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The thalamus and behavior : Effects of anatomically distinct strokes

Emmanuel Carrera and Julien Bogousslavsky Neurology 2006;66;1817 DOI 10.1212/01.wnl.0000219679.95223.4c This information is current as of April 22, 2013

The online version of this article, along with updated information and services, is located on the World Wide Web at: http://www.neurology.org/content/66/12/1817.full.html

Neurology is the official journal of the American Academy of Neurology. Published continuously since 1951, it is now a weekly with 48 issues per year. Copyright 2006 American Academy of Neurology. All rights reserved. Print ISSN: 0028-3878. Online ISSN: 1526-632X.

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The thalamus and behavior


Effects of anatomically distinct strokes
Emmanuel Carrera, MD; and Julien Bogousslavsky, MD

AbstractData on behavioral changes after thalamic lesion are sparse and largely based on isolated reports of patients with thalamic strokes. However, recent findings suggest that behavioral patterns can be delineated on the basis of the four main arterial thalamic territories. The anterior pattern consists mainly of perseverations and superimposition of unrelated information, apathy, and amnesia. After paramedian infarct, the most frequent features are disinhibition syndromes, with personality changes, loss of self-activation, amnesia, and, in the case of extensive lesions, thalamic dementia; this pattern may often be difficult to distinguish from primary psychiatric disorders, especially when neurologic dysfunction is lacking. After inferolateral lesion, executive dysfunction may develop but is often overlooked, although it may occasionally lead to severe long-term disability. After posterior lesion, whereas cognitive dysfunction with neglect and aphasia are well known, no specific behavioral syndrome has been reported. In the future, perfusion CT, functional MRI, and tractography using diffusion imaging in stroke patients may provide a better understanding of the role of the corticothalamic relationship in behavioral changes associated with thalamic stroke.
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The first clinicopathologic study of thalamic stroke was published in 1906 by Dejerine and Roussy,1 who emphasized sensorimotor disturbances. Twenty years later, cognitive deficits after isolated thalamic lesions were described by Hillemand2 and Lhermitte,3 with atypical aphasia in patients with left lesions. Since then, although aphasia, agnosia, amnesia, and neglect have frequently been reported after thalamic strokes,4-6 behavioral changes have been rarely described. More recently, major advances in the understanding of the thalamus and behavior after stroke have been made due to the development of morphologic and functional imaging.
Methods. For the purpose of this review, we selected the patients reported in the literature with an adequate description of behavior secondary to radiologic-proven thalamic lesions. Although MRI is currently the best radiologic technique for stroke localization, patients with only a CT scan were also included because of the limited number of patients described with behavioral changes after thalamic lesion. We then grouped the patients according to the main vascular territories involved7-10 as defined by pathologic data (figure 1): 1) the anterior, tuberothalamic, or polar territory, supplied by the tuberothalamic or polar artery, which originates from the posterior communicating artery, or, in one-third of patients, by the paramedian or thalamoperforating arteries; 2) the paramedian territory, supplied by the thalamoperforating arteries, which originate from the first part of the posterior cerebral artery (P1); 3) the inferolateral or thalamogeniculate territory, supplied by the thalamogeniculate arteries, which originate from the second part of the posterior cerebral artery (P2); and 4) the

posterior territory, supplied by the medial and lateral branches of the posterior choroidal artery, which originates from P2.

