Neurology India
menu-bar5 Open access journal indexed with Index Medicus
  Users online: 863  
 Home | Login 
About Editorial board Articlesmenu-bullet NSI Publicationsmenu-bullet Search Instructions Online Submission Subscribe Videos Etcetera Contact
  Navigate Here 
 Resource Links
  »  Similar in PUBMED
 »  Search Pubmed for
 »  Search in Google Scholar for
 »Related articles
  »  Article in PDF (905 KB)
  »  Citation Manager
  »  Access Statistics
  »  Reader Comments
  »  Email Alert *
  »  Add to My List *
* Registration required (free)  

  In this Article
 »  Abstract
 » Conclusions
 »  References
 »  Article Figures

 Article Access Statistics
    PDF Downloaded66    
    Comments [Add]    

Recommend this journal


Table of Contents    
Year : 2018  |  Volume : 66  |  Issue : 3  |  Page : 772-778

Thalamus and Language: What do we know from vascular and degenerative pathologies

1 Neurological Clinic, Department of Internal Medicine and Neurology, University of Trieste, Cattinara Hospital, Trieste, Italy
2 Italian Liver Foundation, Centro Studi Fegato, Science Park, Trieste, Italy

Date of Web Publication15-May-2018

Correspondence Address:
Dr. Rita Moretti
Neurological Clinic, Department of Internal Medicine and Neurology, University of Trieste, Cattinara Hospital, Strada di Fiume, 447, 34149, Trieste
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.232283

Rights and Permissions

 » Abstract 

Language is a complex cognitive task that is essential in our daily life. For decades, researchers have tried to understand the different role of cortical and subcortical areas in cerebral language representations and language processing. Language-related cortical zones are richly interconnected with other cortical regions (particularly via myelinated fibre tracts), but they also participate in subcortical feedback loops within the basal ganglia (caudate nucleus and putamen) and thalamus. The most relevant thalamic functions are the control and adaptation of cortico-cortical connectivity and bandwidth for information exchange. Despite having the knowledge of thalamic and basal ganglionic involvement in linguistic operations, the specific functions of these subcortical structures remain rather controversial. The aim of this study is to better understand the role of thalamus in language network, exploring the functional configuration of basal network components. The language specificity of subcortical supporting activity and the associated clinical features in thalamic involvement are also highlighted.

Keywords: Basal ganglia, behavioral dysfunction, cortex, language network, speech disorders, thalamus
Key Message:
Language is altered due to different lesions of the anterior and paramedian thalamic nuclei. These alterations are influenced by important thalamo-cortical information exchanges; the adaptive modalities of control of the ongoing cognitive and motor process; and, the focal and remote feedforward and backward connections from the thalamus to the cortical regions.

How to cite this article:
Moretti R, Caruso P, Crisman E, Gazzin S. Thalamus and Language: What do we know from vascular and degenerative pathologies. Neurol India 2018;66:772-8

How to cite this URL:
Moretti R, Caruso P, Crisman E, Gazzin S. Thalamus and Language: What do we know from vascular and degenerative pathologies. Neurol India [serial online] 2018 [cited 2021 Sep 17];66:772-8. Available from:

It is widely believed that neuropsychological functions are not simply localized in specific cortical areas but are rather subserved by a mosaic of neuronal structures,[1],[2],[3],[4] richly interconnected with other cortical regions, but participating in subcortical feedback loops within the basal ganglia [BG] (caudate nucleus and putamen) and the thalamus.[5],[6],[7],[8],[9],[10] Recently, an in-vivo tractography study demonstrated wide connections between the Broca's area and subcortical nuclei in human volunteers. In particular, two functionally distinct regions within the Broca's area, the anterior portion implicated in semantic processing and the posterior portion involved in phonology and syntax, have been shown to project to the anterior putamen.[11],[12]

Previous studies described the role of BG as strongly influencing the increase of the signal-to-noise ratio during language processing.[13],[14] This might be a type of enhancing signal for selected items and of suppression for the competing ones.[15],[16]

Cortico-thalamo-cortical circuitry has been extensively demonstrated.[17],[18],[19],[20],[21],[22] The most significant is the intimate relationship between the BG and the thalamus, in five parallel cortical-thalamic loops, namely, two motor loops (skeletomotor and occulomotor) and three non-motor loops. The non-motor loops include a dorsolateral prefrontal-cortex loop (DLPFC including the BG, thalamus and area 9–10), a lateral orbitofrontal loop (LPFC), and an anterior cingulate loop. The DLPFC loop is involved in executive functions, planning, and working memory. The LPFC mediates empathetic and socially appropriate responses. The anterior cingulate loop is involved in communicating reinforcement signals from the ventral tegmental area (VT) and the substantia nigra pars compacta, reinforcing voluntary engagement and volition.

