Transient memory steal: A rare phenomenon of subclavian steal syndrome

R Shanmugasundaram¹, G Rajendiran¹, MB Pranesh², E Prasanna Venkatesan³,  
¹ Department of Cardiology, PSG Institute of Medical Sciences and Research, Coimbatore, Tamil Nadu, India
² Department of Neurology, PSG Institute of Medical Sciences and Research, Coimbatore, Tamil Nadu, India
³ Department of Internal Medicine, PSG Institute of Medical Sciences and Research, Coimbatore, Tamil Nadu, India

Correspondence Address:
Dr. E Prasanna Venkatesan
Department of Internal Medicine, PSG Institute of Medical Sciences and Research, Coimbatore, Tamil Nadu
India

Full Text

Sir,

We report a 62-year-old hypertensive male on regular treatment who presented to us with recurrent discrete episodes of memory loss for the past 6 months. His complaints followed left arm exercise like leaning against the wall or carrying weight. He also had dull aching pain in his left arm following exercise. While the pain lasted for 10-15 min, it was soon followed by impaired ability to remember new information. During this period, he was restless and repeatedly asked the same questions to his family members. His consciousness was well preserved during the episodes and there was no dysarthria, ataxia, or focal neurological deficits. Most of the episodes were stereotyped, lasting for 1-2 h, but the patient was completely amnesic to that episode after that. He has had several such episodes in the last 6 months, all following exercise of the left arm. There was no past history of migraine or epilepsy.

On clinical examination, his left upper limb pulses was absent. There was no vascular bruit. Cardiovascular and central nervous system examination was normal. On further evaluation, his routine blood tests were normal except for raised erythrocyte sedimentation rate (ESR) and raised C-reactive protein (CRP). Magnetic resonance imaging of brain was normal. Cranial vessel Doppler showed flow reversal in the left vertebral artery. Computerized tomography (CT) angiogram [Figure 1] and digital subtraction angiogram showed a tight lesion of the left subclavian arterial origin with a small aneurysm arising from the arch of aorta involving the origin of the left subclavian artery [Figure 2] and [Figure 3]. The left vertebral artery was filling retrograde and the distal left subclavian artery was filling late. A vasculitis workup was negative. A complex partial seizure versus vascular event was considered. Electroencephalography (EEG) did not reveal any abnormality, even when the patient was exercising his left upper limb. A diagnosis of nonspecific aortitis, with left subclavian steal syndrome presenting as transient global amnesia was made. Patient was initially started on prednisolone and later underwent an aortosubclavian bypass with ligation of the aneurysm. During follow-up, the patient remained asymptomatic on left arm exercise.{Figure 1}{Figure 2}{Figure 3}

For a long time, sudden episodic loss of memory was considered hysterical in origin until Fisher and Adams coined the term "transient global amnesia" in 1964. An individual, during an episode of transient global amnesia (TGA), exhibits only anterograde amnesia and no impairment in cognition or any focal neurological deficits. [1] Since the exact etiology of TGA is not known, there are two accepted theories: The arterial ischemic theory and venous congestion theory. [2],[3] But these theories fail to explain why ischemia or venous congestion selectively affects the mesial temporal lobe.

We found only one case in literature where Blasco et al. described a 56-year-old woman with subclavian steal syndrome who presented with two episodes of TGA. [4] Our case is unique as he had experienced several episodes even on a single day and aortitis presenting as TGA has not been reported in literature so far. We propose that left arm exercise resulted in a retrograde flow of blood in the ipsilateral vertebral artery due to subclavian steal phenomenon. This resulted in vertebrobasilar insufficiency and subsequent ischemia of the inferomedial temporal lobe and hippocampus producing TGA. [5]

References