Scholarly article on 2,2'-dimethoxy-4,4'-benzylidene-di-phenol 111979-72-7 from Chemische Berichte p. 950

DOI: 10.1177/000331970005101101

Source and publish data:

Chemische Berichte p. 950 (1910)

Update date:2022-08-16

Topics:: Authors:

Manchot

Read Full Text PDF DownLoad Join now for total 90,000,000 free articles

Article abstract of DOI:10.1177/000331970005101101

Full text of DOI:10.1177/000331970005101101

Stroke:

and

Pathogenesis, Investigations,

Part II ofIII

Prognosis

Thomas J.

PhD

Tegos,

Evi

Kalodiki,

Michael

Sabetai,

andAndrewN.

Nicolaides,

LONDON, ENGLAND

ABSTRACT

The aimofthis reviewis to

the current

stroke. It will

present

knowledge regarding

appear

in three

(in

the

epidemiology, ^c^lⁱⁿⁱ^c^a^lpicture,

and risk factors were

parts

part

discussed,

while

the

III will consist ofthe

and rehabilitation). In the

(II)

part

management

present part

and

of stroke are described.

_R_e_g_a_r_d_i_n_gthe

pathogenetic

pathophysiologic aspects

from the

and clinal examination and

investigations apart

history

general investigations,

the

and their role are discussed in detail:

following specialized investigations

Computed

resonance

(MRI), xenon-blood-flow,

positron

tomography (CT), magnetic

imaging

emission

tomography (PET), ^c^e^r^e^b^r^a^langiography, magnetic ^r^e^s^oⁿ^aⁿ^c^eangiography

transcranial

(TCD),

Holter moni-

(

MRA), ultrasonography,

Doppler

echocardiography,

and

addition, _t_a_k_i_n_ginto

accountthe information fromthe above-cited

toring,

biopsies.

modalities

for the final outcome is

prognosis

presented.

From the Irvine

for Cardiovascular

and Research,

Technology

of Vascular

Laboratory

_S_u_r_g_e_r_y_,St. Mary’s Hospital, Imperial

Investigation

College ofScience,

Department

and Medicine, London, England.

copy;2000 Westminster Publications, Inc., 708 Glen Cove Avenue, Glen Head, NY11545, U.S.A.

885

Downloaded from ang.sagepub.com at UCSF LIBRARY & CKM on April 17, 2015

selected sites in the extracra-

nial and intracranial arterial vasculature. Two

sclerosis, involving

Pathogenetic-PathophysiologicAspects

mechanisms

First, an

major

may

plaque mayoccur,

implicated.

blood

is ensured

ofthe

cerebrovascular

with

sub-

total

clot

Normally, adequate

supply

enlargement

an efficient

system

ofthe two internal carotid ar-

sequent

compromise. Upon

teries (ICA) (branches ofthe commoncarotid ar-

or near occlusion of the vessel

stagnation

blood to the anterior

canbe

formed, which, ⁱⁿ

the

ofthe cere-

teries), supplying

part

presence

the and the two vertebral arteries

brovascular

can

brain,

(VA),

compromise,

propagate distally

blood to the

ofthe brain.

and

stroke. Second,

supplying

posterior part

produce

dislodgment

Collateral circulation between the ICA and the

plaque fragments (artery-to-artery may

obstruction ofthe smaller ves-

embolus)

VA is ensured via the circle of

followed

Willis, providing

occur,

sels

of this sensitive

the

adequate perfusion

organ,

distally.

brain.

cause results in

The cardioembolic stroke is

Hypoperfusion

any

diagnosed

brain ischemia. In the case ofan

the

demonstration of

embolus and no evidence of

any

cardiac-transcardiac source of

embolism,if

blood

recover and the

in the case of

brain tissues

other causes of

supply

promptly restored,

symptoms disappear. However,

stroke.

Many

cardiac conditions are

implicated.

term de-

collateral

an infarc-

Lacunar infarction is

small ischemic

poor

supply,

pathological

tion is

_p_r_o_d_u_c_e_d_,which results in permanent

ob-

scribing

lesions, produced by

structions ofthe

arteries. These

neurologic damage.

deep penetrating

arteries tend to branch at 90° from the main in-

tracerebral arteries and have collateral con-

is the result ofemboiisml-7 orhe-

Amaurosis fugax

mechanism.8-12

poor

nections. Obstruction of these vessels

and microatheromatosis can

modynamic

by lipo-

hyalinosis

produce

transient ischemic attack (TIA) can also result

distal

and lacunae.

hemodynamic compromise

from embolic 13-15 or

nisms.

mecha-

Diabetes mellitus and

have been

hemodynamic 16-23

hypertension

in the

predominantly implicated

pathogenesis

lacunae.26

and subarachnoid

Parenchymatous

Stroke

level as

be manifested on the

_h_e_m_o_r_r_h_a_g_e_sare produced bymany

factors.

might

pathologic

infarction, parenchymatous hemorrhage,

and subarachnoid

count for 70%ofall

for

Infarctions ac-

he-

hemorrhage.

strokes, parenchymatous

and subarachnoid hemor-

morrhages

13.5%,

for 13.5%.24

factors are

implicated ⁱⁿ

rhage

their

Many

Investigation

pathogenesis.

brain infarction is considered on clinical

to be

It is of

of stroke in order

other causes of focal

cerebral tumors and subdural

to arrive at the

to differentiate it from the

great importance

diagnosis

grounds

produced bythrombotic, embolic,

mechanisms.25

(1)

and

deficits such as

_h_e_m_a_t_o_m_a_,₍₂₎to

hemodynamic

neurologic

thrombotic infarction

occurs when

on an atherosclerotic

usually

thrombus is

infarction from

and

superimposed

in the

distinguish

hemorrhage,

blood

of stroke. The

plaque, occasionally

presence

(3)

identify specific subtypes

Anembolic infarction is due

identification of the acute event that

the

clotting abnormality.

to occlusion ofan

brings

to the attention ofthe

artery by

embolus, originat-

patient

physician

recurrence or a

impor-

from

source.

