Neuropsychological deficits after bithalamic hemorrhages

doi:10.1016/j.jns.2007.01.042

Journal of the Neurological Sciences

Volume 257, Issues 1–2, 15 June 2007, Pages 174-176

https://doi.org/10.1016/j.jns.2007.01.042 Get rights and content

Abstract

Strategic lesions of the thalamus interfere with cognitive functions and produce complex neuropsychological symptoms. Bilateral, simultaneous thalamic hemorrhages are unusual causes of thalamic dementia.

We present clinical, neuropsychological and structural neuroimaging data of a 12-month follow-up period of a patient with bilateral thalamic hemorrhages.

After the operation of pancreatitis acuta hemorrhagico-necroticans, the patient developed coma. Computed tomography (CT) and magnetic resonance (MR) of the brain showed medially situated bithalamic hematomas. During the follow-up period, patient's level of consciousness has improved. Moderate dementia (MMSE 20/30) was found with severe temporal and spatial disorientation. Neuropsychological tests showed that attention and concentration were prominently impaired; there were severe verbal and less prominent, visual memory deficits, with anterograde and retrograde amnesia, accompanied by confabulations. Loss of cognitive flexibility and dysexecutive syndrome were also demonstrated. Dynamic apraxia, visual organization and visual construction deficit and impairment of categorial and phonemic fluency were noted. Language was only moderately impaired (anomia).

A year later, neuropsychological profile was similar with moderate improvement of retrograde amnesia, whereas anterograde deficits persisted.

Neuropsychological syndrome in our patient with bilateral thalamic hemorrhages was characteristic for subcortico-cortical cognitive deficit and was caused by disruption of the cortico-thalamic circuitry.

Introduction

Strategic lesions of the thalamus due to infarction or hemorrhage may cause acute or persistent complex neuropsychological dysfunction and may lead to vascular dementia. The most prominent cognitive deficit and one of the most extensively studied is memory dysfunction [1]. Aphasia, neglect and anosognosia were also frequently reported [1], [2], [3].

Bilateral, simultaneous, symmetrical thalamic hemorrhages are unusual causes of thalamic dementia. Kumral and colleagues [4] studied 100 patients with thalamic hemorrhage, but none of them have had bilateral hemorrhages. Bilateral hemorrhages are mostly a consequence of systematic diseases and conditions.

We present clinical, neuropsychological and structural neuroimaging data of the 12-month follow-up period of a man with bilateral thalamic hemorrhages.

Section snippets

Case report

Sixty-year-old, right-handed, Serbian speaking civil engineer (16 years of education) was admitted to Emergency Unit suffering from pancreatitis acuta hemorrhagico-necroticans. After surgery, the patient developed right hemiparesis and coma (Glasgow Coma Scale 5). Computed tomography (CT) and magnetic resonance (MR) of the brain showed medially situated bithalamic hematomas with rupture into the third ventricle. MR angiography was normal. After 2 weeks level of consciousness had improved, but

Discussion

Neuropsychological deficits due to bilateral thalamic infarctions had been reported previously [5], [6]. Bilateral thalamic hemorrhages are very rare and neuropsychological outcome has not been studied yet. We present a patient with pancreatitis acuta hemorrhagico-necroticans, with developed bilateral, simultaneous, medial thalamic hemorrhages secondary to severe coagulopathia.

At the onset of stroke, coma was observed due to disturbance of the arousal system [4].

After 2 weeks, the patient's

Conclusion

Neuropsychological syndrome in our patient with bilateral thalamic hemorrhages was characteristic for subcortico-cortical cognitive deficit and could be caused by disruption of the cortico-thalamic circuits.