Thalamic relay nuclei are now known to play an important role in changing the dynamics of cortical processing by setting up different oscillation patterns of frequency and synchrony.[23],[24],[25],[26],[27],[28],[29],[30],[31],[32] The “Selective Engagement Model”[33] supports the hypothesis that thalamic nuclei monitor the activity state of distributed cortical areas and control their functional connectivity via connections passing through the inferior thalamic peduncle. In the case of linguistic information, this primarily refers to frontal and temporoparietal cortices between which, for example, phonemic, lexical, and semantic information is exchanged during language perception and production. Corticothalamic language processing is complemented by the BG. However, because there is also a nonreciprocal corticothalamic input to each of these thalamic nuclei, the incoming basal ganglionic information from each circuit is mixed with cortical inputs from a different circuit. The information that the thalamic relay nuclei convey to the cortex is, therefore, not only affected by the parallel pathway through the BG structures but is also modified by the nonreciprocal corticothalamic pathway, resulting in an integrated feed-forward processing similar to that seen in sensory systems.[34]

In the specific context of language processing, the “Response–Release Semantic Feedback Model” claims thalamic and BG functions in language production,[35],[36] controlling the interaction between fronto-opercular and temporocortical cortices for the integration of lexico-syntactic with semantic information. BG are thought to coordinate the release of the provided language plan into speech.

Klostermann [33] referred to thalamus as entering in the “Declarative/Procedural Model,” similar to mnemonic operations,[37],[38] and stated that BG provides the requirements to apply grammatical rules to linguistic raw data, the so-called “world knowledge” into lexical input signals.[33],[39]

Borrowed from the classical model of cortico-striato-thalamo-cortical motor processing,[8],[9] the “Lexical Selection Model” views the BG as a machinery to align word-related input to ongoing language plans. This is mainly conceived as a process in which an excess supply of lexical alternatives need to be monitored for unsuited candidate words to be inhibited from further processing. Only the remaining information will be signaled to the thalamus which then initiates frontocortical word release.[40]

What do we know from clinical cases?

Thalamic aphasia should be considered as 'Nessie', the Loch-Ness creature – nobody has seen her, but nobody can deny its existence.

Many different authors described thalamic aphasia as a consequence of thalamus involvement;[41],[42],[43],[44] however, it is not easy at all to relate a defined language disorder, devotedly related to a specific thalamic region of interest. Deficits have often been described in thalamic infarction; however, owing to a relatively complex and sometimes variant vascular supply,[45],[46],[47],[48],[49],[50] aphasic syndromes have been observed with different locations of damage; mostly, they do not occur in isolation but go along with other neuropsychological deficits, and are often accompanied by further extrathalamic lesions. Hence, the allocation of specific symptoms to particular nuclei is genuinely more difficult at this level than it is for cortical regions with their relatively precise functional description [Figure 1].[51]
Figure 1: Functional diagram for the reappraisal of basal ganglia and thalamus in language; ARAS: Ascending reticular activating system

Click here to view

The arterial supply of the thalamus and midbrain consists of a complex arterial network involving the anterior and posterior cerebral circulation. The anterior and inferior midbrain and thalami are supplied mostly by the internal carotid artery, whereas the medial, lateral, and posterior territories are irrigated by the vertebrobasilar system. Four territories for thalamic vascularization have been identified [Figure 2]:
Figure 2: A schematic supply of the vascular system of thalamus. 1. Internal carotid artery. 2. Basilar artery. 3. Communicating artery P1. 4. Posterior cerebral artery P2. 5. Posterior communicating artery. 6. Tuberothalamic artery. 7. Paramedian pedicle. 8. Inferolateral pedicle. 9. Posterior choroidal artery. VA = Ventralis anterior. VL = Ventralis lateralis. DM = Dorsomedialis. VP = Ventralis posterior. P = Pulvinar. LGB = Lateral geniculate body

Click here to view

  1. Anterior, tuberothalamic, or polar territory (dorsomedian nucleus is usually spared): This territory, supplied by the tuberothalamic artery, accounts for approximately 12–18% of all thalamic infarcts.[52],[53],[54],[55],[56],[57] The most frequent etiology is cardioembolism
  2. Paramedian territory supplied by the paramedian arteries accounts for approximately 22–35% of all thalamic infarcts.[57] The most frequent etiology is cardioembolism [48]
  3. Inferolateral or thalamogeniculate territory. This territory, supplied by the thalamogeniculate arteries, accounts for approximately 45–50% of all thalamic infarcts. The most frequent etiology is microangiopathy
  4. Posterior choroidal territory (pulvinar nucleus): This territory, supplied by the medial and lateral branches of the posterior choroidal arteries, accounts for approximately 7–9% of all thalamic infarcts. The most frequent etiology is microangiopathy.

Bogousslavsky and Carrera,[47],[48],[49] therefore, divided the retrospective case studies of Lausanne into four patterns of clinical presentation – the anterior, paramedian, inferolateral, and posterior syndromes. Clinical practice, however, can often result in mixed-cases, probably due to the occurrence of border zone infarcts or due to variations in the “classical” distribution of the thalamic arteries.[58],[59]

What is astonishing regarding the definition proposed by Bogousslavsky and Carrera [47],[48],[49] is that it relies not only on the vascular supply but also on the regional interconnection: anterior nuclei are the relay centers of the mamillothalamic tract (MTT) in the thalamus. They are reciprocally connected to the anterior limbic system, cingulate gyrus, hippocampus, parahippocampal formation, entorhinal cortex, retrosplenium, and orbitofrontal cortices.[60] Other connections to the medial prefrontal cortices, posterior area of the neocortex, and ventral pallidum have been described.[45],[46]

To be precise, language is involved in all the thalamic lesions, more precisely in those occurring in the anterior and paramedian regions. On the contrary, the inferolateral or thalamogeniculate and the posterior infarcts result in more complex neuropsychological (but not language or speech) alterations.