in-

tant because an

ing

proximal

hemodynamic

early

worsening

farction most

occurs in the

of the acute deficit

rective measures are not taken. In

each and

of risk

_m_a_yoccur

if immediate cor-

commonly

presence

severe stenosis or occlusion of

and absence of collateral

proximal artery

blood

addition,

the identification

stroke

compensatory

every

patient

while the

diminished (for

cerebral

is criti-

flow,

global

perfusion

factors, etiology, and, therefore, potential

in decreased car-

mechanisms of the event is

for avoid-

is based

cally

example,

important

diagnosis

diac

fraction). An ischemic infarction is

_i_n_ga

recurrence. Accurate

ejection

considered to be atherothrombotic,

on the

and

commonly

largely

history

examination, supple-

or infarction ofunknown

mented

use ofblood tests and

cardioembolic, lacunar,

by judicious

imag-

The atherothrombotic

type.

is due to athero-

ofthe brain and its blood vessels.27

type

ing

Downloaded from ang.sagepub.com at UCSF LIBRARY & CKM on April 17, 2015

and when it can

be seen to involve both

and Clinical Examination

clearly

History

Stroke can

and white matter.28

scan betweenthe seventh and tenth

of the CT

grey

Repetition

will

usually

diagnosed clinically, espe-

day

help

over the

of 50

with

to elucidate the mechanism and

cially

person

age

years

ofather-

prognosis. 27

diabetes

an ischemic infarction is trans-

one

hypertension,

osclerosis, or

mellitus,

signs

^O^c^c^a^sⁱ^oⁿ^a^l^l^y^,a

with

known source of

formed into

owing ^t^odisrup-

anyone

hemorrhagic

emboli. Careful auscultation for bruits of the

carotid arteries and their extracranial branches

add evidence to

tion ofthe blood-brain barrier.29

In the acute

hanced CT scan adds

of stroke the contrast-en-

en-

phase

may

support ^adiagnosis.

specificity by showing

hancement of

infarctions but

frequently

early

transformation.28 This

General

produces hemorrhagic

technique is, however,

Investigation

full blood

useful in the

ef-

&dquo;fogging

Chest

fect&dquo;

weeks after the

event)

to de-

radiographs, urinalysis,

sedimentation

count,

period (2

C-reactive

the lesion.28

One

erythrocyte

rate,

pro-

fibrino-

pict

serum

blood

classification schemefor the is-

tein,

lipid profile,

glucose,

proposed

serum

blood

chemic lesions on brain CTfollows30:

gen, calcium,

electrolytes,

clotting

partial

studies

time

activated

[

prothrombin

(PT),

Absence ofinfarct.

_N_o_r_m_a_l_-_a_p_p_e_a_r_i_n_gscan

time

blood urea and cre-

thromboplastin

(aPTT)],

serumuric

sickle cell

immu-

smear,

atinine,

acid,

Watershed/hemodynamic/low perfusion. Hy-

cardiac

(VDRL) and

cortical and subcortical

podensities involving

noelectrophoresis,

enzymes, serologic

tests for

function

An electro-

areas in the

of the middle cerebral

syphilis

thyroid

periphery

might

tests

in the

These

be external

and internal

may

helpful

diagnosis.

artery.

(anterior, pos-

cardiogram (ECG) may

demonstrate conduction

or reveal evidence

terior, superior)

abnormalities and

arrhythmias

Discrete subcortical.

well-circum-

than 1 cmin

noninvolved cere-

Rounded,

ofrecent

_p_r_e_d_i_s_p_o_s_eto

infraction. These conditions

myocardial

lesions

scribed, hypodense

greater

stroke. 27

size, adjacent

apparently

bral cortex in the anterior and middle cerebral

Computed Tomography

artery territory

Computed tomography (CT)

veryimportant

and

Large

cortical.

Mainly

infarcts with cortical

more than 50% of the

order to differentiate between

ischemia and must therefore be

distribution

hemorrhage

occupying

entire anterior and middle cerebral

ritories

_a_r_t_e_r_yter-

rapidly applied

in order to

the

Its

plan

therapy (thrombolysis).

sensitivity ⁱ^snearly

100%

for

he-

parenchymatous

Small cortical. Cortical distribution infarctions

and about 97%for subarachnoid hem-

morrhage

less than 50% of the entire anterior

and middle cerebral

occupying

It can also be

orrhage.28

helpful

identifying

territories

artery

and other conditions mas-

neoplasms, abscesses,

as stroke.28 In

the CTscanwill

with acute

Diffuse white matter

querading

general,

low-density changes.

often not well circum-

area

showareas of

Areas of low

scribed in the

hyperdensity

patients

density

and areas of low

in those

hemorrhage

density

periventricular

with infarction.28 In

with

patients

infarction,

Basal

ischemic lesions. Infarcts

ganglia

(hypo-

normalwhenobtained in

mayappear completely

densities with diameter

lacunae

than 1

greater

cm)

the first several hours.

acute ischemic

after the first 6

Although

with diameterless than

(

hypodensities

lesions

occasionally appear

hours,

cm) in the striatum

infarction

usually may ⁿ^o^t

complete

reliably

may

seen before 24 or 48 hours.28 Even

later,

fail to showsmall ischemic strokes in the

or fossa because of bone artifact.

small infarcts on the cortical surface

Literature review has demonstrated that there is:

firm association between carotid atheroma

or cardioembolism and discrete subcortical or cor-

posteri-

Additionally,

may

(1)

missed.

after the

on the third or fourth

tical infarctions on brain

sociation between

as-

Usually, only

pertinent event,

when its

day

CT,30-33 (2)

strong

can the lesion be seen

infarctions on

collateral circulation in the

hemodynamic

are better de-

brain CTand

circle ofWillis in the presence of carotid athero-

appropriately,

margins

impaired

fined, whenthe attenuation values becomelower,

887

Downloaded from ang.sagepub.com at UCSF LIBRARY & CKM on April 17, 2015

an association betweenbasal

extracranial arteries following transfemoral

catheterization. It remains the most accurate

ma,34-43 (3)

ganglia

infarctions on brain CTwith (i) cardioembolism,

and (iii) carotid

poor

between carotid atheroma and CT-documented

method of

the cerebrovascular system.