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Revisar los principios actuales para el diagnóstico de las categorías de deterioro cognitivo vascular, con énfasis en la nomenclatura, los criterios diagnósticos y los hallazgos clínico-radiológicos diferenciales.
Los principios para el diagnóstico del deterioro cognitivo vascular han evolucionado, pero los criterios disponibles fueron diseñados básicamente para diferenciar la demencia vascular de la demencia tipo Alzheimer, y para propósitos de investigación. Sin embargo, en la práctica clínica se requieren elementos precisos para: 1) el diagnóstico clínico de la demencia y el deterioro cognitivo leve, 2) la identificación clínica y por neuroimagen de las diversas lesiones cerebrovasculares asociadas con la disfunción cognitiva, y 3) la formulación de una relación etiopatogénica entre el deterioro cognitivo y las lesiones cerebrovasculares. Por esta razón se revisaron los elementos diagnósticos de las categorías de deterioro cognitivo vascular, su clasificación y características más relevantes. Se enfatizó en las características que permiten el diagnóstico de la demencia multi-infarto, la demencia por infarto estratégico, la demencia por enfermedad de pequeño vaso cerebral, la demencia mixta y el deterioro cognitivo leve vascular.
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A review of current criteria for the diagnosis of categories related with vascular cognitive impairment, in particular the nomenclature, diagnostic criteria, and differential clinical-radiological findings.
The criteria for the diagnosis of vascular cognitive impairment have evolved, but available criteria were designed basically for differentiating between vascular dementia and dementia due to Alzheimer disease, and for research purposes. Nevertheless, in clinical practice precise elements are required for: 1) Clinical diagnosis of dementia and mild cognitive impairment; 2) Clinical and neuroimaging criteria for identification of the various cerebrovascular lesions associated with cognitive dysfunction, and 3) A formulation of the aetiogenic-pathogenic relationship between cognitive impairment and cerebrovascular lesions. For this reason, a review was carried out on the diagnostic elements of vascular cognitive impairment categories, classification, and their most relevant characteristics. It highlights the characteristic for the diagnosis of multi-infarction dementia, strategic single infarct dementia, small vessel disease with dementia, mixed dementia, and vascular mild cognitive impairment.
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Clinical properties of regional thalamic hemorrhages
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Citation Excerpt :
According to Kirshner,17 this condition is a quasiaphasic abnormality of vigilance, and that the thalamus plays a role in alertness of the speech cortex. In addition, some authors have stated that a mass effect leading to compression of the cortex or its vessels, diaschisis, or disconnection and anterior thalamic involvement may cause aphasia in the thalamic hemorrhage.18,19 Positron emission tomography revealed diffuse hypometabolism in the ipsilateral cerebrum (frontal parietal, temporal, occipital, putamen, and thalamus) in subcortical aphasia after intracranial hemorrhage.20
Thalamic hemorrhage constitutes 6% to 25% of intracerebral hemorrhages. Vascular lesions affecting the thalamus may cause a variety of clinical symptoms. This retrospective study aims to evaluate localization of hemorrhage and clinical symptoms in patients with thalamic hemorrhage.
One hundred and one patients with thalamic hemorrhage were examined retrospectively in our department. Hemorrhages were classified into 5 groups according to computed tomography: medial (thalamoperforate), anterolateral (tuberothalamic), posterolateral (thalamogeniculate), dorsal (posterior choroidal), and global. The relation between volume, localization, and penetration to adjacent structures/ventricles of hemorrhage and risk factors, clinical features, and prognosis were evaluated.
The study group included 101 patients. Eighty-two percent of the patients had hypertension, 19.8% had diabetes mellitus, 14.9% had cardiac disease, and 5.9% had chronic renal failure. Mean blood pressure was 173/101 mm Hg. Decreased Glasgow coma scale was significantly higher in the global hemorrhage group than in all regional groups (Chi-square, 10.54; P = .002). Medial group hemorrhages had a significantly higher rate than anterolateral, posterolateral, and dorsal intraventricular expansion. Out of speech disorders, 49% of patients had a right thalamic lesion (especially dysarthria) and 51% of patients had a left thalamic lesion (mostly aphasia).
