Cases reported "Memory Disorders"

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1/14. Expressive language disorder after infarction of left lentiform nucleus.

    A 53 year old bilingual woman presented with apraxia of speech and writing in English and German after ischaemic infarction of the left posterior lentiform nucleus. Detailed language assessment revealed impairments of articulation, verbal fluency, auditory repetition, interpretation of complex semantic relationships, formulation of definitions and verbal short-term memory. The case illustrates the role of the basal ganglia in speech planning, word retrieval and verbal short-term memory.
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2/14. multiple sclerosis with caudate lesions on MRI.

    A 31-year-old woman displayed sleepiness and impairment of recent memory. T2-weighted MRI revealed high signal intensity lesions in the bilateral basal ganglia, thalamus, and brainstem. Although remission was achieved with corticosteroid therapy, she again displayed memory dysfunction and emotional disturbance one year later, at which time MRI disclosed new lesions in the right caudate nucleus and left frontal white matter. Corticosteroid therapy lead to improvement, and she suffered no recurrence on maintenance steroid therapy. These findings suggest that caudate lesions do occur in multiple sclerosis, the manifestations of which can be abulia and memory dysfunction, as in the present case.
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3/14. Severe personality changes after unilateral left paramedian thalamic infarct.

    personality changes are not uncommon after paramedian thalamic infarction, but usually bilateral or relatively large lesions, often complicated by other neurological or neuropsychological deficits, are present. 'Pure' cases of unilateral lesions are extremely rare. We report that a right-handed, 48-year-old man, who was hypertensive and diabetic but had no prior psychiatric history, developed severe personality changes and a frontal-like syndrome after recovery from acute-onset impairment of consciousness at the age of 43. Other neurological and neuropsychological disturbances, especially verbal and visual amnesia, were unremarkable. MRI showed a very small infarct in the left paramedian area of the thalamus, mainly involving the dorsomedial nucleus.
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4/14. Deficits of memory, executive functioning and attention following infarction in the thalamus; a study of 22 cases with localised lesions.

    The thalamus plays a crucial role in memory, executive functioning and attention. It remains, however, unclear whether thalamic structures have specific roles in each of these functions. We tested 22 cases of thalamic infarction, proven with MR imaging, using experimental and established neuropsychological tests. We performed a lesion-overlap study in standardised stereotactic space of patients sharing a certain deficit, corrected for the lesion distribution of patients without such deficits and determined the regions of interest using an atlas of the human thalamus. We checked for additional, non-thalamic, damage and for deficient comprehension and perception that would preclude interpretation of the results. Non-thalamic damage such as white matter lesions, hippocampal atrophy, sulcal widening and infarctions occur significantly more often in patients aged over 60. The patients with additional damage overlapped to a major degree with those who showed loss of orientation, or lack of comprehension of the test requirements. In the 10 patients judged 'clean', we observed a deficit of episodic long-term memory with relative sparing of intellectual capacities and short-term memory when the mammillo-thalamic tract was damaged. Lesions including the medial dorsal nucleus, midline nuclei and/or intralaminar nuclei accompany executive dysfunctioning. Reduced simple processing speed and attention are associated with age, but not with a particular structure in the thalamus. Complex attention deficits follow damage to the intralaminar nuclei.We conclude that the analysis of structure-function relationships must take into account extra-structure damage which may explain cognitive deficits. Separate thalamic structures are involved in memory, executive functioning and attention.
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5/14. Contributions of the left intralaminar and medial thalamic nuclei to memory. Comparisons and report of a case.

    A patient complained of memory disturbance after a small left thalamic infarction. Neuropsychological testing revealed her memory to be normal provided that she was allowed to rehearse or use semantic encoding strategies. When these strategies were prevented, her performance was impaired. Mapping of the lesion demonstrated involvement of the caudal intralaminar nuclei (centre median and parafascicular nuclei), and portions of the medial nuclei (medioventral [reuniens], centromedial, and the most inferior aspect of the mediodorsal nucleus). The majority of mediodorsal nucleus, the mammillary bodies, the mammillothalamic tract, and the anterior thalamic nuclei, were spared. A comparison among our patient's performances and those of alcoholic Korsakoff patients, patient NA, and amnestic patients with circumscribed diencephalic lesions suggests that there are two distinct behavioral and anatomic types of memory impairment associated with diencephalic lesions. The severe amnesia associated with damage to the mammillary bodies, midline nuclei, mammillothalamic tract, and/or dorsomedial nucleus of the thalamus (eg, Korsakoff and NA) is characterized by encoding deficits that never approximate normal performance. The memory disturbance associated with damage to the intralaminar and medial nuclei of the thalamus is milder and is characterized by severe distractibility.
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6/14. memory dysfunction in caudate infarction caused by Heubner's recurring artery occlusion.

