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.     

Solitary thalamic abscess

Solitary thalamic abscess is a rare entity and very few cases are reported in the literature. A case of congenital heart disease presenting with solitary thalamic abscess and successful management by simple burrhole aspiration is reported.     

Acute thalamic esotropia

Three men developed acute esotropia, stupor, and impaired upward gaze. Vestibulo-ocular stimulation showed that the adducted eye remained immobile while the fellow eye responded normally. The alteration of consciousness, the long-tract neurologic signs, and the esotropia quickly resolved. Upgaze paresis and brief bursts of convergence-retraction nystagmus were the major residual signs. Imaging techniques demonstrated lesions of the contralateral posterior thalamus in each patient. Several mechanisms are proposed to explain the acute esotropia. Impairment of monocular projections in the contralateral posterior thalamus could disinhibit neurons in the oculomotor complex, or ischemia of inputs to neurons involved with vergence control in the midbrain could result in tonic activation of the medial rectus. The clinical and radiographic findings are consistent with infarction in the territory of penetrating branches of the basilar-communicating (mesencephalic) artery. Embolism to the top of the basilar artery is presumed to be the precipitating event.     

Two cases of thalamic infarction presenting with "thalamic astasia"]

We report two cases of so-called 'thalamic astasia', associated with thalamic infarction. A 76-year-old-man suddenly noted to fall down to the left side without severe hemiparesis. An MRI showed an infarction in the superolateral portion of the right thalamus. Over eight weeks, his astasia gradually disappeared. A 69-year-old-man suddenly noted inability to stand with loss of balance. He showed mild hemiparesis, hypesthesia and cerebellar signs on the right side. Although right hemiparesis was slight, he was unable to stand by himself. An MRI demonstrated an infarction in the ventrolateral to ventroposterior portion of the left thalamus. Three weeks later, his symptoms except for cerebellar ataxia remarkably disappeared. The overlapped MRI lesions of these two cases were localized in the ventrolateral thalamus, such as Vimi (nucleus ventrointermedii internus), Vci (nucleus ventrocaudalis internus), Cemc (nucleus centralis thalami magnocellularis). These lesions are so-called 'vestibular thalamic nuclei', in which fibers from vestibulocerebellum are terminated. Involvement of the thalamic connectivity explains that two patients noted inability to stand. Thus we concluded that these two patients had thalamic astasia, described by Masdeu and Gorelick.     

Amnesia in thalamic infarction

Restricted thalamic infarctions are in man a useful model for investigating the consequences of limited diencephalic lesions on memory and verbal or visual learning. Two new cases of amnesia with thalamo-sub-thalamic infarctions are presented, with a general review of the problem. The gathering of the different cases according to the vascular thalamic territories and, as a consequence, to nuclear or associative structures concerned, allows a better approach of the relations between amnesia and infarctions. Uni or bilateral anterior lesions are the cause of more important and pure memory deficits, posterior infarctions are more often associated to language involvement or spatial cognitive problems which interfere with memorizing.     

Hypesthetic-ataxic-hemiparesis in thalamic hemorrhage

Acute onset hypesthetic-ataxic-hemiparesis is described in two hypertensive patients. Computed tomography (CT) showed an area of increased attenuation consistent with blood in contralateral thalamus. The pathophysiologic implications of the cerebellar and pyramidal system in thalamic hemorrhage is discussed.     

Aphasia after left thalamic infarction

We examined a 70-year-old woman who became aphasic after a left thalamic infarction. Computed tomographic scan showed injury that was largely limited to the ventral anterior and rostral ventral lateral thalamic nuclei. Speech was characterized by reduced voice volume, impaired auditory and reading comprehension, perseverations, intermittent use of jargon, fluctuations in the ability to perform confrontation naming, extraneous intrusions, verbal paraphasia, intact repetition skills, and fluent speech that was laconic but grammatically correct. We propose that the deficits after left thalamic injury can be grouped into the following four large clusters: extrapyramidal deficits (decreased or fading voice volume), deficits in lexical access (anomia, verbal paraphasia), deficits in vigilance (neologisms, intrusions, fluctuating performance, jargon, perseverations), and comprehension defects.     

