25 hours ago 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). >> Go To The Portal
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.
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Thalamic aphasia is thought to result from disconnection of cortical language centers from the thalamic nuclei. Strokes in these vascular territories may also cause significant neuropsychological deficits predominantly affecting arousal, memory, and personality changes.
Depending on where the thalamus is damaged, you might experience any of these symptoms:Weakness on one side of the body.Issues with vision.Difficulty swallowing.Loss of memory.Burning.Confusion.Problems thinking or with judgment.Feelings of agitation.More items...•
Patients with lesions affecting the posterior thalamus may present with variable sensory deficits, weakness, memory impairment, aphasia, hand tremor, and dystonia. More specifically, if the inferolateral part of the pulvinar is affected, hemianopsia and quadrantanopsia can be found [2].
After a thalamic stroke, it's common for survivors to experience sensory issues such as numbness, tingling, pins-and-needles sensations, or pain. Sometimes the brain can adapt and regain the ability to process sensory information through a therapy called sensory retraining.
Your thalamus plays a role in keeping you awake and alert. Role in thinking (cognition) and memory. Your thalamus is connected with structures of your limbic system, which is involved in processing and regulating emotions, formation and storage of memories, sexual arousal and learning.
Generally, the thalamus acts as a relay station filtering information between the brain and body. Except for olfaction, every sensory system has a thalamic nucleus that receives, processes, and sends information to an associated cortical area.
Background: Thalamic lesions are seen in a multitude of disorders including vascular diseases, metabolic disorders, inflammatory diseases, trauma, tumours, and infections.
Unfortunately, for most astrocytomas of the thalamus (infiltrative or diffuse Grade II-IV tumors), surgical removal is not an option. In those cases, surgery should be reserved purely for biopsy, to treat hydrocephalus, or to reduce the mass effect.
This means they're caused by a blocked artery in your brain, often due to a blood clot. Hemorrhagic strokes, on the other hand, are caused by a rupture or leakage of a blood vessel into your brain. A thalamic stroke can be either ischemic or hemorrhagic.
Hemorrhagic Strokes The most common cause of a hemorrhagic stroke is uncontrolled hypertension (high blood pressure). 5 High pressure damages the small vessels, known as lacunae, in the brain over time. Eventually, these small vessels can break open leading to a hemorrhagic stroke known as a lacunar stroke.
"The ultimate reality is that without thalamus, the cortex is useless, it's not receiving any information in the first place," said Theyel, a postdoctoral researcher. "And if this other information-bearing pathway is really critical, it's involved in higher-order cortical functioning as well."
Complications of thalamic stroke. Another name for thalamic stroke is thalamic infarct, which basically occurs when the thalamus portion of the brain sustains any type of trauma or physical damage.
Between the cerebral cortex and the mid-brain is a double-lobed mass called the thalamus. This mass controls sensory perception, movement and consciousness. A left thalamic stroke occurs when the blood supply is cut off in the left side of the thalamus. This affects the opposite side of the body.
A stroke in the thalamus can have unique effects for every survivor. To understand how a thalamic stroke affects the body, it helps to look at what a stroke is and what functions the thalamus controls. This article will explain just that, along with an overview of the recovery process. Use the links below to … Understanding Thalamic Stroke: Effects, Treatment, and Recovery Read More »
Dr. Umair Afzal: acquisition of data, analysis and interpretation, drafting the manuscript. Dr. Muhammad U. Farooq: critical revision of the manuscript for important intellectual content and study supervision.
The authors report no disclosures relevant to the manuscript. Go to Neurology.org for full disclosures.
Thalamic lesions are associated with aphasia and hemineglect. It is possible the mechanisms and such neuropsychological may be different depending on the size and site of the thalamic lesion. Keywords: Aphasia; Hemineglect; Stroke; Thalamus.
Abstract. Purpose of review: When the thalamus is damaged, not only are there neurological symptoms such as sensory impairment, hemianopia, or motor control disorders, but there are also various neuropsychological symptoms.
