Localization in neurology

1. cortex

56 AF

.
localization

MCQ
?
1. 56 risk
cardiovascular cancer
2. AF cardioembolic stroke
ischemic stroke warfarin DDx
intracerebral hemorrhage setting
3. vascular cause
etiology localization
4. global aphasia lesion
frontotemporal lobe left dominant hemisphere
80% dominant hemisphere language ability

frontotemporal lobe Broca's Wernicke's area

5. different
anatomy motor strip area frontal lobe leg area medial
parasagittal area supply anterior cerebral artery arm area
dorsolateral area supply middle cerebral artery vascular cause
lesion
MCA cortex subcortical subcortical area
internal capsule fiber

6. focal secondary to GTCs
lesion cortex lesion
arm area motor strip area propagate
7. cortical lesion 1/3 hemisphere
brain hypoxia
cortical lobe signs
1.
2. seizure
3.
4. aphasia
5.agnosia

6.apraxia
7.visual field defect
basic . Gerstmann syndrome
dominant parietal lobe left right confusion, finger agnosia, acalculia,
agraphia

2. subcortical lesion
56 underlying disease hypertension 3


localization

1. hypertension risk cardiovascular risk factor
stroke MI
2.
brainstem lesion
brainstem ipsilateral lesion
lesion
lesion thalamic lesion
subcortical area right thalamic lesion thalamus

lesion internal capsule

 lesion subcortical area; internal capsule and thalamic

lesion right side
3. vascular cause stroke
4. cortical involvement

subcortial area
1. pure motor weakness contralateral lesion; internal capsule
cortical
lesion leg arm area supply vessel
? motor power 1 different
2. pure sensory loss contralateral lesion; thalamus lesion
3. dysarthria clumsy hand; internal capsule ; genu
bulbar involvement corticobulbar tract genu of internal capsule
lesion motor
weakness lesion internal capsule
4. ataxic hemiparesis; pons, corona radiata, internal capsule cerebellar
signs lesion vertigo ataxia
5. mixed motor and sensory loss lesion ; subcortial area; internal
capsule+thalamus

 5 lacunar syndrome stroke small vessels

occlusion
long standing hypertension

2. brainstem
localization 3 cortical and subcortical lesion
brainstem lesion
. brainstem 90%
RS CVS . 20
misconcept brainstem structure
cranial nucleus, fasicle, cerebellar tract, corticospinal
tract, spinothalamic tract. RS, CVS lesion
1 level
brainstem reticular activating system(RAS), RS, CVS center

1.cranial nucleus, fasicle involvement; LMN type, ipsilateral lesion
2. cerebellar signs; ipsilateral lesion
3. motor weakness; lesion medullar decussation
contralateral lesion lesion medullar decussation

 fiber
brainstem
characteristics

. " right pontomedullary lesion CN7

palsy palsy upper motor neuron lower motor neuron"
. " uppermotor neuron
lesion " 90% brainstem cranial
nucleus fasicle nuclear control muscle lower motor
neuron nucleus cranial nerve anterior horn cell control
level brain stem
uppermotor neuron anterior
horn cell cranial nucleus brain stem lower motor
neuron type lesion fiber
corticospinal tract motor strip area subcortical internal capsule
brain stem cross medullar decussation
spinal cord lesion medullar decussation
lesion

upper motor neuron CN involvement LMN type

lesion+ lesion+ cerebellar signs lesion
brain stem lesion !!!

4. spinal cord lesion

localization 4 spinal cord lesion
35 10 5
spastic tone both legs ,
motor power grade 0 both legs, DTR 4+ clonus present, BBK dorsiflexion,
sensory loss up to T10 level , loose sphincter tone.