(

ii) middle cerebral arterylesions

assessing

atheroma44-48

(4)

association

It can differentiate embolism from large artery

thrombosis. It can detect atherosclerotic plaque

stenoses and ulcers, arterial dissections, arteri-

and, finally,

diffuse white matter lesions or lacunae. 32,49,50

the cerebral

tis, vasospasm, Moyamoya disease,

collateral circulation, and the occlusion of

large

Resonance

Magnetic

Imaging

and small arteries. It

strate somevascular mural

however, to demon-

fails,

resonance

(MRI) documents

that

in-

may

Magnetic

imaging

changes

development

the extent and location of infarction earlier after

tervene in the

of clinical manifes-

in all areas ofthe brain,

the

tations, such as

thrombus. These

ultrasound.

and

onset,

including

pos-

intraplaque hemorrhage

terior fossa and the cortical surface, and has

canbe identified

pathologies

better resolution than the CTscan. This

modality

can

with

the vascular malforma-

is not recommended in the

of acute ischemic stroke, ex-

depict

accuracy

Angiography

tions

arteriovenous malformation,

hemangiomas) frequently

(

aneurysms,

early investigation

and cavernous

on routine

not seen

in the case of

cept

cerebral em-

early diagnosed

It is

useful to define

bolism where intraarterial

angiography.

very

thrombolytic therapy

the extent ofdeadversus

tissue when

modali-

can be

dence of

Overall, the inci-

salvageable

immediately applied.52

with diffusion and

amount

employed

perfusion

complications

angiography

ties. The use of intravenous

such as

to 1.2% (ACAS).28 These

be due to stroke,

contrast,

facilitates the

might

reactions to the contrast medium, and

gadopentate dimeglumine,

early

allergic

renal failure.28

detection (within few hours) of the lesion.28 The

MRIcan

on the

the

ofthe

based

The evaluation of the

of stenosis con-

identify

age

hemorrhage

degree

in the vascular

transformation

stitutes

world. TheNorthAmerican

hemoglobin

sequence: oxy-

confusing aspect

surgical

Carotid

hemoglobin, deoxyhemoglobin, methemoglobin,

hemosiderin.

Symptomatic

Trial Collaborators53

the ratio of diameter measurements of the nar-

Endarterectomy

adopted

The

increas-

T2-weightedparenchymal signal

es in most cases after 24 hours from the onset of

the ischemic event as

with CT. TheTl-

rowest residual lumen to the

normal-appearing

carotid

well

the bulb based onthe

compared

lower

profile

beyond

where

has

(50%)

formula: 1 - N/D

is the diameter

weighted sequence

sensitivity

100,

the diameter of the

the bulb where the walls are

for the detection of ischemia

the first 24

stenosis and D

during

artery beyond

hours.28 In

precisely

lacunae are

The

addition,

depicted

parallel.

on MRI as

with CT.28

Carotid

Trial Collaborators54

compared

European

Surgery

the

ofMRIon an

for the ratio of diameter measurements of

the narrowest residual lumen to the theoretical

However,

availability

emergent

andre-

opted

basis is

since it is more

limited,

expensive

time for

diameter of the carotid bulb at this

based

is the

quires considerably longer

image acqui-

point

sition than CT does. In

the

on the formula: 1 - N/D

diameter stenosis and

ameter bulb. Other institutions

where

imaging

addition,

100,

detection of intracerebral

the estimated normal di-

the use of

early

problematic.28

hemorrhage

prefer

diameter as the de-

the common carotid

artery

nominator : 1 - N/C

100 where

is the diam-

Xenon-Blood-Flow and

eter stenosis and

the diameter of the common

Positron Emission

Tomography

carotid

artery.28

Xenon-blood-flow and

emission

used for research.

Conventional

been

in _m_a_n_ycases has

positron

tomog-

angiography

raphy (PET) ^a^r^egenerally

subtraction

They

replaced bydigital

angiography

can assess cerebral blood flow. PET

can

(DSA) or

and

resonance

angiography

(MRA)

scanning

magnetic

also assess metabolism and brain function.28,51

ultrasonography.

Cerebral

Resonance

Angiography

Magnetic

Angiography

Cerebral

tion of an

the

This

and noninvasive tech-

of arterial flow of the

angiography

performed by

injec-

rapidly developing

contrast medium into selected

x-ray

nique provides imaging

888

Downloaded from ang.sagepub.com at UCSF LIBRARY & CKM on April 17, 2015

vessels. With use

^o^fhigh ^fⁱ^e^l^dstrengths

(1.5

large

Ultrasonography

Stenoses at the of the internal carotid

tesla) and different pulse sequencing, blood flow

may

also

in the intracranial arteries.

imaged

origin

can be

MRAcan demonstrate the basilar

identified and

Thus,

artery,

artery (ICA)

reliably

quan-

the circle of

and their main branches and

tified

B-mode

Willis,

by ultrasonography, by utilizing

candetect the

ofocclusion. It is

ultrasound

combined with

ul-

presence

valuable for

particu-

image

Doppler

lesions of the ex-

trasound assessment of flow. Different criteria

larly

identifying

tracranial carotid circulation.55 This

can be used for

the ICA stenosis. Peak

modality

grading

tends to overestimate the

_d_e_g_r_e_eof

stenosis28 and

between

end diastolic

systolic velocity (PSV ICA),

velocity

also cannot

and

confirms the

or their ratios: (a) PSVICA/PSVCCA

ICA),

distinguish reliably

complete

(EDV

and

Table

carotid occlusion. The MRA

anatom-

PSVICA/EDVCCAare some ofthem.5~-63

near-complete

(b)

shows

scheme for the

Doppler findings, provides

proposed

grading

ical

and detects tandemlesions from

of carotid stenosis of more than 50%

information,

hemody-

the aortic arch to the circle of

sometimes

The evaluation of the less than 50%

stenosis canbe done

Willis,

namically.

the

Color flow

altering

surgical management.56

many

visually.

imaging,

MRA combined with ultrasound studies

cases,

eliminates the need for cerebral

on the other

the location and

can be

hand,

helpful

identifying

turbulence

area and in

angiography

pattern

secondary

carotid

lesions. The combina-

to a

evaluating

artery

adjacent

poststenotic

ofthe

assessing

ultra-

tion of the two methods is less

than

the

expensive

morphology

plaque.64

cerebral

and can be used as

As to the carotid

angiography

pri-

plaque morphology,

tool for intracranial and extracra-

sound can

necrotic core

and

maryscreening

identifyhemorrhage, calcification,

nial arterial occlusive diseases.

ultra-

satisfactorily. 65-71 However,

TableI

Evaluation

_o_fCarotid Stenosis

PSV:

EDV: end diastolic

ICA: internal carotid

artery,

peak systolic velocity,

velocity,

CCA: commoncarotid

artery.

