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The case of the forgotten address
Case Report
The case of the forgotten address Shanika Samarasekera, Paul J Dorman Lancet 2006; 367: 1290 Department of Neurology (S Samarasekera MRCP, P J Dorman FRCP), Royal Victoria Infirmary, Newcastle upon Tyne, NE1 4LP, UK Correspondence to: Dr Shanika Samarasekera [email protected]
1290
A 39-year-old right-handed community nurse presented to us on the neurology ward in April, 2005, after a telephone call from her work colleagues. They expressed concern that she had appeared subdued before starting the afternoon shift and that, when asked, she could not recall her home address. She had apparently carried out her morning duties as normal and could not understand her colleagues’ concerns. However, she agreed to be reviewed. The nurse’s symptoms had begun 48 h previously, when she woke with a bitemporal headache, similar in character to previous episodes of migraine. Her vision then “flipped 180°” so that all images appeared inverted. She was able to crawl back to bed and on waking 6 h later, her vision had returned to normal and the headache had subsided. There were no further symptoms, and she continued engagements over the weekend as planned. She had experienced a similar episode while at work 12 years previously. Her vision had “flipped”, again occurring in combination with a migraine. The symptoms resolved within hours. Apart from a long history of infrequent migraines for which she had not received any treatment, there was no other significant medical history. She was a non-smoker, was not taking any medications (including oral contraceptives), and denied alcohol or illicit drug use. On presentation, she appeared withdrawn. General medical examination was unremarkable, and she was normotensive. There were no focal abnormalities on neurological examination. She was still unable to recall her home address, although she was able to give a detailed account of her activities over the preceding 48 h, including dates and times of consultations with patients. We did an Addenbrooke’s cognitive assessment, which showed a score of 66/100, with marked deficits in anterograde memory and verbal fluency. EEG showed a moderate number of slow delta transients and theta slowing in the left temporal region. MRI showed a defined lesion on T2 imaging in the left medial thalamus, with high signal on FLAIR and diffusion-weighted imaging (figure). There was a much smaller lesion in the right thalamus, without corresponding acute signal change. These images were consistent with an acute left medial thalamic and older right thalamic infarct. The focus of high signal on the diffusion-weighted imaging trace showed hypointensity on the apparent diffusion coefficient map (not shown), confirming an area of restricted diffusion indicating an acute infarction. On MR angiography, both vertebral and carotid arteries appeared normal. A transoesophageal echocardiogram showed an aneurysmal interatrial septum with a large patent foramen ovale. Plasma homocysteine concentration, and results of a thrombophilia and an extended autoantibody screen were normal, so anticoagulant treatment with warfarin was started. Although she continued to experience anterograde
Figure: T2-weighted MRI scan showing bilateral thalamic infarcts
memory disturbance after discharge, this improved substantially. She was last reviewed in January, 2006; she had no new symptoms and had returned to work. The subtle changes in our patient’s behaviour and memory could easily have been missed by her colleagues. Such changes are well recognised with anteromedian thalamic infarcts; a loss of self-activation and initiative has been described, with patients appearing to “resemble robots”.1 Anterograde memory disturbance, usually accompanied by dysphasia or aphasia, is another established feature with dominant hemisphere involvement.1,2 The infarct is likely to have arisen from embolisation of thrombus within the aneurysmal septum or a paradoxical embolus from a venous source. Patients with both a patent foramen ovale and an atrial septal aneurysm are at increased risk of recurrent stroke compared with patients presenting with either one of these abnormalities. Longterm oral anticoagulation or surgical closure of the foramen ovale is therefore recommended.3 Our patient described a 180° rotation of her vision, known as reversal of vision metamorphopsia, which was first described by Winslow in 18684—the exact mechanism remains unclear. Our case highlights an atypical presentation of acute stroke and the value of a cognitive assessment as part of the neurological examination. References 1 Carrera E, Michel P, Bogousslavasky J. Anteromedian, central and posterolateral infarcts of the thalamus. Stroke 2004; 35: 2826–31. 2 Schmahmann J. Vascular syndromes of the thalamus. Stroke 2003; 34: 2264–78. 3 Mas J, Arquizan C, Lamy C, et al. Recurrent cerebrovascular events associated with patent foramen ovale, atrial septal aneurysm, or both. N Engl J Med 2001; 345: 1740–46. 4 Winslow F. On obscure diseases of the brain and disorders of the mind, 4th edn. London: John Churchill & Sons, 1868.
