Thalamocortical diaschisis: positron emission tomography in humans.

Baron, Jean‐Claude; Levasseur, M.; Mazoyer, Bernard; Legault-Demare, F.; Mauguière, F; Pappatà, Sabina; Jedynak, Piotr; Derome, P; Cambier, J; Tran-Dinh, S.

doi:10.1136/jnnp.55.10.935

Cited by 144 publications

(69 citation statements)

References 32 publications

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“…Data presented in histograms are means + standard error of the mean. Group differences: * * P , 0.01, * * * P , 0.005. thalamic damage can sometimes be sufficient to disrupt both verbal and nonverbal memory (e.g., Carlesimo et al 2011; see also Baron et al 1992). For these reasons, the observed pattern of findings (Cipolotti et al 2008) need not be inconsistent with the model of Aggleton and Brown (1999).…”

Section: Intralaminar and Midline Thalamic Nucleimentioning

confidence: 91%

Unraveling the contributions of the diencephalon to recognition memory: A review

Aggleton¹,

Dumont²,

Warburton³

2011

Learn. Mem.

139

111

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Both clinical investigations and studies with animals reveal nuclei within the diencephalon that are vital for recognition memory (the judgment of prior occurrence). This review seeks to identify these nuclei and to consider why they might be important for recognition memory. Despite the lack of clinical cases with circumscribed pathology within the diencephalon and apparent species differences, convergent evidence from a variety of sources implicates a subgroup of medial diencephalic nuclei. It is supposed that the key functional interactions of this subgroup of diencephalic nuclei are with the medial temporal lobe, the prefrontal cortex, and with cingulate regions. In addition, some of the clinical evidence most readily supports dual-process models of recognition, which assume two independent cognitive processes (recollective-based and familiarity-based) that combine to direct recognition judgments. From this array of information a "multi-effect multinuclei" model is proposed, in which the mammillary bodies and the anterior thalamic nuclei are of preeminent importance for recollective-based recognition. The medial dorsal thalamic nucleus is thought to contribute to familiarity-based recognition, but this nucleus, along with various midline and intralaminar thalamic nuclei, is also assumed to have broader, indirect effects upon both recollective-based and familiarity-based recognition.Clinical studies repeatedly show that diencephalic pathology can impair recognition memory. Even so, there is no agreed locus within the diencephalon responsible for this memory loss and, hence, no agreed mechanism to explain the impairment. The present review examines both clinical and animal findings, and from this information a multi-effect multi-nuclei (MEMN) model emerges to explain the contributions of the diencephalon to recognition memory.At the outset, it is necessary to refine the focus of this review and to define some of its principal terms. The diencephalon comprises the thalamus and hypothalamus but, as will be explained, only the more medial parts of the diencephalon will be considered in detail. Recognition memory refers to the ability to detect whether a stimulus (e.g., a word, face, picture, object, or sound) has previously been encountered. As a consequence, this review is not about item identification (sometimes also confusingly referred to as recognition). Likewise, conditions that have broad disruptive effects on cognition, e.g., dementia, will not be considered even though recognition is typically impaired. Distinctions will be made between "item recognition," where the task is to determine if an individual item is novel or familiar, and "associative recognition," where all the individual items being experienced are familiar, but their particular combination is novel. A further, distinct ability is "recency" discrimination-the ability to determine which of two familiar stimuli has been experienced more recently. Both studies of amnesia and electrophysiological recordings show how recency memory and recogniti...

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Section: Intralaminar and Midline Thalamic Nucleimentioning

confidence: 91%

Unraveling the contributions of the diencephalon to recognition memory: A review

Aggleton¹,

Dumont²,

Warburton³

2011

Learn. Mem.

139

111

View full text Add to dashboard Cite

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“…This manifests not only as loss of the behavior subserved by that circuit but also as altered metabolism on functional neuroimaging techniques (positron emission tomography and singlephoton emission CT) that evaluate the integrity of the circuit. Depressed levels of metabolic activity in cerebral hemispheres have been observed after discrete thalamic infarction 81,82 and thalamotomy. 82 This diaschisis phenomenon depends on thalamocortical interconnections and provides corroborating physiological evidence for the hypothesis of distributed neural circuits and a mechanism for the behavioral deficits in patients with focal thalamic lesions.…”