889

Downloaded from ang.sagepub.com at UCSF LIBRARY & CKM on April 17, 2015

sound cannot

between

bolus is defined as

blood flow

short transient, within the

to the ear

always distinguish reliably

carotid

and

complete

near-complete

occlusion,

velocity spectrum, sounding

distinction in some clinical situa-

or &dquo;moan,&dquo; and

having ^a

du-

very important

&dquo;snap,&dquo; &dquo;chirp,&dquo;

tions. This distinction can be made

_b_ycerebral angiography.

ration ofless than 300msec, with an

reliably only

amplitude

more than

dB above the

background

(blood

flow

within the

andwith

unidirectional

signal)

appearance

Dopplervelocity spectrum.

Transcranial

Doppler

The detection ofmicroemboli is based onthe

measurementofthe backscatter from the emboli.

Transcranial

in the

(TCD) can assess the flow

and the

Doppler

the

useful

in the detection of emboli is

which is the ratio

middle,

anterior,

posterior

parameter

cerebral arteries and in the vertebrobasilar

the relative

sys-

is detected

intensity increase,

term. 12 The anterior cerebral

ofthe acoustic

bolus to that of the

backscattered fromthe em-

blood

artery

windowat

power

the

from

through

transtemporal

depth

moving

surrounding

0-80 mmand has

direction offlow

it. 78 This relative

lated to the embolic

increase is

re-

away

intensity

directly

the

latter

creases

and mean

of50 cm/sec. The

material (air >

platelet aggregates)

Therefore, TCDcannot

locity.79,80 identify

athero-

andve-

the size

probe

velocity

size,

decrease as the carotoid stenosis in-

fat >

might

ma, thrombus,

data from our

(

unpublished

laboratory -

stenosis evaluation based on NASCETcrite-

and the nature ofemboli at

present.

patients

ria~3~~4~.

with carotid

population

The middle cerebral

the

is detected

TCD-detected emboli are more

artery

atheroma,

preva-

windowat

lent in the

prevalence

and their

related to

through

transtemporal

depth

symptomatic group8 1-91

0-60 mmand has

direction offlowtoward the

of 55 cm/sec. The PI

or their numberis

inversely

and

mean

the time from the event. 85,86,90-93 It has also been

probe

velocity

ofthe

the

cerebral is detect-

shown that TCD-detected emboli were

segment

posterior

transtemporal

artery

positively

windowat

direction of flow toward

of 39 cm/sec. The

associated with carotid

These noninvasive tests constitute

ulceration. 84,91,94-96

through

depth

plaque

of 60-70 mmand has

inex-

useful,

the

and

mean

risk-free methods to evaluate an athero-

and to document the

probe

velocity

pensive,

sclerotic

ofthe

cerebral

is de-

segment

posterior

the

artery

patient

presence

tected

window at

and

ofintracranial stenosis.

through

transtemporal

direction of flow

of 40

progression

of 60-70 mmand has

depth

away

from the

and

a mean

probe

velocity

Echocardiography

cm/sec. The ophthalmic artery is detected

the transorbital window at

0-60mmand has

test for

hypoki-

through

depth

echocardiogram

good screening

direction offlowtoward the

of 21 cm/sec. The in-

intraventricular cardiac thrombi,

large

and

mean

netic wall

to thrombus for-

and

sep-

probe

velocity

segmentspredisposing

tracranial

tected

of the vertebral arteries are de-

valvular

tal abnormalities

atrial

parts

mation,

lesions,

myxomas,

the transforaminal window at

em-

through

allowing paradoxical

of 60-90 mmand have

direction of flow

of 38

bolism.97

in endocarditis and clots in

depth

away

Vegetations

from the

and

mean

atrial

are

visualized. In such

poorly

probe

velocity

appendages

cm/sec. Thebasilar artery is detected through the

cases, transesophageal echocardiography is rec-

ommended.98

transforaminalwindowat

of80-120mm

depth

and has

mean

direction

from the

and

away

probe

of41 cm/sec.~2

velocity

Holter

Monitoring

TCD can

stenotic lesions in the mid-

identify

dle cerebral

and the basilar

the distal vertebral

24- to 48-hourcontinuous

in the detection ofcardiac

canassist

associated

stem,

arteries,

monitoring

arrhythmias

because such lesions in-

It can also assess

artery,

crease

flow

with embolic stroke.99

systolic

velocity.75

the collateral flow across the anterior or

posteri-

reactivi-

ofthe circle ofWillis via the

part

CO2

Biopsies

transient

ty. 76

addition, high-intensity

signals

of microembolic

on clinical

(

HITS), suggestive

material,

Temporal artery biopsy

performed

havebeenidentified in

with extracranial

of arteritis or

arteritis and stroke.loo,101 Relevant

patients

suspicion

temporal

granulomatous

vascular or cardiac disease.77

TCD-detected em-

are

findings

Downloaded from ang.sagepub.com at UCSF LIBRARY & CKM on April 17, 2015

arteritis and stroke.loo,101 Relevant

are

and male

strokes fared better in the

Vertebrobasilar

findings

hypertension,

gender.

term as

of inflammation

cells) in

patchy segments

(giant

long

compared

the vessel wall of the

are

arteries. 102 Brain

to carotid

survival in

strokes. In terms of

the

temporal

artery

hemorrhages,

long-term

on clinical

factors in-

biopsies

performed

suspicion

following

cerebral

and CADASIL disease

dicated an unfavorable

consciousness

amyloidosis 103

prognosis:

(

cerebral autosomal dominant arteriopathy with

level

and

age.

