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Cognitive, affective and behavioural disturbances following vascular thalamic lesions: A review
Abstract
During the last decades, many studies have shown that the thalamus is crucially involved in language and cognition. We critically reviewed a study corpus of 465 patients with vascular thalamic lesions published in the literature since 1980. 42 out of 465 (9%) cases with isolated thalamic lesions allowed further neurocognitive analysis. On the neurolinguistic level, fluent output (=31/33; 93.9%), normal to mild impairment of repetition (=33/35; 94.3%), mild dysarthria (=8/9; 88.9%) and normal to mild impairment of auditory comprehension (=27/34; 79.4%) were most commonly found in the group of patients with left and bilateral thalamic lesions. The taxonomic label of thalamic aphasia applied to the majority of the patients with left thalamic damage (=7/11; 63.6%) and to one patient with bithalamic lesions (=1/1). On the neuropsychological level, almost 90% of the left thalamic and bithalamic patient group presented with amnestic problems, executive dysfunctions and behaviour and/or mood alterations. In addition, two thirds (2/3) of the patients with bilateral thalamic damage presented with a typical cluster of neurocognitive disturbances consisting of constructional apraxia, anosognosia, desorientation, global intellectual dysfunctioning, amnesia, and executive dysfunctions associated with behaviour and/or mood alterations. Our study supports the long-standing view of a 'lateralised linguistic thalamus' but restates the issue of a 'lateralised cognitive thalamus'. In addition, critical analysis of the available literature supports the view that aphasia following left or bithalamic damage constitutes a prototypical linguistic syndrome.
... Lesions in the thalamus, mostly in the left hemisphere, have long been linked to what is known as thalamic aphasia with symptoms primarily including naming deficits (problems of word finding and retrieval such as semantic paraphasia) with relatively preserved repetition, fluency and grammar (Crosson 2013;De Witte et al. 2011;Nadeau and Crosson 1997), while these language impairments frequently co-occur with symptoms in other domains such as amnestic problems, executive dysfunctions and behavior and/or mood alterations (De Witte et al. 2011). This involvement of the thalamus with language processing is consistent with the literature on functional imaging of the thalamus, a review of which correlated thalamic activation mostly with language production tasks (e.g., word or sentence production) and naming, with stronger activation in the left than the right thalamus (Llano 2013). ...
... Lesions in the thalamus, mostly in the left hemisphere, have long been linked to what is known as thalamic aphasia with symptoms primarily including naming deficits (problems of word finding and retrieval such as semantic paraphasia) with relatively preserved repetition, fluency and grammar (Crosson 2013;De Witte et al. 2011;Nadeau and Crosson 1997), while these language impairments frequently co-occur with symptoms in other domains such as amnestic problems, executive dysfunctions and behavior and/or mood alterations (De Witte et al. 2011). This involvement of the thalamus with language processing is consistent with the literature on functional imaging of the thalamus, a review of which correlated thalamic activation mostly with language production tasks (e.g., word or sentence production) and naming, with stronger activation in the left than the right thalamus (Llano 2013). ...
... This functional characterization is in accord with the distribution of paradigm classes ( Table 2), which shows greater contribution of experiments from semantic (semantic monitoring/discrimination, naming) and production (word generation, reading, naming) tasks to the coactivation analysis. The association of the left thalamus with semantics is consistent with the literature on thalamic aphasia which occurs usually after left thalamic lesion and involves naming deficits (problems of word finding and retrieval such as semantic paraphasia) with relatively preserved repetition (Crosson 2013;De Witte et al. 2011;Nadeau and Crosson 1997). Consistently, the thalamus (particularly ventral anterior nucleus and the pulvinar) and its connections with the prefrontal structures including Broca's area have been associated with lexicalsemantic processing, with the thalamus mediating transfer of semantic (pars triangularis/orbitalis) and phonological (pars opercularis) information between these anterior/posterior subdivisions of Broca's area during lexical-semantic processing (Bohsali et al. 2015;Crosson 2021). ...
Background: Despite a pervasive cortico-centric view in cognitive neuroscience, subcortical structures including the thalamus have been shown to be increasingly involved in higher cognitive functions. Previous structural and functional imaging studies demonstrated cortico-thalamo-cortical loops which may support various cognitive functions including language. However, large-scale functional connectivity of the thalamus during language tasks has not been examined before. Methods: The present study employed meta-analytic connectivity modeling to identify language-related coactivation patterns of the left and right thalami. The left and right thalami were used as regions of interest to search the BrainMap functional database for neuroimaging experiments with healthy participants reporting language-related activations in each region of interest. Activation likelihood estimation analyses were then carried out on the foci extracted from the identified studies to estimate functional convergence for each thalamus. A functional decoding analysis based on the same database was conducted to characterize thalamic contributions to different language functions. Results: The results revealed bilateral frontotemporal and bilateral subcortical (basal ganglia) coactivation patterns for both the left and right thalami, and also right cerebellar coactivations for the left thalamus, during language processing. In light of previous empirical studies and theoretical frameworks, the present connectivity and functional decoding findings suggest that cortico-subcortical-cerebellar-cortical loops modulate and fine-tune information transfer within the bilateral frontotemporal cortices during language processing, especially during production and semantic operations, but also other language (e.g., syntax, phonology) and cognitive operations (e.g., attention, cognitive control). Conclusion: The current findings show that the language-relevant network extends beyond the classical left perisylvian cortices and spans bilateral cortical, bilateral subcortical (bilateral thalamus, bilateral basal ganglia) and right cerebellar regions.
... Thus, lesions to the thalamus can result in sensory deficits and neglect, but also in visuo-spatial deficits, pain-syndromes, or even hemiparesis [23]. Additionally, thalamic lesions can lead to a multitude of attentional and cognitive deficits such as amnesia, vigilance impairment, executive dysfunction, apraxia, anosognosia, behavioral and mood alterations, as well as aphasia [24][25][26]. Similar to its role in sensory processing, the role of the thalamus in language is suggested to be that of a moderator conducting the transfer of lexical information to cortical areas [27]. ...
... For instance, patients that display significantly impaired word retrieval do not necessarily meet the cutoff criteria for "aphasia" in standard diagnostics, such as the "standard language test of aphasia" (SLTA) [32,61]. This underlines the idea that typical routine language assessments might underestimate the subtle impairments in patients with thalamic aphasia [24,32]. So even when standard diagnostic tools are administered, thalamic aphasia might be underdiagnosed, a concern that could be addressed by more sensitive aphasia examinations, or a stronger focus on separate language domains in the assessment of thalamic aphasia. ...
... The notion of such a lateralization of language in the thalamus is challenged by studies showing bilateral [54], or even only right-thalamic activity during active or passive language tasks [55]. Unfortunately, handedness was often not tested, and language impairment was often assessed in patients with left-sided thalamic lesions only, limiting these results [24,38]. Additionally, selection criteria are not always precisely reported, and such results might partially be due to a selection bias, as more patients with left sided (thalamic as well as cortical) lesions are being detected and hospitalized overall [82]. ...
Purpose of Review
Thalamic aphasia is a rare language disorder resulting from lesions to the thalamus. While most patients exhibit mild symptoms with a predominance of lexical-semantic difficulties, variations in phenotype have been described. Overall, the exact mechanisms of thalamic aphasia await empirical research. The article reviews recent findings regarding phenotypes and possible underlying mechanisms of thalamic aphasia.
Recent Findings
Variations in phenotype of thalamic aphasia may be related to different lesion locations. Overall, the thalamus’ role in language is thought to be due to its involvement in cortico-thalamic language networks with lesioning of certain nuclei resulting in the diachisis of otherwise interconnected areas. Its possible monitoring function in such a network might be due to its different cellular firing modes. However, no specific evidence has been collected to date.
Summary
While recent findings show a more distinct understanding of thalamic aphasia phenotypes and possible underlying mechanisms, further research is needed. Additionally, as standard language testing might oftentimes not pick up on its subtle symptoms, thalamic aphasia might be underdiagnosed.
... There are several reports on aphasia associated with thalamic lesions (termed thalamic aphasia), most of which were associated with thalamic stroke [4]. A role for the thalamus in language function was confirmed in deep brain stimulation studies [5]. ...
... Thalamic aphasia is usually associated with left thalamic lesions, with the left hemisphere being dominant for language function. The incidence of aphasia associated with left thalamic hemorrhage was reported as 33%-87.5% [4,6]. This wide range may be attributed to differences in the assessment methods for detecting aphasia. ...
... In that study, the types of aphasia included Broca's aphasia (four patients, 7.1%), transcortical motor aphasia (two patients, 3.6%), total aphasia (four patients, 7.1%), amnesic aphasia (15 patients, 26.8%), transcortical sensory aphasia (seven patients, 12.5%), Wernicke's aphasia (26 patients, 46.4%), and dysgraphia (one patient, 1.8%). De White et al. [4] also reported that hemorrhage was frequently located in the posterior lateral portion of the left thalamus, which is consistent with our case. Ischemic stroke confined to the left thalamus also causes aphasia. ...
Background
Mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) with aphasia is a rare disorder, with the associated aphasia reported as either Wernicke’s or Broca’s. Herein, we report a patient with MELAS complicated by thalamic aphasia.
Case
A 15-year-old right-handed girl presented with headache, nausea, right homonymous hemianopsia, and aphasia. She could repeat words said by others, but had word-finding difficulty, paraphasia, and dysgraphia. Brain MRI revealed abnormal signals from the left occipital lobe to the temporal lobe and left thalamus, but Wernicke’s area and Broca’s area were not involved. Additionally, she had short stature, lactic acidosis, bilateral sensorineural hearing loss, and a maternal family history of diabetes and mild deafness. Based on clinical findings and the presence of a mitochondrial A3243G mutation, she was diagnosed with MELAS. With treatment, the brain MRI lesions disappeared and her symptoms improved. Her aphasia was classified as amnesic aphasia because she could repeat words, despite having word-finding difficulty, paraphasia, and dysgraphia. Based on MRI findings of a left thalamic lesion, we diagnosed her with thalamic aphasia.
Conclusion
Thalamic aphasia may be caused by MELAS. Assessment of whether repetition is preserved is important for classifying aphasia.
... In order to cover each of these nuclei, we introduce the overall semiological fingerprint of thalamic aphasia: De Witte et al. [94] reviewed a sample of 465 thalamic infarction patients and described their foremost traits: out of "1) fluent output, 2) normal or mildly impaired comprehension skills, 3) normal or mildly impaired repetition, 4) moderate to severe anomia characterized by semantic paraphasias, neologisms, and perseverations, 5) hypophonia and/or mild articulation deficits and 6) reduction of spontaneous speech or verbal aspontaneity", 63.6% of left infarction cases conformed to at least four of these criteria. In full accordance, aphasia resulting from thalamic insult is best recognized for its fluent, paraphasic production, which may degenerate into jargon, with perseverations and preserved repetition skills [56,67,85,107]. ...
... In full accordance, aphasia resulting from thalamic insult is best recognized for its fluent, paraphasic production, which may degenerate into jargon, with perseverations and preserved repetition skills [56,67,85,107]. Although the non-fluent language is not as prevalent, it is important to note that word-finding is harshly affected, and spontaneous speech often plummets [56,85,94]. ...
... Giraldez et al. [93] Left pulvinar (1) -Paraphasias, mild comprehension deficits. De Witte et al. [94] Left thalamus (465) -Normal or mildly impaired comprehension skills, normal or mildly impaired repetition, moderate to severe anomia, semantic paraphasias, neologisms and perseverations, hypophonia and/or mild dysarthria, and reduction of fluency. ...
Purpose of Review
Subcortical structures have long been thought to play a role in language processing. Increasingly spirited debates on language studies, arising from as early as the nineteenth century, grew remarkably sophisticated as the years pass. In the context of non-thalamic aphasia, a few theoretical frameworks have been laid out. The disconnection hypothesis postulates that basal ganglia insults result in aphasia due to a rupture of connectivity between Broca and Wernicke’s areas. A second viewpoint conjectures that the basal ganglia would more directly partake in language processing, and a third stream proclaims that aphasia would stem from cortical deafferentation. On the other hand, thalamic aphasia is more predominantly deemed as a resultant of diaschisis. This article reviews the above topics with recent findings on deep brain stimulation, neurophysiology, and aphasiology.