Anterior territory infarction. Infarcts in the anterior thalamic territory account for about 12% of all thalamic infarcts (figure 2).6 Because these involve the anterior nuclei, which receive projections from the mamillothalamic tract (MTT) and are connected to the anterior limbic system (including the cingulate gyrus, hippocampus, parahippocampal formation, and orbitofrontal cortex) and to the medial and prefrontal cortex,11,12 most patients with anterior infarcts show a unique behavioral pattern, including superposition of unrelated information and perseverations (anterior behavioral syndrome), apathy, and amnesia. According to the largest case series on anterior strokes,13 which included 12 patients and was based on CT and MRI, one of the more characteristic behavioral changes after anterior infarcts is the superposition of unrelated information, which has been named palipsychism from the Greek palin (again) and psyche (soul),13 with parallel expression of mental activities, irrespective of sequential order. The disorganization of output speech, with grammatically correct phrases, is usually characterized by intrusions of themes previously discussed with the medical staff or patients relatives unrelated to the

From the Department of Neurology, University Hospital, Lausanne, Switzerland. Disclosure: The authors report no conflicts of interest. Received August 24, 2005. Accepted in final form March 1, 2006. Address correspondence and reprint requests to Dr. E. Carrera, Department of Neurology, University Hospital, BH 13, 1011 Lausanne-CHUV, Switzerland; e-mail: emmanuel.carrera@chuv.ch Copyright 2006 by AAN Enterprises, Inc. 1817

Figure 1. Schematic view of the arterial supply to the thalamus. (A) Lateral view; (B) view from above; (C, D) detailed relationship between the arterial territories and nuclear subgroups within the thalamus. 1 carotid artery; 2 posterior communicating artery; 3 basilar artery; 4 thalamogeniculate arteries; 5 tuberothalamic artery; 6 posterior choroidal artery; 7 paramedian pedicle; 8 posterior cerebral artery. Main thalamic nuclei and tracts: CL central lateral; CM centromedian; Co commissural; Cp commissural posterior; DM dorsomedian; MTT mamillothalamic tract; Pua pulvinar anterior; Pum pulvinar medial; Pul pulvinar lateral; Pf parafascicularis; R reticular; VA ventral anterior; VLa ventral lateral anterior; VLp ventral lateral posterior; VPLa ventroposterolateral anterior; VPLp ventroposterolateral posterior; VPM ventroposteromedian.

Figure 2. (A) Diffusion-weighted MRI of a left anterior thalamic infarct involving the anterior nuclei and mamillothalamic tract in a 58-year-old patient who presented with perseverations, incoherent speech with intrusion of previous topics, and distorted memories. (B) Schematic representation (see figure 1 for legend).

current topic. This pattern was found in one of our patients with an MRI-proven right anterior infarct who correctly solved a calculation problem and simultaneously talked about his garden or explained the sequences of a journey while talking about family problems. In another patient with a left anterior infarct (figure 2), intrusions of previous topics and distorted memories were particularly noteworthy, in addition to short-term amnesia, ideomotor apraxia, and executive dysfunction. The pattern of palipsychism seems to be predominant in unconstrained speech, for example, in comments on news or historical facts and in the definition of words, contrasting with a relative preservation in performing automatic
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series. Frequently associated with perseverations in thought and output speech, palipsychism is reminiscent of confusion of ideas and should not be confused with aphasia or confusional state due to other causes.14 Anterograde amnesia, with better performance for recognition, is a constant finding and may persist several years after stroke. In some cases, visuospatial impairment is prominent after right lesions15 and verbal impairment after left lesions.16 After a left infarct, thalamofrontal disconnection was responsible for a distinctive mnesic pattern, with disorganization of autobiographic recollection and newly

