Thalamic infarct presenting with thalamic astasia

Astasia, inability to stand unsupported despite good strength, resembles the marked balance impairment of patients with vestibulocerebellar disease. We describe a patient with unilateral thalamic infarct that presented with astasia. A 76-year-old hypertensive woman was admitted to our hospital because of marked unsteadiness. On neurological examination, she could not stand unsupported and the woman's body swayed back and forth markedly. The swaying was not compensated for by her taking a step forward or backward, and she frequently collapsed when support was withdrawn. Diffusion-weighted magnetic resonance image revealed a discrete infarct within the right posterolateral thalamus. Brain single photon emission computerized tomography revealed markedly decreased regional cerebral blood flow within in the right thalamus with concomitant left superior cerebellar region. We discuss the possible pathomechanisms of thalamic astasia.     

Astasia in a patient with unilateral thalamic infarction: clinical and MRI study]

We report a 82-year-old woman who developed difficulty in standing and sitting in the morning. She had no other complaints and stayed in the bed. The next day, she was admitted to the hospital and neurological examination revealed that she was alert, with no other motor or sensory abnormalities. Finger to nose test, and knee to heel test were normal. No dysdiadochokinesia was seen. Astasia was the only observed abnormal finding. MRI showed a small infarction (14 x 8mm) in the posterolateral portion of the left thalamus (VPL-LP nucleus). During the following 15 days, her imbalance has gradually improved and then disappeared. We diagnosed the patient as astasia occurring from a small unilateral infarction in the thalamus. It is thought that thalamic astasia is caused by the disruption of afferent pathway from the vestibulocerebellum; however, this case is based on just clinical and MRI study, so physiological and pathological studies will be necessary in the future.     

Ataxic hemiparesis following thalamic infarction

We describe a 73-year-old man with ataxic hemiparesis following infarction of the ventrolateral nucleus of the thalamus demonstrated by computed tomography and magnetic resonance imaging. Cerebellar ataxia was most likely due to interruption of the dentatorubrothalamocortical fibers at the level of the injured ventrolateral nucleus. Hemiparesis was probably caused by local edema compressing the corticospinal tract in the adjacent posterior limb of the internal capsule. We believe this to be the first reported case of classic ataxic hemiparesis following thalamic infarction.     

Combined thalamic ptosis and astasia

Isolated cases of astasia or ptosis have each been reported in ischemic or hemorrhagic strokes involving the thalamus. We report a 70-year-old man with a medical history of hypertension who presented with left ptosis and gait disturbance despite intact motor strength in the legs and normal sensory function. MRI of the brain showed an evolving subacute infarction confined to the anteromedial-medial part of the left thalamus with no other areas of recent infarction identified. To our knowledge, combined ptosis and astasia in thalamic infarction has not been reported in the English literature. We identified 11 patients with thalamic ptosis and 21 with thalamic astasia in the literature. Patients who had ptosis, or gait abnormality which would not be related to thalamic stroke, were excluded; for example, evidence of infarction in the hypothalamus, midbrain, pons, cerebellum, or cingulate gyrus.     

Cerebellar ataxia and unilateral asterixis caused by thalamic hematoma. Presumed mechanisms

A 76 year-old hypertensive man developed an acute inability to stand due to a right cerebellar ataxia. Somatosensory performances were normal, but a transient and mild weakness of the right arm and leg with Babinski's sign was observed. There was a prominent asterixis of the right hand. CT scan showed a hemorrhage of the thalamus with surrounding edema of the adjacent internal capsule. Initial median nerve somatosensory evoked potentials showed a mild reduction of left parietal responses with absent left frontal SEPs (P22 and N30). Fourty days later the cerebellar ataxia was persisting while asterixis had disappeared. A second recording of SEPs showed a complete recovery of all cortical components. MRI performed at the same time showed a left postero lateral thalamic lesion. CT, MRI and SEPs findings suggested that asterixis could result from interruption of somatosensory fibres projecting to the motor cortex.     

Thalamic astasia: inability to stand after unilateral thalamic lesions

Inability to stand in the absence of motor weakness or marked sensory loss is usually considered to reflect midline cerebellar disease. However, the 15 patients reported here had astasia related to unilateral thalamic lesions, documented by autopsy and computed tomography in 2 patients and by computed tomography in 13. The lesions, including infarction (6), hemorrhage (7), and tumor (2), involved primarily the superoposterolateral portion of the thalamus, but spared the rubral region. Alert, with normal or near-normal strength on isometric muscle testing and a variable degree of sensory loss, the patients could not stand and 7 of them could not sit up unassisted. They fell backwards or toward the side contralateral to the lesion. They appeared to have a deficit of overlearned motor activity of an axial and postural nature. In the vascular cases, the deficit improved in a few days or weeks. However, these patients had a tendency to sustain falls during the rehabilitation period.     