In these no difference ex-

settings,

subcortical infarcts and

isted between the

and the infratentorial

in neural

leukoencephalopathy).1o4

supra-

Some

hemorrhages.lo5

improvement

function

the end of the sec-

may

apparent by

ond week after the event, and

_b_ythe

end of the

month the maximum will have

recovery

Prognosis

eighth

been reached.lo6

the

of either

or com-

Recurrence ofcerebral infarction is

During

early days

neither

evolving

relatively

to add to

nor ultimate

common and each recurrence is

pleted stroke,

progression

In one

likely

outcome can be

the

deficit. An overview

re-

predicted.

study

1,013

neurologic

analysis

with acute ischemic

survival was

vealed that in individuals with atherothrombotic

patients

stroke,

significantly _l_o_n_g_e_rafter

cerebral infarction than

cerebrovascular

the annual rate of sub-

disease,

after cerebral

The

mor-

stroke was 6.1% in

stroke and 9% in

with minor

hemorrhage.lo5

30-day

sequent

patients

rate was 17% for carotid

infarc-

with

stroke.107

tality

tion,

territory

patients

major

8%for vertebrobasilar

The same

has shownthat the annual rate of

territory infarction,

study

3% for infratentorial

and 57% for

stroke was 1.3%in

hemorrhage,

subsequent

asymptomaticpa-

In terms of short-

tients (carotid

2.2% in those with amau-

supratentorial hemorrhage.

bruit),

termsurvival in

infarctions,

the

factors

rosis

chemic attack.107

and 3.7% in those with transient is-

following

fugax,

indicated an unfavorable

prognosis: depressed

consciousness, conjugate-gaze palsy, limb weak-

advanced

heart

and

ness,

age,

disease,

stroke. Vertebrobasilar strokes fared worse than

T. J. Tegos,

carotid

infarction in the first 10

the difference

territory

days,

NeurologyDepartment

but at 30

terms of

Hammersmith

150 Du Cane Rd

days

disappeared.

Hospital

survival in

factors indicated an unfavorable

the fol-

long-term

infarctions,

LondonW12

lowing

progno-

0HS,

sis : levels of

from the

activity

age,

discharge

hospi-

advanced

heart

E-mail:

tal,

disease, previous stroke,

t.tegos@ic.ac.uk

References

6. Hollenhorst RW: Vascular status of

Hollenhorst RW:

who

Significance

the retinal arterioles. JAMA

bright plaques

1961.

patients

78:23-29,

have cholesterol emboli in the retina. Am

thalmol 61:1159-1165, 1966.

Oph-

Ross Russell RW: Observations onthe retinal blood

vessels in monocular blindness. Lancet 30:1422-

Dyll

LM,

Margolis M,

David NJ: Amaurosis

fugax.

428, 1961.

Neurology 16:135-138, 1966.

N, Lorentz

et al: Recurrent tran-

12:894-897,

8. Furlan

JP,

Whisnant Kearns TP: Unilateral visu-

bright light.

Ashby

Oakley

AJ,

sient monocular blindness. Br Med

al loss in

1979.

Arch Neurol

36:675-676,

963.

Ross Russell RW: Atheromatous retinal embolism.

Lancet 28:1354-1356, 1963.

9. Donnan GA,

FW, WhisnantJP: Carotid

Sharbrough

occlusive disease: Effect of

on visual

bright light

Arch Neurol 39:687-689, 1982.

evoked

response.

McBrien DJ,

RD: The nature ofretinal em-

Bradley

boli in stenosis ofthe internal carotid

Lancet

10. Ross Russell RW,

NGR: Critical

_p_e_r_f_u_s_i_o_nof

artery.

Page

brain and retina. Brain 106:419-434, 1983.

0:697-699, 1963.

891

Downloaded from ang.sagepub.com at UCSF LIBRARY & CKM on April 17, 2015

1. Ross RT, MorrowIM: Ocular and cerebral ischemic

mechanisms in disease of internal carotid

Stroke Council, American HeartAssociation. Stroke

28:1480-1497, 1997.

artery.

Can

2. Wiebers DO, Swanson JW, Cascino TL, et al:

Stroke

Neurol Sci 11:262-268, 1984.

9. Davis KR, AckermanRH, Kistler JP, et al: Computed

of cerebral infarction:

contrast enhancement, and time of

tomography

Hemorrhagic,

appearance.

Bilateral loss of vision in

0:554-558, 1989.

bright light.

Comput Tomogr 11:71-86, 1977.

3. Harrison MJG, Marshall J: TIA

ofthrombus

30. Stevens

Barber

Kerslake

et al: Extended

finding

JM,

CJ,

at carotid

and its

use of cranial CT in the evaluation of

stroke and transient ischaemic attacks. Neuroradiol-

ogy 33:200-206, ¹⁹⁹¹^.

with

endarterectomy

relationship

patients

the

_t_i_m_i_n_gofsurgery. Br J Surg

64:511-512, 1977.

4. Barnett HJM, Peerless SJ, KaufmannJCE: Stump of

internal carotid source for further cere-

31.

F: Centrum ovale infarcts:

artery—a

Bogousslavsky J, Regli

bral embolic ischemia. Stroke 9:448-456, 1978.

Subcortical infarction in the

the middle cerebral

superficial territory

42:1992-

artery. Neurology

5. Beal MF, Williams RF, Richardson EP, et al:

1998, 1992.

Cholesterol embolism as

a cause of transient is-

chemic attacks and cerebral infarction.

32.

Shi

F, _M_o_r_g_a_nT: Carotid stenosis in la-

Neurology

Tegeler CH,

1:860-865, 1981.

cunar stroke. Stroke 22:1124-1128, 1991.

LR,

Sergay ^S^:

Positional cerebral ischemia.

33. Boiten

Lodder J: Lacunar infarcts:

Caplan

Neurol

Pathogenesis

Stroke

39:385-391, 1976.

and

of the clinical

Neurosurg Psychiatry

validity

syndromes.

2:1374-1378, 1991.

7. Ruff RL, Talman WT, Petito F: Transient ischemic

attacks associated with

with carotid

hypotension

hypertensive

34.

Weiller

EB,

Reiche

of low flow infarcts.

_W_,et al. Clinical

Ringelstein

stenosis. Stroke 12:353-

patients

55, 1981.

artery

and

hemodynamic aspects

Stroke 22:1117-1123, 1991.

8. Somerville ER: Orthostatic transient ischemic at-

E, Grace PA,

separate

_B_o_u_c_h_i_e_r_-_H_a_y_e_sD: Are CTin-

Meagher

tacks :

large ^v^e^s^s^e^l

occlusion. Stroke

symptom

farcts

risk factor in

with tran-

patients

5:1066-1067, 1984.

sient cerebral ischaemic

5:165-167, 1991.

Eur

Vasc

Surg

episodes?

DG, Klass DW:

Repetitive

Yanagihara

involuntary

Piepgras

movement associated with cerebral is-

36.