Therefore, infarcts in the anterior territory frequently lead to a perseverative pattern of speech with inappropriate maintenance of the category in all memory and executive tasks, with increased sensitivity to interferences.[48] Many patients show a superimposition and “telescoping” of unrelated information with parallel expression of mental activities called palipsychism from Greek palin (again) and psychê (soul).[61] The output speech after an anterior territory infarct is characterized by grammatically correct phrases, but unpredictable topic shifts, which are usually intrusions on previous topics (introduced by the patient or the examiner); correct phrases are often strung together in a nonsensical or illogical fashion and punctuated by paraphasias or neologism.[62],[63] Perseverations were also found [Figure 3].
Figure 3: A schematic presentation of thalamic nuclei by functional grouping. (a) Anterior nulcei of the thalamus, (b) Paramedian thalamic nuclei, (c) Posterior nuclei of thalamus

Click here to view

Some patients show a spectacular pattern of speech with “impersistance de la pensée,” which may be reminiscent of the “psychotic” speech found in schizophrenics. These speech disturbances are mainly found in the unconstrained speech with relative maintenance of the performance of an automatic series or in reciting poems known by heart.

Single-photon emission computed tomography (SPECT) images show a diffuse hypoperfusion of the left hemisphere, especially prominent in the medial and lateral frontal lobes. Bogousslavsky and Carrera [48],[49] have inferred that these behavioral changes with perseverations and frequent topic shifts in output speech result from a disconnection of the ipsilateral cortex, mainly the medial and lateral frontal regions, which seems to be coincident with what we have previously described.[64],[65],[66],[67],[68],[69],[70]

Aphasia was never found to be the main neuropsychological dysfunction after anterior nuclei infarction, and, when present, it is usually consistent with a moderate form of transcortical motor aphasia associated with hypophonia and dysarthria.[61] Aphasia usually occurs with left or bilateral infarcts, although Bogousslavsky et al.,[53] found four patients (two left-handed and two right-handed) with an infarct limited to the right anterior territory, and whose principal clinical manifestation was transcortical motor aphasia. Spontaneous speech is usually reduced, with a lack of speech initiation and the usage of short sentences. Occasional phonemic paraphasias are found (”anassin”/”assassin”) as well as semantic paraphasias (”clock”/”watch”) or neologisms. Repetition and comprehension are rarely impaired. Phonemic paralexias as well as calculation and writing impairment are rarely found.[71]

Numerous intrusions, perseverations, and false recognition are frequently found. Intrusions during the recall of a word list (provoked confabulations) are more frequent than during spontaneous speech (spontaneous confabulations).[48],[49],[61],[72],[73],[74]

Paramedian nuclei infarcts produced (in physically and emotionally active patients before the occurrence of stroke) a severe apathy; the patients become indifferent as if they have lost motor and affect drive, especially after bilateral lesions,[75] needing constant external programming, which makes them look like robots. The term, “loss of psychic self-activation,” has been proposed to describe this peculiar behavioural pattern.[76],[77]

Akinetic mutism is considered when the patients, who appear to be awake and follow the examiner's eyes, fail to respond or become active after a relevant stimuli has been given. The location of the thalamic lesion is quite similar in patients who present with a loss of self-activation and in those with akinetic mutism. However, the involvement of intralaminar nuclei, especially the centromedian and parafascicular nuclei, may be more extensive in patients presenting with akinetic mutism than in those with “psychic loss of self-activation.”[78]

To make things even much more complicated in clinical practice, another variant requires a merger with these thalamic disorders of speech: the Percheron' artery supply, an anatomical variant of the paramedian artery supply,[79],[80],[81] that does not have a bilateral supply but is derived from a single thalamic perforating artery, arises from the proximal posterior cerebral artery (PCA), between the basilar artery and the posterior communicating artery. It supplies the rostral mesencephalon and both paramedian thalami. If there is an occlusion of the Percheron's artery, bilateral paramedian thalamic infarction occurs, and the consequences, as mentioned above, are dramatic.[82],[83]

Inferolateral or thalamogeniculate territories damage, involving the major part of the ventral posterior nuclei as well as the ventral and lateral parts of the ventrolateral nucleus more rostrally, are the most common (45%) disorders, and lead to the thalamic pain syndrome, as described by Dejerine and Roussy, or a contralateral ataxia and hypesthesia [Figure 2].[84],[85]

The posterior choroidal arteries (arising from the posterior cerebral artery) supply the subthalamic nucleus and midbrain, the medial half of the medial geniculate nucleus, the posterior parts of the intralaminar nuclei and pulvinar nuclei, and usually produce neglect, apathy, and impaired comprehension.[79],[86],[87],[88]

