Search

Selective impairment in recognition of faces (prosopagnosia) resulting from certain localized cortical lesions has been advanced as an argument for a face specific brain module. The argument is claimed to be strengthened by the discovery of an inversion superiority effect in the recognition of faces by a prosopagnosic patient (Farah et al., Vis Res 1995b;35:2089-2093). The present paper reports an inversion superiority effect in the recognition of faces and shoes in a visual agnosic patient. The finding raises the possibility that several classes of orientationally polarized objects, of which shoes and faces are examples, will exhibit inversion superiority.

A brain-damaged patient is described whose pattern of performance provides insight into both the functional mechanisms and the neural structures involved in visual mental imagery. The patient became severely agnosic, alexic, achromatopsic and prosopagnosic following bilateral brain lesions in the temporo-occipital cortex. However, her mental imagery for the same visual entities that she could not perceive was perfectly preserved. This clear-cut dissociation held across all the major domains of high-level vision: object recognition, reading, colour and face processing. Our findings, together with other reports on domain-specific dissociations and functional brain imaging studies, provide evidence to support the view that visual perception and visual mental imagery are subserved by independent functional mechanisms, which do not share the same cortical implementation. In particular, our results suggest that mental imagery abilities need not be mediated by early visual cortices.

In this study we report a patient, MG, who following rupture of left posterior communicating artery exhibited an amnesic-confabulatory syndrome. Neuropsychological examination showed severe impairment on episodic memory tasks, which were marred by florid but plausible and semantically appropriate confabulation. Performance on tasks involving various kinds of semantic knowledge was normal or only mildly impaired. Performance on tasks traditionally considered sensitive to frontal dysfunction was severely impaired with the exception of Cognitive Estimates where MG's performance was completely normal. There was no evidence of structural (CT scan) or metabolic (SPECT) damage to the frontal lobe. It is argued that tasks traditionally considered sensitive to frontal dysfunction are not specifically implemented by cognitive resources based on frontal structures. MG's confabulation is discussed in terms of a possible disruption of cognitive functions involved in the control of the subjective experience of feeling of remembering.

We report the case of a patient who, after sequential bilateral strokes in the occipital regions sparing the primary visual cortex, developed a severe deficit of colour perception. At variance with other reports of acquired achromatopsic patients, she showed a perfectly vivid visual imagery for colours. These findings, together with similar data in domains other than colour processing, challenge the theories which posit that the same cognitive processes are involved in both the perception and the retrieval from memory of a given stimulus.

We report a case of neuromuscular disease overlap between myasthenia gravis and Lambert-Eaton syndrome (LES). Clinical features were those of LES and occurred insidiously in this 68-year old man: proximal weakness predominant in the lower limbs, generalized areflexia, dryness of the mouth and partial right eye palsy. Investigations disclosed a small cell lung cancer. On the other hand, an electrophysiological study showed low amplitude of all motor evoked potentials, and significant decrement in the median nerve at repeated 3 Hz stimulation, but failed to disclose any increment of the motor evoked potential in abductor digiti minimi pedis muscle after both maximal voluntary contraction and repeated 20 Hz stimulation. In addition, the patient improved under anticholinesterase drugs, but failed to respond to guanidine. Titres for both anti-acetylcholine-receptor antibodies and calcium channel antibodies were negative. The relationship between our case and recently reported cases of co-existence of the Lambert-Eaton myasthenic syndrome and myasthenia gravis is discussed.