1. characteristic spinal cord lesion 3
1.1 motor weakness; quadri, paraparesis level
hemiparesis, monoparesis Brown-Sequad
syndrome C or T
1.2 sensory loss; sensory loss dermatome

 extrinsic cord level dermatome intrinsic

cord lesion Hanging or cape like pattern
complete cord dermatome level
1.3 autonomic involvement; bowel bladder involvement, anhidrosis, loss of
hair, loss of morning erection
set cord lesion exclude
cord

2. 35 CNT dz
sexual active life risk HIV demyelinating
disease multiple sclerosis .
requirement resident med diag
DDx
3. 10 post viral
syndrome transverse myelitis
4. sensory loss up to T10 level , level of
lesion T10 dermatome MRI level
whole spine
5. loose sphincter tone. autonomic
involvement

6.spastic tone both legs , DTR 4+ clonus present, BBK dorsiflexion,

upper motor neuron weakness
lesion corticospinal tract involvement
brain, brain stem, spinal cord brainstem is
upper motor neuron corticospinal tract

intrinsic VS extrinsic cord lesion resident
555

5. polyneuropathy
localization 5 nerves lesion; polyneuropathy
polyneuropathy symmetry , asymmetry
4,5,6 symmetric lesion
asymmetric lesion
mononeuritis multiplex nerve entrapment resident
. Guillain Barre syndrome(GBS)
focus resident symmetry GBS

and its variant(MFS, overlaping, AMAN,AMSAN, pandysautonomia, pure sensory,

oropharyngeal type, Bickerstaff's encephalitis) .
hiso
video 555

nerve characteristics lower motor neuron lesion

1. flaccid tone
2. areflexia ( nerve lesion )
3. sensory involvement( pure motor involvement
motor nerve)
4. muscle atrophy( acute atrophy)
5. muscle fasiculation
exclude GBS
Myasthenia gravis MG neuromuscular junction disease

 40 10 5


dysarthria, nasal voice,
motor weakness grade 3 all, decrease sensation at both palms and feet, facial
diplegia. DTR 0 all

1. 40 active sexual life risk HIV asso. GBS
Hx of CNT dz
2. infectious diarrhea

degree of dehydration

GBS most common organism asso
campylobacter jejuni diarrhea metabolic
disturbances ; hypokalemia, hyponatremia

 ..... cranial nerve

3. decrease sensation at both palms and feet sensory
involvement sensory dermatome spinal cord lesion
nerve lesion
4. motor weakness grade 3 all
generalized muscle weakness with gradually progressive course
vascular cause vascular cause sudden
onset fluctuation
neuromuscular disease (MG)
5.dysarthria, nasal voice bulbar
involvement(lower CN )

6. facial diplegia
facial nerve bilateral lesion lower motor neuron type
7. DTR 0 areflexia nerve lesion
8. respiratory involvement
typical GBS sensory and motor involvement
key nerve areflexia, sensory impaired, motor
weakness without fluctuation GBS investigation
LP cell protein albuminocytologic dissociation

 nerve conduction
velocity
IVIG,
plasma exchange

6.

neuromuscular junction
localization 6 neuromuscular junction
Myasthenia gravis Lambert
Eaton myasthnia gravis characteristic
1. pure motor proximal weakness
2. normoreflexia
3. fluctuation/fatiquability
localization
38

facial diplegia, partial ptosis both eyes, proximal muscle weakness grade3,
DTR 2+, limited EOM, sensory; intact, dyspnea,

.....
1. 38 asso CNT dz, HIV

2. facial diplegia facial palsy lower motor neuron
3. limited EOm, ptosis(CN3) Cranial nerve
involvement 3,4,6
4. fatiquability

NMJ lesion
5. proximal muscle weakness grade3,
generalized proximal weakness
6. bulbar involvement
7. dyspnea respiratory involvement MG
diaphragmatic muscle weakness
8. DTR 2+ normoreflexia
9. sensory intact pure motor weakness

 neuromuscular junction clue

NMJ lesion myasthenia gravis
multiple cranial nerves involvement, RS involvement
brain stem level cranial nerve lesion
brain stem cerebellar
symptoms

7. muscle
localization 7 basic neurology
muscle core feature muscle disorder
1. muscle pain exclude
2. pure motor weakness
3. normoreflexia severe muscle destruction
hyporeflexia
4. proximal muscle weakness proximal part
muscle mass select distal part
. common
proximal muscle
5. creatinine phosphokinase
early
very chronic CPK


6. EMG; myopathic pattern resident neuro
newbie 5
basic

63 HCTZ,
simvastatin, fenofibrate, glipizide

1 proximal muscle
weakness grade 2, DTR 2+ , sensory; intact, CN; intact, generalized muscle
tenderness, CPK 5,678 mg/dl

1. 63
cardiovascular disease
2. HCTZ, simvastatin, fenofibrate, glipizide ;
side effect drug interaction
HCTZ
hypokalemia, hyponatremia proximal part

