Hypesthetic ataxic hemiparesis in a thalamic lacune

Right hemiparesis with an ipsilateral hypesthesia and ataxia developed in a 57-year-old man. Magnetic resonance imaging showed a left thalamic lacune bordering the medial portion of the posterior limb of the internal capsule. This finding implicated some pathogenetic mechanism of ataxic hemiparesis.     

Pure sensory stroke due to a pontine lacune

A 53-year-old hypertensive man presented with the sudden onset of an isolated lemniscal sensory syndrome of the entire left side of his body. Magnetic resonance images showed a small lacune in the right paramedian pons corresponding to the location of the medial lemniscus.     

The fallacy of ex-consequentia reasoning and the persistence of PTSD

Many individuals experience psychological distress after a potentially traumatic event, but only a minority develops chronic posttraumatic stress disorder (PTSD). According to the cognitive model of Ehlers and Clark (Behaviour Research and Therapy 38 (2000) 319), chronic PTSD results from distorted beliefs about the trauma or its sequelae. Given the availability of disconfirming information, why do such distorted beliefs persist? A recent promising line of research focuses on the "ex-consequentia" reasoning fallacy: "if I feel anxiety, there must be danger". Ex-consequentia reasoning may start a vicious circle in which subjective fear responses are used to erroneously validate thoughts of impending doom, which intensifies distress, etc. In other words, false alarms are not recognized and irrational beliefs are maintained. We previously found that other anxiety patients (Behaviour Research and Therapy 33 (1995) 917) and PTSD patients (Behaviour Research and Therapy 39 (2001) 1139) show ex-consequentia reasoning, that is, they appear to believe that anxiety symptoms imply the presence of danger. Interestingly, this was not restricted to situations relevant to the individual's anxiety disorder. Tentative data suggest that ex-consequentia reasoning is causally involved in the persistence of PTSD and anxiety disorders. These are presented and possible underlying mechanisms are discussed.     

The history of the cholinergic hypothesis

The cholinergic hypothesis of cognitive impairment and Alzheimer's disease has been for decades a “polar star” for studies on dementia and neurodegenerative diseases. Aim of the present article is to briefly summarize its birth and its evolution throughout years and discoveries. Putting the cholinergic hypothesis in an historical perspective, allows to appreciate the enormous amount of experimental and clinical research that it has stimulated over years and the impressive extent of knowledge generated by this research. While some of the assumptions at the basis of its original formulation are disputable in the light of recent developments, the cholinergic hypothesis has, however, constituted an invaluable stimulus to better understand not only the anatomy and the biochemistry of the cholinergic systems of brain connections but also its developmental biology, its complex relationships with trophic factors, its role in cognitive functions. Thus, rather than being consigned to history, the cholinergic hypothesis will likely contribute to further understanding dementia and neurodegenerative diseases and will hopefully be integrated in novel therapies and treatments.     

The neuroanatomical basis of the Gambler's fallacy: A univariate and multivariate morphometric study

Human decision‐making can be irrational, as in the case of the gambler's fallacy (GF). Converging evidence from behavioral and functional neuroimaging studies has suggested that a hyperactive cognitive system and a hypo‐active affective system contribute to the false world model that generates the GF. However, the neuroanatomical basis underlying the GF remains unclear. The current study addressed this issue by collecting high‐resolution magnetic resonance anatomical images from a large sample of 350 healthy Chinese adults. Univariate voxel‐based morphometry (VBM) analysis suggested that the gray matter volume (GMV) in the anterior cingulate cortex (ACC) and medial temporal lobe (MTL) (two regions of the cognitive system) showed negative correlations with the degree of GF, while the GMV in the striatum and orbitofrontal cortex (OFC; two regions of the affective system) showed positive correlations. Further multivariate VBM analysis showed that the GMV in these regions could potentially predict the degree of GF. Moreover, a mediation analysis suggested that the GMV in MTL, ACC, and OFC mediated the relationships between the cognitive abilities or affective decision‐making performance and the GF. Results of our study help us to understand the potential neural bases of the cognitive system's constructive role and the affective system's destructive role in decision making.     

Intrusions in schizophrenic speech: The immediacy hypothesis vs the lapse of attention hypothesis

Speech samples emitted by schizophrenics and individually matched normals were compared to test whether the immediacy hypothesis or the lapse-of-attention view explains the basis of schizophrenic verbal behavior more effectively. Intrusions in speech were employed as indicators of fluctuating attention, and the guessability of words deleted from speech (“cloze”) was used as a measure of general communicability. Since the inclusion or exclusion of intrusions made no difference with respect to the differential communicability of the speech of normals and schizophrenics, we concluded that the immediacy hypothesis was more consonant with the data than the lapse-of-attention view.     

The vesicular hypothesis questioned

Roger Marchbanks considers John Heuser's evidence in favour of the vesicular hypothesis for the release of transmitter from the presynaptic terminal, and compares this evidence with the biochemists data. He concludes that the evidence is more strongly in favour of a membrane channel gating theory for the release of transmitter from the presynaptic cytoplasm, for which the vesicles serve as a reserve pool of transmitter.     

The gabaergic hypothesis of depression

1. GABAergic mechanisms have been generally ignored in the study of mood disorders and antidepressant drug (AD) action. Recently data have accumulated indicating that GABAergic mechanisms may be involved in both of these. 2. Mood disorders: GABA levels are reported to be low in the CSF and plasma of depressed patients and are related to mood changes. GABAB receptors are decreased in the frontal cortex in two rodent behavioral models of depression and GABA release is reported diminished in the hippocampus. GABAergic drugs (progabide, fengabine) reverse the behavioral deficits in the rodent models and exert clear therapeutic effects in depressed patients. 3. AD action: In behavioral models imipramine upregulates GABAB receptors only in those animals which respond behaviorally to the AD. In naive rats repeated administration of varied ADs upregulates GABAB receptors in the frontal cortex whereas non-ADs (including amphetamine) do not. Bicuculline inhibits the action of imipramine in the learned helplessness model. GABAA receptor stimulation enhances noradrenaline release in the ventral NA pathway. 4. Conclusions: GABAergic mechanisms likely play a role in the modulation of mood and increasing GABAergic tone exerts and antidepressant effect. Actions at GABA synapses appear to be a fundamental facet of ADs, perhaps together with beta-adrenoceptor mediated events.     

The amyloid cascade hypothesis

The amyloid deposits in the brains of patients with Alzheimer's disease have attracted attention and are now considered not only an essential requirement for pathological diagnosis but also an important clue to the pathogenesis of the disease. This article looks critically at the basis of the “amyloid cascade hypothesis” to conclude that there are many issues that need to be resolved since they are inconsistent with the hypothesis.