Recent Findings
The more recent approach conceptualizes non-thalamic aphasias as the offspring of unpredictable cortical hypoperfusion. Regarding the thalamus, there is mounting evidence now pointing to leading contributions of the pulvinar/lateral posterior nucleus and the anterior/ventral anterior thalamus to language disturbances. While the former appears to relate to lexical-semantic indiscrimination, the latter seems to bring about a severe breakdown in word selection and/or spontaneous top-down lexical-semantic operations.
Summary
The characterization of subcortical aphasias and the role of the basal ganglia and thalamus in language processing continues to pose a challenge. Neuroimaging studies have pointed a path forward, and we believe that more recent methods such as tractography and connectivity studies will significantly expand our knowledge in this particular area of aphasiology.
... The term "thalamic aphasia" is widely accepted. It is considered to result from "diaschisis", which implies that anatomically intact cortical structures involved in language are impaired through disruption of cortico-subcortical connections caused by thalamic lesions [4]. ...
... So far, our knowledge on "thalamic aphasia" is based on case reports and case series with heterogenous study populations (e.g. ischemic and hemorrhagic stroke, Parkinson's disease with deep brain stimulation) and various language assessment methods with different time intervals between symptom onset and language assessment [4][5][6]. Some of these studies were limited by lacking details on the affected thalamic subregions. ...
... The variation of frequency mostly depended on the type of language assessment methods. Studies using less detailed examinations reported lower frequencies [4,5,[7][8][9][10]. More sophisticated language assessment methods acknowledge that communication impairments extend beyond verbal deficits and that aphasic symptoms might not result solely from a faulty language system. ...
Background
Aphasia is a recognized presenting symptom of thalamic lesions. Little is known regarding its frequency and phenotype. We examined the frequency of thalamic aphasia following Isolated Acute unilateral ischemic Lesions in the Thalamus (IALT) with respect to lesion location. Furthermore, we characterized thalamic aphasia according to affected language domains and severity.
Methods
Fifty-two patients with IALT were analyzed [44% female, median age: 73 years (IQR: 60–79)]. Lesion location was determined using 3-Tesla magnetic resonance imaging and categorized as anterior, posterior, paramedian or inferolateral. Standardized language assessment was performed using the validated Aphasia checklist (ACL) directly after symptom onset. Aphasia was defined as an ACL sum score of < 135 (range: 0–148).
Results
Of 52 patients, 23 (44%) fulfilled the ACL diagnostic criteria for aphasia, including nearly all lesion locations and both sides. The average ACL sum score was 132 ± 11 (range: 98–147). Aphasia was characterized by deficits within domains of complex understanding of speech and verbal fluency. Patients with left anterior IALT were most severely affected, having significantly lower ACL scores than all other patients (117 ± 13 vs. 135 ± 8; p < 0.001). In particular, aphasia in patients with left anterior IALT was characterized by significantly worse performance in the rating of verbal communication, verbal fluency, and naming (all p ≤ 0.001).
Conclusion
Aphasia occurs in almost half of patients with focal thalamic lesions. Thalamic aphasia is not confined to one predefined thalamic lesion location, but language deficits are particularly pronounced in patients with left anterior IALT presenting with a distinct pattern.
... Isolated thalamic infarction occurs in 2-4% of stroke patients, mostly involving the posterolateral area of the thalamus [9]. While case reports have described aphasic symptoms after ischemic lesions in the anterior, paramedian as well as posterolateral thalamus, the possible importance of specifically the anterior thalamus in language has been stressed early on [10,11]. Clinically, patients are commonly described as presenting with a lack of fluency, mild anomia and semantic paraphasia while comprehension, grammatical functions and repetition remain mostly intact [7,12]. ...
... We could demonstrate, that (1) aphasic symptoms after ILT are rare (6/52 patients) and that (2) aphasic symptoms after ILT are strongly associated with isolated left anterior thalamic lesion location (p < 0.001). So far, reports on aphasic symptoms following thalamic damage were confined to case presentations and case series [10,21]. Description of lesion location included mostly left-but also right-sided areas of the thalamus involving the anterior, the posterolateral and the paramedian thalamus. ...
... Description of lesion location included mostly left-but also right-sided areas of the thalamus involving the anterior, the posterolateral and the paramedian thalamus. While the anterior thalamus has been considered important in language functions, coherent analysis has been missing [10,11]. ...
Background
Aphasic symptoms are typically associated with lesions of the left fronto-temporal cortex. Interestingly, aphasic symptoms have also been described in patients with thalamic strokes in anterior, paramedian or posterolateral location. So far, systematic analyses are missing.
Methods
We conducted a retrospective analysis of consecutive patients admitted to our tertiary stroke care center between January 2016 and July 2017 with image-based (MRI) proven ischemic stroke. We evaluated stroke lesion location, using 3-T MRI, and presence of aphasic symptoms.
Results
Out of 1064 patients, 104 (9.8%) presented with a thalamic stroke, 52 of which (4.9%) had an isolated lesion in the thalamus (ILT). In patients with ILT, 6/52 had aphasic symptoms. Aphasic symptoms after ILT were only present in patients with left anterior lesion location (n = 6, 100% left anterior vs. 0% other thalamic location, p < 0.001).
Conclusions
Aphasic symptoms in thalamic stroke are strongly associated with left anterior lesion location. In thalamo-cortical language networks, specifically the nuclei in the left anterior thalamus could play an important role in integration of left cortical information with disconnection leading to aphasic symptoms.
... The thalamus is a heterogeneous structure located deep in the brain, and at least two types of thalamic relays have been proposed: "first order thalamic relays" which transmit and modulate sensory information from peripheral sensory organs to sensory cortices, and "higher order thalamic relays" which can receive input of cortical information and involvement in the regulation of cortico-thalamo-cortical circuits [6][7][8]. As a higherorder thalamic relay nucleus, the mediodorsal thalamus (MD) is involved in processing various sensory, emotional, cognitive and behavioral motivations [9][10][11][12]. In addition, imaging studies have demonstrated decreased activity, increased volume, and the presence of changes in white matter microstructure in the MD of depressed Parkinson's patients compared with non-depressed Parkinson's patients [13,14], suggesting a possible underlying pathological relationship between MD dysfunction and depression. ...
... First, our study provides evidence that MD acts as a key brain region in CSDS-induced depression-like behavior. MD has been reported to play an important role in major brain functions, including attention, execution, cognition, emotion, learning and memory [9][10][11][12]. Human brain imaging studies suggest that MD activity is reduced in Parkinson's disease (PD) patients with depression, supporting the critical roles of the MD in depression [14]. ...
Clinical studies have shown that the mediodorsal thalamus (MD) may play an important role in the development of depression. However, the molecular and circuit mechanisms by which the mediodorsal thalamus (MD) participates in the pathological processes of depression remain unclear. Here, we show that in male chronic social defeat stress (CSDS) mice, the calcium signaling activity of glutamatergic neurons in MD is reduced. By combining conventional neurotracer and transneuronal virus tracing techniques, we identify a synaptic circuit connecting MD and medial prefrontal cortex (mPFC) in the mouse. Brain slice electrophysiology and fiber optic recordings reveal that the reduced activity of MD glutamatergic neurons leads to an excitatory-inhibitory imbalance of pyramidal neurons in mPFC. Furthermore, activation of MD glutamatergic neurons restores the electrophysiological properties abnormal in mPFC. Optogenetic activation of the MD-mPFC circuit ameliorates anxiety and depression-like behaviors in CSDS mice. Taken together, these data support the critical role of MD-mPFC circuit on CSDS-induced depression-like behavior and provide a potential mechanistic explanation for depression.
... However, the literature contains discrepant reports of the symptoms of individuals with thalamic aphasia. De Witte et al. [26] found, for example, that 14 of 32 (43.8%) patients with acute LH thalamic lesions presented with language comprehension problems (although only 3 of these cases were severe). Strikingly, the authors report that 69% of patients (n = 26) with LH thalamic lesions had moderate to severe naming problems. ...
... Hillis et al. [32], for example, found that 0 of 5 patients with isolated LH thalamic strokes were aphasic. On the other hand, Karussis et al. [70] reported aphasia in 88% (n = 8) of acute left thalamic stroke patients, and a meta-analysis by De Witte et al. [26] reported aphasia in 64% (n = 11) of patients with acute left thalamic lesions. Further, Sebastian et al. [35] found that among a sample of 10 patients with isolated left hemisphere thalamic stroke, half were aphasic. ...
Aphasia, the loss of language ability following damage to the brain, is among the most disabling and common consequences of stroke. Subcortical stroke, occurring in the basal ganglia, thalamus, and/or deep white matter can result in aphasia, often characterized by word fluency, motor speech output, or sentence generation impairments. The link between greater lesion volume and acute aphasia is well documented, but the independent contributions of lesion location, cortical hypoperfusion, prior stroke, and white matter degeneration (leukoaraiosis) remain unclear, particularly in subcortical aphasia. Thus, we aimed to disentangle the contributions of each factor on language impairments in left hemisphere acute subcortical stroke survivors. Eighty patients with acute ischemic left hemisphere subcortical stroke (less than 10 days post-onset) participated. We manually traced acute lesions on diffusion-weighted scans and prior lesions on T2-weighted scans. Leukoaraiosis was rated on T2-weighted scans using the Fazekas et al. (1987) scale. Fluid-attenuated inversion recovery (FLAIR) scans were evaluated for hyperintense vessels in each vascular territory, providing an indirect measure of hypoperfusion in lieu of perfusion-weighted imaging. We found that language performance was negatively correlated with acute/total lesion volumes and greater damage to substructures of the deep white matter and basal ganglia. We conducted a LASSO regression that included all variables for which we found significant univariate relationships to language performance, plus nuisance regressors. Only total lesion volume was a significant predictor of global language impairment severity. Further examination of three participants with severe language impairments suggests that their deficits result from impairment in domain-general, rather than linguistic, processes. Given the variability in language deficits and imaging markers associated with such deficits, it seems likely that subcortical aphasia is a heterogeneous clinical syndrome with distinct causes across individuals.
... According to a previous review [13] of vascular thalamic damage 3 weeks to 4 months post-stroke, almost 90% of the left thalamic and bilateral thalamic patient group presented with memory disturbances, inattention, executive dysfunctions and behaviour and/or mood alterations. Difficulty in fluency (6.4%), repetition (15.1%), naming (72.2%), auditory comprehension (43.8%), reading (25%), and writing (65%) were found in patients with left (n = 37), and comprehension (1/2), repetition (1/2), and naming (2/2) with bilateral thalamic lesions (n = 3). ...
... Crosson (1984) described three cardinal features of thalamic aphasia: (1) fluent output with frequent paraphasia, (2) almost intact auditory-verbal comprehension, (3) slightly impaired repetition [34]. Llano [11] summarized the commonly noted features of thalamic aphasia as 1) deficits in naming, with relative preservation of repetition [13], 2) a high frequency of semantic paraphasic errors [9,35], and 3) perseverations [9,36,37]. ...
Thalamic stroke may result in cognitive and linguistic problems, but the underlying mechanism remains unknown. Especially, it is still a matter of debate why thalamic aphasia occasionally occurs and then mostly recovers to some degree. We begin with a brief overview of the cognitive dysfunction and aphasia, and then review previous hypotheses of the underlying mechanism. We introduced a unique characteristic of relatively transient “word retrieval difficulty” of patients in acute phase of thalamic stroke. Word retrieval ability involves both executive function and speech production. Furthermore, SMA aphasia and thalamic aphasia may resemble in terms of the rapid recovery, thus suggesting a shared neural system. This ability is attributable to the supplementary motor area (SMA) and inferior frontal cortex (IFG) via the frontal aslant tract (FAT). To explore the possible mechanism, we applied unique hybrid neuroimaging techniques: single-photon emission computed tomography (SPECT) and functional near-infrared spectroscopy (f-NIRS). SPECT can visualize the brain distribution associated with word retrieval difficulty, cognitive disability or aphasia after thalamic stroke, and f-NIRS focuses on SMA and monitors long-term changes in hemodynamic SMA responses during phonemic verbal task. SPECT yielded common perfusion abnormalities not only in the fronto–parieto–cerebellar–thalamic loop, but also in bilateral brain regions such as SMA, IFG and language-relevant regions. f-NIRS demonstrated that thalamic stroke developed significant word retrieval decline, which was intimately linked to posterior SMA responses. Word retrieval difficulty was rapidly recovered with increased bilateral SMA responses at follow-up NIRS. Together, we propose that the cognitive domain affected by thalamic stroke may be related to the fronto–parieto–cerebellar–thalamic loop, while the linguistic region may be attributable to SMA, IFG and language-related brain areas. Especially, bilateral SMA may play a crucial role in the recovery of word retrieval, and right language-related region, including IFG, angular gyrus and supramarginal gyrus may determine recovery from thalamic aphasia.
