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Behavioral neurology in the emergency room Language testing brain imaging and acute stroke therapy.

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EDITORIAL
Behavioral Neurology in the Emergency
Room: Language Testing, Brain Imaging,
and Acute Stroke Therapy
Behavioral neurology has often been considered the
most theoretical and least practical area of neurology,
the province of armchair philosophers and students of
the mind–brain relationship. Detailed structure–function analyses, such as the anatomical basis of language
comprehension or of lexical–semantic relationships
(words and their meanings), have held limited interest
for practicing neurologists. Aphasiology has been controversial, with some experts finding little consistent relationship between specific sites of brain injury and
aphasic phenomena.1 Functional brain imaging of cortical networks promises to clarify these inconsistencies
in brain–language correlation.2 Imaging of acute stroke,
before recovery and compensation for damaged areas,
may provide another window into the relationships of
language function and brain structure.
The advent of acute stroke interventions has brought
behavioral neurology into the acute treatment arena,
just as it has forced practicing neurologists out of the
office and into the emergency room. Revascularization
therapies, such as intravenous3 and intraarterial4 thrombolytic therapy, have highlighted the need to identify
brain areas at risk of irreversible damage, but that are
still salvageable if flow can be restored. Speech, language, and cognition are among the most critical functions to preserve in a stroke patient.
New parameters of magnetic resonance imaging
(MRI) have aided the diagnosis of acute stroke.
Perfusion-weighted imaging (PWI) identifies ischemic
tissue at risk of infarction, whereas diffusion-weighted
imaging (DWI) indicates tissue with cytotoxic edema,
already infarcted or on the verge of infarction. The difference between the diffusion and perfusion defects,
the “diffusion–perfusion mismatch,” is thought to represent the “ischemic penumbra.”5,6 This oft-quoted
theory of the diffusion–perfusion mismatch, however,
requires correlation with clinical outcome measures.
In previous research, Hillis and colleagues7 demonstrated that behavioral detection of aphasic deficits or
neglect in acute stroke patients correlated with hypoperfusion on PWI and that improved perfusion by
blood pressure elevation or carotid endarterectomy resulted in both recovery of the clinical deficit and reduction of the PWI defect. Thus, the authors demonstrated that testing of cognitive functions and the
finding of a diffusion–perfusion mismatch have practi-
cal value in the treatment of acute stroke patients. Hillis and colleagues8 presented a patient with a left frontotemporal stroke in whom hypotension appeared to
worsen both the perfusion of Wernicke’s area and language deficits; blood pressure elevation improved both
perfusion and language function. In this issue of the
Annals of Neurology, Hillis and colleagues9 provide
quantitative evidence that the perfusion defects noted
on MRI correlate with the clinical deficits in a specific
language function. The authors correlated delayed perfusion (time to peak on PWI) of Brodmann’s area 22,
the traditional Wernicke’s area, relative to the analogous right hemisphere area, with deficits in spoken
word–picture (lexical–semantic) matching in 50 patients with acute left middle cerebral artery territory
ischemia; 29 additional patients were excluded because
of a diffusion defect indicating an infarct, in which the
degree of perfusion would not be expected to correlate
with language function. The delay in perfusion of area
22 correlated quantitatively with the degree of lexical–
semantic deficit; a delay of longer than 2.5 seconds to
peak perfusion was predictive of loss of lexical–semantic ability.
The implications of this research are important both
for the understanding of language function and for the
scientific basis of acute stroke therapy. First, these results clearly establish the critical importance of the cortical Wernicke’s area for single word comprehension, a
finding also supported by poststroke CT research.10,11
Second, they show that a perfusion defect on MRI indicates a loss of function of the affected cortex. PWI,
along with clinical examination, should guide the use
of thrombolytic agents. For the future, further research
is needed to prove that revascularization of a hypoperfused area on PWI will restore function and improve
clinical outcome. Kidwell and colleagues (University of
California at Los Angeles)12 have shown that diffusion
MRI does not always indicate irreversibly infarcted
brain and that thrombolytic therapy can reduce the diffusion defect. Use of thrombolytic therapy has not
been proved effective beyond the 6-hour window of
the PROACT II study,4 although a potential may exist
in patients who continue to show a diffusion–perfusion
mismatch beyond this time. As Hillis and associates7,8
have shown, simpler measures, such as induced hypertension, improve perfusion in such cases.