Thalamic nuclei and the supplementary motor region (SMR)[89],[90] have been proposed to form the fifth functional area, a functional unit in language processing. The impairment of these interconnecitons often leads to a transcortical sensory aphasia. Further, it should be mentioned that in cases with extended lesions confined to the thalamus, permanent global aphasia has been observed [Figure 3].[91],[92]

Apart from the work on language reported on patients who have developed ischemia in various parts of the brain, more recent data has been derived from in-vivo imaging studies on normal subjects and in subjects with other neurological disorders. A left thalamic activation has been found during the differentiation of distinct speech sounds, alongside with activity in the planum temporale, the superior temporal and Heschl's gyri of the dominant hemisphere.[93]

Moreover, the medial geniculate body (thalamic auditory nucleus) has been shown to be active during the recognition of speech sounds. A cortical feedback loop has been found to be involved, which was found impaired in dyslexic persons.[94],[95] Further, thalamus, specifically in the dorsomedial and pulvinar regions, as well as with frontotemporal involvement, has been seen to be activated during lexico-semantic operations and object recall.[96],[97],[98],[99]

Moreover, a chronometrical sequence of activations has been established during the performance of respective tasks. The dorsomedial thalamus and presupplementary motor areas are engaged in the concept formation of perceived vocal signals, whereas the subsequent pulvinar activity reflects the downstream processes for the semantic alignment of this activity with the ongoing input.[100],[101],[102]

Moreover, Anastasia et al., described two functionally distinct regions within the previously imagined unique area, the Broca's area, whose anterior portion was activated during the semantic processing, and the posterior portion could be activated during the phonology and syntax processing; both these areas project to the anterior putamen and are involved in language processing.[18],[103] In addition to studies on the Broca's area, new information has been reported by Ardila et al., with regard to the peripheral zone around the Wernicke's area involved in language associations, particularly the areas BA20, BA37, BA38, BA39, and BA40. These are considered as a part of the “extended Wernicke's area” that projects diffusely to the thalamic nuclei, in particular in the putamen.[104],[105],[106]

 » Conclusions Top

The control and adaptation of cortico-cortical connectivity and providing the bandwidth for information exchange have been shown to be the most relevant thalamic functions. Three properties of thalamocortical neurons are known:[33] first, the presence of local, and remote feed-forward and feedback connections with almost every cortical region are prerequisites for establishing flexible network constellations; second, the ability to convey information in distinct discharge modes is essential for regulating the likelihood with which messages are passed from one cortical region to another; third, a sequential circuitry of thalamocortical information allows the adaptation of the final messages in an iterative process involving various downstream relay nuclei.

Thalamic neurons notify that a specific area has become active so that a functionally related regions can be engaged. In turn, thalamic neurons will receive the output message from the activated downstream cortex. How this iterative process should be adapted to the ongoing demands, particularly in the context of rapidly changing cognitive operations, as required for language processing, is the subject of further research.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

