Hippocampal–anterior thalamic pathways for memory: uncovering a network of direct and indirect actions

This review charts recent advances from a variety of disciplines that create a new perspective on why the multiple hippocampal–anterior thalamic interconnections are together vital for human episodic memory and rodent event memory. Evidence has emerged for the existence of a series of parallel temporal–diencephalic pathways that function in a reciprocal manner, both directly and indirectly, between the hippocampal formation and the anterior thalamic nuclei. These extended pathways also involve the mammillary bodies, the retrosplenial cortex and parts of the prefrontal cortex. Recent neuropsychological findings reveal the disproportionate importance of these hippocampal–anterior thalamic systems for recollective rather than familiarity-based recognition, while anatomical studies highlight the precise manner in which information streams are kept separate but can also converge at key points within these pathways. These latter findings are developed further by electrophysiological stimulation studies showing how the properties of the direct hippocampal–anterior thalamic projections are often opposed by the indirect hippocampal projections via the mammillary bodies to the thalamus. Just as these hippocampal–anterior thalamic interactions reflect an interdependent system, so it is also the case that pathology in one of the component sites within this system can induce dysfunctional changes to distal sites both directly and indirectly across the system. Such distal effects challenge more traditional views of neuropathology as they reveal how extensive covert pathology might accompany localised overt pathology, and so impair memory

Parietal motor syndrome: a clinical description in 32 patients in the acute phase of pure parietal strokes studied prospectively.

We prospectively studied motor symptoms in 32 patients with CT- or MRI-proven acute pure parietal stroke. A transient, mild, 'pseudoparesis' of the hand (90%), was noted, improved by visual attention and prompting, associated with non-awareness of muscle power (53%), transient soft pyramidal signs (50%), unilateral akinesia (100%) and motor hemineglect (37%) in non-dominant lesions. Lower motoneurone-type atrophy was not observed in this acute phase. We called 'poikilotonia' the striking unpredictable variations in muscle tone, ranging from extreme hypertonia to hypotonia, found in all patients. When maintaining postures, patients showed large oscillations (100%), laterodeviation or levitation of the arm (60%), especially in the case of large or posterior lesions, or, occasionally (3%), motor persistence or even hemicatalepsy (3%). Limb kinetic and manipulatory apraxia, with inadequate organization and anticipation of motor sequences and synergies, motor arrests, perplexity, unrecognizable gestures and loss of bimanual coordination, was a constant finding (100%). Other apraxias (62%) and difficulty in copying intransitive gestures of the hand (84%) were associated with posterior lesions involving the supramarginal gyrus. When reaching towards objects, all patients showed abnormal anticipatory hand shaping, but visuomotor ataxia (3%) was only seen with bilateral posterior stroke. Sensory (70%) or pseudocerebellar (4%) ataxia, was seen in both anterior and posterior lesions. Avoidance behaviors (34%) were not uncommon, but had no localizing value. Of the dyskinesias, hand dystonia (84%) was frequent, but athetosis (16%), asterixis (15%), postural tremor (15%), myoclonus (9%) and stereotypia (9%), were uncommon. The abnormal eye movements were unilateral hypo-akinesia of exploratory saccades (43%), abnormal ipsilateral pursuit and contralateral optokinetic nystagmus in the case of posterior lesions, and oculomotor apraxia with bilateral posterior lesions. In conclusion, parietal motor syndrome can be recognized during bedside examination, and probably reflects the loss of multiple sensory feedback to motor programs, especially those directed to the extrapersonal space

Démence callosale. trouble du comportement lors de myalinolyse centro- et extra-pontique

Introduction et Objectif. Un tableau démentiel lors de syndrome de Marchiafava-Bignami ou de myélinolyse centro-pontique est signalé. Le but de nos observations est d'en mieux définir les caractéristiques comportementales. Patients et Résultats. Nous avons étudié l'atteinte neuropsychologique et comportementale d'un homme de 57 ans souffrant d'un syndrome de Marchiafava-Bignami et d'une femme de 44 ans avec une myélinolyse centro- et extrapontique. Nous pouvons ainsi définir un tableau clinique que nous appelons démence callosale, caractérisé par : 1) une atteinte fronto-limbique avec une tendance à de fréquentes interjections grossières, des comportements répétitifs à connotation asociale, et l'alternance d'un manque d'incitation avec des périodes d'agitation; 2) certains éléments d'un syndrome de Balint (participation calleuse postérieure), dont un aspect pseudo-halluciné avec errance du regard ; 3) des signes de dysconnexion interhémisphérique et 4) des éléments suggérant une atteinte de la substance blanche, tels un faciès figé et une voix monotone. Conclusions. L'identification précoce d'une démence callosale apporte un indice précieux au diagnostic de myélinolyse centro- et extrapontique, en motivant la recherche clinique d'une dysconnexion interhémisphérique et la pratique d'une IRM cérébrale. La confirmation rapide d'une telle affection, parfois létale, permet la prise immédiate des mesures thérapeutiques indispensables (abstinence, correction électrolytique et carentielle)