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Neurology High Yield ( http://www.neuroanatomy.ca/module_list.

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Ischemic Brain Disease

IRREVERSIBLE DAMAGE after 5 minutes


Most vulnerable Hippocampus pyramidal, cerebellum purkinjie cells,
watershed areas
Risks: diabetes, smoking, ATRIAL FIBRILLATION, cocaine
Transient attack: less than 24 hours neurological deficit
Types or stroke
1. Thrombotic/atherosclerotic: MOST COMMON
-pale liquifactive necrosis (NO REFERFUSION)
-causes reactive Gliosis cystic cavity
-usually MCA therefore at periphery
2. Embolic
-Hemorrhagic red infarct (DUE TO REPERFUSION)
-usually atrial fibrillation or atherosclerotic plaques
-MCA
3. Lacunar Infarct
-small perforating vessels (at BASAL GANGLIA ) hyaline
arteriosclerosis
-Causes: diabetes, HTN
4. Hemorrhagic stroke
-from aneurysm
-CharcotBouchard microaneursym at basal ganglia
of lenticulostriate arteries
-from reperfusion of ischemic
5. Watershed Infarct
-prolonged HYPOTENSION
-damage usually bilateral deep cortical areas btw border of two
vessels
-ACA- MCA Top
-MCA- PCA Bottom

Ischemic stroke
Diminished blood flow
Leads to Gliosis
Watershed infarct
Artery
MCA

ACA

Hemorrhagic stroke
Hemorrhage aneurysm
Embolic
Reperfusion

Deficient
-Aphasia (Wernicke or brocas),
-Neglect syndrome (if right parietal, so ignore left side)
-hemiparesis weakness ( arm and face)
-homonymous hemianopsia (temporal more common, so superior
quadrant)
-LEG paresis
-hemiplegia (total paralysis)

PCA
Basilar
Lacunar
stroke

urinary incontinence
-homonymous hemianopsia with macular sparing (since MCA give
blood)
Affect pons ( cranial nerves, coma, apnea, vertigo)
-Pure motor ( internal capsule)
-Pure sensory (thalamus) but the smell intact (since only sensory
that bypass)
-dysarthria
-Ataxic hemiparesis (ipsilateral clumpsy

Imaging:
ACUTE do CT to see if hemorrhagic (dark on CT after 24 hours)
MRI shows up bright in 3-30 min and remain bright 10 days
Histology
12-24 H : RED neurons
24-72: necrosis + PMN
3 -5 day : macrophage
1-2 week : reactive gliosis + vascular proliferation
>2 week: glial scar
Treatment
tPA for occlusive (give within 3 hours)
warfarin/ aspirin for embolic once hemorrhage has been ruled out

Alzheimers

Diffuse cortical atrophy (widen sulci, narrow gyri, expand ventricles, ex


vacuo hydrocephalus )
Nucleus basalis of Meynert ( low ACH)
MOST COMMON cause of dementia ( 2nd is stroke)
Causes
1. Apolipoprotein E 2protective ( 2 serve and protect)
2.
E4 increases risk
3. Down Syndrome, chromosome 21 has APP (amyloid precursor
protein) * will stain with Congo red
-usually get it before 40
4. Presenilin
-Presenilin 1 (chromosome 14)
-
2 (chromosome 1)
Clinical diagnosis (confirmed on autopsy)
Histology
Senile/ neuritic plaques : ABETA-amyloid (beta cleavage of APP)
EXTRACELLULAR
-normal cleavage if ALPHA
Neurofibrillary tangles INTRACELLULAR in neurons
-HYPER phosphorylated Tau proteins which are microtubule
associated

-amount of tangles CORRELATED WITH DEGREE OF


DEMENTIA
Death: infection, penumonia

Diseases of myelination
Guillain- Barre Syndrome/ Acute inflammation Demylinating
polyradiculopathy (PNS and motor + autonomic)
Endoneurium and Schwann cells attacked = autoimmune demyliantion
1-3 weeks post GI infection OR RESPIRATORY (campylobacter jejuni) or
herpes
SYMMETRIC Ascending paralysis MOTOR AND AUTONOMIC
Physical exam:
Decrease or absent reflex
Facial paralysis if ascended to face
Autonomic dysfunction : cardiac and blood pressure fluctuation
Need to give respiratory support
Lumbar puncture: high protein, normal cell count (albuminocytologic
dissociation)
-this high protein is also seen in intracranial cancer
Progressive Multifocal Leukoencephalopathy( PML) (CNS )
Demylination by destruction of oligodendrocytes
Associated with JC virus reactivation in AIDS patients (polyomavirus,ds
DNA)
Dementia and neurological deficits with RAPID PROGRESSION
Typically fatal
Histology: widespread demylination, astrogliosis, lymphohistiocytosis
* associated with Natalizumab ( drug against alpha-integrin used in Crohns
and MS) *MS also demylination oligodendrocytes
Usually seen on one side more