 » References Top

Damasio AR. Descartes' error: Emotion, reason and the human brain. New York: Putnam; 1994.  Back to cited text no. 1
Damasio AR, Damasio H, Rizzo M, Varney N, Gersh F. Aphasia with nonhemorrhagic lesions in the basal ganglia and internal capsule. Arch Neurol 1982;39:15-24.  Back to cited text no. 2
McCarthy RA, Warrington EK. Cognitive neuropsychology: A clinical introduction. Orlando, FL: Academic Press; 1990.  Back to cited text no. 3
Shallice T. From neuropsychology to mental structure. Cambridge, UK: Cambridge University Press; 1988.  Back to cited text no. 4
Goldman-Rakic PS, Selemon LD. New frontiers in basal ganglia research. TINS 1990;13:266-71.  Back to cited text no. 5
Goldman-Rakic PS. Cellular and circuit basis of working memory in prefrontal cortex of nonhuman primates. Prog Brain Res 1990;85:325-36.  Back to cited text no. 6
Signoret JL, Castaigne P, Lhermitte F. Rediscovery of Leborgne's brain: Anatomical description with CT scan. Brain Lang 1984;22:303-19.  Back to cited text no. 7
Alexander M, Naeser P, Palumbo C. Correlations of subcortical CT lesion sites and aphasia profiles. Brain 1987;110:961-91.  Back to cited text no. 8
Alexander M. Clinical-anatomical correlations of aphasia following predominantely subcortical lesions. In: Boller F, Grafman J, editors. Handbook of Neuropsychology. Vol. 2. Amsterdam: Elsevier; 1989. Pp. 47-66.  Back to cited text no. 9
Alexander GA. Basal ganglia thalamocortical circuits: Their role in control of movement. J Clin Neurophysiol 1994;11:420-31.  Back to cited text no. 10
Rolls E, Johnstone S. Neuropsychological analysis of striatal function. In: Vallar G, Cappa SF, Wallesch CW, editors. Neuropsychological disorders associated with subcortical lesions. Oxford: Oxford Associated Press; 1992.  Back to cited text no. 11
Saint-Cyr JA, Taylor AE, Trepanier LL, Lang AE. The caudate nucleus: Head ganglion of the habit system. In: Vallar G, Cappa SF, Wallesch CW, editors. Neuropsychological disorders associated with subcortical lesions. Oxford: Oxford Associated Press; 1992.  Back to cited text no. 12
Mink JW. The basal ganglia: Focused selection and inhibition of competing motor programs. Prog Neurobiol 1996;50:381-425.  Back to cited text no. 13
Nambu A, Tokuno H, Hamada I, Kita H, Imanishi M, Akazawa T, et al. Excitatory cortical inputs to pallidal neurons via the subthalamic nucleus in the monkey. J Neurophysiol 2000;84:289-300.  Back to cited text no. 14
Crosson B, Benefield H, Cato MA, Sadek JR, Moore AB, Wierenga CE, et al. Left and right basal ganglia and frontal activity during language generation: Contributions to lexical, semantic, and phonological processes. J Intern Neuropsych Soc 2003;9:1061-77.  Back to cited text no. 15
Crosson B. Subcortical functions in language and memory. New York: Guilford; 1992.  Back to cited text no. 16
Werring DJ, Toosy AT, Clark CA, Parker GJ, Barker GJ, Miller DH, et al. Diffusion tensor imaging can detect and quantify corticospinal tract degeneration after stroke. J Neurol Neurosurg Psychiatry 2000;69:269-72.  Back to cited text no. 17
Theyel BB, Lee CC, Sherman SM. Specific and nonspecific thalamocortical connectivity in the auditory and somatosensory thalamocortical slices. Neuroreport 2010;21:861-4.  Back to cited text no. 18
Rowan A, Vargha-Khadem F, Calamante F, Tournier JD, Kirkham FJ, Chong WK, et al. Cortical abnormalities and language function in young patients with basal ganglia stroke. NeuroImage 2007;36:431-40.  Back to cited text no. 19
Guillery RW. Anatomical evidence concerning the role of the thalamus in corticocortical communication: A brief review. J Anat 1995;187:583-92.  Back to cited text no. 20
Sherman SM, Guillery RW. The role of the thalamus in the flow of information to the cortex. Philos Trans R Soc Lond B Biol Sci 2002;357:1695-708.  Back to cited text no. 21
Sherman SM, Guil1ery RW. Functional organization of thalamocortical relays. J Neurophysiol 1996;76:1367-95.  Back to cited text no. 22
Haber SN. The primate basal ganglia: Parallel and integrative networks. J Chem Neuroanat 2003;26:317-30.  Back to cited text no. 23
Haber SN, Goenewegen HJ, Grove EA, Nauta WJ. Efferent connections of the ventral pallidum in the rat: Evidence of a dual striato-pallidofugal pathways. J Comp Neurol 1985;238:322-35.  Back to cited text no. 24
Haber SN. Integrating cognition and motivation into the basal ganglia pathways of action. In: Bedard MA, et al. Editors. Mental and behavioural dysfunction in movement disorders. Totowa NJ: Human Press Inc.; 2003. pp. 35-50.  Back to cited text no. 25
Jones EG. The thalamus of primates. In: Bloom FE, Bjorklund A, Hokfelt T, editors. The Primate Nervous System, Part II. VoI. 14. Amsterdam: Elsevier Science; 1998. pp. 1-298.  Back to cited text no. 26