Furthermore, the pulvinar, part of the thalamus, may be associated with hemineglect. General linguistic tasks activated the thalami, depending on the difficulty, as well as the frontal and temporal lobes.
We summarized the current knowledge of aphasia and hemineglect caused by thalamic lesions. Nadeau et al. [ 39] showed five mechanisms attributable to thalamic lesions with regard to cognitive dysfunction: (1) the thalamus is an important component of the brain network that forms the basis of cognitive processes, (2) local cerebral blood flow and metabolism in anatomically connected cortical areas decrease due to diaschisis or impaired thalamic function, (3) occlusion or stenosis of large cerebral blood vessels independently cause thalamic and cortical hypoperfusion, (4) there is a cortical infarct not detected by imaging examination, and (5) output is impeded due to the release of language area formed in the cortical area. On the other hand, Mohr et al. [ 27] has described “dichotomous state” due to thalamic lesions. That is, when awake they speak fairly clearly, when sleepy they become very paraphasic. Luria [ 40] also called thalamic aphasia “quasiaphasic disturbance of vigilance”. These terms imply that the thalamus is somehow keeping the language cortex awake, and when the patient is sleepy the language cortex does not work properly. As shown here, we do not fully understand the mechanism of thalamic aphasia and neglect. Although language function and visuospatial function cannot be discussed in the same way, it is possible that the mechanisms and the symptoms may be different depending on the size and site of the thalamic lesion. A detailed assessment on a case-by-case basis and research to accumulate knowledge on the subject are required for further development in the field. Additionally, thalamic lesions are also rather closely tied to the development of dementia after strokes in the vascular dementia literature, recently. Our interest in the relationships between thalamus and cognition is never exhausted.
The thalamic nuclei are roughly divided into the anterior, medial, and lateral nuclei of the thalamus by white matter, namely the internal medullar lamina,that enters the thalamic nuclei. They are further divided into other additional nuclei, which include the medial and lateral geniculate body located in the posteroinferior area (Fig. 1 ). The anterior nuclei of the thalamus receive fibers from the mammillary body and join the cortical regions, including the cingulate gyrus and parahippocampal gyrus. These nuclei communicate with the limbic system and are associated with emotion and memory. The medial nuclei of the thalamus, of which the main nucleus is the dorsomedial nucleus, communicate with the striatum in the cerebral nuclei and integrate and project somatic/visceral information to the frontal lobe. These nuclei are associated with sensory-based emotions and act on the autonomic nervous system via the hypothalamus. The lateral nuclei of the thalamus are comprised of the lateral dorsal and lateral posterior nucleus, and the pulvinar. They receive input from the midbrain, and other brain regions, and project to the cortical association cortex through output fibers. These nuclei are related to the limbic system and are involved in the formation of memory and emotion. The lateral posterior nucleus receives fibers from other nuclei of the thalamus and communicates with the parietal association cortex. Thus, sensory information is analyzed and integrated in the association cortex. The ventral nuclear group includes the ventral anterior (VA), ventral lateral (VL), and ventral posterior (VP) nuclei. The VA and VL nuclei receive input from the cerebral basal ganglia and the cerebellum, respectively, and they communicate with the motor-related areas of the cerebral cortex through fibers. The VP nuclei are comprised of the ventral lateral, ventral posterior medial, and the ventral posterior inferior nucleus, and receive and communicate somatosensory information input to the sensory area of the cerebral cortex.