... Regarding the thalamus, a "lateralized linguistic" syndrome characterized by severe anomia and little change in repetition or auditory comprehension was identified in 64% of left thalamic lesions (De Witte et al., 2011). Thalamic influence on frontal and temporal cortices may be attributed to the connectivity between prefrontal cortex and medial pulvinar nucleus, which could account for the effects of thalamic lesions on language dysfunction such as anomia (Nadeau, 2021). ...
... Previous studies found that electrical stimulation in the dorsal lateral thalamus and pulvinar could produce symptoms of object anomia and lexical memory disorders, whereas repetitive misnaming was observed under anterior ventrolateral thalamus stimulation (Fedio & Van Buren, 1975). Structurally, the medial pulvinar of the thalamus in the macaque has reciprocal connections with the superior temporal and posterior parietal cortex, which form the peri-Sylvian language cortex in humans (Jones, 2007); pathologically, thalamic lesions can lead to linguistic symptoms characterized by wordfinding difficulties and paraphasias (De Witte et al., 2011;Kuljic-Obradovic, 2003); electrophysiologically, both the thalamus and language eloquent cortices, including Wernicke's area, present increased amplitude of high gamma rhythms in language tasks, indicating language processing activities (Crosson, 2019;Edwards et al., 2010;Steriade, Contreras, Amzica, & Timofeev, 1996). Moreover, the basal ganglia-thalamocortical circuitry connected with Broca's area was reported to play a role in naming processing by supporting lexical retrieval and semantic information (Ullman, 2006). ...
Naming is a commonly impaired language domain in various types of aphasia. Emerging evidence supports the cortico-subcortical circuitry subserving naming processing, although neurovascular regulation of the non-dominant thalamic and basal ganglia subregions underlying post-stroke naming difficulty remains unclear. Data from 25 subacute stroke patients and 26 age-, sex-, and education-matched healthy volunteers were analyzed. Region-of-interest-wise functional connectivity (FC) was calculated to measure the strength of cortico-subcortical connections. Cerebral blood flow (CBF) was determined to reflect perfusion levels. Correlation and mediation analyses were performed to identify the relationship between cortico-subcortical connectivity, regional cerebral perfusion, and naming performance. We observed increased right-hemispheric subcortical connectivity in patients. FC between the right posterior superior temporal sulcus (pSTS) and lateral/medial prefrontal thalamus (lPFtha/mPFtha) exhibited significantly negative correlations with total naming score. Trend-level increased CBF in subcortical nuclei, including that in the right lPFtha, and significant negative correlations between naming and regional perfusion of the right lPFtha were observed. The relationship between CBF in the right lPFtha and naming was fully mediated by the lPFtha-pSTS connectivity in the non-dominant hemisphere. Our findings suggest that perfusion changes in the right thalamic subregions affect naming performance through thalamo-cortical circuits in post-stroke aphasia. This study highlights the neurovascular pathophysiology of the non-dominant hemisphere and demonstrates thalamic involvement in naming after stroke.
... In particular, specific cingulofrontal areas dysfunctions , damages involving primarily the temporoparietal junction (Devinsky, 2008), the lateral ventricles, the frontal horns, and diencephalic regions (Starkstein et al., 1992)-such as the thalamus and the basal ganglia (Starkstein et al., 2010)-might contribute to a reduced self-awareness (Devinsky, 2008;Starkstein et al., 2010;Palermo et al., 2014;Bourlon et al., 2017), also in terms of interoceptive awareness (i.e., the perception of heartbeat, breathing, hunger, thirst, and visceral sensations) (Raimo et al., 2019). De Witte et al. (2011) confirmed that the thalamus might be considered an attractive "hub" for the study of reduced self-awareness of cognitive deficits in ABI. Those authors reviewed 465 patients with vascular thalamic lesions, finding that two thirds of those with bilateral thalamic damage presented specific cognitive and behavioral deficits, such as reduced self-awareness and executive dysfunction, disrupted memory, constructional apraxia, disorientation, and global cognitive deficits associated with behavioral abnormalities (De Witte et al., 2011). ...
... De Witte et al. (2011) confirmed that the thalamus might be considered an attractive "hub" for the study of reduced self-awareness of cognitive deficits in ABI. Those authors reviewed 465 patients with vascular thalamic lesions, finding that two thirds of those with bilateral thalamic damage presented specific cognitive and behavioral deficits, such as reduced self-awareness and executive dysfunction, disrupted memory, constructional apraxia, disorientation, and global cognitive deficits associated with behavioral abnormalities (De Witte et al., 2011). Stroke in the left dorsomedian thalamus (Lanna et al., 2012) and bilateral paramedian thalamus (Rusconi et al., 2014) had been previously associated with anosognosia. ...
Reduced self-awareness is a well-known phenomenon investigated in patients with vascular disease; however, its impact on neuropsychological functions remains to be clarified. Importantly, selective vascular lesions provide an opportunity to investigate the key neuropsychological features of reduced self-awareness in neurocognitive disorders. Because of its rarity, we present an unusual case of a woman affected by a combined polar and paramedian bilateral thalamic infarction. The patient underwent an extensive neuropsychological evaluation to assess cognitive, behavioral, and functional domains, with a focus on executive functions. She was assessed clinically in the acute phase and after 6 months from the stroke, both clinically and by magnetic resonance imaging. The patient developed a cognitive impairment, characterised by prevalent executive dysfunction associated with reduced self-awareness and mood changes, in terms of apathy and depression. Such condition persisted after 6 months. In May 2020, the patient underwent the serology test in chemiluminescence to detect IgG antibodies against SARS-CoV-2. The result of the quantitative test highlighted a high probability of previous contact with the virus. We suggest that reduced self-awareness related to executive dysfunction and behavioral changes may be due to combined polar and paramedian bilateral thalamic lesion. Metacognitive–executive dysfunction affecting the instrumental abilities of everyday life might make people less able to take appropriate precautions, facilitating the risk of SARS-CoV-2 contagion.
... Many studies have shown that there may be more brain regions involved in language function than in the classical language center. Recent studies have shown that the basal ganglia (10,11), cerebellum (8), thalamus (12), and pons (13) are all involved in language function. ...
... As we know, the thalamus is a center of speech processing between Broca's area and Wernicke's area, its injury can lead to changes in cognition and speech. Aphasia can occur in unilateral thalamic injury, indicating that thalamus plays an important role in the process of language generation (12). Our results show that bilateral thalamus with an alteration in FC suggesting the procession of speech in thalamus also is bilateral. ...
Background:
Dysarthria is one of the common symptoms of facial paralysis (FP). This study aimed to investigate functional alterations in the brain language network in early idiopathic peripheral FP patients with dysarthria using resting-state functional magnetic resonance imaging (fMRI).
Methods:
A total of 45 cases of FP (left 22, right 23) and 34 cases of healthy control (HC) were recruited into this study. The data of patients with left-side FP and matched controls (17 cases) were flipped from left to right, and the brain regions were defined as ipsilateral and contralateral regions. The FC of 16 ROIs in classical language centers and regions that may be involved in language function were calculated. After identifying the differences of FC between the two groups, the correlation analysis between altered FC and TFGS score of oral muscle movement in FP group were analyzed.
Results:
The FC between bilateral language regions has a significantly decreased trend in FP group compared with HC group (P<0.05). The ipsilateral inferior frontal gyrus, superior temporal gyrus, and middle temporal gyrus exhibited significantly decreased FC with multiple brain regions. In addition, we found that thalamus and cerebellum also with a significant alteration in FC in FP patients indicating that these two regions may also be involved in the mechanism of dysarthria in FP. The correlation analysis results indicated that the decrease of FC was positively correlated with the severity of oral paralysis.
Conclusions:
Idiopathic peripheral FP with dysarthria induces several FC alterations in the brain language network. The severity of oral paralysis is associated with these functional alterations.
... Obwohl verschiedene patholinguistische Muster auftreten können und der Einfluss weiterer, nach Thalamusläsionen auftretender kognitiver Defizite berücksich-tigt werden sollte, wird von den meisten Autoren die semantisch-lexikalische Störung nach Thalamusläsionen als zentral angesehen [10]. Beschrieben wird hier eine nur gering beeinträchtigte, flüssige Sprachproduktion mit ungestörtem Nachsprechen bei deutlichen Benenn-und teilweise Verständnisstörungen [11]. ...
... Welches Areal des Thalamus besonders relevant für Sprachprozesse sein könnte, ist dabei nicht abschließend geklärt. Zahlreiche Einzelfallberichte und Fallserien zeigen eine klare Häufung von aphasischen Störungen nach linksseitigen Läsionen [11]. Hinweise für eine linksseitige Lateralisation von Sprachfunktionen im Thalamus ergeben sich auch aus Studien bei Patienten mit essenziellem Tremor, die spezifisch während einer Stimulation links-thalamischer Kerngebiete, im Rahmen einer tiefen Hirnstimulation (DBS, deep brain stimulation), Sprachstörungen zeigten [12,13]. ...
ZUSAMMENFASSUNG
Aphasie ist ein typisches Symptom links fronto-temporaler Läsionen. Nicht selten werden aphasische Symptome jedoch auch nach subkortikalen Läsionen z. B. im Thalamus beschrieben. Als Ursache für aphasische Symptome bei Thalamusschädigungen vermutet man die Störung eines thalamo-kortikalen Sprachnetzwerkes. Die Rolle des Thalamus in Sprachfunktionen wird in einer Rekrutierung sprachrelevanter, kortikaler Areale im Sinne einer Monitorfunktion vermutet. Wir berichten über einen 72-jährigen Patienten, der nach einem isolierten, links-anterioren Thalamusinfarkt eine expressiv betonte Aphasie gezeigt hat, und geben einen Überblick zu pathophysiologischen Konzepten.
... However, the exact thalamic site involved in language processing remains elusive, especially with respect to affected language subdomains. Interestingly, while specifics vary, there is consensus that thalamic structures are involved in word fluency tests, anomia in spontaneous language and confrontation naming, while comprehension and repetition mostly remain well preserved [9][10][11] . These findings suggest that the thalamus is embedded in language tasks that rely on involvement of the frontal lobe networks. ...
Thalamic aphasia results from focal thalamic lesions that cause dysfunction of remote but functionally connected cortical areas due to language network perturbation. However, specific local and network-level neural substrates of thalamic aphasia remain incompletely understood. Using lesion symptom mapping, we demonstrate that lesions in the left ventrolateral and ventral anterior thalamic nucleus are most strongly associated with aphasia in general and with impaired semantic and phonemic fluency and complex comprehension in particular. Lesion network mapping (using a normative connectome based on fMRI data from 1000 healthy individuals) reveals a Thalamic aphasia network encompassing widespread left-hemispheric cerebral connections, with Broca’s area showing the strongest associations, followed by the superior and middle frontal gyri, precentral and paracingulate gyri, and globus pallidus. Our results imply the critical involvement of the left ventrolateral and left ventral anterior thalamic nuclei in engaging left frontal cortical areas, especially Broca’s area, during language processing.
... Anomalous crossed aphasia refers to cases in which the features of aphasia do not correspond to the lesion site in the left hemisphere. Although various types of aphasia can occur with left thalamic damage, De Witte et al. [14] described six typical features of thalamic aphasia: reduced spontaneous speech or lack of language initiation; decreased volume and/or mild dysarthria; moderate-to-severe naming impairment characterized by semantic paraphasia, neologism, and perseveration; normal or mild repetition impairment; normal or mild language comprehension impairment; and speech fluency. The patient exhibited reduced spontaneous speech and volume. ...
... PTG following acquired brain injury may lead to psychological outcomes despite actual or perceived physical functional deficits [19,24]. Further, for some individuals with acquired brain injury, diminished insight into some of their deficits may be present [25,26]; poor insight may result in a discrepancy between objective level of functional impairment and higher levels of subjective mental health. Attention on physical function deficits may also overshadow attention on mental health difficulties for many. ...