Acute Disseminated /post infectious Encephalomyelitis


Multifocal PERIVENULAR inflammation and demyelination immune
activation
-after infection : chickenpox, measles
-Vaccination: rabies, smallpox
Similar to Multiple Sclerosis + constitutional (fever etc)
-mental status change, seizure coma
*usually in children and adolescents (but anyone can get it)
Metachromic Leukodystrophy ( CNS and PNS, myelin accumulate in lysosome)
Autosomal recessive lysosomal disease due to ARYLSULFATASE A
deficiency . cant metabolise sphingolipids
Impaired myelin sheath
Diverse psychiatric and neurological problems
Presents at different times depends on the form inherited
-infantile
-juvenile
-Adult
Krabbe Disease
A.R. lysosomal storage disease due to deficiency of GALACTOCEREBROSIDE
See globoid cells
Peripheral neuropathy, developmental delay, optic atrophy
AdrenoLeukoDystrophy
X linked disrupted metabolisim of VERY LONG chain Fatty acids
Build up Fatty acids in adrenal gland, testes, nervous system
Coma/ death, and adrenal crisis occur( not enough cortisol )
Charcot- Marie- Tooth Disease/ Hereditary motor and sensory neuropathy
Defective protein for structure and function of peripheral nerves or myelin
Onset less than 30 years old
Slow progressive weakness of distal limbs with loss of proprioception and
vibration
Autosomal Dominant usually. Associated with Scoliosis and foot deformity
(HGH ARCH OR FLAT)
PRESENT FOOT DROP, and loss of foot and hands motor and sensory first
Central Pontine Myelinolysis
Demylination in the pons : loss of corticospinal and corticobulbar tracts
Due to rapid correction of HYPONATREMIA
Seen in malnourished or alcoholics
Locked in presentation
Often fatal

Sodium
from low to high, pons will die
from high to low, brain will blow (edema/ herniation)

Multiple sclerosis
destruction of oligodendrocytes by CD8 T cells
anti-myelin Basic protein ( high protein IgG in CSF)
white matter plaque form in brain and spinal cord
in white women 20-40 onset in temperate climates.
HLA-DR2
CN2 is the only cranial nerve that is mylinated by oligodendrocytes therefore
affected in MS
Presentation
Optic neuritis (sudden loss vision)
Marcus Gunn: swinging flashlight test . Affected CN2
-normal eye pupil reflex normal,
-abnormal eye, both eyes dilate.
Intranuclear opthalmoplegia (MLF) : ipsilateral MLF to the CN3 that
cant Adduct . Nystagmus other eye when it Abducts . can be bilateral.
CONVERGENCE INTACT
Hemisensory symptoms
Intention tremor
Hemiparesis (weakness)
Bladder/bowl incontinence
SIN : Charcot classic triad of MS
-Scanning speech
-intention tremor, incontinence, intranuclear opthalmoplegia
-nystagmus
Evalutation
MRI gold standard : PERIVENTRICULAR plaques
Two demyelinating lesions separated in time and place
Lumbar puncture: high Leukocytes, oligoclonal banding (high IgG),
high Mylein basic protein, normal glucose
Treatment
IFN-beta : decreases the amount of inflammatory cells crossing BBB
And thought to increase Nerve growth factor
High dose steroids
Natalizumab : humanized monoclonal antibody against Alpha-integrin
a cell adhesion molecule

Neurophysiology
Neuronal cells
Astrocytes: GFAP stain, K+ metabolism, cause REACTIVE GLIOSIS, BBB,
remove excess neurotransmitter
Ependymal cells : line ventricles and maintain flow of CSF With cilia
Microglia : from MESODERM migrate here
-macrophages
-not seen on Nissl stain
-multinucleated with HIV infection
-rods in neurosyphilis
-perivascular in viral encephalitis
Oligodendrocytes : fried egg appearance. CNS myelination
-each mylinated up to 30 axons
-Multiple sclerosis destroys these
Schwann cells : peripheral myelination ( one axon/ Schwann)
-Schwannoma bilateral in NF-2 , at internal acoustic meatus affect CN 7 and 8
-destroyed in Guillian Barre syndrome

