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Neurology India, Vol. 58, No. 6, November-December, 2010, pp. 954-955 Letter to Editor Dramatic improvement following an acute stroke: Is it a transient ischemic attack ? Dheeraj Khurana, Snigdhendu Ghosh Department of Neurology, Postgraduate Institute of Medical Education and Research, Chandigarh, India Date of Acceptance: 17-Aug-2010 Code Number: ni10268 PMID: 21150070 Sir, Dramatic improvement following acute ischemic stroke is a known but incompletely understood phenomenon. [1] Most of these cases would possibly end up being labeled as transient ischemic attacks (TIA). Multimodal imaging may however provide insight into the intricacies of this phenomenon. We report a patient who presented with signs of acute stroke followed by spontaneous recovery. A 55-year-old nondiabetic, hypertensive woman, and previously diagnosed case of rheumatic heart disease (mitral stenosis and mitral regurgitation), not on anticoagulation, presented with sudden-onset weakness of left half of body of 6 hours' duration. Her admission National Institute of Health Stroke Scale (NIHSS) score was 10, and she had a motor power of grade 0/5 in the left upper limb and 1/5 in the left lower limb. At admission, her pulse was 88 /min, regular; blood pressure was 130/86; and random blood sugar was 140 mg%. Cranial noncontrast CT scan was normal, while a CT angiography (CTA) showed a right proximal middle cerebral artery (M1) occlusion [Figure - 1]a. Since she was beyond the window period for intravenous thrombolysis and she did not consent for intra-arterial thrombolysis, she was started on medical treatment with anti-platelet medication (aspirin/dipyridamole), statins and heparin for deep venous vein thrombosis prophylaxis. At 12 hours of the onset of stroke, she started improving and the NIHSS score decreased to 2, while the power in the left upper and lower limbs increased to grade 4/5. At 24 hours, the NIHSS was 0, and a repeat CTA showed a complete recanalization of the right middle cerebral artery (MCA) [Figure - 1]b. She did not have any subsequent worsening of weakness. Cranial magnetic resonance imaging (MRI) done at 12 hours of the onset of stroke showed restricted diffusion in the right basal ganglia [Figure - 2] on diffusion-weighted imaging. Spontaneous recanalization is an intriguing phenomenon and has been clearly documented by cerebral angiography, transcranial Doppler and autopsy studies. [2],[3] An accurate assessment of this phenomenon may not be possible since most studies describing it have a heterogenous patient population, and most studies tend to exclude patients with resolving or resolved symptoms. [4] Embolic strokes are known to recanalize spontaneously more often than occlusion caused by a local thrombosis, [5] while MCA clots resolve spontaneously more often than internal carotid artery clots. [6] The precise prevalence of spontaneous recanalization is not known. The Prolyse in Acute Cerebral Thromboembolism (PROACT) 2 study showed a recanalization rate of 17% in the placebo arm. [4] A study on patients with cardioembolic strokes reported early (<6 hours) and late (>6 hours) spontaneous MCA recanalization rates of 18.8% and 52.8%, respectively, using transcranial Doppler (TCD). [7] Recanalization of cerebral arteries as seen with TCD or MR angiography occurs in 50% of acute ischemic strokes within 8 days. [8] Spontaneous recanalization of major intracranial arteries occurring beyond 6 hours of the stroke is usually predictive of a hemorrhagic transformation. [7] Our patient's stroke was cardioembolic in nature, and her occlusion spontaneously recanalized without a hemorrhagic transformation. Knowledge of spontaneous recanalization has important consequences. In stroke trials, these rates have to be considered in planning, such as sample size calculations, if recanalization is to be taken as an end point. It is imperative that "spontaneously recovered" strokes should acquire a new terminology for better understanding of this entity and appropriate treatment. Inclusion of vascular imaging in the acute stroke imaging is a useful tool to determine stroke pathophysiology, especially in rapidly recovering deficits following an acute stroke, which may be inappropriately labeled as TIA. References
Copyright 2010 - Neurology India The following images related to this document are available:Photo images[ni10268f2.jpg] [ni10268f1.jpg] |
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