Thalamic spindles in an isolated and perfused preparation in vitro

Intracellular recordings were obtained from thalamic nuclei neurones in isolated and perfused whole brains of adult guinea pigs in vitro. Thalamic neurones presented the same basic membrane properties in this preparation as in slices. The majority of cells displayed, in addition, spontaneous spindle oscillations similar to those observed in the cat in vivo. This activity could be blocked by the cholinergic agonist carbachol perfused at 10(-4) M. Thalamic spindles could also be recorded in decorticated preparations, in which perfusion to the cerebral cortex was interrupted. Such preparations could be useful for studying in vitro the spindle generating mechanism in rodents as well as some aspects of brainstem/diencephalic interactions related to the control of sleep and arousal.     

Developmental topographical disorientation: case one

Topographical disorientation is the inability to orient within the environment, usually acquired from lesions to different cerebral regions participating in the attentional, perceptual or memory functions involved during navigation. We present the first case of a patient with topographical disorientation in the absence of any structural lesion and with intact sensory and intellectual function. Experimental tests in both real and virtual environments revealed a selective impairment in forming a mental representation of the environment, namely a cognitive map. Consistent with the patient's behavioural findings, a functional magnetic resonance imaging (fMRI) study showed lack of activation in the hippocampal complex and the retrosplenial cortex while forming a cognitive map of the environment. Although the lack of neural activity results in a negative finding that generally has low interpretative value, in this specific case our findings may provide useful information. First, in a group of healthy control subjects performing the same task, activity within the hippocampal complex and retrosplenial cortex were detected in each individual participant. Second, we found that within the same regions (showing lack of neural activity while forming a cognitive map of the environment) increased neural activity was detected while the patient was performing a different navigation task. This case is the first evidence reported in the literature showing that topographical disorientation may occur as a developmental defect causing a lifelong disorder affecting daily activities.     

Global spatial disorientation: Clinico-pathologic correlations

Two patients presenting with the acute onset of bilateral parietal lobe damage showed initially the features of Balint's syndrome. After most of its manifestations had cleared, both patients exhibited severe disorders of spatial orientation: acoustic ataxia, inability to localize objects in space. In addition, 1 patient showed a topographical disorientation and abnormalities of whole body movements. This patient came to post-mortem examination, which revealed bilateral and fairly symmetrical old and recent infarctions of the superior parietal lobules.In the light of these observations and previous reports, it is suggested that the reported abnormalities of whole body movements can be explained on the basis of a visuo-motor intrahemispheric disconnection due to the bilateral lesion of the dorsal parietal lobe. In addition, the global spatial disorientation is analyzed and is thought to be the manifestation of a derangement of a specific function centered in the parietal lobe. Moreover, it is pointed out that topographic disorientation does not require the concomitant failure of oculomotor mechanisms for its production.The topography of the anatomical lesion is considered in relation to current concepts on brain damage after severe hypotension and cardiac arrest. It is concluded that this group of patients is most likely at risk of developing behavioural abnormalities akin to the ones here reported.     

Transient topographical disorientation

Transient topographical disorientation (TTD) is a short-lasting inability to find one's way in a familiar environment, while the patient remains conscious and is able to recall what happened. We report the study of 10 patients with episodes of TTD, studied on the days following the last episode. The episodes of TTD could be separated into two types: the patients either reported difficulties in spatial orientation with preserved abilities to recognize landmarks and objects, or the difficulties appeared with the recognition of landmarks. Tests exploring spatial orientation, as well as higher visuoperceptive capacities were altered in most of the patients and brain SPECT showed hypoperfusion of the right hemisphere in all patients, which could also be demonstrated 2 years later in some cases. Altogether, our findings suggest that TTD is frequently associated with a more persistent right hemisphere dysfunction of unknown cause. This chronic alteration could represent either a sequel of the acute episode or a preexisting right hemisphere deficit, which inclined the acute insult to be manifested as TTD.     

Thalamic hemorrhage: clinical-CT correlations

We studied 50 patients with thalamic hemorrhage, 84% with hypertension. Five patients had hematomas less than 8 mm and signs that resolved within 4 days. Two patients had headache, papilledema, and hemorrhage contiguous with the lateral ventricles. Twenty-four had hemiparesis, parenchymal hemorrhage 9 to 30 mm, and no ventricular blood. Nineteen had a larger hemorrhage and intraventricular hemorrhage, impaired consciousness, hemiparesis, and pupillary abnormalities; 12 had vertical gaze impairment, and all 19 patients died.     