Muscle Spindles/ Golgi Tendon Organs


Muscle Spindle
Ia
Parallel to extrafusal muscle fibers
Stimulates the A alpha to contract
muscle
Detect stretch

Golgi tendon
Ib
Series to intrafusal muscle
Inhibits A alpha motor neurons to relax
muscle
Detect tension

GABA: accumbens : GRABA cucumber


Raphe nucleus serotonin: RAP SIR
Norepinephrin: Nor-mally LOOK SERIOUS

Blood Brain Barrier

Tight junctions btw endothelial cells + astrocyte foot processes


Vasogenic edema: infarction destroy tight juntions
Transport
o Diffusion: water and nonpolar
o Carrier transport: glucose, amino acids
o Active transport: weak acids, K+
Areas without BBB because they have fenestrated capillaries
-POSSuM Path
(posterior pituitary, OVLT, Subforniceal organ, subcommissural,
median eminence, Pineal gland)
o Choroid plexus
o Area Postrema : vomiting post chemo
o OVLT ( organum vasculosum of lamina terminalis) :osmotic
sensing
o Neurohypophysis: ADH release from brain to circulation

CSF
-Normal
0-4 lymphocytes or macrophage (PMN ALWAYS ABNORMAL)
low protein (high in tumor, Guillain-Barre, and MS = albuminocytologic
dissociation)
equal NA+ to serum
low PH since lower HCO3 higher Cl-, Mg2+ High Mg2+ Cleanse (causes diahrea)
lower K+, Ca2+, Hco3-, glucose
-Made by Choroid plexus in all ventricles (lateral, 3rd , 4th )
-recycled 2-3 times/day
Communicating hydrocephalus Made too much CSF (choroid plexus tumor)
Low absorption (arachnoid granulations scar
following meningitis)
Noncommunication
Blockage
Normal Pressure
Decrease reabsorption with ventricle dilation
therefore no increase in pressure
3W : wet, wacky weird old people
Ex Vacuo
Decreased brain size (stroke, HIV, Alzheimers,,
trauma)
Venticles larger, but CSF pressure normal

Sleep

Suprachiasmatic nucleus Ne pineal gland melatonin


Gaba agonist Alcohol, benzo, barbituates, NE decrease REM and delta
Benzos are useful in night terror and sleep walking.
Bed wetting treat with desmopressin

Stages
BATS Drink Blood
-Awake eyes open : beta ( highest frequency, lowest amplitude)
-Awake eyes closed: alpha
-Stage 1 NON-REM: Theta
-Stage 2: Spindle and K complex
* teeth grinding (Buxism)
-Stage 3: delta (lowest frequency, highest amplitude)
*sleep walking, night terror, bed wetting
-REM: beta
* dreams, and erection
REM sleep
dreaming, penile/clitoris erection
loss motor tone
memory processing function
high O2 use brain, high and variable pulse and BP
extraocular movements due to PPRF
EEG beta (paradoxical sleep)
Every 90 min and increase in duration every cycle
Decrease with age
Ach promote it, NE decrease it
Narcolepsy : start off with REM sleep
-Catplexy: loss all motor tone after strong emotional stimulus
-treat with amphetamines
Sleep Apnea
Types
Obstructive sleep apnea
-Obesity, Craniofacial, nasal congestion, large tonsils
Central sleep apnea : low CNS drive to breath
Symptoms
-excess daytime sleepiness (like narcolepsy) + unrestful sleep(narcolepsy
is restful)
-loud snoring
-small jaw, large neck circumference
-high EPO on labs, because chronic hypoxia
Treatment

-Weight loss
-Continuous positive airway pressure
Complication
-arrhythmia
-pulmonary hypertension

Anatomy
Head and neck
Thoracic Outlet
Subclavian vien and phrenic ON anterior scalene
Btw Anterior and middle scalene above is subclavian artery and below is
trunks brachial plexus
-Thoracic outlet syndrome : compression of brachial plexus and
subcleavian artery btw the anterior and middle scalene
Causes
-due to pancoast tumor
-cervical rib
-hypertophy of scalene muscles : body builders
Symptoms
-numbness and weakness on medial forearm and hand.
-claw hand ( ulnar affected most)
-decreased radial pulse
-Horners syndrome, and recurrent laryngeal n.
Pharyngeal apparatus
Pharyngeal pouch (endoderm) 1,2,3,4,6
Pharyngeal arch (mesoderm and neural crest cells)
Pharyngeal groove/ cleft (ectoderm)
Pharyngeal groove btw 1 and 2 : external ear (only groove)
Pharyngeal pouch 1 : middle ear
2nd pharyngeal arch grows over the other grooves ( if dont fuse properly then
pharyngeal/ lateral cervical/ brachial cyst on lateral part neck)