 CPK
fenofibrate group simvastatin drug interaction
rhabdomyolysis
CPK
3.
proximal muscle weakness grade 2 generalized muscle
tenderness generalized proximal muscle weakness with muscle
pain proximal pain muscle disorder

4. ; fluctuation or fatique NMJ

5. sensory; intact ; pure motor weakness muscle
6.CN; intact; cranial nerve involvement
nerve or NMJ
7. 1 ; etiology
progressive ongoing destruction
8.DTR 2+ ; normoreflexia muscle/NMJ
muscle
9. CPK 5,678 mg/dl active muscle injury lesion
muscle


rhabdomyolysis drugs interaction
inflammatory myopathy ; polymyositis DDx
3-5 CPK

resident long case short case
dermatomyositis polymyositis inclusion body myositis
basic localization in neurology
point

neuro point basic
resident neuro deep
reference

reference 5555


reference
like

. resident .


goodnight la

How to approach acute ischemic stroke version;

Happy New Year !! .

approach stroke

. "
" .
approach approach
TOAST classification google
trial stroke
mechanism . ischemic stroke
localization ( )

 approach etiology
1. Infection
2. Trauma
3. Tumors/ neoplasm
4. Metabolic
5. Toxin/ drugs
6. Vascular
7. Demyelinating
8. Neurodegenerative
9. Congenital
10. Inflammatory
1. etiology sudden focal
neurodeficits vascular cause key sudden
2. ischemia or hemorrhage ischemia brain
edema develop increased intracranial pressure
symptoms 48-72 . stroke large area
infarcts observe neurosigns NPO complication brain
herniation, hemorrhagic transformation tube aspirate
hemorrhage space occupying lesion expand

 increased intracranial pressure small

hemorrhage ischemic stroke

3. vessel territory

- anterior circulation : internal carotid a. > MCA , ACA
- posterior circulation: vertebrobasilar system: PCA
vessel basic anatomy motor strip area
parasagittal area dorsolateral supply ACA supply MCA
1 motor grading MCA get
subcortical MCA
lenticulostriate a. lacunar infarcts proximal MCA
PCA visula field defect homonymous hemianopia with macular
sparing( macular supply MCA ) vertebrobasilar
brain stem lesion
4. resident venous infarcts arterial infarcts
.... iphone
5. TOAST classification
TOAST classification
1. cardioembolism

2. Large vessel atherosclerosis subtype arterial to arterial

emboli fixed intracranial stenosis
3. lacunar infarction or small vessel occlusion
4. determined cause
5. undetermined cause

1. cardioembolism source emboli heart proximal source emboli

clot emboli anterior
posterior circulation emboli

multiple site
brain infarcts
involve anterior territory
posterior fixed
cardioembolism
high risk factor mechanical valve, AF, SSS,
MS, LA clot
2. Large vessels atherosclerosis plaque
atherosclerosis risk factor DM, HT, DLP, obesity, old
age , smoking metabolic syndrome subtype 2
2.1 arterial to arterial emboli vessel carotid artery
internal carotid
ACA, MCA

circle of Willis carotid system anterior circulation

structure supply vertebrobasillar system
occipital lobe ( macular supply MCA), brain stem
anterior posterior circulation anterior
communication artery posterior communication artery circle of
Willis MCA, ACA, PCA
emboli

Indiana Jones


MCA, ACA, PCA
distal
cortex
cortex
embolism heart artery wedge
shape
a. to a. emboli carotid system
left internal carotid stenosis flow
turbulent flow plaque plaque rupture
vessel brain
emboli P. com A. com

 posterior cir. ?
!!!
" "
repeated stroke
carotid bruit
carotid stenosis
transient monocular
blindness or amarousis fugax
*** characteristics a. to a. emboli
1. metabolic syndrome
2. transient monocular blindness or amarousis fugax
3. carotid bruit
4. repeated stroke; same side ACA or MCA
posterior circulation carotid bruit
2.2 fixed intracranial stenosis; fixed lesion vessel brain
MCA left
brain neurodef
diarrhea with
shock ( ) BP drop
vessel constrict BP cerebral blood flow

 extern ( extern on
duty ) low knowledge treat shock staff
infarct
resuscitate volume TIA


!!! vessel
style!!!

