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://ihs-

classification.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://ihs-

classification.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