Jones EG. Correlation and revised nomenclature of ventral nuclei in the thalamus of human and monkey. Stereotact Funct Neurosurg 1990;54/55:1-20.  Back to cited text no. 27
Destexhe A, Contreras D, Steriade M. Mechanisms underlying the synchronizing action of corticothalamic feedback through inhibition of thalamic relay cells. J Neurophysiol 1998;999-1016.  Back to cited text no. 28
Steriade M. Coherent oscillations and short-term plasticity in corticothalamic networks. Trends Neurosci 1999;22:337-45.  Back to cited text no. 29
Destexhe A, Contreras D, Steriade M. Mechanisms underlying the synchronizing action of corticothalamic feedback through inhibition of thalamic relay cells. J Neurophysiol 1998;79:999-1016.  Back to cited text no. 30
Destexhe A, Contreras D, Steriade M. CorticalIy-induced coherence of a thalamic-generated oscillation. Neuroscience 1999;92:427-43.  Back to cited text no. 31
Bal T, Debay D, Destexhe A. Cortical feedback controls the frequency and synchrony of oscillation in the visual thalamus. J Neurosci 2000;20:7478-88.  Back to cited text no. 32
Klostermann F, Krugel LK, Ehlen F. Functional roles of the thalamus for language capacities. Front Syst Neurosci 2013;7:32.  Back to cited text no. 33
McFarland NR, Haber SN. Thalamic relay nuclei of the basal ganglia form both reciprocal and nonreciprocal cortical connections linking multiple frontal cortical areas. J Neurosci 2002;22:8117-32.  Back to cited text no. 34
Murdoch BE. Subcortical brain mechanisms in speech and language. Folia Phoniatr Logop 2001;53:233-51.  Back to cited text no. 35
Murdoch BE, Whelan BM. Speech and language disorders associated with subcortical pathology. Chichester: Wiley-Blackwell; 2009.  Back to cited text no. 36
Mishkin M, Suzuki WA, Gadian DG, Vargha-Khadem F. Hierarchical organization of cognitive memory. Philos Trans R Soc Lond B Biol Sci 1997;352:1461-7.  Back to cited text no. 37
Eichenbaum H. Remembering: functional organization of the declarative memory system. Curr Biol 2006;16:R643-5.  Back to cited text no. 38
Ullman MT. Contributions of memory circuits to language: The declarative/procedural model. Cognition 2004;92:231-70.  Back to cited text no. 39
Norris D, McQueen JM. Shortlist B: A Bayesian model of continuous speech recognition. Psychol Rev 2008;115:357-95.  Back to cited text no. 40
Sherman SM, Guillery RW. Distinct functions for direct and transthalamic corticocortical connections. J Neurophysiol 2011;106:1068-77.  Back to cited text no. 41
Lam YW, Sherman SM. Functional organization of the somatosensory cortical layer 6 feedback to the thalamus. Cereb Cortex 2010;20:13-24.  Back to cited text no. 42
Nadeau SE, Crosson B. Subcortical aphasia. Brain Lang 1997;58:355-402.  Back to cited text no. 43
Assaf M, Calhoun VD, Kuzu CH, Kraut MA, Rivkin PR, Hart J Jr, et al. Neural correlates of the object recall process in semantic memory. Psychiatry Res 2006;147:115-26.  Back to cited text no. 44
Schmahmann JD, Pandya DN. Anatomical investigation of thalamic projections to the posterior parietal cortices in rhesus monkey. J Comp Neurol 1990;295:299-326.  Back to cited text no. 45
Schmahmann JD, Pandya DN. Cerebral white matter fiber pathways. Am Acad Neurol 2005;114-130.  Back to cited text no. 46
Carrera E, Michel P, Bogousslavsky J. Anteromedian, central and posterolateral territory infarcts. Three variant types. Stroke 2004;35:2826-34.  Back to cited text no. 47
Bogousslavsky J, Carrera E. Structure function correlations in behavioural neurology. The thalamus. American Academy of Neurology, 2005, Minneapolis; pdf. 1-16.  Back to cited text no. 48
Bogousslavsky J, Carrera E. Structure function correlations in behavioural neurology. The thalamus. American Academy of Neurology (AAN) Acts of the Congress. San Francisco; 2005. 1-16.  Back to cited text no. 49
Hebb AO, Ojemann GA. The thalamus and language revisited. Brain Lang 2012;126:99-108.  Back to cited text no. 50
Bruyn RPM. Thalamic aphasia. A conceptional critique. J Neurol 1989;236:21-5.  Back to cited text no. 51
Bogousslavsky J, Ferrazzini M, Regli F, Assal G, Tanabe H, Delaloye-Bischof A. Manic delirium and frontal-like syndrome with paramedian infarction of the right thalamus. J Neurol Neurosurg Psychiatry 1988;51:116-9.  Back to cited text no. 52
Bogousslavsky J, Regli F, Assal G. The syndrome of unilateral tuberothalamic artery territory infarction. Stroke 1986;17:434-41.  Back to cited text no. 53
Bogousslavsky J, Regli F, Delaloye B, Delaloye-Bischof A, Assal G, Uske A. Loss of psychic self activation with bithalamic infarction. Acta Neurol Scand 1991;83:309-16.  Back to cited text no. 54
Bogousslavsky J, Regli F, Uske A. Thalamic infarcts: Clinical syndromes, etiology, and prognosis. Neurology 1988;38:837-47.  Back to cited text no. 55
Bogousslavsky J, Van Melle G, Regli F. The Lausanne Stroke Registry: Analysis of 1,000 consecutive patients with first stroke. Stroke 1988;19:1083-92.  Back to cited text no. 56