(skip 2) 579 , then 2 10


*DI George : 3rd pharyngeal POUCH (thymus and inferior calcitonin) + 4th fail to
differentiate NEURAL crest cell involves.
*thyroglossal cyst : remnant of thyroglossal duct that didnt fuse. Midline cyst that
moves on swallow and tongue protrusion
* Cleft lip and palate :
-develop from the mesoderm neural crest cells of 1st pharyngeal arch
-Cleft lip : maxillary processes dont fuse
-cleft palate: palatine shelves fail to fuse
First arch syndromes : abnormal formation of first arch (where mandible and
maxilla from) with abnormal neural crest migration

-Treacher Collins : small jaw, eyes slanted down, malformed ears and
hearing loss, colobomas
-Pierre Robin sequence : very small jaw , cleft palate, posterior displaced
tongue
Pharyngeal fistula : 2nd groove and pouch persist, fistula on anterior border
SCM

Nervous system development

Rostral neuropore close first ( 25 day) : high alpha feto protein +


POLYHYDRAMINOS
Caudal neuropore ( 27 day) : high alpha feto protein

Neural crest cells derivatives


CAlifornia MOTEL PASS
-craniofacial structure (1st arch maxilla and mandible)
-Arachnoid, and pia (dura is mesoderm)
-Melanocytes
-Odontoblasts
-Tracheal cartilage
-Enterochromaffin cells (adrenal medulla)
-Laryngeal cartilage
-Parafollicular cells , psueounipolar
-All ganglia, DRG, celiac
-Schwann
-Spiral septum (aorticopulomary septum) , also endocardial cushions

Neurons

Voluntary movement : 2 neuron system


Sensory : 3 motor neuron
Spinothalamic tracts always lateral in brainstem
Costicospinal always medial and ventral in brainstem
Medial lemniscus is medial in medullar and moves laterally in the midbrain
bc need to join spinothalamic since going to thalamus together

Dural Venous Sinus

Reflection of DURA mater


Cavernous sinus contains : CN 3,4, 5V1 and V2, 6, internal carotid
-lateral to sella tunica
-cavernous sinus thrombosis or carotid artery aneurysm affect CN6
first
-drains eyes, nose, upperlip, Danger triangle

Return blood to INTERNAL jugular vien at JUGULAR FORAMEN


-combo of sigmoid sinus and inferior petrosal sinus

Circle of Willis and arteries damage clinical


Mnemonics:
PICA and AICA are both lateral
o Face and body pain and temp split
o PIKA-CHEW : cant chew CN 9 and 10
o AICA is FACIAL : CN7 affected lower and upper face bc the nucleus
Medial in medulla and pons : medial lemniscus = touch, vibration,
proprioception opposite body
o Medial medulla: anterior spinal
o Paramedical branches of basilar artery
Anterior spinal Artery = Medial Medullary syndrome (CN12)
Medial lemniscus: contralateral touch, vibration, proprioception
CN12 : ipsilateral tongue, and deviate to lesion lick your wound
Pyramid : lower extremity contralateral
PICA = lateral Medullary / Wallenberg Syndrome ( CN 9 and 10)
Dissociated pain and temp : ipsilateral face (spinal V), contralateral body
(spinothalamic)
Descending hypothalamics: ipsilateral HOrners (beside spinothalamic
always)
Nucleus Ambiguus (CN 9 and 10) : ipisilateral dysphagia, dysarthria, loss gag
reflex, hoarsness voice
Vestibular nuclei: vertigo, nausea, nystagmus
Inferior cerebellar peduncle: ipsilateral limb ataxia
Medial Pontine : paramedical branches of basilar artery ( CN6 and 7)
**Corticospinal and medial lemniscus (LIKE MEDIAL MEDULLARY) BUT
HAVE CN 6 AFFECTED ( 7 is more lateral so spared)
AICA= Lateral Pontine

