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(Stroke. 2006;37:915.)
© 2006 American Heart Association, Inc.
Research Reports |
From the Department of Clinical Neurosciences (P.N.S., I.D., A.K., P.F., A.M.D.), University of Calgary, Alberta; and the Advance Medicare & Research Institute (J.R.), Kolkata, India.
Correspondence to Andrew M. Demchuk, MD, FRCPC, Associate Professor, Department of Clinical Neurosciences, University of Calgary, Foothills Medical Centre, Room 1162, 1403 29th St, NW, Calgary, Alberta, Canada. E-mail ademchuk{at}ucalgary.ca
| Abstract |
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Methods Three hundred and twenty six patients underwent noncontrast CT and CTA for acute stroke at our institution over 3 years (June 2002 to April 2005). Of them, 116 had disabling deficits and presented within 3 hours. We reviewed the clinical data, noncontrast CT, CTA, electroencephalogram and outcome of these patients and identified those who presented with presumed seizure activity at stroke onset (seizure or altered consciousness at stroke onset).
Results Nine (7.7%) patients had a concern of seizure at stroke onset. Median age 73 years (range, 31 to 85 years), median National Institutes of Health Stroke Scale (NIHSS) score 12 (range, 5 to 29). CTA showed proximal middle cerebral artery occlusion in 2 and distal middle cerebral artery occlusion in 3 patients. All 5 of these patients had evidence of infarction on follow-up (stroke+early seizure group-intracranial occlusion present). Three of these patients received intravenous tissue plasminogen activator because they were deemed to have "ischemic tissue at risk". Four patients had normal CT and CTA studies and recovered completely in 24 hours (Todds paralysis only group-intracranial occlusion negative).
Conclusion Seizure at stroke onset was relatively uncommon in a consecutive cohort of acute stroke patients. CTA was a useful modality in differentiating Todds paralysis from early seizure and ischemia by detection of intracranial occlusion and may contribute to decision-making for thrombolysis.
Key Words: Todds paralysis
| Introduction |
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We sought to examine this issue and determine whether computed tomographic angiography (CTA) in the acute setting can help to differentiate Todds paralysis without cerebral ischemia from ischemia with early seizures.
| Materials and Methods |
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| Results |
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5) and presented within 3 hours of symptom onset. Nine patients were identified with history of presumed seizure activity at symptom onset. Four patients had witnessed focal motor seizures and 5 had alteration of consciousness with strong suspicion of seizure activity. The clinical, EEG findings and outcome are summarized in the Table. NCCT head showed an ASPECTS of 10 in 7 patients and 7 and 8 in 1 patient each. CTA was normal in 4 patients and showed proximal occlusion of the middle cerebral artery in 2 patients and distal middle cerebral artery branch occlusion in 3 patients. The Figure shows the NCCT, CTA and the follow-up CT of a patient with M1 occlusion. Three of the 5 patients with intracranial occlusion received tPA despite the relative contraindication because there was evidence of ischemia and the deficits were disabling. Two patients showed rapidly improving deficits and hence were not given thrombolysis. Of the 3 who received tPA, 2 had a favorable outcome (mRS 1) and the 1 had a poor outcome (mRS 3). All 4 patients with normal CT and CTA did not receive tPA and recovered completely with no evidence of infarction on follow-up imaging. The 5 patients with evidence of intracranial occlusion on the CTA had infarcts on the follow-up CT.
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| Discussion |
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Seizure at stroke onset is still considered a relative contraindication for thrombolysis.1,11 This is based on the fear of risking treatment in a patient with Todds paralysis. Todds paralysis is a condition characterized by brief period of partial or complete paralysis with or without aphasia after a seizure. It usually subsides in 48 hours. All the patients in our series presented with disabling right- or left-sided weakness with or without aphasia. In a setting of history of focal seizures or patient in altered consciousness in an anterior circulation stroke, it is important to differentiate postictal Todds paralysis alone from early ischemia with seizure. The exact frequency of seizure at stroke onset is not known. The study by Shinton et al showed a frequency of 5.7% with single or recurrent seizures at stroke onset.7 Intravenous tPA given within 3 hours of symptom onset is a proven effective therapy for acute ischemic stroke. Seizure at stroke onset hinders the option of thrombolytic treatment; hence, an investigation that can help to differentiate Todds paralysis from deficit attributable to early ischemia is necessary in the decision-making.
CTA is quickly gaining widespread use for triaging acute stroke patients. It has become widely available because of new generation spiral CT scanners and only takes 10 additional minutes to perform to diagnose intracranial occlusion. CTA offers information on the vascular status12,13 and extent of parenchymal ischemic injury with the CTA source imaging information.10,14 Studies have shown its role in selection of patients for thrombolytic therapy, and its diagnostic accuracy is in good agreement with the angiographic findings.12 It appears ideally suited to assist in this clinical scenario. EEG is a sensitive neurodiagnostic tool in the detection of acute cerebral ischemia and epileptic activity, but its specificity is low.15 Focal slowing and epileptiform activity can occur in both ischemia and seizures; hence, it does not help in the differentiation of these entities as was seen in our patients. Specific EEG findings of seizure still do not distinguish seizure with Todds paralysis versus ischemic seizures. Multimodal MRI techniques may also be useful in this setting by providing information regarding presence of ischemia (diffusion-weighted imaging) as well as perfusion information or status of intracranial vessels (magnetic resonance angiography). One would anticipate similar differences between Todds paralysis alone versus early seizure with ischemia. One challenge in treating patients with seizure and stroke relates to an acceleration of ischemia which may hasten evolution to infarction attributable to increased cerebral glucose metabolic demand caused by excessive neuronal activity from seizures. This could lead to extension of infarction and worse outcome as shown in a positron emission tomography study.16,17 This rapid evolution to infarction may limit thrombolysis benefit unless treatment can be given early.
In conclusion, seizure at stroke onset is an uncommon clinical scenario facing clinicians in the emergency room. CTA is useful in differentiating patients with Todds paralysis alone from those with early seizure and stroke. Thrombolysis could be carefully contemplated in patients with stroke and presumed seizure and intracranial occlusion, but more safety data may be required.
Received November 28, 2005; accepted December 6, 2005.
| References |
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2. Kilpatrick CJ, Davis SM, Tress BM, Rossiter SC, Hopper JL, Vandendriesen ML. Epileptic seizures in acute stroke. Arch Neurol. 1990; 47: 157160.
3. So EL, Annegers JF, Hauser WA, OBrien PC, Whisnant JP. Population based study of seizure disorders after cerebral infarction. Neurology. 1996; 46: 350355.
4. Arboix A, Garcia-Eroles L, Massons JB, Oliveres M, Comes E. Predictive factors of early seizures after acute cerebrovascular disease. Stroke. 1997; 28: 15901594.
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16. Bladin ChF, Alexandrov AV, Norris JW. Seizures after stroke. In: Fisher M, Bougousslavsky J, eds. Current Review of Cerebrovascular Diseases. Philadelphia: Current Medicine, 1996; 107117.
17. De Reuck J, Decoo D, Algoed L, Boon P, Van Maele G, Lemahieu I, Strijckmans K, Goethals P. Epileptic seizures after thromboembolic cerebral infarcts: a positron emission tomographic study. Cerebrovasc Dis. 1995; 5: 328333.
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