acquired information.16 Anatomic studies suggest that the amnesia results from interruption of the MTT and its projections to the cingulate gyrus, hippocampus, and orbitofrontal and prefrontal cortex.17 In patients with anterior infarcts,13 interruption of frontal projections may also explain the fantastic and bizarre confabulations, which are similar to those found after medial frontal lobe lesion.18 Aphasia is rare and usually consistent with transcortical motor aphasia. Spontaneous speech is reduced, with lack of speech initiation, hypophonia, and dysarthria.13,19 Poetic, fantastic, or extravagant paraphasias and neologisms may also be found. Visual neglect, topographic disorientation (after right19 or left or bilateral13 lesions), and constructional apraxia (after left lesion)19 are more rare. Paramedian territory infarction. Infarcts in the paramedian territory account for about 35% of all thalamic infarcts6 and involve mainly the dorsomedian and intralaminar nuclei (figures 3 and 4). The dorsomedian nucleus, divided into the anteromedial magnocellular nucleus, and posterolateral parvocellular nucleus, receives projections from the amygdala and has connections to the prefrontal cortex and ventral pallidum.20 The intralaminar nuclei, including the centromedian, parafascicular nuclei, central medial, paracentral, and central lateral nuclei, project to the orbitofrontal and mediofrontal cortex, the motor and premotor cortex, and the internal globus pallidus.21 The classic features of acute paramedian infarcts include a decreased level of consciousness, vertical gaze paresis, and cognitive impairment.6,22,23 The behavioral changes become apparent when the decreased level of consciousness resolves. They consist mainly of personality changes with disinhibited behavior associated with apathy, loss of self-activation, and amnesia. After paramedian strokes, several distinct personality changes with disinhibition syndromes, resulting from thalamofrontal disconnection, have been reported. These patterns may be difficult to distinguish from psychiatric pathologies. Cyclical psychosis and manic delirium, classically found in schizophrenic patients, have been reported in detail in two patients with paramedian strokes. The first patient showed episodes of delirium, joking, and improper comments with fantastic stories24 interrupted by intervals of severe apathy. This fluctuation between periods of hyperactivity and periods of lack of spontaneity was also seen in another patient25 described as a zombie, sleeping and eating excessively, who, every 3 months, became, for a period of about 36 hours, frankly manic, cried, and had a labile affect, with fuite des ide es. In the first patient, the CT scan showed a right paramedian stroke, but MRI was not performed. In the second patient, MRI revealed bilateral paramedian stroke involving mainly the dorsomedian nucleus. Thus, it is not established whether a unilateral lesion is sufficient to induce cyclical psychosis and mania. In several psy-

Figure 3. (A) T2-weighted MRI showing a bilateral paramedian stroke predominantly on the left side in a 39-yearold woman. This patient presented with improper behavior and inadequate and disinhibited comments to her husband. Three hours later, she complained she was not able to control her eyes, then rapidly became comatose. Cognitive tests, performed 3 days later, showed persistent loss of self-activation and severe amnesia. (B) Schematic representation (see figure 1 for legend).

chiatric studies, the role of the dorsomedian nucleus in schizophrenia has been emphasized, with anatomic26 and radiologic27 data showing a reduction in dorsomedial volume and functional imaging28 revealing thalamofrontotemporal cortex disconnection on PET studies in schizophrenic patients. Additionally, frontal-like syndromes secondary to thalamofrontal disconnection have been described in several patients with paramedian strokes. Utilization behavior, with excessive use of objects and inability to
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Figure 4. (A) T2-weighted MRI of a unilateral left paramedian infarct in a 54-year-old man who, during coronary angiography, presented sudden vertical diplopia and transient hypersomnolence. Cognitive tests, performed 2 days later, were entirely normal except for loss of selfactivation. (B) Schematic representation (see figure 1 for legend).