www.thelancet.com Vol 367 April 15, 2006
The case of the forgotten address Shanika Samarasekera, Paul J Dorman Lancet 2006; 367: 1290 Department of Neurology (S Samarasekera MRCP, P J Dorman FRCP), Royal Victoria Infirmary, Newcastle upon Tyne, NE1 4LP, UK Correspondence to: Dr Shanika Samarasekera [email protected]
1290
A 39-year-old right-handed community nurse presented to us on the neurology ward in April, 2005, after a telephone call from her work colleagues. They expressed concern that she had appeared subdued before starting the afternoon shift and that, when asked, she could not recall her home address. She had apparently carried out her morning duties as normal and could not understand her colleagues’ concerns. However, she agreed to be reviewed. The nurse’s symptoms had begun 48 h previously, when she woke with a bitemporal headache, similar in character to previous episodes of migraine. Her vision then “flipped 180°” so that all images appeared inverted. She was able to crawl back to bed and on waking 6 h later, her vision had returned to normal and the headache had subsided. There were no further symptoms, and she continued engagements over the weekend as planned. She had experienced a similar episode while at work 12 years previously. Her vision had “flipped”, again occurring in combination with a migraine. The symptoms resolved within hours. Apart from a long history of infrequent migraines for which she had not received any treatment, there was no other significant medical history. She was a non-smoker, was not taking any medications (including oral contraceptives), and denied alcohol or illicit drug use. On presentation, she appeared withdrawn. General medical examination was unremarkable, and she was normotensive. There were no focal abnormalities on neurological examination. She was still unable to recall her home address, although she was able to give a detailed account of her activities over the preceding 48 h, including dates and times of consultations with patients. We did an Addenbrooke’s cognitive assessment, which showed a score of 66/100, with marked deficits in anterograde memory and verbal fluency. EEG showed a moderate number of slow delta transients and theta slowing in the left temporal region. MRI showed a defined lesion on T2 imaging in the left medial thalamus, with high signal on FLAIR and diffusion-weighted imaging (figure). There was a much smaller lesion in the right thalamus, without corresponding acute signal change. These images were consistent with an acute left medial thalamic and older right thalamic infarct. The focus of high signal on the diffusion-weighted imaging trace showed hypointensity on the apparent diffusion coefficient map (not shown), confirming an area of restricted diffusion indicating an acute infarction. On MR angiography, both vertebral and carotid arteries appeared normal. A transoesophageal echocardiogram showed an aneurysmal interatrial septum with a large patent foramen ovale. Plasma homocysteine concentration, and results of a thrombophilia and an extended autoantibody screen were normal, so anticoagulant treatment with warfarin was started. Although she continued to experience anterograde
Figure: T2-weighted MRI scan showing bilateral thalamic infarcts
memory disturbance after discharge, this improved substantially. She was last reviewed in January, 2006; she had no new symptoms and had returned to work. The subtle changes in our patient’s behaviour and memory could easily have been missed by her colleagues. Such changes are well recognised with anteromedian thalamic infarcts; a loss of self-activation and initiative has been described, with patients appearing to “resemble robots”.1 Anterograde memory disturbance, usually accompanied by dysphasia or aphasia, is another established feature with dominant hemisphere involvement.1,2 The infarct is likely to have arisen from embolisation of thrombus within the aneurysmal septum or a paradoxical embolus from a venous source. Patients with both a patent foramen ovale and an atrial septal aneurysm are at increased risk of recurrent stroke compared with patients presenting with either one of these abnormalities. Longterm oral anticoagulation or surgical closure of the foramen ovale is therefore recommended.3 Our patient described a 180° rotation of her vision, known as reversal of vision metamorphopsia, which was first described by Winslow in 18684—the exact mechanism remains unclear. Our case highlights an atypical presentation of acute stroke and the value of a cognitive assessment as part of the neurological examination. References 1 Carrera E, Michel P, Bogousslavasky J. Anteromedian, central and posterolateral infarcts of the thalamus. Stroke 2004; 35: 2826–31. 2 Schmahmann J. Vascular syndromes of the thalamus. Stroke 2003; 34: 2264–78. 3 Mas J, Arquizan C, Lamy C, et al. Recurrent cerebrovascular events associated with patent foramen ovale, atrial septal aneurysm, or both. N Engl J Med 2001; 345: 1740–46. 4 Winslow F. On obscure diseases of the brain and disorders of the mind, 4th edn. London: John Churchill & Sons, 1868.
www.thelancet.com Vol 367 April 15, 2006