    We report five cases with caudate infarction due to Heubner's recurring artery occlusion, in which we conducted detailed memory examinations in terms of explicit memory and implicit memory. We performed the auditory verbal learning test as explicit memory tasks, and motor and cognitive procedural memory tasks, developed by Komori, as implicit memory tasks. Comparing normal control subjects with patients with left caudate infarction due to Heubner's recurring artery occlusion demonstrated lower scores on both declarative and motor procedural memory tasks. These results suggest that the left caudate nucleus may be related with both declarative memory and procedural memory.
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7/14. language disturbances from paramedian thalamic infarcts: a CT method for lesion location.

    The authors describe the case of three patients suffering from language disorder secondary to mesencephalo-thalamic infarcts. One of them showed the clinical features of transcortical motor aphasia, while the other two presented the typical pattern of the so-called "thalamic aphasia". The CT-stereotaxic method for lesion localization disclosed that the dorso-medial was the mostly involved thalamic nucleus in each case. Since this nucleus is connected both with Broca's and Wernike's areas, the authors suggest that the more or less extensive involvement of the fibres connecting these structures may be responsible for the different aphasic features presented in these cases.
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8/14. The syndrome of unilateral tuberothalamic artery territory infarction.

    The study of 3 personal cases and 5 published cases of unilateral infarct limited to the territory of the tuberothalamic artery suggests that this syndrome should be differentiated from the other thalamic syndromes. The onset is usually sudden, with moderate contralateral weakness. Sensory changes may be present but remain mild. The patients are apathetic, show perseveration and may be disoriented. In left-sided infarcts, transcortical aphasia, verbal and visual memory impairment and sometimes acalculia are found. In right-sided infarcts, hemispatial neglect, visual memory impairment and disturbed visuospatial processing are common. A decreased level of consciousness, disturbed ocular movements, severe motor weakness and delayed abnormal movements do not occur. Involvement of the ventral lateral and dorsomedial nucleus with sparing of the intralaminar nuclei, posterolateral formation and upper midbrain may explain this picture. The fact that the tuberothalamic artery arises from the posterior communicating artery, which often receives its supply from the carotid system, further justifies considering unilateral tuberothalamic infarcts as a syndrome.
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9/14. Left thalamic infarction and disturbance of verbal memory: a clinicoanatomical study with a new method of computed tomographic stereotaxic lesion localization.

    A 41-year-old right-handed man developed disturbances of language and memory after a discrete thalamic infarction. Detailed neuropsychological assessment revealed deficits in verbal fluency, word finding, confrontation naming, and anterograde memory for verbal material. High-resolution computed tomography with stereotaxic lesion localization permitted the determination of the thalamic nuclei involved in the infarction. We suggest that the patient's problem in language and verbal memory reflected a defect in memory processing for verbal material during registration, retention, and retrieval, and that this defect probably resulted from a left anterior thalamic lesion affecting the ventrolateral nucleus, centromedian-parafascicular nuclei complex, internal medullary lamina, or mamillothalamic tract.
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10/14. Subcortical prosopagnosia and anosognosia.

    A 59-year-old right-handed woman with acute hemorrhage affecting the head of the left caudate nucleus exhibited prosopagnosia and anosognosia. It is suggested that these symptoms are due to a disconnection syndrome affecting a putative cortico-limbic reticular loop involved in attention. prosopagnosia can occur with lesions outside the main central visual pathways and is a material-specific motivational neglect to faces: alternatively prosopagnosia in this patient may represent abnormal gating sensory limbic activity since sensory (visual) modulated memory related cholinergic fibers arising from the nucleus basalis of the substantia innominata (Meynert's) were likely involved by surrounding edema.
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