... In the linguistic aspect, it has been a matter of debate whether the thalamus plays a role in language [148,149]. According to a previous review [150], almost 90% of the left thalamic and bilateral thalamic patients 3 weeks to 4 months post-stroke presented with memory disturbances, inattention, executive dysfunctions, and behavioral and/or mood alterations. Linguistic difficulties, such as fluency (6.4%), repetition (15.1%), naming (72.2%), auditory comprehension (43.8%), reading (25%), and writing (65%) were found in patients with left thalamic lesions (n = 37), and comprehension (1/2), repetition (1/2), and naming (2/2) were found in those with bilateral thalamic lesions (n = 3). ...
It is well known that cortical damage may affect cognitive functions, whereas subcortical damage, especially brainstem stroke, would be far less likely to cause cognitive decline, resulting in this condition being overlooked. Few studies have focused on cognitive dysfunction after a pontine stroke. Here, we begin with describing our nine new case reports of in-depth neuropsychological findings from patients with pontine stroke. The dominant domain of cognitive dysfunction was commonly characterized by executive dysfunction, almost in line with previous studies. The severity was relatively mild. We give an overview of the available literature on cognitive decline following a pontine stroke. This is followed by discussions regarding the prognosis of the cognitive disabilities. Based on previous neuroimaging findings, we would like to get to the core of the neuropathology underlying the cognitive declines in the context of “diaschisis”, a phenomenon of a broad range of brain dysfunctions remote from the local lesions. Specifically, our unique paper, with two modalities of neuroimaging techniques, may help us better understand the pathology. SPECT scans yield evidence of frontal and thalamic hyper-perfusion and cerebellar hypo-perfusion in patients with pontine stroke. Functional near-infrared spectroscopy, when focusing on the supplementary motor area (SMA) as one of the hyper-perfusion areas, exhibits that SMA responses may be subject to the severity of cognitive decline due to a pontine stroke and would also be related to the recovery. Finally, we posit that cognitive decline due to pontine stroke could be explained by the failure of hierarchical cognitive processing in the fronto–ponto–cerebellar–thalamic loop.
... Симптомы нарушения поведения у обезьян при повреждении MD сходны с теми, которые наблюдаются у них при разрушении дорсолатеральной [Isseroff et al., 1982] и орбитальной [Mitchell et al., 2007;Izquierdo, Murray, 2010] префронтальной коры. Пациенты с локальными нарушениями кровообращения в области MD или таламофронтального тракта демонстрируют нарушения УФ, дезориентацию и потерю критичности [Калашникова, Гулевская, 1998;Van der Werf et al., 2003;De Witte et al., 2011]. В обзоре [Ouhaz et al., 2018] представлены клинические данные и результаты экспериментальных исследований на животных, которые свидетельствуют о совместном вкладе PFC и MD в обеспечение избирательного контроля когнитивных процессов. ...
В книге обобщены исследования коллектива авторов, посвященные актуальным проблемам мозгового обеспечения регуляции поведения и когнитивной деятельности в подростковом возрасте.
Морфологические, нейрофизиологические и нейропсихологические исследования, представленные в книге, свидетельствуют о существенных преобразованиях мозговой организации процессов регуляции познавательной деятельности и поведения у подростков. При этом направленность таких изменений — прогресс или снижение функциональных возможностей — различна для разных звеньев мозговых регуляторных систем и меняется с возрастом. Наиболее существенные изменения в подростковом возрасте претерпевают системы эмоционально-мотивационной регуляции, что в значительной степени увеличивает риск учебной и социальной дезадаптации.
Книга предназначена для физиологов, психологов, педагогов и студентов биологического, психолого-педагогического и клинико-психологического профиля.
... The medio-dorsal nucleus and other anterior thalamic nuclei are reciprocally connected with prefrontal regions through the anterior thalamic radiations (Fig. 3 and Table 1) and lesions cause similar dysexecutive deficits to those observed following prefrontal lesions (De Witte et al., 2011;Van der Werf et al., 2003). The use of a delayed-response task to test working memory in non-human primates has shown changes in firing rates in prefrontal and anterior thalamic regions (Fuster & Alexander, 1971). ...
Attention, working memory, and executive control are commonly considered distinct cognitive functions with important reciprocal interactions. Yet, longstanding evidence from lesion studies has demonstrated both overlap and dissociation in their behavioural expression and anatomical underpinnings, suggesting that a lower dimensional framework could be employed to further identify processes supporting goal-directed behaviour. Here, we describe the anatomical and functional correspondence between attention, working memory, and executive control by providing an overview of cognitive models, as well as recent data from lesion studies, invasive and non-invasive multimodal neuroimaging and brain stimulation. We emphasize the benefits of considering converging evidence from multiple methodologies centred on the identification of brain mechanisms supporting goal-driven behaviour. We propose that expanding on this approach should enable the construction of a comprehensive anatomo-functional framework with testable new hypotheses, and aid clinical neuroscience to intervene on impairments of executive functions.
... Le thalamus joue un rôle important sur le plan du contrôle des processus linguistiques lexico-sémantiques, syntaxiques et morphologiques (Klostermann et al., 2013). L'infarctus du thalamus peut ainsi être l'origine d'une aphasie fluente, parfois appelée aphasie « thalamique » (Nadeau & Crosson, 1997), caractérisée par des troubles légers de compréhension et de répétition, de l'anomie et des troubles de la lecture et de l'écriture (de Witte et al., 2011). Le noyau caudé est une autre structure sous-corticale connue pour jouer un rôle dans le contrôle du langage, notamment sur le plan de l'inhibition et de la sélection des représentations linguistiques (Friederici, 2006). ...
... Language-related terms were all associated with thalamo-cortical pairs of left cluster 1 (medial-lateral nuclei). While thalamic participation in language is widely described in the neuropsychological literature (Brown 1974;Crosson 1984Crosson , 2021De Witte et al. 2011), the evidence from functional neuroimaging is limited (Klosterman et al. 2013;Llano 2013Llano , 2016. When imaging studies have reported involvement of the thalamus in language processes, they either feature very broad anatomical labels (e.g., "thalamus") for reporting activation peaks or utilize anatomical regions of interest that do not discriminate between thalamic nuclei, which limits the available evidence to the issue of hemispheric specialization (Indefrey and Levelt 2004;Garn et al. 2009;Seghier and Price 2010). ...
The human thalamus relays sensory signals to the cortex and facilitates brain-wide communication. The thalamus is also more directly involved in sensorimotor and various cognitive functions but a full characterization of its functional repertoire, particularly in regard to its internal anatomical structure, is still outstanding. As a putative hub in the human connectome, the thalamus might reveal its functional profile only in conjunction with interconnected brain areas. We therefore developed a novel systems-level Bayesian reverse inference decoding that complements the traditional neuroinformatics approach towards a network account of thalamic function. The systems-level decoding considers the functional repertoire (i.e., the terms associated with a brain region) of all regions showing co-activations with a predefined seed region in a brain-wide fashion. Here, we used task-constrained meta-analytic connectivity-based parcellation (MACM-CBP) to identify thalamic subregions as seed regions and applied the systems-level decoding to these subregions in conjunction with functionally connected cortical regions. Our results confirm thalamic structure–function relationships known from animal and clinical studies and revealed further associations with language, memory, and locomotion that have not been detailed in the cognitive neuroscience literature before. The systems-level decoding further uncovered large systems engaged in autobiographical memory and nociception. We propose this novel decoding approach as a useful tool to detect previously unknown structure–function relationships at the brain network level, and to build viable starting points for future studies.
... Moreover, Indefrey and Levelt [65] in a metanalysis of eighty-two fMRI studies identified brain areas which appear to be critical for the various steps of single word production, including, beyond traditionally languagerelated areas, the supplementary motor areas, the insula and the thalamus. The role of the thalamus and the insula has been well-established in language sub-processes [46,[66][67][68][69]. Posterior left ventrolateral and pulvinar thalamic lesions have been shown to result in severe word-finding deficits, along with mild disturbances in reading, repetition and auditory comprehension [70]. ...
Despite the relative scarcity of studies focusing on pharmacotherapy in aphasia, there is evidence in the literature indicating that remediation of language disorders via pharmaceutical agents could be a promising aphasia treatment option. Among the various agents used to treat chronic aphasic deficits, cholinergic drugs have provided meaningful results. In the current review, we focused on published reports investigating the impact of acetylcholine on language and other cognitive disturbances. It has been suggested that acetylcholine plays an important role in neuroplasticity and is related to several aspects of cognition, such as memory and attention. Moreover, cholinergic input is diffused to a wide network of cortical areas, which have been associated with language sub-processes. This could be a possible explanation for the positive reported outcomes of cholinergic drugs in aphasia recovery, and specifically in distinct language processes, such as naming and comprehension, as well as overall communication competence. However, evidence with regard to functional alterations in specific brain areas after pharmacotherapy is rather limited. Finally, despite the positive results derived from the relevant studies, cholinergic pharmacotherapy treatment in post-stroke aphasia has not been widely implemented. The present review aims to provide an overview of the existing literature in the common neuroanatomical substrate of cholinergic pathways and language related brain areas as a framework for interpreting the efficacy of cholinergic pharmacotherapy interventions in post-stroke aphasia, following an integrated approach by converging evidence from neuroanatomy, neurophysiology, and neuropsychology.
... In a recent review, it has been shown that patients with vascular syndrome of the thalamus had cognitive impairment in subdomains such as attention, orientation, memory, praxis, executive functions, concentration, global intellectual functions, behavior, and mood [21]. In another study, neuropsychological tests were performed on healthy people, and their thalamic volume was evaluated by magnetic resonance imaging [22]. ...
Background:
The thalamus is known as the central sensory and motor relay station of the brain generally. However, cognitive decline due to thalamic lesions has been previously reported in different studies. Also, it has been observed that different cognitive subdomains are affected according to the localization of the lesion in the thalamus.
Objectives and methods:
Detailed neurophysiological tests were performed on 28 patients with thalamic hemorrhage and the control group. Patients were grouped according to lesion localization. The results were compared with both the control group and the hemorrhage groups themselves.
Results:
The performance of patients in all neuropsychological tests was significantly worse than that of the control group. Of the 28 patients, 15 had anterolateral, 5 had posterolateral, 5 had dorsal, and 3 had an anteromedial thalamic hemorrhage. The anteromedial group had the worst scores of almost all tests. Also, 2 situations came to notice in these tests. First, the posterolateral group achieved a remarkably low mean in the recall subgroup of the MMSE tests and verbal memory process tests. Second, the anterolateral group was found to have a low mean in both the language subgroup of the MMSE tests and the phonemic subgroup of the verbal fluency tests.
Conclusion:
It was concluded in this study that thalamic hemorrhages affect cognition entirely regardless of the lesion localization. It was also observed that the lateral part of the thalamus was associated with language, the posterior part with memory, and the anteromedial part with the rest of the cognitive subdomains.
... In 2011, De Witte et al., critically reviewed 465 patients with vascular thalamic lesions published in the literature since 1980. [33] 75% had a thalamic infarction, 25% haemorrhage, and 90% patients had a left thalamic lesion. Those who met at least four out of the following six operational criteria: 1) fluent output, 2) normal or mildly impaired comprehension skills, 3) normal or mildly impaired repetition, 4) moderate to severe anomia characterised by semantic paraphasias, neologisms and perseverations, 5) hypophonia and/or mild articulation deficits and 6) reduction of spontaneous speech or verbal aspontaneity, were given the diagnosis of thalamic aphasia. ...
The field of language research has seen tremendous progress in the last two decades. Advances in neuro-imaging and stimulation mapping have changed the way we conceive the neural basis of speech and language processing. In the past, the Wernicke-Lichtheim model was the most influential model explaining the neuro-anatomical basis of language. More recently, the concept of dual stream language processing has emerged, wherein separate dorsal and ventral networks are synergistically involved in phonological (sound to articulation) and semantic (sound to meaning) processing respectively. In this review article, we highlight new insights and approaches to the neurobiology of language, across different aspects of language processing like perception, comprehension, production, hemisphere lateralization, role of subcortical structures and effect of damage to language networks.
... Stuss and Benson (1984) proposed that prefrontal thalamocortical connections provide a selective gating mechanism involved in alerting and orienting processes. The medio-dorsal (MD) nucleus and other anterior thalamic nuclei are reciprocally connected with prefrontal regions through the anterior thalamic radiation (Figure 4) and lesions cause similar dysexecutive deficits to those observed following prefrontal lesions (De Witte et al., 2011;Van der Werf et al., 2003). The use of a delayed-response task to test working memory in non-human primates has shown changes in firing rates in prefrontal and anterior thalamic regions (Fuster & Alexander, 1971). ...
