TRANSIENT ISCHAEMIC ATTACKS

Definitions and mimics

CONTENTS

Dr Charles Miller Fisher

Terms before TIA

Clinical concept of TIA

Stendhal’s Aphasia

Changing Definitions

Flawed definitions

Mimics

Tissue based diagnosis

DR CHARLES MILLER FISHER (1913-2012).

Dr. C. Miller Fisher, a Neurologist at

Massachusetts General Hospital

whose pioneering discoveries in the

causes and treatment of strokes

created the basis for modern stroke

treatments.

He authored more than 200

publications detailing his

observations.

“strokes do not occur at random”,

DR CHARLES MILLER FISHER (1913-2012).

In his most famous

observation, he

repeatedly noted“premonitory fleeting symptoms”

(including limb sensory

symptoms, and monocular

visual loss) experienced by

patients prior to a ischaemic

stroke, and made the crucial

link to carotid artery

atheromatous disease.

SO WHAT TERM CAME BEFORE TIA

cerebral arterial spasms:

This hypothesis put forward by Raynaud (1862) to

account for the transient loss of vision was

accepted by many authors (Weiss, 1882; Bland,

1889; Peabody, 1891; Osier, 1896) as the most

convincing pathophysiological explanation of

cerebrovascular transient episodes.

THE CLINICAL CONCEPT OF T.I.A

During the 2nd Princeton Conference: intermittent vascular insufficiency,

ischemic recurrent attacks

recurrent focal cerebral ischemic attacks

transient cerebral ischemia

Defined by Dr Miller-Fisher in 1958:

“Transient Ischemic Attack”

in 1958 the ‘Ad hoc Committee’ NIH indicated the transient episodes as ‘transient cerebral ischemia’

1961 3rd Princeton Conference the term: ‘focal intermittent insufficiency or

ischemic attack’ was still used,

It was only in the 4th Princeton Conference of 1965, however, that the definition gained unanimous acceptance.

“transient ischemic attacks”

(Carolie et al,. 1998)

HENRI-MARIE BAYLE (STENDHAL) 1781 - 1842

Stendhal’s Aphasic spells:

The first report of TIA’s followed by a stroke.

Famous French novelist of the 19th

Century.

Had a series of short lived speech impairments, reported in his correspondence.

Stendhal’s TIA’s occurred a few months before a fatal stroke.

Forgot how to speak French, had word finding problems.

Bogousslavsky, J. (Lausanne) ,Boller, F. (Paris) 2005

Frontiers of Neurology and Neuroscience,Vol. 19Neurological Disorders in Famous ArtistsISBN: 978-3-8055-7914-8e-ISBN: 978-3-318-01206-4DOI:10.1159/isbn.978-3-318-01206-4

Stendhal by Soedermark in 1840

STENDHAL’S LAST PORTRAIT

Portrait by Henry

Lehmann Aug 1841 Exactly 20 years before Broca’s

presentation at the Society

d’Anthropologie

Right hand and face

weakness,(Del Litto, 1968)

Dominant right hand

Stendhal never reported right

hemiparesis.

1958 DEFINITION OF TIA

Cerebral Ischemic episode that:

“may last from a few

seconds up to several

hours, the most common

duration being a few

seconds up to five or ten

minutes”.

Fisher, C.Miller ,Oct 1958,

Cerebrovascular diseases: pathophysiology, diagnosis, and

treatment ,Journal of Chronic Diseases ,Volume 8 , Issue 4 , 419

- 447

EARLIER TIA DEFINITIONS

1975 NATIONAL INSTITUTE OF NEUROLOGICAL AND COMMUNICATIVE DISORDERS AND STROKE. 1988,WHO DEFINITION

“Episodes of temporary and

focal dysfunction of vascular

origin, which are variable in

duration, commonly lasting

from 2-15 minutes, but

occasionally lasting as long

as 24 hours; they leave no

persistent neurologic deficit”.

“Sudden focal cerebral

dysfunction lasting less than

24 hours of presumed

vascular origin confined to

the area of brain or eye

perfused by a specific

artery”WHO MONICA Project Principal Investigators. The World Health Organization

MONICA Project (monitoring trends and determinants in

cardiovascular disease): a major international collaboration. J Clin

Epidemiol. 1988;41(2):105–114

WHERE ARE THE FLAWS?

Time dependency!

The probability of infarct

on MRI, DWI increases as

the symptom duration

increases,

Observed brain infarcts

with symptoms lasting for

30 seconds

As well as normal DWI

despite symptoms lasting

for several hours.

Sorensen et al, 2011:

WHERE ARE THE FLAWS?- 2

Resolution of symptoms

TIA is not necessarily

transient at the tissue

level

1/3 of traditionally

defined TIAs have had

infarcts.

Giles MF, Albers GW, Amarenco P, et al. Addition of brain

infarction to the ABCD2 Score (ABCD2I): a collaborative

analysis of unpublished data on 4574

patients. Stroke. 2010;41:1907–1913.

SIZE OF TIA RELATED INFARCTS

The most important characteristic of TIA-related infarcts on DWI is their small size, Koroshetz WJ, Benner T, et al. 2005.