The organization of thalamic connections

Connections ascending to the thalamus. Contrary to classical opinion, all thalamic nuclei receive extrathalamic afferents. Segregation or convergence within a topographically defined nucleus represent two modalities of thalamic afferents. In addition, certain topographically organized thalamic afferents possess "privileged" or primary "targets" in the thalamic nucleus while others possess supplementary "targets" in other thalamic nuclei (see cerebellar, pallidal and spinothalamic projections). Ascending connections from several brain stem structures can converge on the same nucleus or diverge to several thalamic nuclei. Thalamic connections with the telencephalon. Methods for determining axonal transport have demonstrated that all thalamic nuclei, with the exception of the reticular nucleus and the ventral part of the lateral geniculate body, project towards the cerebral cortex. Four nuclear complexes can be recognized in the cat as a function of the different modalities of localization, concentration and lamination of the projections towards the cortex and the central grey nuclei. In general, the thalamocortical connections have reciprocal ipsilateral corticothalamic projections originating in the infragranular layers of the cerebral cortex. The reticular nucleus and the ventral part of the lateral geniculate body, which is not projected to the cerebral cortex, are exceptions. Each cortical area receives a "privileged" connection from a thalamic nucleus and a supplementary connection- from one or several other thalamic nuclei. The "privileged" connections usually pass to the fourth and third layers of the neocortex, and sometimes also to the first layer. In contrast, the supplementary connections pass to different superficial or deep cortical layers. Each nucleus is formed of subunits which possess different hodologic and topographic characteristics as a function of the nucleus considered. Convergence or divergence of thalamocortical and corticothalamic projections on the different thalamic nuclei, as well as the laminar distribution of efferents in the cerebral cortex, are related strictly to the hodologic organization of different cellular subunits constituting the nuclei. Concentration or diffusion of thalamic projections on cerebral cortex is related more to the single or multiple projection of cell populations belonging to a thalamic nucleus than to widespread collateralization of thalamocortical axons.     

Cheiro-oral-pedal syndrome in thalamic infarction

Sensory disturbance around the corner of the mouth, in the palm of the hand and in the foot on the same side (cheiro-oral-pedal syndrome) has been reported only in 2 patients with brainstem lesion. We report 2 cases of cheiro-oral-pedal syndrome; the causative lesion was revealed by magnetic resonance imaging to be in the ventral posterolateral and ventral posteromedial nuclei of the thalamus.     

Surgical approaches to thalamic tumors

The paper summarizes the results of surgical treatment of patients with thalamic tumors of different topographic variants. Since 1985 till 2010 127 patients were operated, 147 direct surgical interventions were performed. Repeated surgeries were required due to partial resection of a tumor or recurrence. In most cases resection of tumors was performed via transcallosal (48%) and occipital interhemispheric (29%) approaches. Less common approaches included transcortical (frontal, temporal, parietal) (14%), pterional through lateral and basal parts of Sylvian fissure (6%) and subtentorial supracerebellar (3%). Selection of approach is based on topographic features of tumor within thalamus, direction of its growth and relations with adjacent structures (internal capsule, brainstem, hypothalamus, ventricular system). Each approach has its own advantages and drawbacks which are highlighted in the paper.     

Motor neglect of thalamic origin

The clinical picture of thalamic motor neglect is identical to those of motor neglect in general, the major symptom of which being an underutilization of one side of the body in the absence of sensory-motor defect. Several thalamic nuclei can be implicated on the grounds of pathological and experimental data, most frequently the ventro-lateral nucleus. The prevalence of left neglect is not so obvious in the case of thalamic than in the case of other sites of lesions. Motor neglect appears as a disorder in the triggering of the brain structures network which program and prepare movement in several circumstances; attentional tasks are only a particular circumstance. Some thalamic nuclei are the site of hypoactivity in the case of frontal motor neglect in the monkey, as shown by anatomical and functional studies; this emphasizes the strong participation of thalamus to the motor network, the dysfunction of which can induce a motor neglect.