Saez de Ocariz M, Nader JA, Santos JA, Bautista M. Thalamic vascular lesions. Risk factors and clinical course for infarcts and hemorrhages. Stroke 1996;27:1530-6.  Back to cited text no. 57
Labauge R, Pages M, Marty-Double C, Blard JM, Boukobza M, Salvaing P. Occlusion of the basilar artery. A review with 17 personal cases. Rev Neurol 1981;137:545-71.  Back to cited text no. 58
Yamamoto Y, Georgiadis AL, Chang HM, Caplan LR. Posterior cerebral artery territory infarcts in the New England Medical Center Posterior Circulation Registry. Arch Neurol 1999;56:824-32.  Back to cited text no. 59
Yakovlev PI, Locke S. Limbic nuclei of the thalamus and connections of limbic cortex, III: Corticocortical connections of the anterior cingulated gyrus, the cingulum, and the subcallosal bundle in monkey. Arch Neurol 1961;5:34-70.  Back to cited text no. 60
Ghika-Schmid F, Bogousslavsky J. The acute behavioural syndrome of anterior thalamic infarction: A prospective study of 12 cases. Ann Neurol 2000;48:220-7.  Back to cited text no. 61
Chatterjee A, Yapundich R, Mennemeier M, Mountz JM, Inampudi C, Pan JW, et al. Thalamic thought disorder: On being “a bit addled”. Cortex 1997;33:419-40.  Back to cited text no. 62
Tatemichi TK, Desmond DW, Prohovnik I, Cross DT, Gropen TI, Mohr JP, et al. Confusion and memory loss from capsular genu infarction. A thalamocortical disconnection syndrome? Neurology 1992;42:1966-79.  Back to cited text no. 63
Moretti R, Torre P, Antonello RM, Capus L, Gioulis M, Zambito Marsala S, et al. “Speech start-hesitation” following subthalamic nucleus stimulation in Parkinson Disease. Eur Neurol 2003;49:251-3.  Back to cited text no. 64
Moretti R, Torre P, Antonello RM, Capus L, Zambito Marsala S, Cattaruzza T, et al. Neuropsychological changes after subthalamic nucleus stimulation: A 12-month follow-up in nine patients with Parkinson Disease. Parkinsonism Relat Disord 2003;10:73-9.  Back to cited text no. 65
Moretti R, Torre P, Antonello RM, Cattaruzza T, Cazzato G, Bava A. Frontal lobe dementia and subcortical vascular dementia: A neuropsychological comparison. Drugs Aging 2004;21:931-7.  Back to cited text no. 66
Moretti R, Torre P, Antonello RM, Cazzato G, Bava A. Subcortical-cortical lesions and two-step aplasia in a bilingual patient. In: Shohov SP, editor. Advances in psychology research. Vol. 23. New York: Novascience Publisher; 2003. pp. 33-44.  Back to cited text no. 67
Moretti R, Torre P, Antonello RM, Capus L, Gioulis M, Zambito Marsala S, et al. Cognitive changes following subthalamic nucleus stimulation in two patients with Parkinson disease. Percept Motor Skills 2002;95:477-86.  Back to cited text no. 68
Moretti R, Torre P. La demenza frontale. Aprilia-Roma: Stampa Grafica-2000; 2003.  Back to cited text no. 69
Moretti R, Torre P, Antonello RM, Capus L, Gioulis M, Zambito Marsala S, et al. Effects on cognitive abilities following subthalamic nucleus stimulation in Parkinson Disease. Eur J Neurol 2001;8:726-7.  Back to cited text no. 70
Malamut BL, Graff-Radford NR, Chawluk J, Grossman RI, Gur RC. Memory in a case of bilateral thalamic infarction. Neurology 1992;42:163-9.  Back to cited text no. 71
Kapur N, Coughlan K. Confabulations and frontal lobe dysfunction. J Neurol Neurosurg Psychiatry 1980;43:461-3.  Back to cited text no. 72
Benson DF, Djenderedjian A, Miller BL, Pachana NA, Chang L, Itti L, et al. Neural basis of confabulation. Neurology 1996;46:1239-43.  Back to cited text no. 73
Schnider A, Gutbrod K, Hess CW, Schroth G. Memory without context: Amnesia with confabulations after infarction of the right capsular genu. J Neurol Neurosurg Psychiatry 1996;61:186-93.  Back to cited text no. 74
Engelborghs S, Marien P, Pickut BA, Verstraeten S, De Deyn PP. Loss of psychic self-activation after paramedian bithalamic infarction. Stroke 2000;31:1762-5.  Back to cited text no. 75
Laplane D, Levasseur M, Pillon B, Dubois B, Baulac M, Mazoyer B, et al. Obsessive-compulsive and other behavioural changes with bilateral basal ganglia lesions. A neuropsychological, magnetic resonance imaging and positron tomography study. Brain 1989;112(Pt 3):699-725.  Back to cited text no. 76
Laplane D. La perte d'auto-activation psychique. Rev Neurol 1990;146:397-404.  Back to cited text no. 77
Van Domburg P, Ten Donkelaar HJ, Notermans S. Akinetic mutism with bithalamic infarction. Neuropsychological correlates. J Neurol Sci 1996;139:58-65.  Back to cited text no. 78
Schmahmann J. Vascular syndromes of the thalamus. Stroke 2003;34:2264-78.  Back to cited text no. 79
Lamot U, Ribaric I, Popovic KS. Artery of Percheron infarction: Review of literature with a case report. Radiol Oncol 2015;49:141-6.  Back to cited text no. 80
Castaigne P, Lhermitte F, Buge A, Escourolle R, Hauw JJ, Lyon-Caen O. Paramedian thalamic and midbrain infarcts: Clinical and neuropathological study. Ann Neurol 1981;10:127-48.  Back to cited text no. 81