Section: A Note On Diaschisismentioning

confidence: 99%

Vascular Syndromes of the Thalamus

Schmahmann

2003

Stroke

772

589

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Background-This article reviews the anatomy, connections, and functions of the thalamic nuclei, their vascular supply, and the clinical syndromes that result from thalamic infarction. Summary of Review-Thalamic nuclei are composed of 5 major functional classes: reticular and intralaminar nuclei that subserve arousal and nociception; sensory nuclei in all major domains; effector nuclei concerned with motor function and aspects of language; associative nuclei that participate in high-level cognitive functions; and limbic nuclei concerned with mood and motivation. Vascular lesions destroy these nuclei in different combinations and produce sensorimotor and behavioral syndromes depending on which nuclei are involved. Tuberothalamic territory strokes produce impairments of arousal and orientation, learning and memory, personality, and executive function; superimposition of temporally unrelated information; and emotional facial paresis. Paramedian infarcts cause decreased arousal, particularly if the lesion is bilateral, and impaired learning and memory. Autobiographical memory impairment and executive failure result from lesions in either of these vascular territories. Language deficits result from left paramedian lesions and from left tuberothalamic lesions that include the ventrolateral nucleus. Right thalamic lesions in both these vascular territories produce visual-spatial deficits, including hemispatial neglect. Inferolateral territory strokes produce contralateral hemisensory loss, hemiparesis and hemiataxia, and pain syndromes that are more common after right thalamic lesions. Posterior choroidal lesions result in visual field deficits, variable sensory loss, weakness, dystonia, tremors, and occasionally amnesia and language impairment. Conclusions-These vascular syndromes reflect the reciprocal cerebral cortical-thalamic connections that have been interrupted and provide insights into the functional properties of the thalamus.

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“…Five possible explanations were considered: (1) 41 have emphasized the evidence of transhemispheric diaschisis. Second, there was no heart failure, orthostatic hypotension, or other severe systemic circulatory disturbances present in our patients.…”

Section: Discussionmentioning

confidence: 99%

Relation of cerebral blood flow to motor and cognitive functions in chronic stroke patients.

Mori

Sadoshima

Ibayashi

et al. 1994

Stroke

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The aim of this study was to examine the levels of cerebral blood flow in relation to motor and cognitive functions in 300 chronic unilateral stroke patients (age, 64 +/- 12 years; mean +/- SD). Cerebral blood flow was measured by the 133Xe inhalation method, adjusted for age, sex, and PCO2 level. Motor function was scored according to Brunnstrom hemiplegic staging and cognitive function according to the Hasegawa dementia rating scale tested in Japanese. Asymmetries of blood flow between affected and nonaffected hemispheres increased with lesion size and were highest in 11 embolic strokes (20 +/- 9%) and higher in 80 nonembolic cortical infarctions (11 +/- 11%) and 76 hemorrhages (9 +/- 7%) than in the group of 133 subcortical infarctions (2 +/- 6%) or 16 control subjects (1 +/- 2%). Severity of hemiparesis correlated with decreased cerebral blood flow in the affected hemisphere (P < .01) and increased hemispheric asymmetries of blood flow (P < 001). Cognitive impairments, after adjusting for age, correlated with decreased cerebral blood flow in the nonaffected hemisphere (P < .0001), left hemispheric lesions (P < .0005), and embolic stroke (P < .005) but not with asymmetries of blood flow. Among 67 patients having bilateral reductions of cerebral blood flow, 25 patients with left hemispheric lesions showed more severe cognitive impairments than among 42 patients with right hemispheric lesions (P < .05). We confirmed that severity of hemiparesis correlated with the degree of asymmetries of cerebral blood flow, reflecting the extent and location of the lesions. Bilateral reductions of cerebral blood flow in patients with left hemispheric lesions may in part contribute to cognitive impairments, indicating reductions of global neuronal activities in the contralateral hemisphere or diffuse cerebrovascular changes. Further studies of cerebral metabolism and follow-up of cerebral circulation are required to reveal the pathophysiology and clinical consequences.

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Thalamocortical diaschisis: positron emission tomography in humans.

Cited by 144 publications

References 32 publications

Unraveling the contributions of the diencephalon to recognition memory: A review

Unraveling the contributions of the diencephalon to recognition memory: A review

Vascular Syndromes of the Thalamus

Relation of cerebral blood flow to motor and cognitive functions in chronic stroke patients.

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