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Diencephalic amnesia and apraxia after left thalamic infarction
  1. Department of Neurology, Royal Adelaide Hospital, Adelaide, South Australia
  2. University Department of Medicine
  1. Professor PD Thompson, University Department of Medicine, Royal Adelaide Hospital, Adelaide, South Australia 5000, Australia
  1. Department of Neurology, Royal Adelaide Hospital, Adelaide, South Australia
  2. University Department of Medicine
  1. Professor PD Thompson, University Department of Medicine, Royal Adelaide Hospital, Adelaide, South Australia 5000, Australia

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Amnesia and apraxia are unusual manifestations of unilateral thalamic lesions. A patient in whom severe amnesia and apraxia were the presenting features of a left thalamic infarct is presented. The findings support the concept that memory and praxis both utilise circuits which include the dominant thalamus.

A 78 year old right handed Hungarian woman presented with memory loss and disorientation. She had been well and conversed normally with her daughter on the evening before presentation. The next morning, her daughter was alarmed to find her mother's house in a state of disarray. Dishes were unwashed, lights left on, and doors open. The patient seemed baffled by eating utensils, attempting to scoop food with her knife. Later that morning, she failed to recognise longstanding Hungarian friends. She was unable to recall her address, the name of the city in which she lived, or the names of her grandchildren. She subsequently failed to recognise her family doctor of 7 years. History included non-insulin dependent diabetes, hypertension, hyperlipidaemia, and atrial fibrillation. Medications were digoxin, glibenclamide, and metoprolol. Captopril had been prescribed 4 weeks previously but was ceased 2 days before presentation due to presyncopal symptoms. The patient consumed no alcohol. There was no history of cerebrovascular events.

Cognitive functions were examined at the bedside with the assistance of an interpreter, as the patient spoke no English, although she conversed freely in her native Hungarian. She had no recollection of events since emigrating to Australia 50 years previously, gave her correct maiden name, and could not recognise or name her grandchildren, although she recognised her daughter. She acknowledged she was in a hospital, but maintained it was in Budapest and the year was 1947. Although her recollections regarding her early life and wartime Hungary seemed accurate, she confabulated when asked for details of recent events. Short term recall of verbal material and people was poor. The patient was able to name objects such as a pencil and a watch, and obey two and three stage commands. She wrote her name and copied simple designs correctly, and could imitate gestures such as waving goodbye or blowing a kiss. However, she was unable to use eating utensils or a toothbrush, either in pantomime or when provided with the object itself. Movements of the face and limbs were normal, and there were no sensory abnormalities. Knee and ankle jerks were absent bilaterally and both plantar responses were extensor. General examination revealed atrial fibrillation and mild cardiomegaly.

The patient continued to display severe impairment of anterograde memory. She was reluctant to leave her bed, and quickly became lost unless supervised. She did not recognise familiar staff members and was unable to use ward landmarks to reorientate herself. She required assistance to feed herself, brush her teeth, and shower. When reviewed 3 months later, her memory disturbance and apraxia for simple activities of daily life (such as brushing her teeth) persisted, necessitating care in a supervised environment.

Brain MRI (figure) showed a left anterior thalamic lesion consistent with lacunar infarction and periventricular white matter disease.

T2 weighted axial MRI brain slice showing ischaemic infarction of the left anterior thalamus and periventricular white matter ischaemic changes.

Deficits of anterograde and retrograde memory after thalamic lesions are well recognised.1 The syndrome of diencephalic amnesia after bilateral medial thalamic lesions typically involves striking disorientation for time, loss of autobiographical information (often extending back for many years), confabulation, and severe anterograde amnesia for verbal and visual material, including recognition of familiar faces.1 These features were well illustrated by our patient, who became “marooned” in an earlier place and time. Amnesia after unilateral thalamic lesions is rare.2 There is increasing evidence that thalamic lesions interrupt the multiple brain networks which form the anatomical substrate of memory,1-4 encompassing the hippocampus, medial thalamus, frontal and cingulate cortices, and overlapping with the language areas of the left hemisphere.3 The thalamus is activated in retrieval of episodic (autobiographical) and semantic (encyclopaedic) information from long term storage4 and execution of learned motor tasks,5 which may reflect its widespread connections with other subcortical and cortical structures.

The patient's ability to name or identify objects was not tested systematically. However, on the evidence available, it seems likely that her difficulty in utilising common objects was a manifestation of apraxia for daily tasks rather than, for example, agnosia for the objects involved. Apraxia is a rare manifestation of isolated thalamic lesions.5 The ability to access stored motor representations is thought to be crucial for normal execution of learned actions.5 These motor representations or “engrams” are analogous to motor memories. Although praxis is generally regarded as a function of distributed cortical regions in the left hemisphere, apraxia in association with thalamic amnesia has not been emphasised in previous reviews of this syndrome.1-2 Involvement of deep hemispheric white matter in association with basal ganglia pathology is thought to be critical for the development of apraxia after lesions of subcortical structures.5 The conjunction of diencephalic amnesia and apraxia after thalamic infarction in the present case may be interpreted as further evidence that retrievial of episodic, semantic, and motor memories is mediated by overlapping functional networks in the dominant hemisphere.1 3 4


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