Damage to the dorsomedial thalamic nucleus, central lateral intralaminar thalamic nucleus, and midline thalamic nuclei on the right-side impair executive function and attention under conditions of high demand but not low demand.

This study reports a patient, OG, with a unilateral right-sided thalamic lesion. High resolution 3T magnetic resonance imaging revealed damage to the parvicellular and magnocellular subdivisions of the dorsomedial thalamus (DMT), the central lateral intralaminar nucleus (also known as the paralamellar DMT), the paraventricular and the central medial midline thalamic nuclei. According to the neuropsychological literature, the DMT, the midline and intralaminar thalamic nuclei influence a wide array of cognitive functions by virtue of their modulatory influences on executive function and attention, and this is particularly indicated under conditions of low arousal or high cognitive demand. We explored this prediction in OG, and compared his performance on a range of low and high demand versions of tests that tapped executive function and attention to a group of 6 age- and IQ-matched controls. OG, without exception, significantly under performed on the high-demand attention and executive function tasks, but performed normally on the low-demand versions. These findings extend and refine current understanding of the effects of thalamic lesion on attention and executive function.

Stimulus timing by people with Parkinson's disease.

Previous literature suggests that Parkinson's disease is marked by deficits in timed behaviour. However, the majority of studies of central timing mechanisms in patients with Parkinson's disease have used timing tasks with a motor component. Since the motor abnormalities are a defining feature of the condition, the status of timing in Parkinson's disease remains uncertain. Data are reported from patients with mild to moderate Parkinson's disease (both on and off medication) and age- and IQ-matched controls on a range of stimulus timing tasks without counting. Tasks used were temporal generalization, bisection, threshold determination, verbal estimation, and a memory for duration task. Performance of patients was generally "normal" on all tasks, but significant differences from performance of controls were found on the memory for duration task. Among the "normal" effects noted were arithmetic mean bisection, asymmetric temporal generalization gradients, and subjective shortening on the memory for duration task. The results suggest (a) that some previous reports of timing "deficits" in Parkinson's patients were possibly due to the use of tasks requiring a timed manual response and (b) small differences between patients and controls may be found on tasks where two stimuli are presented on each trial, whether patients are on medication or off it.

A cognitive neuropsychological and psychophysiological investigation of a patient who exhibited an acute exacerbated behavioural response during innocuous somatosensory stimulation and movement.

We report findings from a cognitive neuropsychological and psychophysiological investigation of a patient who displayed an exacerbated acute emotional expression during movement, innocuous, and aversive somatosensory stimulation. The condition developed in the context of non-specific white matter ischaemia along with abnormalities in the cortical white matter of the left anterior parietal lobe, and subcortical white matter of the left Sylvian cortex. Cognitive neuropsychological assessment revealed a pronounced deficiency in executive function, relative to IQ, memory, attention, language and visual processing. Compared to a normal control group, the patient [EQ] displayed a significantly elevated skin conductance level during both innocuous and aversive somatosensory stimulation. His pain tolerance was also significantly reduced. Despite this, EQ remained able to accurately describe the form of stimulation taking place, and to rate the levels of pain intensity and pain affect. These results suggest that EQ's exaggerated behavioural response and reduced pain tolerance to somatosensory stimulation may be linked to cognitive changes, possibly related to increased apprehension and fear, rather than altered pain intensity or pain affect per se.

Recognition memory abnormalities in asymptomatic biological parents of a patient with schizophrenia.

BACKGROUND: Recognition memory dysfunction has been frequently reported in schizophrenic populations, and has been linked with the development of delusions and thought disorder. A range of neuropsychological abnormalities have also been documented in the biological asymptomatic relatives of patients with schizophrenia; however, recognition memory has not been one of them. AIM: This study was carried out in order to investigate: (i) verbal and facial recognition memory in terms of accuracy and false alarm rates; and (ii) contributions from the episodic and semantic memory systems to recognition memory, in the biological asymptomatic parents of a reported schizophrenic patient and a set of male and female psychotic controls. RESULTS: Gender differences failed to emerge between the psychotic controls on any of the recognition measures (discrimination accuracy, response bias, hit and false alarm rates, 'remember' and 'know' recognition memory decisions). However, there was evidence of recognition dysfunction in the female relative, and to a lesser extent, in the male. Both parent's recognition memory performance profiles were marked by a pathologically elevated false alarm rate, and an increased dependence 'remember' judgements, i.e. input from the episodic memory system, to drive recognition memory decisions. CONCLUSIONS: These findings are discussed in the context of models of episodic and semantic memory impairment in schizophrenia.

Contribution of the left dorsomedial thalamus to recognition memory: a neuropsychological case study.

