Thalamic dementia is an infrequent condition characterized by memory deficits and frontal-like behavioral disturbances which are usually due to bilateral (anterior or paramedian) thalamic lesions of various origin. Cases due to a unilateral infarct have only been reported rarely and are the subject of discussion. Here we describe the case of a 67-year-old man, retired, showing the typical clinical and neuropsychological features of thalamic dementia as a consequence mainly of unilateral infarct of the anterior and paramedian part of the left thalamus. At the onset, the patient presented with transient diplopia and vertigo, drowsiness, severe ideomotor slowing, general disorientation, reduced verbal fluency, and both retro- and anterograde amnesia. The neurological examination at admission also showed mild dysmetria at the right upper limb and unsteady gait. During the following weeks, there was a progressive recovery of retrograde memory and of spatial, temporal and personal orientation; ideomotor slowing and hypersomnia partially abated. Anterograde memory deficits, behavioral disturbances, and changes in personality became prominent. The patient appeared considerably apathetic, and indifferent to the environment and presented with a prevalent anxiety-depression mood state, associated with occasional subeuphoric and jocular attitudes. Formal neuropsychological testing was performed 1 year after the onset of symptoms. The patient appeared distractable and showed moderate reduction of psychomotor speed; he was partially aware of his memory problems, even if unconcerned. Spontaneous speech was poor, but grammatically intact. At the MMSE the patient lost points for time orientation and on recall of three items (corrected total score = 26.5/30). The memory tasks revealed a marked reduction in verbal memory ability; performance at attention and fluency tasks were low-average. There was no evidence of aphasia, apraxia, agnosia, and visuospatial deficits. The Neuropsychiatric Inventory mainly revealed the presence of intense abulia, anxiety and depression, irritability, and dishinibition. Three serial contrasted CT scans, performed during hospitalization, were normal, whereas a subsequent (7 months later) brain MRI showed an infarct involving the anterior and paramedian part of the left thalamus and lacunar lesions located in the lenticular nuclei and in the cerebellar hemispheres bilaterally. The present report contributes to the clarification of organization and physiology of thalamus and thalamocortical pathways involved in memory and behavior dynamics.
Isella, V., Santoro, P., Frattola, L., Ferrarese, C., Appollonio, I. (2000). Thalamic dementia: Report of a case due to unilateral paramedian infarct of the left thalamus. NEUROLOGICAL SCIENCES, 21(4 (supplement)), S163-S163.
Thalamic dementia: Report of a case due to unilateral paramedian infarct of the left thalamus
ISELLA, VALERIA;Frattola L;FERRARESE, CARLO;APPOLLONIO, ILDEBRANDO
2000
Abstract
Thalamic dementia is an infrequent condition characterized by memory deficits and frontal-like behavioral disturbances which are usually due to bilateral (anterior or paramedian) thalamic lesions of various origin. Cases due to a unilateral infarct have only been reported rarely and are the subject of discussion. Here we describe the case of a 67-year-old man, retired, showing the typical clinical and neuropsychological features of thalamic dementia as a consequence mainly of unilateral infarct of the anterior and paramedian part of the left thalamus. At the onset, the patient presented with transient diplopia and vertigo, drowsiness, severe ideomotor slowing, general disorientation, reduced verbal fluency, and both retro- and anterograde amnesia. The neurological examination at admission also showed mild dysmetria at the right upper limb and unsteady gait. During the following weeks, there was a progressive recovery of retrograde memory and of spatial, temporal and personal orientation; ideomotor slowing and hypersomnia partially abated. Anterograde memory deficits, behavioral disturbances, and changes in personality became prominent. The patient appeared considerably apathetic, and indifferent to the environment and presented with a prevalent anxiety-depression mood state, associated with occasional subeuphoric and jocular attitudes. Formal neuropsychological testing was performed 1 year after the onset of symptoms. The patient appeared distractable and showed moderate reduction of psychomotor speed; he was partially aware of his memory problems, even if unconcerned. Spontaneous speech was poor, but grammatically intact. At the MMSE the patient lost points for time orientation and on recall of three items (corrected total score = 26.5/30). The memory tasks revealed a marked reduction in verbal memory ability; performance at attention and fluency tasks were low-average. There was no evidence of aphasia, apraxia, agnosia, and visuospatial deficits. The Neuropsychiatric Inventory mainly revealed the presence of intense abulia, anxiety and depression, irritability, and dishinibition. Three serial contrasted CT scans, performed during hospitalization, were normal, whereas a subsequent (7 months later) brain MRI showed an infarct involving the anterior and paramedian part of the left thalamus and lacunar lesions located in the lenticular nuclei and in the cerebellar hemispheres bilaterally. The present report contributes to the clarification of organization and physiology of thalamus and thalamocortical pathways involved in memory and behavior dynamics.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.