Professor Yasser Metwallywww.yassermetwally.com INDEX                                                     INTRODUCTION   ...
Professor Yasser Metwallywww.yassermetwally.com       Periventricular abnormality       Cortical-subcortical        abno...
Professor Yasser Metwallywww.yassermetwally.com hypertensive individuals (61%). The incidence of a cardiogenic source for ...
Professor Yasser Metwallywww.yassermetwally.com References    1. Bhatt DL, Kapadia SR, Yadav JS, Topol EJ: Update on clini...
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Radiological pathology of transient ischemic attacks

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Radiological pathology of transient ischemic attacks
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Radiological pathology of transient ischemic attacks

  1. 1. Professor Yasser Metwallywww.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. 2. Professor Yasser Metwallywww.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. 3. Professor Yasser Metwallywww.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. SUMMARYType Incidence Age Carotid Hypertension Possible aetiology stenosisPeriventricular Common in 73.8 Low 75% Microvascular brainwhite matter Egypt incidence diseasechanges(leukoaraiosis)Cortical- Common in 66.6 Low 61% Microvascular brainSubcortical Egypt incidence diseaseWatershed Rare in 70.8 High Low Carotid bifurcation Egypt incidence diseaseNormal Common in 58.6 Low 76 % Microvascular brain Egypt incidence disease www.yassermetwally.com
  4. 4. Professor Yasser Metwallywww.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

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