This study reports a patient with a unilateral left thalamic lesion which was centred on the dorsomedial thalamic nucleus. Cognitive neuropsychological assessment revealed a severe impairment in verbal memory and symptoms of executive dysfunction, in the presence of relatively intact visual and facial recognition, working memory, praxis, language and IQ. Verbal and visual recognition memory were investigated using the remember-know paradigm. The results indicated a profound impairment in recollection-driven verbal recognition memory. These results are discussed in the context of the role of the dorsomedial thalamic nucleus in recognition memory, and functional models of memory.

The delusions of Capgras and intermetamorphosis in a patient with right-hemisphere white-matter pathology.

Previous neuropsychological studies have demonstrated an association between person misidentification and right-hemisphere dysfunction. In the study reported here, we explore the contribution of facial and visual recognition impairments in a patient with right-hemisphere subcortical white-matter pathology in the frontal and parietal lobes and a diagnosis of vascular cognitive impairment. The patient displayed false recognition of unfamiliar faces and deficient retrieval of key biographic detail for famous faces. These results are discussed in the context of the contribution of deficiencies in the visual system and subcortical white-matter lesions to the development of Capgras delusion.

A review of the phenomenology and cognitive neuropsychological origins of the Capgras syndrome.

In this article the epidemiology, aetiology, neuroanatomy and neuropsychology of the Capgras syndrome (CS) are reviewed in detail. CS is characterized by the delusional belief that one or a few highly familiar people have been replaced by impostors who are physically very similar to the original/s. The patient acknowledges that the double and known person look alike, but maintains the belief that the significant person, in psychological terms, is absent. CS is relatively rare, occurring predominantly in the context of schizophrenia, and was traditionally considered to have its origins in psychodynamic conflict. More recently, however, it has been estimated that between 25 and 40% of cases are associated with organic disorders, which include dementia, head trauma, epilepsy and cerebrovascular disease. Neuroimaging evidence suggests a link between CS and right hemisphere abnormalities, particularly in the frontal and temporal regions. Neuropsychological research has provided empirical support for these findings, by consistently reporting the presence of impairments in facial processing--an established right hemisphere function. It is likely that the study of this symptom will lead to a greater understanding of the neurological basis of psychotic experiences and may provide a paradigm for how the psychoses should be investigated.

A neuropsychological perspective on three schizophrenic patients with midline structural defects.

BACKGROUND: The relationship between midline structural defects and schizophrenia remains unclear, although a number of neuroradiological studies have reported an association between schizophrenia and a range of anomalies. METHOD: Three patients are reported, each diagnosed with schizophrenia and neuroradiological evidence of midline structural anomalies. MRI scans are reported in conjunction with performance over a range of neuropsychological tests designed to assess frontal and lateralised cognitive functions. RESULTS: Evidence of anterior dysfunction was present in all three cases, while on an individual basis patients displayed varying patterns of preserved and dysfunctional cognitive processing. CONCLUSION: The reported findings raise a number of interesting issues regarding the nature of hemispheric involvement in schizophrenia.

Visual processing in patients with Frégoli syndrome.

We investigated four paranoid schizophrenic patients diagnosed with Frégoli delusion, and four matched psychotic controls. Neuropsychological testing included visual and verbal recognition memory, in addition to a comparison of left and right hemispheric processing of two different classes of stimuli, animate and inanimate objects. Performance on the recognition memory test failed to discriminate between the two psychotic groups on the basis of facial recognition, however, the patients with Frégoli delusion failed to show the right hemisphere processing advantage for the animate class of stimuli found for the set of norms and also present in the psychotic control group. These results are discussed in the context of both current theories of the delusional misidentification syndromes in general, and models of facial recognition in particular.

Relationship between cortical lamination and texture sensitivity in complex neurones of the striate cortex in cats.

The present study provides detailed anatomical evidence that the strongly texture-sensitive complex neurones of the cat's striate cortex constitute a discrete subset of all complex neurones, and lie in two bands, deep in lamina III and in lamina V. Physiological properties of simple and complex striate cortical neurones were characterized extracellularly in lightly anaesthetized cats by use of micropipettes filled with 12% Fast Green FCF dye in 2.0 M sodium chloride. Complex neurones were further subdivided on the basis of their length-summating properties for an optimally oriented bar into "standard," "special," or "intermediate" categories and on the basis of their tuning and degree of sensitivity to motion of random texture. Extracellular dye marks were made at strategic locations along each microelectrode track, especially at the site of recording from strongly texture-sensitive complex neurones. Tracks were reconstructed with the aid of the histologically recovered dye marks in sections counterstained with cresyl violet to reveal cortical lamination. The results confirm and refine the inference made by Hammond and MacKay (Exp. Brain Res. 22:427-430, '75; Exp. Brain Res. 30:275-296, '77) and the gross observations from 2-deoxyglucose uptake studies by Wagner, Hoffmann, and Zwerger (Brain Res. 224:31-43, '81) concerning the laminar distribution of texture-sensitive complex neurones in the cat's striate cortex.