Aphasia caused by left paramedian thalamic infarction. Anatomo-clinical case

A 67 year-old right-handed man presented with an aphasia of acute onset associated to paralysis of vertical eye movements, mild cerebellar right dysmetria and right hemiparesis without hemianopia. CT scan showed two low density areas in the left thalamus and left occipital lobe. Neuropsychological examination revealed a non fluent aphasia with normal repetition, semantic paraphasias, perseverations and good comprehension of verbal and written commands. There was no alexia. Writing was impaired only by motor disturbances. Three weeks after the onset, tetraparesis and impairment of consciousness followed by a locked in syndrome supervened. Death occurred four months after onset. Neuropathological examination showed a left paramedian thalamic infarct involving the ventrolateral, dorso-medial and intralaminar nuclei, sparing the pulvinar. There was an occipital infarct sparing the calcarine scissura and multiple infarctions in the pons and the cerebellum. Broca's and Wernicke's areas were spared. We suggest that the involvement of medial nuclei could be partly responsible of language disturbances in thalamic aphasia.     

Non-persistent "doll phenomenon" in a patient with right thalamic infarction]

An 81-year-old right-handed woman was admitted because of acute dysarthria and left hemiparesis. She had lived herself without aids until the admission. On neurological examination she was confused and disoriented. She was ambulant, but had mild dysarthria and mild left hemiparesis. Neuropsychological tests showed severe impairment of memory, mild impairment of visual cognition, decreased fluency of word recall and mild paramnesia, but no acalculia, agraphia, aphasia or apraxia. MRI of the brain showed small infarction in the right anterior thalamus. 123I-IMP SPECT demonstrated a decrease in CBF of the thalamus, basal ganglia and frontal lobe on the right. During admission, she always played with a doll as if she took it as a real baby. This peculiar symptom. "doll phenomenon" continued for approximately three months later. The "doll phenomenon" usually appears in demented patients with diffuse mental deterioration or dysfunction of the frontal lobe. The present patient had not been demented until the onset of the thalamic infarction, and disturbance of cognition caused by the right thalamic infarction probably produced the "doll phenomenon".     

Lateral thalamic infarcts

A patient with occlusion of the proximal posterior cerebral artery (PCA), a lateral thalamic infarct, and hemisensory loss later developed hemianopia and hemiparesis and had extensive PCA territory infarction in the midbrain, the lateral portion of the thalamus, and the occipital lobe noted at necropsy. Two other patients had lateral thalamic infarcts on computed tomography, normal angiographic findings, and presumed thalamogeniculate artery branch occlusion. There are three clinical syndromes associated with lateral thalamic infarction: (1) hemisensory loss, hemiataxia, and involuntary movements; (2) pure sensory stroke; and (3) sensory-motor stroke. Ataxia, adventitious movements, and sensory loss are due to infarction of the lateral, posterolateral, and posteromedial ventral nuclei caused by occlusion of the PCA proximal to the thalamogeniculate artery branches or by occlusion of large thalamogeniculate arteries. Pure sensory and sensory-motor strokes are due to smaller infarcts in the posterolateral-posteromedial ventral complex and adjacent internal capsule caused by occlusion of penetrating artery branches of the thalamogeniculate arteries.     

Left antero-medial thalamic infarction and symptoms of amnesia, aphasia, and dementia

Three cases of left antero-medial thalamic infarction who showed amnesia, aphasia and dementia were studied comparatively in terms of clinical features and the MRI findings. Case 1 and Case 2, who showed transient amnesia and aphasia respectively, had a single lesion in the left antero-medial thalamus. Case 1 had a lesion in a more ventral part than Case 2, suggesting that Case 1 had a lesion of the bundles into the anterior and dorsomedial thalamic nuclei while Case 2 had a lesion of the ventrolateral thalamic nucleus. On the other hand, Case 3 who showed persistent dementia had multiple lesions in addition to the left antero-medial thalamic infarction. A review of the previous reports and investigations of the present cases suggest that a single ischemic lesion in the left antero-medial thalamus will cause amnesia and/or aphasic symptom while in cases with other multiple lesions it may cause persistent dementia.     