regulate the interaction with the environment, was extensively described in two patients with right or bilateral thalamic intralaminar and dorsomedian nuclei infarcts.29 The hypothesis of a thalamocortical disconnection was supported by SPECT studies revealing hypoperfusion of the right cerebral cortex, with some predominance of the frontal area. Another young patient with bilateral dorsomedian nuclei and intralaminar nuclei infarction on MRI showed characteristics of utilization behavior when she started to eat and smoke compulsively and only stopped when food or cigarettes were out of sight.30 Disinhibition
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behavior was also diagnosed, with inappropriate jokes and lack of shame. She was highly distractible and reacted to every auditory, visual, and tactile cue. Interestingly, disconnection of the temporal lobes, in addition to the frontal lobes, was revealed by PET studies, suggesting that frontal-like syndromes after paramedian infarcts may result from disconnection of a wider cortical area than the frontal lobe. This spectacular behavior may persist several months after stroke.31 After unilateral, but especially after bilateral, infarcts, patients may become severely apathetic and aspontaneous, as if they have lost motor and affective drive. Two patients with bilateral lesions of the dorsomedian and intralaminar nuclei, assessed by CT scan in one patient32 and by MRI in the other,33 have been described in detail. Both showed no concern for their relatives and their illness and required constant external programming, appearing like robots. The term of loss of psychic self-activation has been proposed.34 The intralaminar nuclei, especially the centromedian and parafascicular nuclei,21 seem to play an important role in arousal and motivation, with involvement of the striatalventral pallidal frontomesial motivational and limbic loop and interruption of the posterior orbital and mesial frontal cortex projections, which project to the anterior cingulate gyrus and back to the striatum. A SPECT study highlighted the impact of paramedian structures on the frontomesial cortex.33 In patients with extensive involvement of the centromedian and parafascicular nuclei who appear awake, fail to respond, and become active after relevant stimuli, akinetic mutism should be suspected and may represent a severe form of loss of psychic self-activation. Amnesia is a frequent sign after paramedian infarcts. The role of the intralaminar and dorsomedial nuclei is debated. Patients with a lesion restricted to the intralaminar nuclei present with discrete amnesia, but severe distractibility,35 which suggests that the intralaminar nuclei are probably not memory structures per se, but part of a functional system regulating attention for simultaneous activities. The role of the dorsomedian nucleus is more controversial.36 Patients with lesions limited to the dorsomedian nucleus present with less severe amnesia than those with an anterior lesion.10 The dorsomedian nucleus is involved in executive processes and in processing the contents of the stimuli for storage and recall, whereas the anterior nuclei influence the selection of material to be stored and remembered.37 More anecdotal is the description of transient global amnesia after left paramedian infarcts, with repetitive queries and temporary inability to form new memories.38 Anatomic studies suggest that the anterior nuclei have numerous connections to the hippocampal formation, whereas the dorsomedian nucleus has more connections to the amydala (amygdalofugal tract).39,40 Differential involvement of these two limbic circuits may explain the differences in amnesia after MTT or anterior nuclei lesions or after

dorsomedian lesions. Damage to both circuits may result in the most severe amnesia. Aphasia after paramedian infarcts, with reduced fluency sparing comprehension and repetition, is suggestive of transcortical motor aphasia. Exceptionally, with extensive left lesions, comprehension and repetition are impaired.41 Hypophonia associated with loss of initiative may be found, as well as semantic and phonologic paraphasias.42 Dysarthria is particularly severe after bilateral lesions.43 Vascular dementia usually results from multiple lesions of the white matter.44 Dementia due to a single lesion is rare but can occur after thalamic lesion, especially in the case of bilateral paramedian or anterior lesions. The diagnosis of dementia is made when impaired attention, apathy, and poor motivation have resolved. Subacute and progressive thalamic dementia45 may also occur after venous thrombosis (figure 5). Total recovery after bilateral paramedian infarct is rare. The evolution is, in most cases, neither severe nor good.23 Inferolateral territory infarction. Infarcts in the inferolateral territory account for about 45% of all thalamic infarcts (figure 6).6 This territory includes the ventrolateral nucleus, ventroposterior nuclei (ventroposterolateral, ventroposteroinferior, and ventroposteromedian nuclei), and ventromedian nucleus. The ventrolateral nucleus has connections to the cerebellum and the motor and prefrontal cortex.46 The ventroposterolateral nucleus receives inputs from the medial lemniscal and spinothalamic pathways, whereas the ventroposteromedial nucleus receives inputs from the trigeminothalamic pathway. The most common clinical pattern after inferolateral infarct is ataxia and hypesthesia.6 However, behavioral changes such as executive dysfunction and cognitive signs such as aphasia are often undiagnosed. Executive functions relate to the planning, initiation, and regulation of goal-directed behavior,47 and their dysfunction can lead to long-term disability. In contrast to amnesia, they are not restricted to a specific thalamic structure, as tests used to assess executive functions draw on several functions such as working memory and attentive processes.48 Executive dysfunction and affective changes were described in six of nine patients with inferolateral lesions (all confirmed by MRI) with impairment of verbal and figural fluencies and performances in Stroop-like tasks.49 These behavioral changes showed similarities with those found after cerebellar lesions,50 emphasizing the impact of the lateral thalamus on cerebellofrontal connections. Aphasia is rarely reported after vascular lesion of the lateral nuclei,51 which is surprising given their numerous projections to the temporal and parietal lobes.52 However, in a recent study,10 mild transcortical motor aphasia with reduced fluency was found in almost one-third of patients. Ideomotor apraxia was demonstrated in a patient with a right lesion when he was asked to do common tasks such as brushing his teeth or using a screwdriver.53 Another patient