** same as PICA with the spinothalamic, dissociated pain and temp, and
hypothalamic
CN 7 and 8
Middle peduncle : ipsilateral aaxia
Vestibular nuclei : vertigo, nausea, vomiting, nystagmus

Pontocerebellar Angle: is CN7 and 8 only! NO OTHER TRACTS. (unilateral loss of


hearing)
Medial Midbrain = PCA (posterior cerebellar artery)
CN3 ipsilateral
Corticospinal and corticobulbar tracts : contralateral body and lower face
cn7
Dorsal Midbrain: Parinaud syndrome (pineal gland tumor)
Superior colliculus : vertical conjugate gaze
Pretectal : pupillary reflex
Cerebral aqueduct : hydrocephalus non communicating
PCA
Middle cerebral

Anterior cerebral
Posterior
communicating
Lenticlostriate
(lentiform and stratum)
Basilar
Anterior communicating

Homonymous hemianopsia with macular sparing


Contralateral face paralysis and sensory

arm

aphasia if on the left side


left side neglect if on right side (parietal lobe)
Contralateral leg and foot motor and sensory
CN3 down and out
Pure motor ( internal capsule)
Pure sensory (thalamus)
Locked in
Visual field

Spinal cord

Notochord nucleus pulposus


-posterior lateral herniate due to posterior ligament
31 nerves , C1-7 exit above, others exit below
spinal cord ends at L2, subarachnoid ends at S2 (children cord ends at L3-L4)
-Lumbar puncture at L4-L5 *do my iliac crest L4
Cauda Equina: S2-S 5 affect
o SADDLE SENSORY DISTURBANCE
o Lower back pain
o Lower extremity motor and sensory loss ( from sciatic) L4-S3
UNILATERAL ( therefore not much incontinence and impotence bc
only one side)
o Pelvic splanchnic

o Disk slip L4-L5 L5-S1, tumors, trauma


Conus medullaris UMN and LMN ( cauda equine ONLY LMN) +
BILATERAL SIGNS, INCONTINENCE, IMPOTENENCE

Basal Ganglia

Function : regulation of movements by modulation of cortical output


The basal ganglia usually feedback on cortex
DOPAMINE :
o D1 CAUSES MOVEMENT by activating inhibited pathway: excitatory
pathway (therefore Parkinsons decreases movement, bradykinesia
etc)
o D2 causes movement by INHIBITING inhibitory pathway
-parkinsons no dopamine here, causes activation inhibitory
pathway so low movement

Striatum : caudate and Putamen


-Activated by cortex,
-Direct: inhibit the internal Globus pallidus, so Thalamus activated
-indirect (D2) : inhibits externus Globus pallidus so subthalamus
activated activate internal globus pallidus inactivate thalamus
- D1 activate direct, D2 inactivate indirect = BOTH promote move
-Ach activate indirect therefore DECREASE MOVE
* Lesion direct = decrease movement ( Parkinsons)
* lesion indirect = chorea, athetosis, dystonia, tics ( EX: hemiballismus if
subthalamus lesion)
-Wilsons copper in basal ganglia (wing beating tremor) especially
putamen ( lenticulo= putamen and globus pallidus)

Cerebellum
-Input

- IPSILATERAL spinocerebellum via inferior


-CONTRALATERAL Cortical middle cerebellar peduncles
-Output
-Purkinjie fibers deep cerebellar nuclei superior cerebellar peduncle
contralateral cortex
- Regions
Region
Function
Input from
Deep cerebellar
nuclei
Vermis
Proximal muscles
Input spinal cord
Fastigial nucleus
Intermediate
Distal muscles
Input spinal cord
Eboliform and
zone
globose
Lateral
Planning and
Cortex and inferior Dentate nucleus
hemisphere
coordination
olivary nucleus
thalamus VA, VL
Flocculonodular
Balance and eye
CN8 vestibular
FastigialLateral
lobe
movement
vestibular
-dont eat greasy foods lateral to medial
Pathology
Damage vermis : truncal ataxia and dysarthria
Damage cerebellar hemisphere : ipsilateral intention tremor and lImb ataxia
-fall towards side lesion
-DYSMETRIA, dysdiadochokinesia, dysarthria, nystagus, HYPOTONIA
Anterior Vermis : alcohol leading to gait ataxia
Posterior vermis: medulloblastoma, ependymomas causing truncal ataxia

Hypothalamus
1. Hunger

2.
3.
4.
5.
6.
7.
8.