Amnesia, confabulation and nonaphasic misnaming after left thalamic infarct]

A 72-year-old right handed woman developed amnesia, confabulation and abnormal (bizarre) verbal response after the left thalamic infarction. Clinical features including disorientation, euphoria and various kinds of paraphasia coincided in nonaphasic misnaming. MR images showed that lesions involved the genu of the internal capsule, the anteroventral nucleus, the lateroventral nucleus, intralaminar nuclei, the mamillothalamic tract and the region around the ventral thalamus. 99mTc-HMPAO-SPECT revealed decreased uptake in the left frontal lobe, probably due to the disconnection from the thalamus. These findings suggest that the dysfunction of the thalamus (mainly ventrolateral) and the left frontal lobe caused the disturbance of the self-monitoring in the language use, which generated confabulation and nonaphasic misnaming in our case.     

The lacteridian reticular thalamic nucleus projects topographically upon the dorsal thalamus: Experimental study in Gallotia galloti

The projection pattern of the ventral thalamic reticular nucleus onto the dorsal thalamus was studied in the lizard Gallotia gallotiusing in vitro horseradish peroxidase and fluorescent carbocyanine labelling techniques. Localized label deposits at three dorsoventrally spaced sites in the dorsal thalamus elicited retrograde transport into separate, though partly overlapping, medial, dorsolateral and ventrolateral sectors within an extended cytoarchitectonic complex which may be globally identifiable as the reticular nucleus. Neurons found in the dorsolateral and ventrolateral sectors mainly corresponded to the cell group named nucleus ventromedialis (or nucleus of the dorsal supraoptic decussation) in the literature, whereas neurons labelled in the medial sector corresponded to the so-called dorsal hypothalamic nucleus. Sparser cells appear labelled in the superficially placed nucleus suprapeduncularis. Thalamotelencephalic fibers arising from the injected dorsal thalamic nuclei also project on the corresponding retrogradely labeled sectors within the reticular nucleus. These findings reveal a rough topographic organization in the connections of the extended reticular nucleus complex with the whole dorsal thalamus. This supports the hypothesis of hodological homology between this ventral thalamic formation in Gallotiaand the mammalian thalamic reticular nucleus. © 1994 Wiley-Liss, Inc.     

Disappearance of essential tremor after thalamic infarction]

Stereotactic thalamotomy has been used with some benefit in the treatment of essential tremor. We report a 73-year-old woman whose essential tremor of the right hand spontaneously disappeared after thalamic infarction. She had suffered hand tremor of the right hand for seven years. One morning, she noticed mild muscular weakness in her right upper and lower extremities, numbness around her mouth and paresthesia in her right arm. Simultaneously, she noticed disappearance of the tremor of her right hand. Several days later, right hemiplegia and paresthesia completely resolved. Neurological examination revealed no postural tremor or resting tremor. T 2-weighted brain MR imaging showed a high-intensity signal in the left thalamus that involved the ventralis intermedius nucleus. Clinical recovery from the effect of the infarct on essential tremor was complete. Therefore, it seems that thalamic infarction in this patient had an effect on essential tremor similar to that achieved with thalamotomy.     

Isolated crossed superior rectus palsy in a midbrain infarction]

A 61-year-old man suddenly heard tinnitus and diplopia at night during watchinng television. A few days later he visited at our hospital. Neurologically he exibited marked isolated right superior rectus palsy which was also indicated by the Hess test. No other neurological abnormalities were found such as other ocular muscle paresis, cranial nerve palsies, hemiparesis, sensory impairement or cerebellar ataxia. MRI showed a left medial thalamic infarction extending to a rostral part of the midbrain anterolateral to the cerebral aqueduct at the superior colliculi level. Unilateral superior rectus palsy can rarely be caused by a contralateral midbrain infarction, because fibers from the subnucleus subserving the superior rectus decussate within the oculomoter nerve complex. In this case the crossing fibers toward the contralateral superior rectus may have been selectively involved by a tinny lesion in the area of the oculomotor nucleus. The patient had a slightly narrowed right palpebral fissure. It is indicated that crossing fibers toward the contralateral levator muscle of the eyelid may be also involved. The patient's diplopia completely resolved two months later after the onset.     

Persistent pure verbal amnesia and transient aphasia after left thalamic infarction

A 57-year-old right-handed man suffered persistent pure verbal amnesia (PPVA) and transient aphasia after left thalamic infarction. A neuroanatomical study with magnetic resonance imaging to identify the site of the lesion showed destruction of the internal medullary lamina (IML), mammillothalamic tract (MTT), the ventrolateral nucleus (VL) and the lower one-third of the medial nucleus. As regions critical for PPVA are unknown, we reviewed the cases of PPVA after left thalamic infarction reported in the literature. These suggest that confined destruction of the IML, MTT and VL in the left thalamus can produce PPVA.     