Attention, working memory, and executive control are commonly considered distinct cognitive functions with important reciprocal interactions. Lesion studies pioneered by Donald Stuss have demonstrated both overlap and dissociation in their behavioral expression and anatomical underpinnings. Here, we provide an overview of cognitive models as well as recent data from lesion studies and both invasive and noninvasive multimodal neuroimaging and brain stimulation, in order to provide an updated perspective on the relationship between attention, working memory, and executive control. Specifically, we address the functional and anatomical correspondence between these processes, toward the goal of identifying whether a lower dimensional theoretical framework should be employed to understand executive control (Karolis et al., 2019). We conclude by emphasizing that one avenue for moving the field, pioneered by Donald Stuss, forward consists of studying this low-dimensional space with a multi-method approach to identify converging evidence regarding the interaction between subfunctions, allowing to construct a model of executive control as the emergent consequence of efficient implementation of these processes.
... The initial semiology of our patient, including sensorimotor deficit, in-coordinate limb movements, slurred speech, sleep-like attacks, visual impairments and unilateral spatial neglect, was suggestive of a right thalamic syndrome [11,12]. The initial SPECT indeed revealed a right thalamic hypoperfusion, coherent with this initial clinical presentation. ...
Background:
In the nineteenth century, Jean Martin Charcot explained functional neurological disorder (formerly called conversion disorder) as a "psychodynamic" lesion. Numerous advances in neuroimaging have permitted identification of the neural underpinnings of this disorder.
Case presentation:
Herein we describe a case of functional neurological disorder (FND) with initial left sensorimotor deficit, in-coordinated limb movements, neglect, clouded consciousness, slurred speech and a semiology of visual impairment. A single photon emission computed tomography (SPECT) showed a right thalamic hypoperfusion, which is rather concordant with the initial semiology. Later, the semiology changed, presenting with a predominantly neurovisual complex presentation. The second SPECT showed no more thalamic abnormalities but an hypoperfusion in the right temporo-occipital junction, right inferior parietal lobe and left superior frontal lobe, which is also rather concordant with the changing semiology.
Conclusions:
This case illustrates the evolving neuroimaging patterns of FND but also the concordance between semiology and neuroimaging findings in FND supporting Charcot's theory of "dynamic lesion".
... Based on the theoretical background, the aim of the present study was to examine whether there are differential profiles of Cc decline in older adults with VRF and older adults with MCI [101,102], which can also differentiate them from healthy controls. Taking into account what has been mentioned above, the hypothesis of the study was formulated as follows: ...
Cardiovascular health declines with age, due to vascular risk factors, and this leads to an increasing risk of cognitive decline. Mild cognitive impairment (MCI) is defined as the negative cognitive changes beyond what is expected in normal aging. The purpose of the study was to compare older adults with vascular risk factors (VRF), MCI patients, and healthy controls (HC) in main dimensions of cognitive control. The sample comprised a total of 109 adults, aged 50 to 85 (M = 66.09, S.D. = 9.02). They were divided into three groups: 1) older adults with VRF, 2) MCI patients, and 3) healthy controls (HC). VRF and MCI did not differ significantly in age, educational level, or gender as was the case with HC. The tests used mainly examine inhibition, cognitive flexibility, and working memory processing. Results showed that the VRF group had more Set Loss Errors in drawing designs indicating deficits in establishing cognitive set and in cognitive shifting. MCI patients displayed lower performance in processing. Hence, different types of specific impairments emerge in vascular aging and MCI, and this may imply that discrete underlying pathologies may play a role in the development of somewhat different profiles of cognitive decline.
Background and objectives
Emotional and cognitive deficits are prevalent in strokes involving the thalamus. In contrast to cognitive deficits, emotional deficits have not been studied prospectively in isolated thalamic stroke.
Methods
In 37 ischemic thalamic stroke patients (57.0 [50.0; 69.5] years [median (Q1; Q3)], 21 males, 5 anterior, 12 paramedian, 20 inferolateral vascular territory), and 37 non-stroke control patients matched for age and sex, we prospectively examined depression, anxiety, activities of daily living, and quality of life at 1, 6, 12, and 24 months post-stroke using the Hospital-Anxiety-and-Depression Scale (HADS), Nürnberger-Alters-Alltagsaktivitäten scale (NAA), and Short Form-36 (SF36) questionnaire. Voxel-based lesion-symptom mapping (VLSM) and lesion-subtraction analyzes were performed to determine associations between questionnaire scores and thalamic stroke topography.
Results
At 1 month post-stroke, anterior thalamic stroke patients had higher depression scores [8.0 (7.5; 10.5)] than paramedian [4.5 (1.0; 5.8)] and inferolateral [4.0 (1.0; 7.0)] thalamic stroke patients. Furthermore, anterior thalamic stroke patients had higher anxiety scores [11.0 (8.0; 14.5)] than their matched controls [2.5 (2.0; 2.5)], paramedian [4.5 (1.0; 5.8)] and inferior [4.0 (1.0; 7.0)] thalamic stroke patients. Depression and anxiety scores in anterior thalamic stroke patients remained high across the follow-up [depression: 9.0 (3.5; 13,8); anxiety:10.05 (2.8, 14.5)].
Physical health assessed by SF36 was intact in anterior [1 month post-stroke: T-score = 55.9 (37.0; 57.6)] but reduced in inferolateral [44.5(32.4; 53.1)] thalamic stroke, whereas mental health was reduced in anterior thalamic stroke [32.0 (29.8; 47.3)].
VLSM confirmed that voxels in the anterior thalamus around Montreal Neurological Institute (MNI) coordinates X = −8, Y = −12, Z = 2 were more often affected by the stroke in depressed (HADS-score ≥ 8) than non-depressed (HADS-score < 8) patients and voxels around coordinates X = −10, Y = −12, Z = 2 were more often affected in anxious (HADS-score ≥ 8) than non-anxious (HADS-score < 8) patients.
Conclusion
Anterior, but not paramedian or inferolateral thalamic stroke was associated with depression and anxiety. Even though our results are mostly significant in the left thalamus, this observation on stroke laterality might be confounded by the fact that the right hemisphere was underrepresented in our study.
Vascular cognitive impairment (VCI) encompasses a wide range of conditions, including cognitive impairment associated with stroke or vascular brain injury, mild vascular cognitive impairment, and vascular dementia (VD). Knowledge of language impairment associated with VD is far less extensive than that of Alzheimer's disease. Although not prevalent in VD, impairment in language skills has been reported. A better understanding of the neurolinguistic features associated with the different presentations of VD could facilitate medical diagnosis. In this article, we report data on language impairment in VD, with particular attention to their primary or secondary functional origin. To better appreciate this functional origin, we also outline the main characteristics of impairment in other cognitive functions. Key elements that should be considered in the speech-language assessment of individuals with possible or proven VD are also highlighted.
Background:
Schizophrenia is regarded as a brain network or connectome disorder that is associated with neurodevelopment. Children with early-onset schizophrenia (EOS) provide an opportunity to evaluate the neuropathology of schizophrenia at a very early stage without potential confounding factors. But dysfunction in brain networks of schizophrenia is inconsistent.
Purpose:
To identify abnormal functional connectivity (FC) in EOS patients and relationships with clinical symptoms, we aimed to reveal neuroimaging phenotypes of EOS.
Study type:
Prospective, cross-sectional.
Population:
Twenty-six female/22 male patients (age:14.3 ± 3.45 years) with first-episode EOS, 27 female/22 male age- and gender-matched healthy controls (HC) (age:14.1 ± 4.32).
Field strength/sequence:
3-T, resting-state (rs) gradient-echo echo-planar imaging and three-dimensional magnetization-prepared rapid gradient-echo imaging.
Assessment:
Intelligence quotient (IQ) was measured by the Wechsler Intelligence Scale-Fourth edition for Children (WISC-IV). The clinical symptoms were evaluated by the Positive and Negative Syndrome Scale (PANSS). FC strength (FCS) from rs functional MRI (rsfMRI) was used to investigate functional integrity of global brain regions. In addition, associations between regionally altered FCS and clinical symptoms in EOS patients were examined.
Statistical tests:
Two-sample t-test controlling for sample size, diagnostic method, brain volume algorithm, and age of the subjects, Bonferroni correction, Pearson's correlation analysis. A P-value <0.05 with a minimum cluster size of 50 voxels was considered statistically significant.
Results:
Compared with HC, EOS patients had significantly lower total IQ scores (IQ:91.5 ± 16.1), increased FCS in the bilateral precuneus, left dorsolateral prefrontal cortex, left thalamus, and left parahippocampus (paraHIP), and decreased FCS in the right cerebellum posterior lobe and right superior temporal gyrus. The PANSS total score of EOS patients (PANSS total score:74.30 ± 7.23) was found to be positively correlated to FCS in the left paraHIP (r = 0.45).
Data conclusion:
Our study revealed that disrupted FC of brain hubs illustrate multiple abnormalities in brain networks in EOS patients.
Evidence level:
1 TECHNICAL EFFICACY STAGE: 2.
This up-to-date, superbly illustrated book is a practical guide to the effective use of neuroimaging in the patient with sleep disorders. There are detailed reviews of new neuroimaging techniques – including CT, MRI, advanced MR techniques, SPECT and PET – as well as image analysis methods, their roles and pitfalls. Neuroimaging of normal sleep and wake states is covered plus the role of neuroimaging in conjunction with tests of memory and how sleep influences memory consolidation. Each chapter carefully presents and analyzes the key findings in patients with sleep disorders indicating the clinical and imaging features of the various sleep disorders from clinical presentation to neuroimaging, aiding in establishing an accurate diagnosis. Written by neuroimaging experts from around the world, Neuroimaging of Sleep and Sleep Disorders is an invaluable resource for both researchers and clinicians including sleep specialists, neurologists, radiologists, psychiatrists, psychologists.
The human thalamus relays sensory signals to the cortex and facilitates brain-wide communication. The thalamus is also more directly involved in sensorimotor and various cognitive functions but a full characterization of its functional repertoire, particularly in regard to its internal anatomical structure, is still outstanding. As a putative hub in the human connectome, the thalamus might reveal its functional profile only in conjunction with interconnected brain areas. We therefore developed a novel systems-level Bayesian reverse inference decoding that complements the traditional neuroinformatics approach towards a network account of thalamic function. The systems-level decoding considers the functional repertoire (i.e., the terms associated with a brain region) of all regions showing co-activations with a predefined seed region in a brain-wide fashion. Here, we used task-constrained meta-analytic connectivity-based parcellation (MACM-CBP) to identify thalamic subregions as seed regions and applied the systems-level decoding to these subregions in conjunction with functionally connected cortical regions. Our results confirm thalamic structure–function relationships known from animal and clinical studies and revealed further associations with language, memory, and locomotion that have not been detailed in the cognitive neuroscience literature before. The systems-level decoding further uncovered large thalamic-centered systems engaged in autobiographical memory and nociception. We propose this novel decoding approach as a useful tool to detect previously unknown structure–function relationships at the brain network level, and to build viable starting points for future studies.
We mapped the left hemisphere cortical regions and fiber bundles involved in picture naming in adults by integrating task-based fMRI with dMRI tractography.
We showed that a ventral pathway that “maps image and sound to meaning” involves the middle occipital, inferior temporal, superior temporal, inferior frontal gyri, and the temporal pole where a signal exchange is made possible by the inferior fronto-occipital, inferior longitudinal, middle longitudinal, uncinate fasciculi, and the extreme capsule.
A dorsal pathway that “maps sound to speech” implicates the inferior temporal, superior temporal, inferior frontal, precentral gyri, and the supplementary motor area where the arcuate fasciculus and the frontal aslant ensure intercommunication.
This study provides a neurocognitive model of picture naming and supports the hypothesis that the ventral indirect route passes through the temporal pole. This further supports the idea that the inferior and superior temporal gyri may play pivotal roles within the dual-stream framework of language.
Thalamocortical dysfunction is thought to underlie the pathophysiology of chronic pain revealed by electroencephalographic studies. The thalamus serves as a primary relay center to transmit sensory information and motor impulses via dense connections with the somatosensory and motor cortex. In this study, diffusion tensor imaging (probabilistic tractography) and resting-state functional magnetic resonance imaging (functional connectivity) were used to characterize the anatomical and functional integrity of the thalamo-sensorimotor pathway in chronic low back pain (cLBP). Fifty-four patients with cLBP and 54 healthy controls were included. The results suggested significantly increased anatomical connectivity of the left thalamo-motor pathway characterized by probabilistic tractography in patients with cLBP. Moreover, there was significantly increased resting-state functional connectivity (rsFC) of bilateral thalamo-motor/somatosensory pathways in patients with cLBP as compared to healthy controls. We also detected a significant positive correlation between pain intensity during the MRI scan and rsFC of the right thalamo-somatosensory pathway in cLBP. Our findings highlight the involvement of the thalamo-sensorimotor circuit in the pathophysiology of cLBP.