-Lateral : makes hunger (inhibited by LEPTIN L=L) (destroy loss weight


laterally first)
-VentroMedial : satiety (damage cause expand from medial)
Temperature
-Anterior: A/C cools body (parasympathetics)
-Posterior : heating (sympathetics)
Suprachiasmatic nucleus
Sex urge : septal nucleus
Supraoptic : ADH
Paraventicular: oxytocin
AUTONOMIC send signal to sympathetic
Arcuate nucleus : release dopamine to inhibit prolactin

Thalamus
* SENSORY RELAY ( except olfactory bypass it )
1. Lateral geniculate : visual ( Lateral= light)
2. Medial geniculate : auditory (medial= music)
3. VPL ( ventral posterior lateral) : all sensory body
4. VPM ( ventral posterior medial) : all sensory face
5. Ventral anterior/ lateral (VL and VL): MOTOR inform from basal ganglia and
cerebellum
Epithalamus: pineal gland
Subthalamus lesion; hemiballismus

Limbic System
5 Fs : feeding, fight or flight, feelings, fuking,
Hunger
Fight or flight
Emotion
Sex
MEMORY
-bilateral destroy Hippocampus : anterograde memory
-bilateral destroy mammilary bodies: anterograde and
retrograde
Limbic contains : cingulate gyrus, fornix, mammillary, amygdala, hippocampus
Kluver- Bucy Syndrome: bilateral lesion amygdala and hippocampus
Anterograde amnesia, hypersexuality, oral behavior
Decreased aggressiveness (they are passive)
Objects in visual field treat inappropriate, human approach lion without fear

Cortex
Prefrontal: organize and planning intellectual and emotional
-cant concentrate, easily distracted, apathy, emergence infantile suckling
and grasp reflex
Premotor: planning motor activities
-Lesion: APRAXIA cant do purposeful movements (even tho motor and
desire there). Cant perform things in correct sequence
Frontal eye field : cant move both eyes to contralateral side (deviate to side of
lesion)
Posterior parietal associated areas(left side): also APRAXIA , cant draw a circle.
(bilateral)
-Astereognosia : cant recognize objects in hand (contralateral)
Internal capsule:

1. Anterior limb : thalamocortical


2. Genu: corticobulbar
3. Posterior: corticospinal, all somatosensory thalamocortical
Aphasia
1. Brocas : broken boca : can understand, cant speak or write (frustrated)
2. Wernikes: Word salad. Speak but dont make sense and dont understand
3. Gerstmann Syndrome: (angular gyrus damage) : alexia( cant read) agraphia
( cant write) but understand spoken language
4. Conduction aphasia : ( arcuate fasiculus) : POOR REPITITION, can
understand and speak
5. Transcortical apraxia: corpus callosum damaged so cant send signal.
Understand command on left but cant move right arm (can move left)
6. Transcortical sensory: poor understanding, CAN SPEAK AND REPEAT
7. Transcortical motor: cant speak, CAN UNSERDTAND AND REPEAT
Right Parietal Lobe: ASOMATOGNOSIA : awareness of body on left side is lost.

Cranial nerve muscle + exceptions

All tongue is hypoglossus ( EXCEPT palatoglossus CN 10)


All palate is vagus ( except tensor veli palitini CN 5 V3)
All pharyngeal muscles vagus (except stylopharyngeus , CN 9)
Carotid sinus and body CN9 afferent, 10 efferent
Aortic arch chemo and baroreceptos CN10 afferent and efferent
Gag reflex lost = cn 9, cough reflex lost- CN 10

Eye
-Lower retinal field lateral geniculate Dorsal optic radiation/
calicarine/parietal lobe SUPRA-calcarine (cuneus)
-upper retinal fieldLG Meyers loop/ Temporal lobe INFRA-calcarine
(lingual)
Additional pathways
Optic tract pretectal area ( light reflex)

superior colliculus ( vertical conjugate gaze)

suprachiasmatic nuclei ( circadian rhythm)
Pupil
Present in cortically blind and unconscious
Constriction : CN2 pretectal bilateral Edinger westphal ciliary
ganglion SHORT CILIARY nerves pupillary sphincter
Dilation: T1 superior cervical ganglion LONG CILIARY
* Adies: dilated pupil slow react light, lack knee jerk reflex (normal accom)

* Argyll Robertson : prostitute, accommodate but dont react (syphilis)


* Marcus Gunn : MS swinging flash light
Conjugate Gaze
Horizontal is by PPRF and MLF
Vertical is superior colliculi

