes have 2 I’s in name).
Local anesthetics
mech
Block Na+ channels by binding to specific receptors on inner portion of channel.
Local anesthetics
mech specifically for 3° amine
3° amine local anesthetics penetrate membrane in uncharged form, then bind to ion
channels as charged form.
Local anesthetics
considerations WRT
infection
In infected (acidic) tissue, anesthetics are charged and cannot penetrate membrane
effectively. Therefore, more anesthetic is needed in these cases.
Local anesthetics
considerations WRT
order of nerve blockade (structure of nerve)
small unmyelinated pain fibers > small myelinated autonomic fibers > large myelinated
autonomic fibers.
Local anesthetics
considerations WRT
order of nerve blockade (function of nerve)
pain (lose first) > temperature > touch > pressure (lose
last).
Local anesthetics
clinical use
Minor surgical procedures, spinal anesthesia
Local anesthetics
and allergies
If allergic to esters (more likely), give amides.
Local anesthetics
Toxicities
-CNS excitation,
-severe cardiovascular toxicity (bupivacaine),
-hypertension, hypotension,
-arrhythmias (cocaine).
Which
Local anesthetic can cause
severe cardiovascular toxicity
(bupivacaine)
Which
Local anesthetic can cause
arrhythmias
(cocaine)
Neuromuscular blocking drugs
uses
Used for muscle paralysis in surgery or mechanical ventilation
Neuromuscular blocking drugs
wrt selectivity
Selective for motor
(vs. autonomic) nicotinic receptor.
Neuromuscular blocking drugs
name the depolarizing ones
Succinylcholine
Neuromuscular blocking drugs
name the nondepolarizing ones
Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rapacuronium.
Succinylcholine.
mech
Neuromuscular blocking drugs
Depolarizing
Depolarizing Neuromuscular blocking drugs
reversal of blockade
Phase I (prolonged depolarization) no antidote. Block potentiated by cholinesterase inhibitors.

Phase II (repolarized but blocked)––antidote consists of cholinesterase inhibitors (e.g., neostigmine).
Mech of Nondepolarizing Neuromuscular blocking drugs
Competitive––compete with ACh for receptors
Nondepolarizing Neuromuscular blocking drugs
reversal of blockade
Reversal of blockade––neostigmine, edrophonium, and other cholinesterase inhibitors.
Dantrolene
uses
treatment of malignant hyperthermia,
and

neuroleptic malignant syndrome
Causes of Malignant Hyperthermia
the concomitant
use of inhalation anesthetics (except N2O) and succinylcholine.
Malignant Hyperthermia
Tx
Dantrolene
causes of neuroleptic malignant syndrome
(a toxicity of antipsychotic drugs).
neuroleptic malignant syndrome
Tx
Dantrolene
Dantrolene
Mech
prevents the release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle.
Brain Locations of Synthesis of neurotransmitters

NE
Locus Ceruleus
Brain Locations of Synthesis of neurotransmitters

Dopamine
Ventral tegmentum and SNc
Brain Locations of Synthesis of neurotransmitters

5-HT
Raphe Nucleus
Brain Locations of Synthesis of neurotransmitters

ACh
Basal nucleus of Mynert
Sensory corpuscles
which ones are in all skin
Free nerve endings (C, A-delta fibers)
Sensory corpuscles
Free nerve endings (C, A-delta fibers)

where and what
all skin and some viscera

Pain and Temp