Over 150 years have passed since the first formal description of aphasia associated with localized neurologic damage. In the years since that time, a significant amount of research has been conducted to identify/explain the locations and functions of the brain regions responsible for (or associated with) language as well as to describe the various types of aphasia resulting from injury to these locations. Many of these attempts to associate somewhat predictable patterns of language deficits with damage to specific structures have been confounded by atypical reports and considerable variability in either the behavioral presentation and/or structural damage that directly contradict/oppose some of the proposed theories. However, considering the aphasias as vascular syndromes, or a collection of symptoms associated with damage to various structures supplied by a specific artery, accounts for both the predictability and the variability seen. This chapter presents a brief history of aphasia classification, the vascular territories commonly associated with aphasia, the different aphasic vascular syndromes, and the typical recovery/evolution of aphasia presentation over time.
The hallmarks of thalamic aphasia based on the previous case reports include word-finding difficulties and verbal paraphasias, in particular, irrelevant verbal paraphasias, despite normal articulation, intact repetition, and mild comprehension deficits. However, no group study has been conducted on whether thalamic aphasia frequently involves irrelevant verbal paraphasias compared with the other types of aphasia and potential mechanisms underlying those irrelevant verbal paraphasias has yet to be elucidated. Here we approached the nature of thalamic aphasia by investigating its accompanying irrelevant verbal paraphasias. Compared with aphasic patients with the other types, patients with thalamic aphasia showed the higher ratio of irrelevant verbal paraphasias among the total errors as well as to the relevant verbal paraphasias. In our previous case report on thalamic aphasia, a close relationship between irrelevant verbal paraphasias and selective attentional dysfunction was observed, suggesting selective attentional dysfunction, which is deeply associated with thalamic damage, led to development of irrelevant verbal paraphasias. With the previously proposed mechanisms behind thalamic aphasia, the characteristic speech found in thalamic aphasia might reflect word-finding errors due to inability to activate semantic fields that is related to the target word as well as inability to suppress words that are irrelevant to the target word.
Background
Stroke lesion size and location are understood to be more accurate predictors of recovery from aphasia than demographic variables such as age, education, or socioeconomic status.
Aims
We hypothesise that markedly high premorbid language function can influence functional recovery from aphasia.
Methods & Procedures
This case study reports the recovery of a 64-year-old right-handed male, with large left posterior cerebral artery territory infarct involving the thalamus, occipital lobe and posteromedial temporal lobe. The report is informed by retrospective review of clinical notes, language assessment, and interviews with the participant and his family. Premorbidly, he had acquired fluency in five additional languages in early adulthood, followed by a career in senior roles within corporate communications.
Outcomes & Results
Following severe expressive aphasia in the acute period, the subacute and chronic phases were characterised by residual mild anomia and cognitive communication difficulties apparent on formal assessment, yet masked in functional contexts through compensatory strategies and preservation of an authoritative premorbid communication style.
Conclusions
The current report provides single-case evidence that individuals with markedly high premorbid metalinguistic skills may, in functional contexts, be able to compensate for expressive aphasic deficits and preserve their communicative competence. The discrepancy between the participant’s performance on formal versus informal language assessment underscores the necessity for both perspectives for accurate diagnosis of aphasia. Consideration of premorbid language function can usefully guide clinical decision-making about intervention for individuals with aphasia.
Abstract Background More patients with left-hemispheric than right-hemispheric strokes are admitted to hospitals. This is due to the easier recognition of cortical symptoms of the dominant-hemisphere. The thalamus constitutes a “micro-model” of the brain cortex with structure-function relationships known to be asymmetric, especially for language, memory, and visuo-spatial neurocognitive functions. The goal of this study was to characterize clinical symptoms and lesion distribution patterns of patients with acute isolated thalamic stroke (ITS) and to evaluate whether left-sided lesions are overrepresented in the hospital. Methods We performed a radiological database search including all brain scans performed in the Center of Neurology and Neurosurgery of the University Hospital Frankfurt between 2010 and 2019. A total of 5733 patients presenting with acute ischemic stroke were screened for ITS. Based on the MRI data, a lesion-overlap map was then generated to visualize the ITS lesion distribution. Results Fifty-eight patients with unilateral ITS were identified. A majority of 38 patients (65.5%) showed left-sided ITS, whereas only 20 patients (34.5%) had right-sided ITS (p = 0.012). A particular difference was found for ITS lesions in the anterior thalamus of the anterolateral (n = 10) and anteromedian (n = 3) vascular territory, which were located in the left thalamus in 85% of patients (p = 0.011). No distribution difference was found for ITS lesions in the inferomedial (n = 7), central (n = 8), inferolateral (n = 23) and posterior (n = 7) vascular territories. The neuropsychological symptoms of thalamic aphasia (n = 8), neurocognitive impairment (n = 6), behavioral changes (n = 2), neglect (n = 2) and memory deficits (n = 3) were described predominantly in patients with left-sided ITS (p
Modelling stroke in animals remains a challenge for translational research, especially for the infraction of small subcortical arteries. Using combined fibre optics and photothrombosis technologies, we developed a novel model of optically-induced infarcts (Opto-STROKE). Combining our model with electrophysiological recordings in freely-behaving mice, we studied early and late consequent patho-physiological changes in the dynamics of sleep-wake circuits and cognitive performance. Here, focusing on inducing Opto-STROKE lesions in the intralaminar thalamus (IL), which in humans cause severe impairments of arousal, cognition, and affective symptoms, our model recapitulated important deficits on sleep disorders presented in humans including arousal instability, concurrent to an augmented slow-wave activity and a reduction gamma power bands during wakefulness. Moreover, during NREM sleep, spindle density was decreased and topographically shifted to frontal cortices when compared to control animals. Remarkably, gamma power and spindle density were correlated with decreased pain threshold and impaired prefrontal cortex- dependent working memory in Opto-STROKE mice relative to controls. Collectively, our combined method influences both anatomical and functional outcomes of the classical stroke procedures and offers new insights on the fundamental role of the media thalamus as a hub for the regulation of both sleep-wake architecture and cognition.
A 71-year-old, right-handed woman was admitted to our hospital due to a sudden difficulty with conversation. On admission, she was alert, but had a euphoric mood, disorientation, and a disturbance of recent memory. Her speech was fluent. Her repetition and auditory word cognition were excellent, but she had a slight difficulty with naming visual objects. She frequently showed word-finding difficulty and irrelevant paraphasia during free conversation and a word fluency task. Her irrelevant paraphasia was observed more frequently when she was asked to explain her outbreak of anger at the hospital, i.e., it was situation-dependent. She also had anosognosia. MRI showed an infarct in the territory of the left tuberothalamic artery. Single-photon emission computed tomography revealed low-uptake lesions in the left thalamus and orbital frontal, medial frontal, and medial temporal lobes. The patient was diagnosed with non-aphasic misnaming. The clinical characteristics of patients with non-aphasic misnaming in the literature were reviewed. All of the patients with non-aphasic misnaming had word-finding difficulty and irrelevant paraphasia. Additionally, they had either emotional disturbance or anosognosia.
Background: Previous studies utilized lesion-centric approaches to study the role of the thalamus in language. In this study, we tested the hypotheses that non-lesioned dorsomedial and ventral anterior nuclei (DMVAC) and pulvinar lateral posterior nuclei complexes (PLC) of the thalamus and their projections to the left hemisphere show secondary effects of the strokes, and that their microstructural integrity is closely related to language-related functions. Methods: Subjects with language impairments after a left-hemispheric cortical and/or subcortical, early stroke (n = 31, ≤6 months) or late stroke (n = 30, ≥12 months) sparing thalamus underwent the Boston Naming Test (BNT) and diffusion tensor imaging (DTI). The tissue integrity of DMVAC, PLC, and their cortical projections was quantified with DTI. The right-left asymmetry profiles of these structures were evaluated in relation to the time since stroke. The association between microstructural integrity and BNT score was investigated in relation to stroke chronicity with partial correlation analyses adjusted for confounds. Results: In both early stroke and late stroke groups, left-sided tracts showed significantly higher mean diffusivities (MDs), which were likely due to Wallerian degeneration. Higher MD values of the cortical projections from the left PLC (r = -0.5, p = 0.005) and DMVAC (r = -0.53, p = 0.002) were correlated with lower BNT score in the late stroke but not early stroke group. Conclusion: Nonlesioned thalamic nuclei and thalamocortical pathways show rightward lateralization of the microstructural integrity after a left hemispheric stroke, and this pattern is associated with poorer naming. Impact statement To the best of our knowledge, our study is the first diffusion tensor imaging study suggesting that the thalamic nuclei and pathways of the left hemisphere spared by direct ischemic insult undergo secondary degeneration over time that is associated with poorer picture naming. Our study may pave the way for targeted interventions such as invasive or noninvasive brain stimulation techniques that engage these spared pathways to prevent secondary degeneration and lead to better outcomes in poststroke aphasia.
Visual cortical disorders are often encountered in clinical practice but frequently misunderstood and misdiagnosed. Visual cortical syndromes that occur as a result of a stroke are more readily recognized by clinicians compared to the non-syndromic and generalized dysfunction of the visual cortex that occurs with neurodegenerative disorders that lead to dementia, such as Alzheimer's disease or Dementia with Lewy bodies. Nonetheless, visual cortical disorders are best organized and categorized as neurological syndromes that occur due to disruption of specific visual cortical networks, whether due to vascular insult, neurodegenerative disease, or other lesions that result in visual behavioral dysfunction. An astute clinician can easily misinterpret a patient's visual complaints that are due to posterior cortical dysfunction for ocular disease and the patient can go months to years without a diagnosis, understanding, or care for their visual dysfunction. A careful history and examination are necessary for proper diagnosis, as is an understanding of the most common visual cortical syndromes that impact daily visual functions. The reader should keep in mind the functional specialization and anatomy of the primary and secondary (or association) visual cortical regions while committing to memory the visual cortical syndromes reviewed here and elsewhere in this text. Without an understanding of the underlying functional posterior cortical anatomy, subtle manifestations of visual cortical syndromes, or partial and incomplete syndromes, can be difficult to recognize. Syndromes reviewed in this section include Cerebral Achromatopsia, Simultanagnosia, Constructional Apraxia, and Cerebral Akinetopsia.
The pattern of decreased prefronto-thalamic connectivity and increased sensorimotor-thalamic connectivity has been consistently documented in schizophrenia. However, whether this thalamo-cortical abnormality pattern is of genetic predisposition remains unknown. The present study for the first time aimed to investigate the common and distinct characteristics of this circuit in schizophrenia patients and their unaffected siblings who share half of the patient's genotype. Totally 293 participants were recruited into this study including 94 patients with schizophrenia, 96 their healthy siblings, and 103 healthy controls scanned using gradient-echo echo-planar imaging at rest. By using a fine-grained atlas of thalamus with 16 sub-regions, we mapped the thalamocortical network in three groups. Decreased thalamo-prefronto-cerebellar connectivity was shared between schizophrenia and their healthy siblings, but increased sensorimotor-thalamic connectivity was only found in schizophrenia. The shared thalamo-prefronto-cerebellar dysconnectivity showed an impressively gradient reduction pattern in patients and siblings comparing to controls: higher in the controls, lower in the patients and intermediate in the siblings. Anatomically, the decreased thalamic connectivity mostly centered on the pre-frontal thalamic subregions locating at the mediodorsal nucleus, while the increased functional connectivity with sensorimotor cortices was only observed in the caudal temporal thalamic subregion anchoring at the dorsal and ventral lateral nuclei. Moreover, both decreased thalamo-prefronto-cerebellar connectivity and increased sensorimotor-thalamic connectivity were related to clinical symptoms in patients. Our findings extend the evidence that the decreased thalamo-prefronto-cerebellar connectivity may be related to the high genetic risk in schizophrenia, while increased sensorimotor-thalamic connectivity potentially represents a neural biomarker for this severe mental disorder.
