Radiological pathology of transient ischemic attacks http://yassermetwally.com http://yassermetwally.net

1. Professor Yasser Metwally
www.yassermetwally.com
INDEX
 INTRODUCTION
 Periventricular white matter
changes (leukoaraiosis)
 Cortical-Subcortical
abnormality
 Watershed abnormality
 Normal MRI
 SUMMARY
INTRODUCTION
Most patients with TIAs have normal CT scans. The incidence of associated infarction as
demonstrated by CT has varied from 0 to 20% . These CT abnormalities have frequently
consisted of lacunae or more extensive ill-defined periventricular regions of decreased
density or watershed infarctions. The gray matter enhancement associated with cortical
infarction and cerebral dysautoregulation has been an infrequent finding. Other observed
CT findings have been equally nonspecific, including ventriculomegaly and cortical
atrophy.
The MRI is abnormal in 70% of cases with TIAs. All abnormalities seen by CT are also
visualized by MRI. Moreover, MRI commonly visualized more extensive involvement than
is appreciated by CT. The MRI findings can be divided into four categories according to
their anatomical distribution and morphology as follows.
www.yassermetwally.com

2. Professor Yasser Metwally
www.yassermetwally.com
 Periventricular abnormality
 Cortical-subcortical
abnormality
 Watershed abnormality
 Normal MRI
 Periventricular white matter changes (leukoaraiosis)
This category is composed of the oldest patients (average age 73.8 years) and had the
highest percentage of hypertensives (75%). Of all the groups , this group tended to have a
more Polymorphic appearance, being combined on occasion with cortical and subcortical
abnormalities as well as extending into clear watershed zones. Abnormalities of the
immediate periventricular area, especially bordering the dorsolateral surfaces of the
ventricles, are relatively nonspecific since this region may be injured by a wide variety of
disease states .
The diversity of possible causes (embolic, hemodynamic, and
hypertensive) is present within this group. The incidence of a
cardiac history consisting of arrhythmias (chronic atrial
fibrillation and ventricular arrhythmias), mitral annular
calcifications, and aortic sclerosis, as well as myocardial
infarction and angina is very low in this group. It is of
interest that this group has the lowest degree of
hemodynamically significant carotid stenosis. TIAs and
RINDS in this group is one of the clinical manifestations of
microvascular brain disease.
Figure 1. CT scan image showing leukoaraiosis
Although there are a diverse number of disease states that may cause these periventricular
changes, it seems apparent that the most common etiology would be the vascular changes
associated with hypertension. Such changes perhaps are best illustrated by a common
disease, namely, subcortical arteriosclerotic encephalopathy (SAE). SAE and the high
incidence of lateral periventricular abnormalities encountered have been the topic of much
debate. Although none of the patients in this group have a symptom complex composed of
dementia, stroke, gait disturbance, ventriculomegaly, or urinary incontinence it seems
reasonable to expect that SAE may initially present with TIA or reversible ischemic
neurologic deficit (RIND). This group had the highest percentage of RIND symptoms.
 Cortical-Subcortical abnormality
This is the largest Population of abnormalities found, representing 43% of all abnormal
studies. The average age of this group was 66.6 years, which is considerably lower than that
of the periventricular group. This group also had a relatively large percentage of
www.yassermetwally.com

3. Professor Yasser Metwally
www.yassermetwally.com
hypertensive individuals (61%). The incidence of a cardiogenic source for the emboli such
as atrial fibrillation, ventricular arrhythmias, prolapsed mitral valve, atherosclerotic heart
disease with angina, and recent myocardial infarction is low. The incidence of significant
carotid stenosis defined as greater than 80% by carotid ultrasound or angiography is also
very low in this group. CT scans might be abnormal in this group demonstrating
periventricular lacunae or focal gray matter enhancement. This group has the lowest
percentage of recurrent TIAS. TIAs and RINDS in this group is one of the clinical
manifestations of microvascular brain disease.
 Watershed abnormality
This category has an average age of 70.3 years and, interestingly, the lowest percentage of
hypertension (58%), comparable to the cortical-subcortical group. All of these patients
have abnormalities lying in a deep posterior wedge distribution extending posteriorly and
dorsally from the lateral ventricles. Some of them have abnormalities extending along the
dorsolateral aspect of the lateral ventricles. Others have the abnormality extending along
the cortex and subcortical region between the anterior and middle cerebral arteries.
Abnormalities within watershed zones, within the cerebellum and between the distributions
of the posterior inferior and superior cerebellar arteries is occasionally demonstrated.
Many of these patients have significant carotid stenosis with or without coronary artery
stenosis. Myocardial infarctions or ventricular arrhythmias are occasionally present. This
group has the highest percentage of multiple or recurrent TIAs (67%).
 Normal MRI
This group has the youngest average age (58.6 years), the second highest percentage of
hypertensives (67%), and the second highest number of recurrent TIAS. incidence of
significant carotid disease or cardiac disease is very low.
SUMMARY
Type Incidence Age Carotid Hypertension Possible aetiology
stenosis
Periventricular Common in 73.8 Low 75% Microvascular brain
white matter Egypt incidence disease
changes
(leukoaraiosis)
Cortical- Common in 66.6 Low 61% Microvascular brain
Subcortical Egypt incidence disease
Watershed Rare in 70.8 High Low Carotid bifurcation
Egypt incidence disease
Normal Common in 58.6 Low 76 % Microvascular brain
Egypt incidence disease
www.yassermetwally.com