Figure 5. (A) T2-weighted and (B) diffusion-weighted MRI, showing bilateral venous infarct predominantly on the right side in a 18-year-old woman who, 3 days after unusual headaches, presented a decreased level of consciousness. Cognitive tests showed a lack of self-activation, severe attentional deficits, anosognosia, severe verbal and visuospatial amnesia, and a diminished capacity for abstraction and problem solving. (C) Venous angio-MRI showed absence of the sinus rectus and deep cerebral veins.
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quent signs are hypoesthesia and homonymous horizontal sectoranopsia (involvement of the lateral geniculate body). No specific behavioral syndrome seems to result from a posterior lesion. However, neuropsychological signs have been described in some cases. Spatial neglect is mainly found after a medial pulvinar lesion resulting from thalamotemporal interruption rather than thalamoparietal interruption.58 Aphasia is rarely reported, probably because of compensatory mechanisms. Limitations. There are several limitations that prevent a definitive conclusion from being drawn about the specificity of the different behavioral patterns according to the four main territories. This review is based on a limited number of case reports or small series using different neuroradiologic techniques. Postmortem anatomic descriptions are, unfortunately, rare, as thalamic infarcts are rarely life threatening. Additionally, infarcts in variant territories, resulting from borderzone ischemia or arterial variation, may occur, and several different subcortical cortical loops may therefore be involved simultaneously. In terms of the clinical description of the different case reports, the patients prestroke emotional status is rarely reported, although it may change the behavioral pattern after stroke. Conclusions. After thalamic strokes, behavioral manifestations are multiple, and virtually all cortical syndromes may be mimicked by thalamic strokes, which reflect the role of the little brain of the thalamus in behavior and cognition. Behavioral syndromes with personality changes, associated with anterior and paramedian lesions, may often be difficult to distinguish from primary psychiatric disorders, especially when neurologic dysfunction is lacking. Further description of abnormal behavior after thalamic infarcts, for example, may provide a better understanding of the mechanisms of schizophrenia. New imaging techniques, such as perfusion CT and high-resolution MRI, will help in understanding the impact of thalamic lesion on the cortex. In addition, tractography, together with the more frequent use of functional imaging such as SPECT or PET, may provide important information on connections between the thalamus and cortex59,60 and help determine the role of the different thalamic nuclei in behavior. However, these new techniques will be useless without the close attention of the clinician to the often tenuous changes in behavior in patients with suspected stroke. References
1. Dejerine J, Roussy G. Le syndrome thalamique. Rev Neurol 1906;14: 521532. 2. Hillemand P. Contribution a ` le tude des syndromes thalamiques. The ` se, Paris, 1925. 3. Lhermitte J. Symptomatologie de lhe morragie du thalamus. Rev Neurol (Paris) 1936;65:8993. 4. Fisher CM. The pathologic and clinical aspects of thalamic hemorrhage. Trans Am Neurol Assoc 1959;33:5659.