**** characteristics fixed intracranial stenosis
1. associated with hemodynamic change
2. repeated stroke; same side and same artery. STEREOTYPE!!
3. metabolic syndrome
3. Lacunar infarction or small vessel occlusion
longstanding hypertension evidence long standing
hypertension LVH common basal ganglia, thalamus , pons,
cerebellum vessel cortex
lacunar syndrome
*** characteristics lacunar infarction or small vessel occlusion
1. involve cortex

2. area CT
3. lacunar syndrome
4. asso. long stnading hypertension
4. determined cause rare cause arterial dissection, vasculitis,
hypercoagulability stroke in the young
5. undetermined cause work up
cryptogenic, mechanism work up

How to approach Headache step by step

line approach
100% approach
step
1. identify primary secondary headache
SNOOP4
special condition
workup new onset headache in immunocompromised host HIV,
awakening pain

- primary headache overactivity of

pain-sensitive structures underlying disease


common Migraine, tension type headache, cluster headache and others
trigeminal autonomic cephalgia (SUNCT,cluster, paroxysmal hemicrania)
Chronic daily headaches, hypnic
headache common neurologist

- secondary headache disease
pain sensitive structure encephalitis, aneurysm, tumor
primary brain secondary brain
secondary headache infection, trauma, tumor ,metabolic, toxin
,drugs, vascular, demyelination
2. primary pattern
international
headache society classification !!!! criteria
cluster, tension, migraine classification link
http://ihs-classification.org/en/02_klassifikation/
secondary headache
localization

 focal diffuse
focal localization structure
lesion temporal area meninges, bone, sinus, vessel,
brain parenchyma localization
step etiology
etiology key .......
......
2.1 infection exclude CNS infection

secondary headache
cns infection
cns infection stiffness of
neck , signs of increased intracranial pressure (. signs
symptoms of increased intracranial pressure !!!)
approach CNS infection
!!!
2.2 trauma head injury exclude EDH, SDH, ICH


increased intracranial pressure focal neurological
deficits epidural hematoma lucid interval

 day3-5 focal neurodef

increased intracranial pressure
subdural hematoma bleeding tendency
3

CT
secondary headache ??

specific
pep !!!
2.3 tumor primary brain tumor common
Astrocytomas, Oligodendrogliomas, Ependymomas , Meningiomas,
Craniopharyngiomas neurosurgery
metastatic CA common
Lung ,Breast ,Genitourinary tract cancer, Melanoma,Head and neck cancer
Gastrointestinal cancers, Lymphoma,
CA origin primary source
CA breast abnormal discharge, breast mass CA lung smoking, chronic
cough , wt loss, lung mass
2.4 metabolic cause ;
hypothyroidism

http://ihs-classification.org///10.04.00_homoeostasis.html
hypoglycemia http://ihsclassification.org///10.05.00_homoeostasis.html
2.5 toxin, drugs; common nitric oxide
, carbonmonoxide, alcohol, drugs abuse, medication overuse headache
( ), tropine, digitalis, disulfiram, hydralazine, imipramine,
nicotine, nifedipine, nimodipine
http://ihsclassification.org//03_/08.00.00_substance.html
2.6 vascular cause; stroke ischemia hemorrhage AVM
arterial hypertension dialysis hypotension
... subarachnoid hemorrhage (SAH)
*****
- worst headache
- sudden headache vascular cause sudden
- meningism; stiffness of neck, Kernig positive
subarachnoid hemorrhage irritate meninges
-signs and symptoms of increased intracranial pressure;

papilledema, enlarged blind spot
-subhyaloid hemorrhage

- three tube/glass test positive LP CSF

traumatic tap
- CSF xanthochrome positive
2.7 demyelination focal neurodef
multiple sclerosis
Lhermitte's sign
approach etiology infection , trauma, tumor etc...

approach
long case
infection trauma bla bla
step step how
to approach headache
1. identify ; primary or secondary headache characteristic of
secondary headache
2. if it is primary; pattern primary headache
migraine, tension , cluster, other trigeminal
autonomic cephalgia
3. if it is secondary ; focal or diffuse focal localization
pain sensitive structure meningeal
irritation signs eyeground ********

 sinus diffuse
localization non specifics
4. approach etiology

stroke
investigation
stroke



review paper
standard textbook
anatomy
admit point goodnight

Vertigo
vertigo neuro ENT approach vertigo
true vertigo
dizziness chief complaint
vertigo true
vertigo component retropulsion, spinning sensation true
vertigo vertigo sensory ataxia