Background:
Enteroviruses-associated acute necrotizing encephalopathy (ANE) of childhood is rarely reported in the literature. Clinico-radiological features of ANE are well-recognized and bilateral thalamic nuclei are frequently affected by ANE. Neuropsychiatric symptoms are rarely seen. Thalamic damage can cause psychosis.
Case:
Herein, we present a pediatric case of enterovirus-associated ANE presenting with psychosis related to thalamus damage in whom a favorable response to treatment was achieved.
Conclusion:
Thalamic damage occurs during the Enteroviruses-associated acute necrotizing encephalopathy and it can be related psychiatric sympthoms. Clinicians should be aware of uncommon presentations of ANE, and patients with thalamic damage should be followed for neuropsychiatric manifestations. Early recognition and appropriate treatment of ANE is important to obtain favorable outcomes.
The article is devoted to the specific nature of subcortical aphasia, with particular emphasis on thalamic aphasia. It describes the features of subcortical aphasias which make it possible to differentiate them from cortical aphasias and defines the characteristics of thalamic aphasia which are indicated by researchers seeking its constitutive features. The article also discusses the anatomic aspects of the thalamus and the latest reports on the functions it performs in the language processing process through thalamocortical networks.
Background:
The thalamus has a demonstrated role in language, particularly through its connectivity to frontal language cortices.
Case report:
A 59-year-old man with transient mixed aphasia following resection of a left-sided thalamic cavernous malformation is reported. No operative complications were encountered, and there was no surgical contact with cortical language areas. The patient recovered full language function within a week postoperatively.
Conclusions:
The role of thalamic nuclei in language processes and other reports of transient thalamic aphasia are reviewed.
The Prefrontal Cortex (PFC) is one of the principal brain regions studied in consciousness. Previous investigations suggest that the PFC is an important neural hub in both awareness and the manipulation of the content of consciousness. Despite a consensus in the scientific community regarding PFC function in cortico-cortical networks, there is still intense debate as to its role in the thalamocortical network and the formation of content of consciousness. The objective of this research is to provide a comprehensive review of the possible implications of PFC activity in awareness, with a focus on thalamic neural pathways that could explain perceptual alterations in the content of consciousness. We posit that the PFC and its connection with nonspecific thalamic nuclei could be responsible for the functional integration of sensory perception into a unique conscious content. This cortico-thalamocortical neural loop would denote a small closed-loop subnetwork within the thalamocortical system that organizes the flow of temporal and spatial information to maintain a subjective stream of consciousness. In particular, attentional top-down mechanisms between the PFC and the reticular thalamic nucleus could influence the formation of the content of consciousness through their capacity to regulate thalamic activity. Summarizing, the PFC acts as a dynamic and multifunctional neural hub that recalibrates global neural dynamics and regulates interactive brain processes associated with consciousness.
A case of severe aphasia after right hemisphere stroke, confirmed by CT, in an unambiguously dextral patient is reported. The patient showed no limb apraxia, and performed well on a test of "closure" (Mooney faces). Extensive testing revealed no signs of visuo-spatial neglect. We conclude that "pure" crossed aphasia can occur in the absence of symptoms normally associated with right hemisphere lesions.
A patient with a chronic amnesic state resulting from bilateral paramedian thalamic infarction showed a pattern of retrograde amnesia not previously reported. Personally relevant autobiographical memory was profoundly impaired, whereas knowledge of famous people and public events was relatively spared. Furthermore, knowledge of famous people, including the ability to make accurate temporal judgements, was less affected than knowledge of public events. In addition, we have documented a severe and systematic distortion of personal memory. These findings are not compatible with current accounts of retrograde amnesia based either upon the type of information stored (e.g. episodic versus semantic memory), or upon simple storage versus access models. We propose an explanation based upon an interactive cognitive model in which the patient shows a disorder at the 'thematic retrieval framework' level of memory organization due to a disconnection of frontal and medial temporal memory systems.
The authors report a patient of pure apraxic agraphia with normal praxis due to left thalamic infarction. O-15-gas-PET showed reduced oxygen metabolism in the left thalamus and the left dorsolateral premotor area, while MRI and C-11-fulumazenil-PET showed no remarkable lesions in the frontal cortex. The patient's word imaging remained normal. The authors hypothesize that thalamic destruction causes pure apraxic agraphia by exerting a remote effect on left dorsolateral premotor area and blocking somewhere between graphemic area and motor programming.
Hypersomnolent state, severe amnesia, transient coma and vertical gaze abnormalities are characteristic features of bilateral paramedian thalamic infarcts. Vergence disorders or blepharospasm has recently been reported but there is no study reporting blepharospasm together with exotropia. In this paper, we present a case with bilateral paramedian thalamic infarct who had blepharospasm and acute exotropia. A 60-year-old, right-handed, male patient who was unconscious was admitted to the hospital. His history revealed a speech disorder and a headache preceding his unconsciousness. On physical examination the pulse rate was 86/min/regular, the blood pressure 200/120 mm Hg, and respirations 14 per minute. On neurologic examination, he was stuporous and his pupils were equal and myotic. Bilateral light reaction was diminished. There was bilateral persistent tonic spasm of the eyelids and the eyes were in divergence position. Plantar reflexes were bilateral extensor. Cranial CT disclosed bilateral hypodense infarct areas in the paramedian thalamic localisation. The patient was treated with an antiaggregant, dexamethasone and antihypertensive. No change was found in blepharospasm and divergence position during therapy. The patient died on the seventh day after stroke onset. The supranuclear organisation of the vergence system is not well-known, though conjugate eye movements are mostly understood. Dysfunction of the vergence in structures contributing to neural integration may be due to disordered convergence secondary to organic conditions. Although the anatomic pathway of these signals has not yet been identified, divergence eye movements have been assumed to result from a complementary input from divergence neurons to the lateral rectus motoneurons. Divergence position in our case might be related to convergence paralysis or excessive stimulation of divergence neurons due to involvement of vergence pathways. Data from previous studies indicate that convergence paralysis might be more responsible for acute exotropia in bilateral paramedian thalamic lesions. The pathophysiological mechanism for disorders of eyelid movements is not well known. Bilateral eyelid opening in awake patients by unilateral stimulation in the prefrontal, occipital and rarely precentral cortices has been demonstrated. Reflex blepharospasm or excessive eyelid closure that is provoked by attempts to hold the eyelids open is seen with nondominant hemispheric infarction, brainstem lesions or rarely in thalamic vascular events. In conclusion, we propose that vergence and eyelid functions are already closely linked with the paramedian thalamic area and the descending cortical pathways which pass through the paramedian thalamus and exert an inhibitory input to premotor vergence neurons in the midbrain. We would like to point out the fact that although paramedian thalamic infarcts are considered not to be fatal, our patient died on the seventh day after stroke onset. This case raises the question of whether acute vergence together with eyelid function abnormalities could be a negative prognostic sign.
Ischemic thalamic lesions can be responsible for acute alteration in intellectual functioning. Based on clinical and neuropsychological observation in five patients we were able to confirm the localization of the ischemic lesion in the left or the right thalamus. Left thalamic lesions were characterised by acute general confusion, desorientation and alteration of verbal memory. In right sided thalamic lesions disturbance of visuo-spatial memory was predominant. Bilateral lesions can be responisble for an amnesic Korsakoff syndrome
A case of anterograde amnesia, due to a bilateral symmetrical lesion in the medial part of the thalamus, and discovered by computed tomography, is reported. Behavioural disorders, in the form of motor and verbal lack of spontaneity with affective indifference but without lasting disturbances of attention and reasoning abilities, were associated with the memory disorder. From the results of repeated psychometric examinations it would appear that the memory disturbance is related more to hippocampic amnesia than to thalamo-cingular amnesia. The appearance of the lesions on computed tomography, the changes noted in clinical and electroencephalographic signs, and the results of electrooculographic and somesthetic evoked potential recordings, suggested the presence of an ischemic lesion limited to the 2 thalami and affecting mainly the dorsomedial nuclei, the internal medullary nuclei, and the mamillothalamic bundles. The respective roles of these various structures in the development of memory and behavioural disorders are discussed.
A neuropsychological study was carried out in 4 cases of infarction in the territory of the anterior choroidal artery. In 3 cases the lesions were on the right side. A syndrome of the minor hemisphere was present with severe visual neglect, constructional apraxia, alexia due to disorders of visuo-spatial strategy, anosognosia and motor impersistence. In the case with a left-sided lesion there was no neglect but a mild aphasia with impaired fluency, semantic paraphasias, perseveration and a decreased psycho-linguistic ability. The mechanisms of neglect in right-sided lesions are considered.
A 43-year-old woman developed, during post-partum, an axial amnesia of ischemic origin. Stereotactic correlations were obtained by matching CT scan images with the true reference plane of the examination, according to an original method. This led to the diagnosis of infarction in the territory of a paramedian thalamomesencephalic artery. The amnesia probably resulted from bilateral lesions of Vicq d'Azyr's bundle. Atypical features in this case were the absence of disorder of vigilance and oculomotor disorders. The striking fact in this patient was recovery of some recognition capability contrasting with the persistence of a major evocation disorder.
We used positron emission tomography to study the effects of unilateral vascular thalamic lesions on cortical oxygen or glucose utilisation in 10 patients. There was a significant ipsilateral cortex hypometabolism in 9 of the 10 patients, affecting diffusely the whole cortical mantle. The only patient spared was free of neuropsychological deficit at time of PET study. In 4 patients, the magnitude of ipsilateral cortical hypometabolism was significantly less at follow-up PET study, together with improved neuropsychological function. When plotted altogether, the 14 studies showed a significant tendancy for the hypometabolism to improve with time elapsed since clinical onset. On the whole, these data suggest that the ipsilateral cortical hypometabolism reflects an essentially functional alteration and not only a degenerating process. This most likely indicates a cortical deafferentation due to loss of non-specific thalamo-cortical connections, i.e. a phenomenon akin to 'diaschisis'. However, a causal relationship between cortical hypometabolism and neuropsychological deficit cannot be firmly established from the present data.
Predominantly impairment or preservation of category-specific naming and comprehension is not rare in aphasics. Much less frequent is a selective inability to generate proper names. To our knowledge, only one such case has been reported after a left thalamic lesion, located in the ventral anterior nucleus, the mamillo-thalamic tractus and the genu of the internal capsule. We report a new case of selective inability to generate proper names after a left tubero-thalamic infarct. A 65-year old right-handed man presented with a selective impairment in producing proper names, both from photographies or descriptions and on tests of verbal fluency. The deficit was obvious both for persons names and for geographical names. The rest of the neuropsychological testing was remarkable only for a mild verbal amnesia, affecting only serial material (list of words), a reduced fluency for flowers, fruits and musical instruments, difficulties in learning of new words, and a dissociation between preserved learning for occupations and impaired learning for words on a test of learning of words and occupations (Cohen, 1990). This anomia for proper names could result from an indirect frontal-lobe dysfunction, preventing volontary activation of the phonological representation of proper names.
Twenty-five patients with nonhaemorrhagic infarcts of the thalamus were studied clinically and by neuropsychological testing, computerized tomography and somatosensory evoked response (SER) recordings. Our aim was to determine whether the findings in these different tests would form distinct symptom clusters associated with different anatomical territories of the thalamus.
Infarction conforming to the tuberothalamic arterial territory caused a facial paresis for emotional movements, severe neuropsychological deficits and a delay of the SER after P14. Infarction conforming to the interpeduncular profundus arterial territory caused a supranuclear vertical gaze paresis, severe neuropsychological deficits and a delay in the P60 component of the SER. Infarction conforming to the anterior choroidal territory caused a hemiparesis, moderate neuropsychological deficits and varied sensory evoked responses. Patients with infarctions conforming to the entire geniculothalamic territory had sensory loss in multiple modalities, minimal neuropsychological deficits and absence of sensory evoked responses after P14. A lacune in this territory caused pure hemisensory loss involving part of the body for the modalities of pain and light touch but not proprioception or vibration. Neuropsychological deficits were uncommon and N32 and N60 were delayed in the SER.
We have studied 5 patients having a language disturbance associated with a left thalamic lesion documented by computerized tomography. These patients were submitted to a french adaptation of the Boston Diagnostic Aphasia Examination, originally designed by Goodglass and Kaplan. A quantitative analysis of these language disturbances has shown that they are characterized by reduction of fluency, resembling that of dynamic aphasia, with impaired volume, tone and articulation of speech. There is also a difficulty at finding word categories. Perseverations are frequent while paraphasias are scarce, being then mostly incoherences. Comprehension is impaired, but only at a complex level. Reading and writing are inconsistantly affected. This symptom-complex is coherent enough from case to case to be considered as a recognizable type of aphasia, specially since it is invariably associated with a left thalamic lesion.