4. Professor Yasser Metwally
www.yassermetwally.com
References
1. Bhatt DL, Kapadia SR, Yadav JS, Topol EJ: Update on clinical trials of antiplatelet
therapy for cerebrovascular diseases. Cerebrovasc Dis 2000; 10 Suppl 5: 34-40.
2. Bots ML, van der Wilk EC, Koudstaal PJ, et al: Transient neurological attacks in
the general population. Prevalence, risk factors, and clinical relevance. Stroke 1997
Apr; 28(4): 768-73.
3. Brown RD Jr, Evans BA, Wiebers DO, et al: Transient ischemic attack and minor
ischemic stroke: an algorithm for evaluation and treatment. Mayo Clinic Division of
Cerebrovascular Diseases. Mayo Clin Proc 1994 Nov; 69(11): 1027-39.
4. Culebras A, Kase CS, Masdeu JC, et al: Practice guidelines for the use of imaging in
transient ischemic attacks and acute stroke. A report of the Stroke Council,
American Heart Association. Stroke 1997 Jul; 28(7): 1480-97.
5. Davalos A, Matias-Guiu J, Torrent O, et al: Computed tomography in reversible
ischaemic attacks: clinical and prognostic correlations in a prospective study. J
Neurol 1988 Jan; 235(3): 155-8.
6. Dyken ML, Conneally M, Haerer AF, et al: Cooperative study of hospital frequency
and character of transient ischemic attacks. I. Background, organization, and
clinical survey. JAMA 1977 Feb 28; 237(9): 882-6.
7. Feinberg WM, Albers GW, Barnett HJ, et al: Guidelines for the management of
transient ischemic attacks. From the Ad Hoc Committee on Guidelines for the
Management of Transient Ischemic Attacks of the Stroke Council of the American
Heart Association. Circulation 1994 Jun; 89(6): 2950-65.
8. Forbes CD: Antiplatelet therapy for secondary stroke prevention. Scott Med J 1999
Apr; 44(2): 54-9.
9. Gross SB: Transient ischemic attacks (TIA): current issues in diagnosis and
management. J Am Acad Nurse Pract 1995 Jul; 7(7): 329-37.
10. Gustafsson D, Elg M: The pharmacodynamics and pharmacokinetics of the oral
direct thrombin inhibitor ximelagatran and its active metabolite melagatran: a
mini-review. Thromb Res 2003 Jul 15; 109 Suppl 1: S9-15.
11. Henneman PL, Lewis RJ: Is admission medically justified for all patients with acute
stroke or transient ischemic attack? Ann Emerg Med 1995 Apr; 25(4): 458-63.
12. Johnston SC, Gress DR, Browner WS, Sidney S: Short-term prognosis after
emergency department diagnosis of TIA. JAMA 2000 Dec 13; 284(22): 2901-6.
13. Landi G: Clinical diagnosis of transient ischaemic attacks. Lancet 1992 Feb 15;
339(8790): 402-5.
14. Lanska DJ: Review criteria for hospital utilization for patients with cerebrovascular
disease. Task Force on Hospital Utilization for Stroke of the American Academy of
Neurology. Neurology 1994 Aug; 44(8): 1531-2.
15. Shiozaki T, Hayakata T, Taneda M, et al: A multicenter prospective randomized
controlled trial of the efficacy of mild hypothermia for severely head injured
patients with low intracranial pressure. Mild Hypothermia Study Group in Japan. J
Neurosurg 2001 Jan; 94(1): 50-4.
16. Worrall BB, Johnston KC: Antiplatelet therapy in secondary stroke prevention.
Curr Atheroscler Rep 2000 Mar; 2(2): 104-9.
17. Zweifler RM: Management of acute stroke. South Med J 2003 Apr; 96(4): 380-5.
www.yassermetwally.com