F: Borderzone infarctions

occlusion:

Bogousslavsky

Regli

chemia. Ann Neurol 18:244-250, 1985.

distal to internal carotid

artery

Prognos-

tic

Ann Neurol 20:346-350, 1986.

implications.

GD, Pessin MS, Scott RM: Limb

Baquis

carotid TIA. Stroke 16:444-448, 1985.

shaking:

J, Regli F: Unilataral watershed cere-

Bogousslavsky

bral infarctions.

36:373-377, 1986.

1. Dobkin BH: Orthostatic as

risk fac-

Neurology

Sievers

hypotension

39:30-34, 1989.

tor for

occlusive cerebrovascular dis-

symptomatic

Neurology

38.

Ecker

al:

Ringelstein EB,

ease.

Noninvasive assessment ofCO2inducedvasomotor

in normal individuals and

with

2. Tatemichi TK,

Perfusion

WL, Prohovnik I, et al:

response

patients

Young

insufficiency

internal carotid

occlusions. Stroke 19:963-

in limb

transient is-

artery

shaking

chemic attacks. Stroke 21:341-347, 1990.

969, 1988.

3. KamataT, Yokota T, FurukawaT, et al: Cerebral is-

39. Mull M, Schwarz M,

Thron A: Cerebral haemi-

chemic attacks caused

spheric low flow infarcts in the arterial occlusive

disease: Lesion patterns and angiomorphological

conditions. Stroke 28:118-123, 1997.

bypostprandial hypotension.

Stroke

5:511-513, 1994.

4. Foulkes MA, Wolf PA, Price TR, et al: The Stroke

Data Bank:

methods and baseline charac-

40. Beal MF, Williams RS, Richardson P, et al:

Design,

teristics. Stroke 1988; 19:547-554, 1988.

Cholesterol embolism as

cause of transient is-

chemic attacks and cerebral infarction.

Neurology

from the National Institute of the

Special report

1:860-865, 1981.

Disorders and Stroke: Classification of

Neurological

Cerebrovascular Disease III. Stroke 21:637-676,

41. Torvik A: The pathogenesis ofwatershed infarcts in

the brain. Stroke 15:221-223, 1984.

1990.

6. ChamorroA, Sacco RL, MohrJP, et al: Clinical-com-

42. Pollanen MS, Deck JHN: Directed embolization is

an alternate cause of cerebral watershed infarc-

tions. Arch Pathol Lab Med 113:1139-1141, 1989.

correlations of lacunar infarc-

puted tomographic

tion in the Stroke Data Bank. Stroke 22:175-181,

1991.

3. Graeber MC, Jordan JE, Mishra SK, et al:

Watershed infarction on computer tomographic

7. Donnan GA:

with stroke

Investigation

patients

and transient ischaemic attacks. Lancet 339:473-

scan: An unreliable

of hemodynamic stroke.

sign

Arch Neurol 49:311-313, 1992.

77, 1992.

8. Culebras A, Kase CS, Masdeu JC, et al: Practice

for the use of in transient is-

44. Weiller C, B, Reiche W, et al: The

Ringelstein

large

infarctions:

clinical and

guidelines

imaging

striatocapsular

pathophys-

chemic attacks and acute stroke.

of the

Arch Neurol 47:1085-1091, 1990.

iological entity.

report

892

Downloaded from ang.sagepub.com at UCSF LIBRARY & CKM on April 17, 2015

5. Adams HP, Damasio H, Putman S, et al: Middle

occlusion as

60. Withers CE, Gosink BB, Keighhtley AM, et al:

Duplex carotid sonography. Peak systolic velocity

cerebral

cause ofisolated sub-

artery

cortical infarction. Stroke 14:948-952, 1983.

in quantifying internal carotid artery stenosis.

Ultrasound Med9:345-349, 1990.

6. Ringelstein EB, Biniek R, Weiler C, et al: Type and

extent ofhemispheric brain infarctions and clinical

outcome in early and delayed middle cerebral

61. Moneta GL, Edwards JM,

G, et al:

Papanicolaou

for

_a_s_y_m_p_t_o_m_a_t_i_ccarotid artery

stenosis:

Screening

recanalization.

42:289-298, 1992.

criteria for

60% to 99%

artery

Neurology

Duplex

discriminating

stenosis. J Vasc

21:989-994, 1995.

Surg

Mattos

7. Caplan L, Babikian V, Helgason C, et al: Occlusive

disease of the middle cerebral artery. Neurology

62. Hood

DB,

evaluation of new duplex criteria to identify 70%

internal carotid stenosis. Vasc

23:254-

MA,

Mansour

_A_,et al:

Prospective

5:975-982, 1985.

artery

Surg

8. Araki G, Mihara H, Shizuka M, et al: CTand arteri-

of with transient is-

262, 1996.

ographic comparison

patients

chemic attacks—correlation with small infarction

ofbasal

Stroke 14:276-280, 1983.

63.

Dhanjil S,

Jameel

Nicolades

of internal carotid to end di-

et al: Ratio of

ganglia.

peak systolic velocity

astolic

teria for

ofcommoncarotid: new

cri-

velocity

grading

duplex

9. Pantoni L, Garcia JH: Pathogenesis of leukoareosis.

Stroke 28:652-659, 1997.

internal carotid stenosis. Vasc

Techn 21:237-240, 1997.

S: Clinical and

tures of lacunar versus nonlacunar minor stroke.

Stroke 20:59-64, 1989.

fea-

Norrving

Cronqvist

radiologic

4. Geroulakos G, Ramaswami G, Nicolaides A, et al:

Characterisation of

matic carotid

and

symptomatic

asympto-

plaques using high-resolution

real-

1. Baron JC: Positron

in cerebral is-

tomography

time

1993.

ultrasonography.

Surg 80:1274-1277,

chemia.

985.

review.

27:509-516,

Neuroradiology

5. Picano E, Landini L, Distante A, et al: Fibrosis,

and calcium in human atherosclerotic

lipids

Circ

2. Lownie SP: Cerebral

Conventional

angiography:

plaque.

In Stroke:

angiography.

sis and

Pathophysiology, Diagno-

Res

1985.

6:556-562,

ed. 2, ed.