Infarcts as small as 0.07 ml can occur during a TIA.

96%of all infarcts in TIA are smaller than 1 ml.

Oliveira-Filho et al (2002) describes these infarcts as:

“footprints of transient ischemia”

for lesions on DWI that remain after complete resolution of TIA symptoms,

Ay H, Oliveira-Filho J, Buonanno FS, et al. “Footprints” of transient ischemic attacks: a diffusion-weighted MRI study. Cerebrovasc Dis. 2002;14:177–186.

Ay H, Koroshetz WJ, Benner T, et al. Transient ischemic attack with infarction: a unique syndrome? Ann Neurol. 2005;57:679–686.

WHERE ARE THE FLAWS? - 3

Stroke, TIA & MimicsFocal symptoms identifiable to an arterial territory not always an ischemic mechanism;

Non-ischemic mechanisms include: Seizures,

Subdural haemorrhage,

Intracerebral haemorrhage,

brain tumours,

multiple sclerosis and,

migraine

can cause transient neurological symptoms confined to a vascular territory (Prabhakaran,2008;Sheehan 2009)

TISSUE BASED DEFINITION

TIA STROKE

TIA is a transient episode of

neurologic dysfunction

caused by focal brain, spinal

cord, or retinal

ischaemia, without acute

infarction, AHA 2009

.

Ischaemic stroke is defined as:

An infarction of central nervous

system tissue (brain, spinal

cord, or retinal cell death)

attributable to ischemia, based

on neuropathologic,

neuroimaging, and/or clinical

evidence (ie, persistence of

symptoms or findings) of

permanent injury, AHA 2013..

IMPORTANCE OF ACCURATE DIAGNOSIS

Post TIA Stroke risk 15-30%,(Rothwell et al, 2005).

Misdiagnosis:

Inappropriate treatment

Unnecessary investigations

Long term secondary prevention

Anxiety

Driving restrictions, i.e. HGV

NATURE OF THE SYMPTOMS -1

Positive Symptoms

An excess of CNS Neuronal activity

Visual

Flashing lights

Zigzag shapes

Lines

Shapes

Somatosensory

Pain

Motor

Jerking limb movements

NATURE OF THE SYMPTOMS -2

Negative Symptoms

Loss or reduction in

CNS neuronal function

Visual loss

Hearing loss

Loss of sensation

Reduced limb power

MIMIC VS TIA

MIMICS TIA

Usually Positive symptoms Random symptoms, no respect

for vascular pathways

Slow variable progression, -Jacksonian march

Progressive paraesthesia

LoC

Stereotypical events

Tongue biting

Vomiting

Longer durations

Precipitating factors

Usually negative symptoms

Vascular pathways are

respected

All start together

Abrupt start,

Gradual offset

Not stereotypical events

Short duration <1 hr

ANY QUESTIONS PLEASE?

REFERENCE

Sorensen, A. G., & Ay, H. (2011). Transient ischemic attack: definition, diagnosis, and risk stratification. Neuroimaging clinics of North America, 21(2), 303-13,

Easton JD, Saver JL, Albers GW, et al. Definition and evaluation of transient ischemic attack: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association Stroke Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Nursing; and the Interdisciplinary Council on Peripheral Vascular Disease. The American Academy of Neurology affirms the value of this statement as an educational tool for neurologists. Stroke 2009; 40:2276.

Sacco RL, Kasner SE, Broderick JP, et al. An updated definition of stroke for the 21st century: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2013; 44:2064.

Prabhakaran S, Silver AJ, Warrior L, et al. Misdiagnosis of transient ischemic attacks in the emergency room. Cerebrovasc Dis. 2008;26:630–635.

Sheehan OC, Merwick A, Kelly LA, et al. Diagnostic usefulness of the ABCD2 score to distinguish transient ischemic attack and minor ischemic stroke from noncerebrovascular events: the North Dublin TIA Study. Stroke. 2009;40:3449–3454.

Nadarajan V, et al. Pract Neurol 2014;14:23–31. doi:10.1136/practneurol-2013-000782

Mohr JP, Caplan LR, Kistler JP. In Memoriam: C Miller Fisher. Stroke 2012;43:1739-40.

Greenberg SM. C Miller Fisher: An Appreciation. Stroke 2013;44:171-2.

Caplan LR, Mohr JP, Ackerman RH. In Memoriam: Charles Miller Fisher (1913-2012). Arch Neurol. 2012;69(9):1208-9. doi:10.1001/archneurol.2012.1743.

Caplan LR. Fishers Rules. Archives of Neurology. 1982;39:389-90.

Bogousslavsky, J. (Lausanne) ,Boller, F. (Paris) 2005,Frontiers of Neurology and Neuroscience,Vol. 19.Neurological Disorders in Famous Artists.ISBN: 978-3-8055-

7914-8 e-ISBN: 978-3-318-01206-4 DOI:10.1159/isbn.978-3-318-01206-4

WHO MONICA Project Principal Investigators. The World Health Organization MONICA Project (monitoring trends and determinants in cardiovascular disease): a major international collaboration. J Clin Epidemiol. 1988;41(2):105–114