They report that it is difficult to distinguish hemineglect caused by damage to the thalamus from that caused by the right parietal/temporal lobe. From the viewpoint of the attention/arousal network, the thalamus forms part of the cortico-reticular loop. It is said that hemineglect is caused by blockage of this circuit due to damage to the thalamus [ 9, 19, 20 ]. In addition, Mesulam et al. [ 21] report that “inattention” exists not only in the sensory aspect, but also in the motor and linguistic aspects. Sensory and motor neglect are strongly related, and they are not necessarily independent. The responsible lesion is not confined to the parietal, occipital or the temporal lobe, but extends to the frontal lobe and cingulate gyrus as well as the thalamus. Lesions in the subcortical areas, such as the striatum and substantia nigra, are also involved as a network. Karnath et al. [ 22] conducted a comparative study on the subcortical lesions in patients with or without hemineglect and reported that the putamen, pulvinar, and caudate nucleus were the subcortical structures involved in spatial neglect in humans, and that the anatomical network directly linked to the superior temporal gyrus (STG) was involved. Furthermore, the involvement of the pulvinar in hemineglect has been identified [ 22 ]. In particular, the pulvinar, part of the thalamus, is said to be associated with hemineglect (Fig. 3 ). Following an infarction in the posterior cerebral artery area, there is an increased incidence of hemineglect when there is a lesion in the perforating branches to the thalamus. In summary, the thalamus and hemineglect may be related in some way through the brain network that includes the pulvinar and thalamus.
It has long been known that the thalamus is related to language function [ 23 ]. Since reports of clinical cases on thalamotomy [ 24] and electric stimulation [ 25] for Parkinson’s disease or of thalamic damage [ 26, 27] have been published, the relationship between language and the pulvinar, as well as the VL nuclei has been debated. With advances in diagnostic imaging, aphasia due to thalamic lesions is no longer considered rare. Mori et al. [ 28] reported that the incidence of aphasia due to hemorrhage in the left thalamus was 33%, while Karussis et al. [ 29] reported that the incidence was 87.5%. Discrepancies in the incidence of aphasia are believed to be due to a bias arising from different methods of assessment for detecting aphasia, in addition to the differences in subjects among hospitals and institutions conducting the research. Osawa et al. [ 11 •] conducted a standard language test of aphasia on 71 patients with new-onset acute thalamic hemorrhage, and reported that language disorders were observed in 59 of them. The language disorders included Broca’s (4 patients), transcortical motor (2 patients), total (4 patients), anomic (15 patients), transcortical sensory (7 patients) and Wernicke’s aphasia (26 patients) and dysgraphia (1 patient) (Fig. 4 ).
With regard to hemineglect due to thalamic infarction, Watson et al. [ 9] reported a case of infarction within the lateral part of the right thalamus which was accompanied by an old infarction in the right superior parietal lobe. Small lesions localized in the thalamus rarely cause obvious hemineglect. Normally, right thalamic lesions including the VL nucleus or the intralaminar nuclei cause left hemineglect [ 16 ]. However, in patients with hemineglect due to an infarction localized to the right thalamus, the lesion responsible may not be confined to the right thalamus as hypoperfusion of the cerebral cortex is observed [ 17 ].
There are several studies indicating that thalamic lesions cause hemineglect [ 9 ], but most report cases of hemorrhage and only a few report cases of infarction. In a study by Kumral et al. [ 10 ], hemineglect was observed in 19 of 51 cases with right-sided lesions (37.3%) of the 100 consecutive cases of acute thalamic hemorrhage, while Osawa, et al. [ 11 •] showed that hemineglect was observed in 35 of 44 cases with right-sided lesions (79.5%). In another study, Chung et al. [ 12] classified thalamic hemorrhage into anterior, posteromedial, posterolateral, and dorsal types, and reported that the posterolateral type had a high incidence of hemineglect. However, Kawahara et al. [ 13] reported that, while severe paralysis was noted in the posterolateral type, it was the dorsal type that showed severe hemineglect. Although the majority of reports on hemineglect due to thalamic lesions are cases of hemorrhage spreading out of the thalamus, hemineglect may also be caused by a small number of hematomas and lesions localized in the thalamus. In such cases, the symptoms are transient. The mechanism underlying such cases is believed to be cortical dysfunction due to damaged subcortical fibers, or diaschisis, rather than a direct compression of the cortex [ 6, 14 ]. On the other hand, the expansion of lesions to surrounding tissue is present in cases where hemineglect remains a sequela of thalamic hemorrhage [ 15 ].
Sebastatin et al. [ 17] reported that, while aphasia was observed in 5 of 10 patients with left thalamic infarction, aphasia may appear even in the absence of cortical hypoperfusion as cortical hypoperfusion was observed in only one of them .