Figure 6. (A) T2-weighted MRI of a left inferolateral thalamic infarct in the territory of the thalamogeniculate arteries in a 58-year-old man showing executive dysfunction with verbal fluency difficulties, pathologic response inhibition, and pathologic conceptual ability, in addition to a right sensory and ataxic hemisyndrome. (B) Schematic representation (see figure 1 for legend).

was unable to use a toothbrush either in pantomime or when given the object itself.54 Posterior territory infarction. Infarcts in the posterior territory account for 8% of all thalamic strokes.6 The pulvinar is the main component of the posterior nuclei and can be divided into three main parts,5 the medial pulvinar, with projections to the parieto-occipital cortex,55 prefrontal cortex, cingulum, and parahippocampal cortex,56 and the inferior and the lateral pulvinar, with connections to the occipital, parietal, and temporal lobes.57 The most fre1822 NEUROLOGY 66 June (2 of 2) 2006

5. Schmahmann JD. Vascular syndromes of the thalamus. Stroke 2003;34: 22642278. 6. Bogousslavsky J, Regli F, Uske A. Thalamic infarcts: clinical syndromes, etiology, and prognosis. Neurology 1988;38:837847. 7. Percheron G. Arteries of the thalamus in man; choroidal arteries. Rev Neurol (Paris) 1977;133:547558. 8. Percheron G. Arteries of the human thalamus; arteries and paramedian thalamic territory of the communicating basilar artery. Rev Neurol (Paris) 1976;132:309324. 9. Percheron G. Arteries of the human thalamus; artery and polar thalamic territory of the posterior communicating artery. Rev Neurol (Paris) 1976;132:297307. 10. Carrera E, Michel P, Bogousslavsky J. Anteromedian, central and posterolateral territory infarcts of the thalamus. Three variant types. Stroke 2004;35:28262834. 11. Yakovlev PI, Locke S, Korsoff DY, Patton RA. Limbic nuclei of thalamus and connections of limbic cortex, I: organization of projections of the anterior group of nuclei and of the midline thalamic nuclei of the thalamus to the anterior cingulate gyrus and hippocampal rudiment in the monkey. Arch Neurol 1960;3:620641. 12. 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;5:3470. 13. Ghika-Schmid F, Bogousslavsky J. The acute behavioural syndrome of anterior thalamic infarction: a prospective study of 12 cases. Ann Neurol 2000;48:220227. 14. Chatterjee A, Yapundich R, Mennemeier M, et al. Thalamic thought disorder: on being a bit addled. Cortex 1997;33:419440. 15. Graff-Radford NR, Eslinger PJ, Damasio AR, Yamada T. Nonhemorrhagic infarction of the thalamus: behavioural, anatomic and physiologic correlates. Neurology 1984;34:1423. 