Vestibular System and Hearing

Utricle and saccule : linear acceleration and force of gravity


Semicircular canals: angular acceleration/ deceleration
Vestibular nuclei send info to flocculonodular lobe in cerebellum
Endolymph has HIGH K+ , LOW Na+, like intracell fluid
Nystagmus of vestibular damage
- Vestibular system activates ipsilateral CN 3, contralateral CN6 so
makes eyes GO OPPOSITE DIRECTION
-Lesion causes the other side to over work, so the eyes deviate
TOWARDS lesion
(slow component)
-the fast component back to normal position is by brain
(called the nystagmus)
- Caloric testing (COWS, Cold opposite, warm same)
-cold water (mimicks lesion) slow component to ear with cold
water, nystagmus opposite
-warm water activates that ear, slow component away,
nystagmus towards

Clinical
1. Otosclerosis: conductive hearing loss bc the ossicles dont amplify
sound
2. Hyperacusis: CN7 damage.
3. Presbycusis: loss of hair cell in the base of cochlea (therefore high
frequency sound loss) OLD PEOPLE
4. Lesion at cochlear nucleus or pontomedullary junction= unilateral
sensory hearing loss
5. Lesion anything higher up causes BILATERAL hearing DECREASED
(not lost)

Nucleus + random areas


Nucleus Solitaries: Visceral Sensory ( taste, baroreceptor, Gut distention)
-CN 7, 9, 10
Nucleus AMbiguous : Motor pharynx, larynx, upper esophagus
-CN 9 and 10 swallowing and palate elevation

Dorsal Motor Nucleus : Autonomic to heart, lungs, and upper GI CN10


Spinal nucleus of V: pain temp face
Superior olivary nucleus: lower pons get auditory info
Reticular formation
-Raphe nuceli: Serotonin
-Locus ceruleus : NE . invoved in cortical arousal
-Periaqueductal grey: opiods
Reticular activating system : in the midbrain. Responsible for arousal and
wakefulness. Destruction causes coma
Eyes above ears
-Superior colliculi : conjugate vertical gaze
-inferior colliculi : auditory pathway

MEDBULLETS
KLM SOUNDS
KUH: CN 10
LA-LA-LA : CN 12
MI-MI-MI : CN 7
Lumbar Puncture:
Ends L2 adults, L3 neonates. Do puncture L4-L5 using iliac crest
Aneurysm
RBC in lumbar is acute, with turn yellow (xanthochromia)
Give calcium channel blocker (nimodipine) to prevent secondary vasospasm
which occurs 2-3 days post SUBARACHNOID hemorrhage
Berry aneurysm at anterior communication ( ADPCK, marfan, Ehler danlos,
artery vien malformation)
o Subarachnoid (headache)
Charcot Bouchard aneurysm is lenticostriate vessel at basal ganglia ( HTN
chronic and diabetes)
o Intraparenchimal (usually motor or sensory loss)
Internal carotid
In cavernous sinus
In the foramen lacerum
Parkinsons

Have Lewy Bodies/ alpha- synuclein eosinophilic inclusions ( but so does


Lewy Body Dementia, therefore if dementia is present go with Lewy Body
dementia)
the Lewy body is the round pink dot
the substantianiagra doesnt send dopamine to striatum ( caudate and
Putamen)
Basal ganglia lewy body and late dementia = PARKINSONS
Cortical lewy body and early dementia = Lewy Body Dementia

Huntington
high Dopamine, low ACH and GABA
high Dopamine in nigro-striatal = direct pathway activated so hyperkinesis
high dopamine in meso-limbic = psychotic symptoms
Alzheimers vs Picks Disease
both have Tau protein aggregates intacellularly
-Alzheimers is TANGLES
-Picks disease is ROUND
Poliomyelitis
Fecal- oral infection: replicates in oropharynx and small intestine blood
CNS
Sore throat LMN symptoms
WERDNIG-HOFFMAN DISEASE : autorecessive, destroy anterior horns like
polio. FLOPPY BABY
Friedreich Ataxia
MITOCHONDRIAL FUNCTION INPAIRED
GAA
Macular degeneration
Dry: fat deposits in macula, slow disease course
Wet: neovascularization of the macula, fast disease course
RANDOM
Alpha- feto Protein