Sensory ataxic hemiparesis in thalamic hemorrhage

Ataxic hemiparesis with cerebellar-like features has been reported following infarction or hemorrhage of the thalamus. We describe five patients with incoordination and corticospinal tract signs in the limbs opposite a dorsolateral thalamic hemorrhage. In four patients the hemorrhage extended superiorly into the lateral ventricle, the adjacent paraventricular region, and the upper and medial parts of the posterior limb of the internal capsule. Instead of cerebellar dysfunction, these patients exhibited directional errors of movement that improved distinctly when performed under visual guidance. We explain the incoordination on the basis of conscious deep sensory loss in the involved limbs. Perception of light touch, painful pinprick, and temperature were preserved in all patients. We use the term "sensory ataxic hemiparesis" to distinguish these patients from those with "classic" ataxic hemiparesis and cerebellar-like features, a distinction that may be important when planning functional rehabilitation.     

Bilateral thalamic damage,cortical hypometabolism and behavioural disturbances

Thalamic damage could be responsible for reduced metabolism in anterior cortical areas. In order to investigate an anatomical lesion and impairment of regional blood flow (rCBF) in distant cortical areas, we studied by magnetic resonance imaging (MRI) and single photon emission computed tomography (SPECT) a patient with bilateral thalamic infarction, who presented with sudden consciousness impairment, drowsiness, gaze paralysis, dysphagia and bilateral Babinski sign. Three weeks later the neurological symptoms disappeared, but a severe mental deterioration was evident MRI showed thalamic bilateral damage of posterior and medial areas, involving part of the pulvinar, more evident for the right thalamus. A ^99mTc-HMPAO SPECT showed a decrease of rCBF over frontal and parietal regions, more evident for the right hemisphere. Six months later a severe memory impairment was still evident and MRI and SPECT picture were unchanged. The persistent memory defect could be related to a loss of cortical activation following the thalamic damage. The absence of primary lesions of cortical regions on CT scan and MRI and the neuroanatomical considerations on the diffuse projections running from medial nuclei and pulvinar to large parts of anterior neocortex supported this hypothesis.     

Thalamic hand dystonia: an MRI anatomoclinical study

Focal dystonia has been attributed to lesions involving the basal ganglia and/or thalamus. Hand dystonia was studied in a patient with a unilateral thalamic infarction documented by MRI. A 18-year-old girl presented with severe isolated dystonia of the right hand as a sequel of perinatal infarction. MRI scan revealed infarction affecting part of the dorsomedian, lateral posterior, ventral lateral, ventral posterior lateral nuclei, and centromedian-parafascicular nucleus of the contralateral thalamus. The unique MRI anatomoclinical presentation of this case, taken together with the literature data, could provide evidence that a lesion affecting one or several thalamic nuclei, including the centromedian nucleus, can induce hand dystonia.     

Abnormalities of thalamic activation and cognition in schizophrenia

OBJECTIVE: Functional and structural magnetic resonance imaging (MRI) was used to investigate relationships among structure, functional activation, and cognitive deficits related to the thalamus in individuals with schizophrenia and healthy comparison subjects. METHOD: Thirty-six schizophrenia subjects and 28 healthy comparison subjects matched by age, gender, race, and parental socioeconomic status underwent structural and functional MRI while performing a series of memory tasks, including an N-back task (working memory), intentional memorization of a series of pictures or words (episodic encoding), and a yes/no recognition task. Functional activation magnitudes in seven regions of interest within the thalamic complex, as defined by anatomical and functional criteria, were computed for each group. RESULTS: Participants with schizophrenia exhibited decreased activation within the whole thalamus, the anterior nuclei, and the medial dorsal nucleus. These nuclei overlap with subregions of the thalamic surface that the authors previously reported to exhibit morphological abnormalities in schizophrenia. However, there were no significant correlations between specific dimensions of thalamic shape variation (i.e., eigenvectors) and the activation patterns within thalamic regions of interest. Better performance on the working memory task among individuals with schizophrenia was significantly associated with increased activation in the anterior nuclei, the centromedian nucleus, the pulvinar, and the ventrolateral nuclei. CONCLUSIONS: These results suggest that there are limited relationships between morphological and functional abnormalities of the thalamus in schizophrenia subjects and highlight the importance of investigating relationships between brain structure and function.