© 2001 Wiley-Liss, Inc.
559
Hypotension in the setting of hypoxia or stroke
worsens brain injury in animal models13 and in patients,14 but the use of pressor agents to raise blood
pressure will require specific clinical trial evidence to
become a routine recommendation. Rordorf and colleagues15 have reported encouraging results in 7 of 13
patients treated with phenylephrine. Methods such as
those of Hillis and coworkers7–9 should be at the forefront of research into this treatment strategy, and neurologists interested in cognitive function should emulate their practical application of these techniques in
the emergency room.
Howard S. Kirshner, MD
Department of Neurology
Vanderbilt University School of Medicine
Nashville, TN
References
1. Willmes K, Poeck K. To what extent can aphasic syndromes be
localized? Brain 1993;116:1527–1540.
2. Kirshner HS. Language studies in the third millennium. Brain
Lang 2000;71:124 –128.
3. NINDS rt-PA Stroke Group. Tissue plasminogen activator for
acute ischemic stroke. N Engl J Med 1995;333:1581–1587.
4. Furlan AJ, Higashida R, Wechsler L, et al. Intra-arterial
prourokinase for acute ischemic stroke. The PROACT II study:
a randomized controlled trial. JAMA 1999;282:2003–2011.
560
Annals of Neurology
Vol 50
No 5
November 2001
5. Fisher M, Garcia JH. Evolving stroke and the ischemic penumbra. Neurology 1996;47:884 – 888.
6. Schlaug G, Benfield BS, Baird AE, et al. The ischemic
penumbra: operationally defined by diffusion and perfusion
MRI. Neurology 1999;53:1528 –1537.
7. Hillis AE, Barker P, Beauchamp N, et al. MR perfusion imaging reveals regions of hypoperfusion associated with aphasia and
neglect. Neurology 2000;55:782–788.
8. Hillis AE, Kane A, Barker P, et al. Restoring blood pressure
reperfused Wernicke’s area and improved language. Neurology
2001;56:670 – 672.
9. Hillis AE, Wityk RJ, Tuffiash E, et al. Hypoperfusion of Wernicke’s area predicts severity of semantic deficit in acute stroke.
Ann Neurol 2001;50:561–566.
10. Selnes OA, Niccum N, Knopman DS, Rubens AB. Recovery of
single word comprehension: CT-scan correlates. Brain Lang
1984;21:72– 84.
11. Naeser MA, Helm-Estabrooks N, Haas G, et al. Relationship
between lesion extent in “Wernicke’s area” on computed tomographic scan and predicting recovery of comprehension in Wernicke’s aphasia. Arch Neurol 1987;44:73– 82.
12. Kidwell CS, Saver JL, Mattiello J, et al. Thrombolytic reversal
of acute human cerebral ischemic injury shown by diffusion/
perfusion magnetic resonance imaging. Ann Neurol 2000;47:
462– 469.
13. Kirschner HS, Blank WF Jr, Myers RE. Changes in cortical
subarachnoid fluid potassium concentrations during hypoxia.
Arch Neurol 1976;33:83–90.
14. Lavin P. Management of hypertension in patients with acute
stroke. Arch Intern Med 1986;146:66 – 68.
15. Rordorf G, Koroshetz WJ, Ezzeddine MA, et al. A pilot study
of drug-induced hypertension for treatment of acute stroke.
Neurology 2001;56:1210 –1213.
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testing, stroki, behavior, language, emergency, neurology, room, imagine, brain, acute, therapy
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