-High: neural tube defect, gastroschisis (lateral fold not fuse in


gastralation), omphalocele (the GI doesnt turn back in the 180
degree)
-Low : Downs Syndrome
Metastatic brain tumor if its located at junction grey and white matter
Lesion surrounding MIDBRAIN (RED NUCLEUS )
-ABOVE: decorticate
-Below : decerebrate
UMN high reflexes ( except superficial abdominal and cremaster is lost)
Fasciculus cuneatus is found about T5 only ( fasciculus gracilis at all levels)
Spinocerebellar tracts destroyed in Friedreich ataxia
Romberg sign
1. Eyes open and sway = cerebellum
2. Eyes closed and sway = dorsal column damage
Bladder nerves
1. Spastic : lesion above sacral
2. Atonic : lesion at sacral ( overfill so continuous dribble)
Endolymph is the only EXTRACELL fluid in body that has INTRACELL
electrolytes
Alcoholic thiamine deficiency cause deterioration of : dorsomedial nucleus
thalamus, mammillary bodies, hippocampus, vermis of cerebellum
Layer 4 cortex ( internal granular) : thalamus signals enter here (SENSORY)
Layer 5 cortex ( internal pyramidal): Corticospinal and bulbar ( MOTOR)
Aphasia also comes with AGRAPHIA ( they cant write)

FOOT ARCH IS HIGH OR FLAT


Fredrich ataxia
Charcot Marie tooth
Fragile X

U WORLD
Guillian Barre : segmental demylination , ENDONEURAL inflammation
Werdnig- Hoffman syndrome: anterior horne degeneration in neonates
inherited. FLOPPY BABY
Craniopharyngioma is calcified cystic tumor
ATM : Ataxia Telangiectasis Mutated
-DNA breaks

-reccurent infections pulomary , ataxia, and distended capillaries on


sun exposed areas.
-IgA deficiency therefore sinopulomary infection
Mitochondrial Diseases
-Leber Hereditary optic neuropathy: bilateral vision loss
-Myoclonic epilepsy with ragged red fibers: myoclonic seizures and
myopathy with exercise. Muscle biopsy shows ragged red fibers
-Mytochondrial encephalomyopathy with lactic acidosis and stroke
like episodes (MELAS)
Metabolic encephalopathy
-hypoglycemia
-hyperglycemia
-hepatic encephalopathy (high ammonia levels)
Rabies
-to DRG brain
-killed vaccine give as prophylactic to people who are at high risk of
rabies like veternarians, cave exploerers, lab workers, rabies dog
countries)
Heroin
-Withdrawal: nausea, vomit, abdominal pain, muscle ache
-flu like : dilated pupils, yawn, lacrimation, piloerection, hyperactibe
bowl sounds
Stimulants (cocain, amphetamines) withdrawal
-increased appetite, hypersomnia
-psychomotor retardation
severe depression crash
Alcohol and benzos: seizure, tachycardia, palpitations
Lysosomal alpha 1-4 glucosidase = maltase
47, XXX is clinically silent. May have a little lower IQ
47, XYY is aggressive, criminal, lower IQ, tall, severe acne
Congenital toxoplasmosis: hydrocephalus, intracranial calcification,
chorioretinitis. They are infected in utero across the placenta . avoid cat feces
if pregnant
Sciatic nerve is L4 S3
Spinal cord sections
Look if has the dorsal cuneaus ( above T5)
Look for lateral horn T1-L2
Look for large anterior horn in cervical and lumbosacral
More proximal has more white mater and more ovoid
Nisseria meningitis: from respiratory droplets.
-Pharyn blood choroid meningies
Meniere: tinittus (ringing), vertigo, hearing loss, episodic!
Bi polar: lithium, valproate, carbamazepine and atypical antipsychotics
Screening tests need a high sensitivity (SNOUT)
HSV-1 most common teens and young adults for SPORADIC ENXEPHALITIS,

-reactivation latent virus


-Temporal lobe involved bilaterally.
-fever, headache, mental status changes, Cranial nerves, seizures,
aphasia (temporal) , olfactory hallucination (temporal), personality
(amygdala)
-Cowdry A bodies eosinophilic + multinucleated cells
Neurology
Vascular malformation
o Causes hemorrhage intraventricular
o Seen on microscope as dilated, tortuous worm like channels and can
cause seizure disorder
This is tuberous sclerosis, an autosomal dominant condition characterized by
intellectual disability and seizures beginning early in life. The characteristic
feature is the presence of "tubers" which are enlarged and firm, whitened gyri.

The small petechial hemorrhages in the mammillary


bodies seen here are characteristic for Wernicke
disease, another complication of chronic alcoholism

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