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
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