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ARTICLES: S. Claiborne Johnston, Steve Sidney, Allan L. Bernstein, and Daryl R. Gress A comparison of risk factors for recurrent TIA and stroke in patients diagnosed with TIA Neurology 2003; 60: 280-285 [Abstract] [Full text] [PDF]

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The Syndrome of Recurrent Pure Sensory Episodes

Jeffrey L Saver   (10 April 2003)

Reply to Saver

Clay Johnston   (10 April 2003)

The Syndrome of Recurrent Pure Sensory Episodes 10 April 2003
Jeffrey L Saver, Physician UCLA Stroke Center Send Correspondence to journal: Re: The Syndrome of Recurrent Pure Sensory Episodes jsaver{at}ucla.edu Jeffrey L Saver	We congratulate Johnston et al on their study of risk factors for recurrent cerebral ischemic events in patients presenting with transient ischemic attack (TIA).[1] The authors focus on a distinct subgroup of patients with isolated sensory symptoms with a high risk of recurrent TIA (40%), not progressing to stroke. However, the syndrome of recurrent pure sensory episodes has been documented.[2,3] C. Miller Fisher pioneered its description (the authors cite Fisher’s papers on late life migraine accompaniments, but not on this entity). In a series of 135 cases, Fisher found that isolated, unilateral sensory disturbance presented in two distinct, and equally frequent manners: 1) sudden onset of pure sensory stroke preceded by no or few TIAs; and 2) frequent transient, unilateral hypoesthesia or paresthesias not progressing to permanent deficit.[2] The syndrome of recurrent pure sensory episodes has been associated with ventroposterolateral infarcts on imaging and autopsy.[2,3] Its pathogenesis is speculative, but likely a substantial proportion of cases are due to waxing/waning poststroke paresthesias as a variant manifestion of poststroke pain, and others due to recurrent ischemia beyond a fixed stenosis in a penetrating vessel, migrainous phenomena, hyperventilation paresthesias, and simple partial seizures. Approximately three to five patients a year are referred to our stroke center for sensory spells that recur despite multiple combinations of antithrombotics and anticonvulsants. Making the diagnosis spares patients from repeated invasive imaging, treatment with aggressive combination antithrombotic regimens likely to produce bleeding complications, and undue worry when episodes recur. References 1. Johnston SC, Sidney S, Bernstein AL, Gress DR. A comparison of risk factors for recurrent TIA and stroke in patients diagnosed with TIA. Neurology 2003;60:280-285. 2. Fisher CM. Pure sensory stroke and allied conditions. Stroke 1982;13:434-447. 3. Fernandez-Beer E, Patrick T, Biller J, Saver JL. Recurrent pure sensory transient ischemic attacks: in vivo demonstration of associated thalamic infarction. J Stroke Cerebrovasc Dis 1994;4:174-178.
Reply to Saver 10 April 2003
Clay Johnston UCSF Neurology Send Correspondence to journal: Re: Reply to Saver clay.johnston{at}ucsfmedctr.org Clay Johnston	We are grateful for the comments of Dr. Saver. As he points out, our results extend those of Dr. Fisher by demonstrating that patients initially presenting with pure sensory transient ischemic attacks (TIA) generally have a benign prognosis, with high risk of recurrent transient symptoms but low risk of subsequent stroke. Fisher notes that only 10 of 100 cases of sensory TIA or stroke had both a TIA and a stroke but he provides no information on the timing of events and risks cannot be calculated [1]. We fully agree that escalation to more aggressive and dangerous antithrombotic therapies may not be indicated in patients with recurrent pure sensory TIA. There may be a role for calcium-channel blockers [2] as we have found in two of our patients with such spells, but this requires further study. 1. Fisher CM. Pure sensory stroke and allied conditions. Stroke 1982;13(4):434-447. 2. Winterkorn JM, Kupersmith MJ, Wirtschafter JD, Forman S. Brief report: treatment of vasospastic amaurosis fugax with calcium-channel blockers. N Engl J Med 1993;329(6):396-398.