Bamett HJM,

Management,

6. Picano E, Landini L, Distante A, et al:

Mohr JP, Stein BM, et al. New York: Churchill

Angle depen-

dence of ultrasonic backscatter in arterial tissues:

Livingstone, 1992,

3. North American

215.

_s_t_u_d_yin ^vⁱ^t^r^o^.Circulation 72:572-576, 1985.

Carotid Endarterec-

Symptomatic

7. Aldoori MI, Baird RN, Al-Sam SZ, et al:

Trial Collaborators. Beneficial effect ofcarotid

Duplex

tomy

and

in cerebral is-

with

scanning

plaque histology

endarterectomy

symptomatic patients

high-

chaemia. Eur

Vasc

1:159-164, 1987.

carotid stenosis.

_E_n_g_lJ

Med325:445-453,

Surg

grade

1991.

8. Bendick PJ, Glover JL, Hankin R, et al: Carotid

Correlation of

AnnVasc

4. European Carotid Surgery Trialists’ Collaborative

plaque morphology:

phy with histology.

duplex sonogra-

Surg

2:6-13, 1988.

MRC

Interim results for

Carotid

Trial:

with severe

Group.

European

Surgery

symptomatic patients

Picano

Landini

Lattanzi

et al: Time domain

(

70-99%) or with mild (0-29%) carotid stenosis.

echo

evaluations from normal and athero-

pattern

Lancet 337:1235-1243, 1991.

sclerotic arterial walls:

77:654-659, 1988.

_s_t_u_d_yin ^vⁱ^t^r^o^.

Circulation

5. Anderson CM, Lee RE, Levin DL,

al:

Measurement of internal carotid

from source MR

stenosis

artery

0. Urbani MP, ^Pⁱ^c^aⁿ^oE, Parenti G, et al: In vivo ra-

angiograms. _R_a_d_i_o_l_o_g_y193:219-

ultrasonic tissue characteriza-

diofrequency-based

226, 1994.

tion of the atherosclerotic

1512, 1993.

Stroke 24:1507-

plaque.

6. Saouaf R, Grassi CJ, Hartnell GG, et al:

Complete

and

ultrasound as the sole

angiography

Doppler

RE, Fowler M, et al: Ultrasonic

of carotid

tion. Stroke 27:2173-2177, 1996.

Beletsky VY, Kelley

densitometric

modalities

to carotid

imaging

prior

endarterectomy.

analysis

plaque composi-

Clin Radiol

3:579-586,

1998.

7. Robinson ML, Sacks D, Perlmutter GS, et al:

Diagnostic ^c^rⁱ^t^e^rⁱ^a^f^o^r^c^a^r^o^tⁱ^dduplex sonography.

2. Aaslid R, Markwalder TM, Nornes H: Noninvasive

transcranial

ultrasound

in basal cerebral arteries.

of flow

Doppler

recording

1988.

Am J Roentgenol 151:1045-1048,

velocity

57:769-774, 1982.

Neurosurg

8. Polak JF,

carotid

GR,

DH, et al: Internal

and

Dopkin

O’Leary

stenosis:

artery

Accuracy

reproducibili-

3. FoxJF: Howto measure carotid stenosis.

Radiology

color-Doppler-assisted imaging. Radiology

86:316-318, 1993.

73:793-798, 1989.

4. Eliasziw M, FoxAJ, Sharpe BL, et al: Carotid artery

9. Moneta GL, Taylor DC, Zierler RE, et al: Asymp-

stenosis: External

Carotid

of the North American

validity

tomatic internal carotid

steno-

high grade

artery

risk factors or

Trial

Measurement

Endarterectomy

sis : Is stratification

_a_c_c_o_r_d_i_n_gto

Method.

204:229-233, 1997.

Radiology

75. Caplan LR,

Brass LM, DeWitt LD, et al: Transcranial

Vasc

duplex spectral analysis possible.

Surg

0:475-483, 1989.

893

Downloaded from ang.sagepub.com at UCSF LIBRARY & CKM on April 17, 2015

ultrasound: Present status.

91. Molloy J, Markus HS: Asymptomatic embolization

stroke and TIA risk in with carotid

Doppler

0:696-700, 1990.

Neurology

predicts

patients

stenosis. Stroke 30:1440-1443, 1999.

artery

6. Kleiser B, WidderB: Course ofcarotid

occlu-

artery

cerebrovascular

Stroke 23:171-174, 1992.

sions with

92. Forteza AM, Babikian VL, Hyde C, et al: Effect of

impaired

reactivity.

time and cerebrovascular symptoms on the preva-

lence of microembolic

vical carotid stenosis. Stroke 27:687-690, 1996.

in patients with cer-

signals

7. Eicke BM, vonLorentz J, Paulus W: Embolus detec-

tion in different

of carotid disease. Neurol

degrees

Res 17:181-184, 1995.

93. Sliwka U, Lingnau A, Stohlmann WD, et al: Preva-

lence and time course of microembolic

signals

8. Consensus on microembolus detection by TCD.

Stroke 29:725-729, 1998.

with acute stroke. Stroke 28:358-363,

patients

997.

9. Markus HS, Brown MM: Differentiation between

4. Valton L, Larrue V, Arrue P, et al:

Asymptomatic

with carotid

different

cerebral embolic materials

an in vitro model.

pathological

cerebral embolic

signals

patients

transcranial

_D_o_p_p_l_e_rin

using

stenosis. Stroke 26:813-815, 1995.

Stroke 24:1-5, 1993.

MP:

microembolic

_s_i_g_n_a_l_sfor di-

Spencer

agnosis

Doppler

0. Droste DW, Markus HS, Nassiri D, et al: The effect

of ulcerated carotid

cardiography 13:1-4, 1996.

Echo-

artery plaques.

on the

of embolic

_D_o_p_p_l_e_rmodels.

velocity

studied in transcranial

5:986-991, 1994.

appearance

signals

Stroke

6. Orlandi G, Parenti G, Bertolucci A, et al: Carotid

features on

and

plaque

angiography

asymptomatic

1. Babikian VL,

relates of

V, et al: Clinical cor-

Pochay

Hyde

cerebral microembolism. Acta Neurol Scand

transient

detected

with

high-intensity

signals

6:183-186, 1997.

7. Greenland P, Knopman DS, Mikell FL, et al:

assessment of

on transcranial

Doppler sonography

patients

cerebrovascular disease. Stroke 25:1570-1573,

994.