16. Clarke S, Assal G, Bogousslavsky J, et al. Pure amnesia after unilateral left polar thalamic infarct: topographic and sequential neuropsychological and metabolic (PET) correlations. J Neurol Neurosurg Psychiatry 1994;57:2734. 17. Mori E, Hashimoto M. Diencephalic lesions and memory impairment. Shenkei kenkyu no shinpo (Adv Neurol Sci) 2001;45:198208. 18. Benson DF, Djenderedjian A, Miller BL, et al. Neural basis of confabulation. Neurology 1996;46:12391243. 19. Bogousslavsky J, Regli F, Assal G. The syndrome of the unilateral tuberothalamic artery territory infarction. Stroke 1986;17:434441. 20. Guigere M, Goldman-Rakic PS. Mediodorsal nucleus: areal, laminar, and tangential distribution of afferents and efferents in the frontal lobe of rhesus monkey. J Comp Neurol 1988;277:195213. 21. Groenewegen HJ, Berendse HW. The specificity of the nonspecific midline and intralaminar nuclei. Trends Neurosci 1994;17:5256. 22. Castaigne P, Lhermitte F, Buge A, et al. Paramedian thalamic and midbrain infarct : clinical and pathological study. Ann Neurol 1981;10: 127148. 23. Gentilini M, de Renzi E, Crisi G. Bilateral thalamic artery infarcts: report of eight cases. J Neurol Neurosurg Psychiatry 1987;50:900909. 24. Bogousslavsky J, Ferrazzini M, Regli F, et al. Manic delirium and frontal-like syndrome with paramedian infarction of the right thalamus. J Neurol Neurosurg Psychiatry 1988;51:116119. 25. McGilchrist I, Goldstein LH, Jadresic D, Fenwick P. Thalamo-frontal psychosis. Br J Psychiatry 1993;163:113115. 26. Pakkenberg B. Pronounced reduction of total neuron number in mediodorsal thalamic nucleus and nucleus accumbens in schizophrenics. Arch Gen Psychiatry 1990;47:10231028. 27. Byne W, Buchsbaum MS, Kemether EM, et al. Magnetic resonance imaging of the thalamic mediodorsal nucleus and pulvinar in schizophrenia and schizotypal personality disorder. Arch Gen Psychiatry 2001;58:133140. 28. Mitelman SA, Byne W, Kemether EM, Hazlett EA, Buchsbaum MS. Metabolic disconnection between the mediodorsal nucleus of the thalamus and cortical Brodmanns areas of the left hemisphere in schizophrenia. Am J Psychiatry 2005;162:17331735. 29. Eslinger PJ, Warner GC, Grattan LM, Easton JD. Frontal lobe utilization behavior associated with paramedian thalamic infarction. Neurology 1991;41:450452. 30. Mu ller A, Baumgartner RW, Ro hrenbach C, Regard M. Persistent Klu verBucy syndrome after bilateral thalamic infarction. Neuropsychiatry Neuropsychol Behav Neurol 1999;12:136139. 31. Fukatsu R, Fujii T, Yamadori A, et al. Persisting childish behavior after bilateral thalamic infarcts. Eur Neurol 1997;37:230235.