Percheron G. Arteries of the human thalamus: II. Arteries and paramedian thalamic territory of the communicating basilar artery. Rev Neurol 1976;132:309-24.  Back to cited text no. 82
Lazzaro NA, Wright B, Castillo M, Fischbein NJ, Glastonbury CM, Hildenbrand PG, et al. Artery of Percheron infarction: Imaging patterns and clinical spectrum. AJNR Am J Neuroradiol 2010;31:1283-9.  Back to cited text no. 83
Janssen MP, Schreuder A, Koehler PJ. Delayed dysosmia and dysgeusia after thalamic infarction. J Neurol Sci 2015;348:286-7.  Back to cited text no. 84
Elwischger K, Rommer P, Prayer D, Mueller C, Auff E, Wiest G. Thalamic astasia from isolated centromedian thalamic infarction. Neurology 2012;78:146-7.  Back to cited text no. 85
Van der Werf YD, Witter MP, Uylings HB, Jolles J. Neuropsychology of infarctions in the thalamus: A review. Neuropsychologia 2000;38:613-27.  Back to cited text no. 86
Hermann DM, Siccoli M, Brugger P, Wachter K, Mathis J, Achermann P, et al. Evolution of neurological, neuropsychological and sleep-wake disturbances after paramedian thalamic stroke. Stroke 2008;39:62-8.  Back to cited text no. 87
De Witte L, Brouns R, Kavadias D, Engelborghs S, De Deyn PP, Marien P. Cognitive, affective and behavioural disturbances following vascular thalamic lesions: A review. Cortex 2011;47:273-319.  Back to cited text no. 88
Jonas S. The supplementary motor region and speech emission. J Commun Disord 1981;14:349-73.  Back to cited text no. 89
Jonas S. The thalamus and aphasia, including transcortical aphasia: A review. J Commun Disord 1982;15:31-41.  Back to cited text no. 90
Kumar E, Mashih AK, Pardo J. Global aphasia due to thalamic hemorrhage: A case report and review of the literature. Arch Phys Med Rehabil 1996;77:1312-5.  Back to cited text no. 91
Kumar R, Lozano AM, Montgomery E, Lang AE. Pallidotomy and deep brain stimulation of the pallidum and subthalamic nucleus in advanced Parkinson's disease. Mov Disord 1998;13:73-82.  Back to cited text no. 92
Alain C, Reinke K, McDonald KL, Chau W, Tam F, Pacurar A, et al. Left thalamo-cortical network implicated in successful speech separation and identification. Neuroimage 2005;26:592-9.  Back to cited text no. 93
Von Kriegstein K, Patterson RD, Griffiths TD. Task-dependent modulation of medial geniculate body is behaviorally relevant for speech recognition. Curr Biol 2008;18:1855-9.  Back to cited text no. 94
Diaz B, Hintz F, Kiebel SJ, Von Kriegstein K. Dysfunction of the auditory thalamus in developmental dyslexia. Proc Natl Acad Sci U S A 2012;109:13841-6.  Back to cited text no. 95
Assaf M, Calhoun VD, Kuzu CH, Kraut MA, Rivkin PR, Hart J Jr, et al. Neural correlates of the object-recall process in semantic memory. Psychiatry Res 2006;147:115-26.  Back to cited text no. 96
Van Der Werf YD, Jolles J, Witter MP, Uylings HBM. Contributions of thalamic nuclei to declarative memory functioning. Cortex 2003;39:1047-62.  Back to cited text no. 97
Nadeau SE, Crosson B. Subcortical aphasia. Brain Lang 1997;58:355-402.  Back to cited text no. 98
Kraut MA, Kremen S, Moo LR, Segal JB, Calhoun V, Hart J Jr. Object activation in semantic memory from visual multimodal feature input. J Cogn Neurosci 2002;14:37-47.  Back to cited text no. 99
Slotnick SD, Moo LR, Kraut MA, Lesser RP, Hart J Jr. Interactions between thalamic and cortical rhythms during semantic memory recall in human. Proc Natl Acad Sci U S A 2002;99:6440-3.  Back to cited text no. 100
Klostermann F, Wahl M, Marzinzik F, Schneider GH, Kupsch A, Curio G. Mental chronometry of target detection: Human thalamus leads cortex. Brain 2006;129:923-31.  Back to cited text no. 101
Klostermann F, Wahl M, Schomann J, Kupsch A, Curio G, Marzinzik F. Thalamo-cortical processing of near-threshold somatosensory stimuli in humans. Eur J Neurosci 2009;30:1815-22.  Back to cited text no. 102
Ford AA, Triplett W, Sudhyadhom A, Gullett J, McGregor K, Fitzgerald DB, et al. Broca's area and its striatal and thalamic connections: A diffusion-MRI tractography study. Front Neuroanat 2013;7:8.  Back to cited text no. 103
Mitchell AS, Sherman SM, Sommer MA, Mair RG, Vertes RP, Chudasama Y. Advances in understanding mechanisms of thalamic relays in cognition and behavior. J Neurosci 2014;34:15340-6.  Back to cited text no. 104
Sherman SM. Thalamus plays a central role in ongoing cortical functioning. Nat Neurosci 2016;19:533-41.  Back to cited text no. 105
Ardila A, Bernal B, Rosselli M. how localized are language brain areas? A review of Brodmann areas involvement in oral language. Arch Clin Neuropsychol 2016;31:112-22.  Back to cited text no. 106


  [Figure 1], [Figure 2], [Figure 3]


Print this article  Email this article
Online since 20th March '04
Published by Wolters Kluwer - Medknow