Echocardiography

diagnostic

stroke. Ann Intern Med95:51-53, 1981.

D, Grosset DG, QuinRO, et al: Detection

Georgiadis

B, Polasek P, Voll C, et al:

of intracranial emboli in

with carotid dis-

Cujec

Transesophageal

in the detection of

patients

car-

potential

Stroke

ease. Eur

Vasc

8:309-314, 1994.

echocardiography

Surg

diac source of embolism in stroke

patients.

3. Sitzer M, Siebler M, Steinmetz H: Silent emboli and

2:727-733, 1991.

9. RemJA, Hachinski VC, Boughner DR, et al: Value of

cardiac in TIA

their relation to clinical in extracranial

symptoms

disease. Cerebrovasc Dis 5:121-123,

carotid

artery

and

1995.

monitoring

and stroke

echocardiography

Stroke 16:950-956, 1985.

patients.

4. Sitzer M. Muller W, Siebler M, et al: Plaque ulcera-

tion and lumen thrombus are the main sources of

00.

PC, Burch JG,

Anunusual

FS: Granulomatous

of stroke. Stroke 8:29-

Burger

angiitis.

Vogel

cerebral microemboli in

internal carotid

etiology

high-grade

stenosis. Stroke 26:1231-1233, 1995.

35, 1977.

artery

01. Howard GF III, Ho SU, Kim KS, et al: Bilateral

carotid occlusion

from

5. Markus HS,ThomsonND, BrownMM:

Asymptom-

and

disease. Brain 118:

artery

resulting

giant ^c^e^l^l

ar-

atic cerebral embolic

signals

artery

symptomatic

teritis. Ann Neurol 15:204-207, 1984.

carotid

asymptomatic

005-1011, 1995.

102. Greenfield’s

ed. 4, ed.

Adams

Wiley

Neuropathology,

JH, Corsellis JAN,

Duchen LW. NewYork:

185.

6. Orlandi G, Parenti

Bertolucci

_A_,et ^a^l^:Silent cere-

Medical, 1984,

bral microembolism in

and

symptomatic

stenoses of low and

asympto-

_h_i_g_hde-

matic carotid

103. Gudmundsson

Jonasson

_T_A_,et

artery

gree. Eur Neurol 38:39-43, 1997.

G, Hallgrimsson J,

al: Hereditary cerebral haemorrhage with amyloi-

dosis. Brain 95:387-404, 1972.

7. Babikian VL, Wijman CAC, Hyde C, et al: Cerebral

microembolism and recurrent cerebral or reti-

early

nal ischemic events. Stroke

104. Lammie

GA,

autosomal dominant

Rakshi

Rossor

_M_N_,et al: Cerebral

28:1314-1318,

1997.

arteriopathy

with subcortical

infarcts and

confirmation

Neuropathol 14:201-206, 1995.

(CADASIL) —

leukoencephalopathy

D, LindnerA, ManzM, et al: Intracranial

Georgiadis

microembolic

cardiac or carotid embolic source and normal con-

trols. Stroke 28:1203-1207, 1997.

cerebral

in 2

cases. Clin

biopsy

in 500

with

signal

patients

potential

105. Chambers

Prognosis

BR,

Norris

of acute stroke.

JW,

Shurvell

BL,

Neurology

et al:

37:221-225,

CAC, Babikian VL,

ICA, et al:

Matjucha

Wijman

1987.

Cerebral microembolism in

chemia. Stroke

with retinal is-

patients

9:1139-1143,

1998.

106. Toole JF: Cerebrovascular

_D_i_s_o_r_d_e_r_s_,ed. 4,

ch. 14.

NewYork: Raven Press, 1990,

277-307.

0. MolloyJ, KhanN, Markus HS:

Temporalvariability

embolization in carotid

107. Wilterdink JL, Easton D: Vascular event rates in

pa-

asymptomatic

stenosis and

artery

Stroke

tients with atherosclerotic cerebrovascular disease.

Arch Neurol 49:857-863, 1992.

optimal recording protocols.

9:1129-1132, 1998.

894

Downloaded from ang.sagepub.com at UCSF LIBRARY & CKM on April 17, 2015

Products guided by the article

Product name:2,2'-dimethoxy-4,4'-benzylidene-di-phenol

Cas No:111979-72-7

R&D Labs maybe for 111979-72-7

suzhou BetterBioChem Co., Ltd.

website:http://www.betterbiochem.com

Contact:+86-18013506594

Address:No. 8 Building, 18 nong, Xi Yingnan Road, Pudong, Shanghai,China
Anhui Eapearl Chemical Co., Ltd.

Contact:86-562-5858458

Address:358 South Huaihe Road
Nantong Baokai Chemical Co., Ltd (Hangzhou Baokai Bio-Chemicals Co.,Ltd.)

Contact:+86-513-83886111

Address:No. 68 Suzhou road ,Binjiang Fine Chemical Industrial Park , Beixin town, Qidong city ,Jiangsu province
Shanghai Hanhong Scientific Co.,Ltd.

website:http://www.chemvia.com

Contact:+86-21-64541543,54280654,13918533501

Address:Jiachuan Road 245
Nanjing yieldpharma co.ltd

Contact:13813902930 025-52714267

Address:20 Fengji Road, Yuhua Economic Development Zone, Nanjing, Jiangsu, P. R. China

Relevant to this article

Preparation of membrane-mimicking lamellar structures by molecular confinement of hybrid nanocomposites

Doi:10.1039/c8cc09399g
(2019)
Doi:10.1039/jr9460000503
(1946)
Late-Stage Bromination Enables the Synthesis of Rubrolides B, I, K, and O

Doi:10.1002/ejoc.201600473
(2016)
Convenient substitution of hydroxypyridines with trifluoroacetaldehyde ethyl hemiacetal

Doi:10.1002/jhet.5570380103
(2001)
Doi:10.1007/BF01913383
(1988)
A Convenient Method for the Protection of Amino Groups as Diethyl Phosphoramidates

Doi:10.1055/s-1984-30778
(1984)

Article Doi

DOI: 10.1177/000331970005101101

Source and publish data:

Authors:

Article abstract of DOI:10.1177/000331970005101101

Full text of DOI:10.1177/000331970005101101

Products guided by the article

R&D Labs maybe for 111979-72-7

Relevant to this article

Hot Product