In the study, we detected that the most important risk factor in thalamic hemorrhage is hypertension. The prognosis is worse in global and medial group hemorrhages, especially those which rupture to the ventricle, than the other groups. Thalamic lesions cause a variety of symptoms, including forms of aphasia, such as crossed dextral aphasia.
Vascular dementia with left thalamic infarction: Neuropsychological and behavioral implications suggested by involvement of the thalamic nucleus and the remote effect on cerebral cortex. The Osaki-Tajiri project
2013, Psychiatry Research - Neuroimaging
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The left side effect is thought to be associated with separation of concurrent sounds, contributing to smooth verbal communication in everyday settings (Alain et al., 2005), or syntactic integration of lexical elements in grammatical structure (Dominey et al., 2009). Several studies have also reported the relationship between thalamic lesion and decreased word fluency (Kuljic-Obradovic et al., 2007) or mental flexibility (Swartz et al., 2008). Six patients exhibited depression in this study.
Vascular dementia (VaD) is a condition whereby decreased cerebral perfusion causes cognitive deterioration. We hypothesized that lesions of the anterior nucleus (AN) including the mammillo-thalamic tract cause a decline in the recollection of past episodes/events, and that the left thalamic infarction can cause frontal dysfunction through the “diaschisis.” We investigated 18 VaD cases with only left thalamic infarction. ^99mTc-ECD single photon emission computed tomography (SPECT) was used to assess regional cerebral blood flow (CBF). To test the first hypothesis, the scores on the Cognitive Abilities Screening Instrument (CASI) domain Recent memory or the rating on the Clinical Dementia Rating (CDR) domain Memory were analyzed. To test the second hypothesis, we selected the six regions of interest that correlated with the two measures, i.e., word fluency and/or depressive state, as assessed with the Geriatric Depression Scale (GDS). We found that all patients had amnesia, especially in the AN group, six of the eight patients had scores of 1+ on the CDR Memory scale, and all but one disclosed the CASI domain Recent memory impairment. There were significant correlations between the left anterior cingulate CBF and word fluency scores, and between the right rectal gyrus CBF and GDS scores. We suggest that these observations are due to a remote effect of the thalamic lesion.
Cognitive, affective and behavioural disturbances following vascular thalamic lesions: A review
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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.
Bilateral thalamic necrosis following ingestion of ridge gourd infested with coelomycete fungi (Diplodia)
2010, Journal of the Neurological Sciences
Bilateral thalamic lesions detected on magnetic resonance imaging have a wide differential diagnosis. This report describes a previously healthy young man who developed bilateral thalamic necrosis with seizures, vomiting, hepatitis, neutrophilic leukocytosis and metabolic acidosis following consumption of raw dried fruits of the ridge gourd plant (Luffa acutangula) prescribed by a traditional medicine practitioner. These fruits were subsequently shown to be infested with spores and conidiomata of Diplodia, a coelomycete fungus known to cause neurotoxicity in farm animals. The patient made a partial recovery with supportive care, and has persistent deficits consistent with bilateral medial thalamic damage. This is the first report of neurological toxicity attributable to Diplodia in humans, and this entity should be considered in the differential diagnosis of bilateral thalamic lesions in the appropriate clinical setting.
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Neuropsychological deficits after bithalamic hemorrhages

Abstract

Introduction

Section snippets

Case report

Discussion

Conclusion

J Neurol Sci

J Neurol Sci

Brain Lang

J Neurol Sci

J Neurol Sci

Brain Lang

Brain Lang

Brain Lang

Brain Lang

Thalamic hemorrhage. A prospective study of 100 patients

Stroke

Vascular syndromes of the thalamus

Stroke

Frontal subcortical circuits and human behavior

Arch Neurol

Pure amnesia after unilateral left polar thalamic infarct: topographic and sequential neuropsychological and metabolic (PET) correlations

J Neurol Neuorsurg Psychiatry