32. Bogousslavsky J, Regli F, Delaloye B, et al. Loss of psychic self activation with bithalamic infarction. Acta Neurol Scand 1991;83:309316. 33. Engelborghs S, Marien P, Pickut BA, et al. Loss of psychic selfactivation after paramedian bithalamic infarction. Stroke 2000;31: 17621765. 34. Laplane D. La perte dauto-activation psychique. Rev Neurol 1990;146: 397404. 35. Mennemeier M, Fennell E, Valenstein E, Heilman KL. Contributions of the left intralaminar and medial thalamic nuclei to memory. Arch Neurol 1992;49:10501058. 36. Von Cramon DY, Hebel N, Schuri U. A contribution to the anatomical basis of thalamic amnesia. Brain 1985;108:9931008. 37. Van der Werf YD, Jolles J, Witter MP, Uylings HB. Contributions of thalamic nuclei to declarative memory functioning. Cortex 2003;39: 10471062. 38. Gorelick PB, Amico LL, Ganellen R, Benevento LA. Transient global amnesia and thalamic infarction. Neurology 1988;38:496499. 39. Graff-Radford NR, Tranel D, van Hoesen GW. Diencephalic amnesia. Brain 1990;11:125. 40. Mishkin M. Memory in monkeys severely impaired by combined but not by separate removal of amygdala and hippocampus. Nature 1978;273: 297298. 41. 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;77:13121315. 42. Kennedy M, Murdoch BE. Chronic aphasia subsequent to striatocapsular and thalamic lesions in the left hemisphere. Brain Language 1993;44:284295. 43. Ackermann H, Ziegler W, Petersen D. Dysarthria in bilateral thalamic infarction. A case study. J Neurol 1983;240:357362. 44. Roman GC, Erkinjuntti-Wallin A, Pantoni L, Chui HC. Subcortical ischaemic vascular dementia. Lancet Neurol 2002;1:426436. 45. Krolak-Salmon P, Montavont A, Hermier M, et al. Thalamic venous infarction as a cause of subacute dementia. Neurology 2002;58:1689 1691. 46. Strick PL. Anatomical analysis of ventrolateral thalamic input to primar motor cortex. J Neurophysiol 1976;39:10211031. 47. Van der Werf YD, Scheltens P, Lindeboom J, et al. Deficits of memory, executive functioning and attention in the thalamus; a study of 22 cases with localised lesions. Neuropsychologia 2003;41:13301344. 48. Van der Werf YD, Witter MP, Uylings HB, Jolles J. Neuropsychology of infarctions in the thalamus: a review. Neuropsychologia 2000;38:613 627. 49. Annoni JM, Khateb A, Gramigna S, et al. Chronic cognitive impairment following laterothalamic infarcts. Arch Neurol 2003;60:14391443. 50. Schmahmann JD, Sherman JC. The cerebellar cognitive affective syndrome. Brain 1998;121:561579. 51. Karussis D, Leker RR, Abramsky O. Cognitive dysfunction following thalamic stroke: a study of 16 cases and review of the literature. J Neurol Sci 2000;172:2529. 52. Botez MI, Barbeau A. Role of subcortical structures, and particularly of the thalamus, in the mechanisms of speech and language. A review. Int J Neurol 1971;8:300320. 53. Nadeau SE, Roeltgen DP, Sevush S, et al. Apraxia due to a pathologically documented thalamic infarction. Neurology 1994;44:21332137. 54. Warren JD, Thompson PD, Thompson PD. Diencephalic amnesia and apraxia after left thalamic infarction. J Neurol Neurosurg Psychiatry 2000;68:248. 55. Yeterian EH, Pandya DN. Corticothalamic connections of the posterior parietal cortex in the rhesus monkey. J Comp Neurol 1985;237:408 426. 56. Yeterian EH, Pandya DN. Corticothalamic connections of paralimbic regions in the rhesus monkey. J Comp Neurol 1988;269:130146. 57. Schmahmann JD, Pandya DN. Anatomical investigation of thalamic projections to the posterior parietal cortices in rhesus monkey. J Comp Neurol 1990;295:299326. 58. Karnath HO, Ferber S, Himmlebach M. Spatial awareness is a function of the temporal not the posterior parietal lobe. Nature 2001;411:950 953. 59. Behrens TE, Johansen-Berg H, Woolrich MW, et al. Non-invasive mapping of connections between human thalamus and cortex using diffusion imaging. Nat Neurosci 2003;6:750757. 60. Johansen-Berg H, Behrens TE, Sillery E, et al. Functional-anatomical validation and individual variation of diffusion tractography-based segmentation of the human thalamus. Cereb Cortex 2005;15:3139.

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The thalamus and behavior : Effects of anatomically distinct strokes Emmanuel Carrera and Julien Bogousslavsky Neurology 2006;66;1817 DOI 10.1212/01.wnl.0000219679.95223.4c This information is current as of April 22, 2013
Updated Information & Services References including high resolution figures, can be found at: http://www.neurology.org/content/66/12/1817.full.html This article cites 59 articles, 19 of which can be accessed free at: http://www.neurology.org/content/66/12/1817.full.html#ref-list1 This article has been cited by 12 HighWire-hosted articles: http://www.neurology.org/content/66/12/1817.full.html#relatedurls This article, along with others on similar topics, appears in the following collection(s): All Cerebrovascular disease/Stroke http://www.neurology.org/cgi/collection/all_cerebrovascular_di sease_stroke All Neuropsychology/Behavior http://www.neurology.org/cgi/collection/all_neuropsychology_ behavior Infarction http://www.neurology.org/cgi/collection/infarction Information about reproducing this article in parts (figures, tables) or in its entirety can be found online at: http://www.neurology.org/misc/about.xhtml#permissions Information about ordering reprints can be found online: http://www.neurology.org/misc/addir.xhtml#reprintsus

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