1. identify true vertigo dizziness ataxia

2. true vertigo peripheral central vertigo
anatomy peripheral vertigo ENT
vestibulococchlear
central vertigo cerebellar tracts and its pathway cerebellum
tract brain stem central cerebellum
and brainstem

IT (
)

3. peripheral vertigo central vertigo

3.1 nystagmus nystagmus
quick and slow phase
( horizontal)
(vertical) (rotatory) (multidirectional)
nystagmus google lets say

.
eye deviate nystagmus
????

nystagmus nystagmus
peripheral vertigo nystagmus horizontal rotatory
vertical nystagmus central vertigo nystagmus
specific central vertigo vertical
nystagmus*** multidirectional nystagmus
vertigo nystagmus exclude

3.2 peripheral central

3.3 postural related vertigo

peripheral central central


orthostatic hypotension
vertigo
3.4 hearing problem
vertigo peripheral central
3.5 neurologic deficits central vertigo
cerebellar signs
http://www.osceskills.com//subjects/cerebellar-examination/

scanning speech
nystagmus
hypotonia
overshooting reflex
neuro .
5555


3.6 Dik- Hallpike maneuver

https://www.youtube.com/watch?v=wgWOmuB1VFY
link
-peripheral vertigo ( BPPV benign paraxysmal
positional vertigo) nystagmus
latency 5-20 seconds central
- maneuver peripheral vertigo fatiquability/habituation
nystagmus central
3.7 duration peripheral central

How to approach transient loss of consciousness (TLOC)

Hello 555
AEC extern intern
. .
elective

seniority
1

555 ( )
transient loss of consciousness syncope vs non syncope
syncope
1. Neurally-mediated reflex dysautonomia rare
autonomic involvement reflex

2. Orthostatic hypotension .
BP

3. Cardiac arrhythmia VT, AF with RVR, sick sinus

syndrome , SVT , heart block syncope
4. Structural cardiac or pulmonary disease O2
hypoxia COPD exacerbation , TOF common
syncope
5.cerebrovascular disease minor stroke : lacunar infarction or TIA
non syncope
1. Disorders resembling syncope without any impairment of consciousness
. Pseudoseizure , psychogenic
witness hypoxia bizarre pattern
stereotype secondary gain
3
??? !!
2. Epileptic syndrome generalized seizure complex partial
seizure
common disease transient loss of
consciousness syncope seizure TIA
TIA focal neurodef
impaired conscious lesion brain bilateral lesion

seizure vs syncope

Step 1
Pre symptomatic phase

witness


seizure
SNSD one direction
( )
syncope
prodrome

( senario 555 )






hypogly
Seizure aura lobe

Occipital lobe
Temporal lobe
(de ja vu)
Parietal lobe paresthesia
Frontal lobe orbitofrontal
Step 2
Symptomatic phase
cloudy

1. Duration
absence seizure
complex partial seizure
versive seizure lesion frontal lobe
extremely away from lesion deviate lesion
Syncope seconds
2. Abnormal movement syncope loss of tone or brief muscle
contraction seizure

- stereotype pattern

-rhythmic movement
- jerky component seizure

3. Eye deviation syncope eye deviate nystagmus
sezure
4. Self injury head injury seizure
5. Incontinence loose sphincter seizure
6. Frothing , drooling seizure
7. Hypoxic feature cyanosis seizure
syncope
Step 3
Post symptomatic phase
hypoxia seizure 3-4
brain hypoxia syncope hypoxia

1. Post ictal confusion
2. Post ictal aphasia language deficit primary lesion
dominant hemisphere
3. Todd's paralysis primary lesion
frontal lobe

 step localization
1. Aura lobe
2. Abnormal movement focal secondary to GTCs
primary lesion
3. Eye deviation imply frontal eye field *** remember seizure: look away from
lesion (irritative lesion) stroke: look into the lesion( destructive lesion)
pathway basic eye movement
4. Post ictal aphasia; dominant hemisphere
5. Todd's paralysis


neuro good night good morning