Summary We report two cases of recovery from retrograde amnesia, which occurred almost suddenly, 1 year and 1 month from onset, respectively. Amnesia followed a left thalamic infarction in one patient and a mild head trauma in the other. Full and permanent recovery occurred within a short time after the spontaneous emergence to consciousness of a single autobiographical event, triggered by the specific experience of a very similar new event. Recovery was limited to retrograde amnesia, leaving unaffected the anterograde deficit present in one of the patients. The nature (psychogenic versus organic) of our patients' memory loss is commented upon in the light of a review of previously reported cases of retrograde amnesia. The transient defect of retrograde memory is discussed in terms of a reversible distortion of the neuronal ‘patterned matrices’ suggested by Gloor (Brain 1990; 113: 1673–94).
The long-term prognosis after left tuberothalamic infarction was studied in a selected group of 7 patients who had memory disturbances sufficiently severe to warrant neuropsychological consultation and rehabilitation. The mean age of the patients was 46.7 ± 5.6 years and the mean follow-up time 22.3 ± 15.0 months. At the acute stage 4 patients had dysphasia, 1 hemiparesis, and 1 vertical gaze paresis. These improved well. All 7 had memory disturbances, which remained the dominant disability. Four patients had severe behavioral symptoms (psychosis, depression, anxiety) at the acute stage. The most common residual behavioral symptoms were inactivity and depression. At the end of rehabilitation (mean 15.4 months) clear residual disturbances in verbal memory and learning were still observed. These prevented return to work in all but 1 case. No case of true dementia was found.
OBJECTIVE—White matter lesions are often seen on MR scans of elderly non-demented and demented people. They are attributed to degenerative changes of small vessels and are implicated in the pathogenesis of cognitive decline and dementia. There is evidence that especially periventricular white matter lesions are related to cognitive decline, whereas subcortical white matter lesions may be related to late onset depression. The frequency distribution of subcortical and periventricular white matter lesions according to age and sex reported.
METHODS—A total of 1077 subjects aged between 60-90 years were randomly sampled from the general population. All subjects underwent 1.5T MR scanning; white matter lesions were rated separately for the subcortical region and the periventricular region.
RESULTS—Of all subjects 8% were completely free of subcortical white matter lesions, 20% had no periventricular white matter lesions, and 5% had no white matter lesions in either of these locations. The proportion with white matter lesions increased with age, similarly for men and women. Women tended to have more subcortical white matter lesions than men (total volume 1.45 ml v 1.29 ml; p=0.33), mainly caused by marked differences in the frontal white matter lesion volume (0.89 ml v 0.70 ml; p=0.08). Periventricular white matter lesions were also more frequent among women than men (mean grade 2.5 v 2.3; p=0.07). Also severe degrees of subcortical white matter lesions were more common in women than in men (OR 1.1; 95% confidence interval (95% CI) 0.8-1.5) and periventricular white matter lesions (OR 1.2; 95% CI 0.9-1.7), albeit that none of these findings were statistically significant.
CONCLUSIONS—The prevalence and the degree of cerebral white matter lesions increased with age. Women tended to have a higher degree of white matter lesions than men. This may underlie the finding of a higher incidence of dementia in women than in men, particularly at later age.
Sixteen cases of the anterior choroidal artery syndrome are reported. In its completed form, this rare syndrome combines the triad of hemiplegia, hemianaesthesia, and homonymous hemianopia CT examination confirms the diagnosis by revealing an area of reduced density situated in the posterior limb of the internal capsule, sparing the thalamus medially and encroaching upon the tip of the globus pallidus laterally, and corresponding to the distribution of the anterior choroidal artery. Incomplete forms of the syndrome are more frequent. Left-sided spatial neglect may accompany right-sided lesions, as may slight disorders of speech in left-sided lesions. Clinical-anatomical correlations are discussed.
Objective.
—To report the distribution of Mini-Mental State Examination (MMSE) scores by age and educational level.Design.
—National Institute of Mental Health Epidemiologic Catchment Area Program surveys conducted between 1980 and 1984.Setting.
—Community populations in New Haven, Conn; Baltimore, Md; St Louis, Mo; Durham, NC; and Los Angeles, Calif.Participants.
—A total of 18 056 adult participants selected by probability sampling within census tracts and households.Main Outcome Measures.
—Summary scores for the MMSE are given in the form of mean, median, and percentile distributions specific for age and educational level.Results.
—The MMSE scores were related to both age and educational level. There was an inverse relationship between MMSE scores and age, ranging from a median of 29 for those 18 to 24 years of age, to 25 for individuals 80 years of age and older. The median MMSE score was 29 for individuals with at least 9 years of schooling, 26 for those with 5 to 8 years of schooling, and 22 for those with 0 to 4 years of schooling.Conclusions.
—Cognitive performance as measured by the MMSE varies within the population by age and education. The cause of this variation has yet to be determined. Mini-Mental State Examination scores should be used to identify current cognitive difficulties and not to make formal diagnoses. The results presented should prove to be useful to clinicians who wish to compare an individual patient's MMSE scores with a population reference group and to researchers making plans for new studies in which cognitive status is a variable of interest.(JAMA. 1993;269:2386-2391)
Le syndrome amnésique est analysé dans 6 infarctus restreints de la région thalamique. Les lésions bilatérales s'accompagnaient des déficits les plus francs; l'oubli à mesure n'était net qu'à la phase initiale et touchait la mémoire verbale et la mémoire visuelle. Dans les lésions unilatérales, les déficits étaient beaucoup plus discrets et il n'y avait pas d'argument suffisant pour démontrer une spécialisation hémisphérique stricte, gauche pour la mémoire verbale, droite pour la mémoire visuo-spatiale. Ces cas et les autres de la littérature évoquaient que l'amnésie est plus importante et plus pure dans les infarctus touchant la partie antérieure du thalamus.
The hypothesis is advanced that cerebral dominance includes two elements, interhemispheric specification for language (lateralization) and intrahemispheric language specification (localization). Consequently, each type of aphasia is determined by the degree of dominance establishment (i.e., lateralization and localization) existing at the moment of brain damage. Evidence for this concept is presented through a comparison of aphasia in left handers and 'anomalous' dextrals with aphasia in childhood.
In this volume the authors combine two clinically-oriented approaches to language disorder. The clinical aspects of aphasia syndromes are stressed but the authors also review assessment techniques, linguistic analyses, problems of aphasia classification, and frequently occuring related disorders such as alexia, agraphia and acalculia. In addition, commonly encountered speech disorders, neurobehavioral and psychiatric problems commonly associated with apasia, and the language characteristics of aging and dementia reviewed. A neural basis is proposed for aphasia and related problems. Finally, aspects of rehabilitation and recovery are presented.
Crossed aphasia is caused by a right-hemisphere lesion in a right-handed person. Although this unusual language lateralisation pattern is a defining characteristic, there is disagreement among authors on additional diagnostic criteria. In addition, there is a significant amount of variability between patients as to the associated symptomatology, such as the presence of apraxic or visuospatial signs. Because of the rarity of crossed aphasia, the understanding of this clinical entity depends entirely on the analysis of published case studies. This paper presents two new cases of crossed aphasia, and discusses the major issues related to crossed aphasia diagnosis and symptomatology. Procedures for the assessment of crossed aphasia patients are also suggested.
In this paper, we describe the case of a right-handed man, MR, who after right thalamic haemorrhage presented subtranscortical aphasia. Of the disturbances generally associated with standard left hemisphere functions, the patient presented acalculia but not apraxia. Among the functions attributed to the standard right hemisphere, MR showed impairment in affective language and presented unilateral neglect and a strong position preference.
In this paper we have reviewed the cases of vascular crossed aphasia reported in the literature, in order to check whether deep lesions are really overrepresented in crossed aphasia with respect to standard aphasia. The comparison with a large sample of standard left-hemisphere-damaged aphasics revealed a significantly higher incidence of purely deep lesions in crossed aphasics than in standard aphasics. The overrepresentation of deep lesions in crossed aphasia appears to be contingent on the co-occurrence of aphasia and Unilateral Neglect after right-hemisphere lesion. This suggests an interaction between language and attentional mechanisms in the case of reversed language lateralisation: the overcrowding of these functions in the right hemisphere could make language more vulnerable after right deep lesions.
A case of expressive aphasia resulting from right middle cerebral artery occlusion in a fully right-handed woman without sinistral antecedents is reported. The significance of the findings in relation to cerebral dominance is discussed.RésuméPrésentation d'un cas d'aphasie expressive due à une thrombose de l'artère cérébrale moyenne droite chez une femme totalement droitière et sans antécédent de gaucherie. La signification des constatations est discutée par rapport á la dominance cérébrale.ZusammenfassungMitteilung eines Falles von motorischer Aphasie infolge Schädigung der rechten Hirnhemisphäre durch Mediaverschluss. Es handelte sich bei der Patientin um eine ausgesprochene Rechtshänderin, bei welcher sich auch anamnestisch keinerlei Hinweise für partielle Linkshändigkeit ergaben. Die klinischen Befunde werden in ihrer Bedeutung für das Problem der Hemisphärendominanz diskutiert.
We report a case of persistent anterograde amnesia secondary to an anterior thalamic infarct. A 49-year-old right-handed man is referred for acute anterograde amnesia. Diffusion-weighted imaging performed at 24 hours shows an acute punctiform infarct of the left anterior thalamus, while T2-weighted imaging reveals a contralateral and symmetrical ischemic sequelae in the right anterior thalamus. The two lesions are isolated and remarkably centered with the mamillothalamic tract. We suggest the symptoms are caused by the addition of the two lesions interrupting the mamillothalamic tracts. This is the second clinico-pathological observation of a persistent amnestic syndrome secondary to a bilateral lesion of the mamillothalamic tract.
Ce cas décrit l’évolution vers un trouble psychotique déficitaire d’un patient de 38 ans, sans antécédents psychiatriques, après une ischémie cérébrale au niveau mésencéphalo-thalamique bilatéralement, à prédominance gauche. Les symptômes psychotiques positifs initiaux (délire, hallucinations acoustico-verbales) ont laissé progressivement la place à des symptômes négatifs, qui sont devenus prédominants après quelques mois. Le diagnostic retenu après un suivi psychiatrique de 14 mois a été : trouble psychotique avec idées délirantes, dû à une ischémie cérébrale (DSM IV). L’intérêt du développement d’une échelle spécifique pour des troubles psychotiques survenus après une ischémie cérébrale est suscité à partir des descriptions cliniques isolées, d’autant plus qu’une échelle spécifique pour des troubles dépressifs post-ischémiques a déjà été développée. La nécessité d’un examen psychiatrique et des réévaluations systématiques dans le décours des ischémies cérébrales thalamiques nous semble importante à retenir, tant au niveau du diagnostic différentiel qu’au niveau d’une prise en charge psychiatrique précoce, plus efficace.
Humans can generate and maintain relatively coherent trains of thought in natural discourse. The neural mediation of this ability and the phenomenology of its breakdown are not well understood. We report a case of a woman with paramedian thalamic strokes involving the mammillothalamic tract, intralaminar nuclei, parts of the dorsomedial and ventral lateral nuclei bilaterally. She presented with a dense amnesia and confusion typical of the syndrome of bilateral paramedian thalamic infarcts. Her Tc-99m HMPAO brain SPECT scan showed decreased thalamic and basal ganglia blood flow. General diminution of cerebral blood flow and areas of further diminution in the right frontal, left temporal and left temporoparietal regions were also observed. Although her amnesia was characteristic of diencephalic amnesia, her most striking clinical feature was a bizarre, disconnected and at times incoherent speech output. Analysis of her speech revealed relatively preserved lexical and morpho-syntactic linguistic production. By contrast, analysis of the macrostructure of her discourse revealed frequent unpredictable topic shifts that were completely unconstrained by contextual factors. Many of her shifts were intrusions from previous topics. We interpret her severely disordered speech output as representing the surface manifestations of a thought disorder (rather than as a language disorder per se) characterized by an inability to maintain and appropriately shift themes that normally guide discourse. Median and intralaminar thalamic nuclei appear to be critical for the neurophysiologic regulation of thalamocortical and striatocortical circuits, which in turn may be critical for the functional regulation of contextually appropriate transitions of thought.