Thalamic tumors: clinical presentation

INTRODUCTION: Thalamic tumors (TTs) account for approximately 1% of all intracranial neoplasms. TTs are seen predominantly in children and young adults. Most childhood neoplasms in this location are of glial lineage, a large proportion being low-grade tumors. The evolution of symptoms before diagnosis is characteristically shorter in children than in adults. CLINICAL PRESENTATION: Clinical features of TTs reflect the pressure of the mass on the cerebrospinal fluid pathways, the pyramidal tracts, the thalamic nuclei and the optic radiations. In this paper, we review the clinical data of 20 children with TTs seen at our hospital and compare the findings with those in the current literature. An acute presentation is not rare and was encountered in 20% of our patients, although most individuals had a subacute or slow evolution. Symptoms and signs of raised intracranial pressure (65%), motor deficits (40%), and seizures (35%), alone or in combination, were the most frequent manifestations of TTs. Behavioral and mental changes are not uncommon in TTs and were found in 25% of our patients. Involuntary movements (10%) and the classic thalamic syndrome (5%) were quite exceptional. Infants and young children with TTs may present with macrocephaly, psychomotor delay, and failing vision or disorders of ocular movements.     

Neuropsychological aspects of disorientation

Patients were asked twelve orientation questions before ECT and during the recovery period (the postictal confusional state) following ECT. Disorientation was more severe in the elderly. The different orientation items did not recover simultaneously; different recovery times may enable patients to give responses that are logical contradictions. While certain models (e.g., "person" versus "place" versus "time") may be useful in describing the differential recovery of orientation items, other models based on memory will probably prove more useful in delineating what causes this differential recovery. Patients gave responses to age and current year that were displaced backwards in years from the correct response. It is suggested that this displacement represents retrograde amnesia. As the postictal confusional state cleared, however, these backwardly displaced responses decreased in years of remoteness, thus showing a pattern of "shrinkage" that is similar to shrinking retrograde amnesia following head-injury. It is suggested that this result supports Ribot's law of regression.     

Thalamic neglect

Thalamic lesions can provoke negligence behavior with various, sometimes dissociated manifestations: motor negligence or reduction in use of one half of the body whatever the direction of the gesture or the half-space in which it occurs; extinction phenomena demonstrated without difficulty for visual, somatesthetic and auditory modalities; spatial negligence involving attentional and intentional components, often difficult to distinguish. Negligence of this type is mainly the result of right sided lesions, with several non-exclusive explanations: natural predominance of the left hemisphere, activating role of language with respect to the left hemisphere, capacity of the right hemisphere to be "attentive" to bath half-spaces in contrast to the left hemisphere, attentive to the right half-space only.     

Thalamic neglect

Three patients with right thalamic hemorrhage showed contralateral neglect and limb akinesia. They also had anosognosia, visuospatial disorders, and emotional flattening. In animals, neglect can be induced by lesions along a cortico-limbic-reticular loop including the intralaminar thalamic nuclei. We propose that an activation defect is responsible not only for the neglect and akinesia, but also for the visuospatial and emotional defects usually associated with right-hemisphere cortical dysfunction.     

Thalamic aphasia

Summary Four patients with aphasia due to small circumscribed thalamic lesions are presented. A review of the literature on thalamic aphasia revealed 16 similar cases. While the general consensus that only left-sided thalamic lesions are associated with aphasia is confirmed, analysis of the sites of the thalamic infarctions and the dysphasia elements did not reveal an unequivocal correlation. The explanation of this finding is that (a) disruption of any circuit, whether taking place in the connections or in the nuclei, leads to dysfunction and (b) thalamofrontal connections are not topographically arranged according to the thalamic nuclei, but show a frontal rostrocaudal/thalamic mediolateral interrelationship irrespective of thalamic nuclear masses.     

Thalamic ataxia

Summary Seventeen patients with hemiataxia as a manifestation of thalamic infarction were studied. Hemiataxia had the main clinical characteristics of a cerebellar type of ataxia, though it never occurred in isolation, being associated with ipsilateral sensory disturbance (hemiataxia hypaesthesia) in 7 patients, with ipsilateral sensory disturbance and hemiparesis (hypaesthetic ataxic hemiparesis) in 8 patients, and with hemiparesis (ataxic hemiparesis) in 2 patients. Recovery was good, and in all patients the sensory and motor disturbances improved or cleared before the hemiataxia. All patients had an infarct involving the lateral part of the thalamus (thalamo geniculate territory in 16, tuberothalamic territory in 1), also affecting the posterior limb of the internal capsule (PLIC) in 7 patients. Hemiataxia seemed linked to involvement of the caudal part of the ventral lateral nucleus of the thalamus or the immediately adjacent medial part of the PLIC. These structures are near the corticospinal pathways and the ventral posterior nucleus of the thalamus, explaining why hemiataxia is associated with hemiparesis or hypaesthesia in this type of infarct.