Biomedical subjects

Gordon F Sherman

Publications and source records attributed to Gordon F Sherman.

4 recordsLinked to original sources

PubMed2005

Relative sparing of primary auditory cortex in Williams Syndrome.

Williams Syndrome (WS) is a neurodevelopment disorder associated with a hemizygous deletion on chromosome 7. WS is characterized with mental retardation, severe visual-spatial deficits, relative language preservation, and excellent facial recognition. Distinctive auditory features include musical ability, heightened sound sensitivity, and specific patterns of auditory evoked potentials. These features have led to the hypothesis that the dorsal forebrain is more affected than the ventral. Previously, we reported primary visual area 17 abnormalities in rostral striate cortex, a region contributing to the dorsal visual pathway. Based on the dorsal-ventral hypothesis, and language and auditory findings, we predicted a more normal histometric picture in auditory area 41. We used an optical dissector method to measure neurons in layers II-VI of area 41 in right and left hemispheres of the same 3 WS and 3 control brains used in the area 17 study. There was a hemisphere by diagnosis interaction in cell packing density (CPD) in layer IV and in cell size in layer III between WS and control brains. Post hoc analysis disclosed in control brains, but not WS, a layer IV left > right asymmetry in CPD, and a layer III left < right asymmetry in cell size. WS brains showed more large neurons bilaterally in layer II and in left layer VI. Histometric alterations in area 41 were less widespread than rostral visual cortex. Also, there was less asymmetry in the WS brain. We interpret layers II and VI differences as reflecting increased limbic connectivity in primary auditory cortex of WS.

Adult↗

PubMed2003

Dyslexia linked to talent: global visual-spatial ability.

Dyslexia has long been defined by deficit. Nevertheless, the view that visual-spatial talents accompany dyslexia has grown, due to reports of individuals with dyslexia who possess visual-spatial strengths, findings of elevated incidence of dyslexia in certain visual-spatial professions, and the hypothesis that left-hemisphere deficits accompany right-hemisphere strengths. Studies have reported superior, inferior, and average levels of visual-spatial abilities associated with dyslexia. In two investigations, we found an association between dyslexia and speed of recognition of impossible figures, a global visual-spatial task. This finding suggests that dyslexia is associated with a particular type of visual-spatial talent-enhanced ability to process visual-spatial information globally (holistically) rather than locally (part by part).

Aptitude↗

PubMed2002

Spatial and nonspatial Morris maze learning: impaired behavioral flexibility in mice with ectopias located in the prefrontal cortex.

About half of BXSB/MpJ-Yaa (BXSB) mice have neocortical ectopias (misplaced clusters of neurons located in layer I of cortex). Previous behavioral studies have suggested that ectopic mice have superior spatial, but equivalent nonspatial, reference memory learning. However, since spatial and nonspatial learning were not assessed in the same apparatus and with the same testing procedure, it is unclear if this conclusion is accurate. We have created a new nonspatial Morris maze for mice that differs from the spatial task only in the type of cues that must be utilized to efficiently locate the platform (intra-maze black/white patterns vs. extra-maze room cues) and does not differ in the level of task complexity or the presence of objects within the maze. Ectopic mice were very good in utilizing extra-maze cues when learning the spatial version and in utilizing intra-maze cues when learning the nonspatial version of the Morris maze, while non-ectopics were not, suggesting that ectopics have superior spatial and nonspatial reference memory. Ectopias in BXSB mice are usually located in prefrontal and/or motor cortex. The prefrontal cortex is involved in behavioral flexibility (e.g. being able to easily switch from using spatial to nonspatial cues). Only ectopic mice with ectopias specifically located in the prefrontal region of cortex demonstrated difficulty switching from using extra-maze to intra-maze cues and vice versa. Thus, the presence of one or more ectopias in the prefrontal region of cortex disrupted one of the normal functions of the prefrontal cortex.

Animals↗

PubMed2002

Williams syndrome: neuronal size and neuronal-packing density in primary visual cortex.

BACKGROUND: Williams syndrome (WMS) is a rare, genetically based syndrome associated with a hemideletion in chromosome 7 (7q11.22-23) and characterized by a unique constellation of somatic, brain, and cognitive features. Individuals with WMS demonstrate an unusual and uneven neuropsychological profile showing cognitive and visual spatial deficits juxtaposed with relative language preservation and excellent facial recognition. OBJECTIVES: A neuroanatomical hypothesis for these behavioral findings suggests predominant involvement of the dorsal portions of the hemispheres relative to the ventral portions, including preferential involvement of peripheral visual field cortical representations over central representation. Predominant involvement of magnocellular visual pathways, as opposed to parvocellular pathways, is also suggested by this hypothesis. SUBJECTS: We examined primary visual cortical area 17 in the right and left hemispheres in 6 age- and sex-matched autopsy specimens from 3 WMS-affected brains (1 male and 2 females; mean [SD] age, 44 [14] years) and 3 control brains (1 male and 2 females; mean age, 43 [11] years). DESIGN: Neurons in layers II, III, IVA, IVB, IVCalpha, IVCbeta, V, and VI were measured using an optical dissector method to determine possible differences between WMS-affected and control brains in cell-packing density, neuronal size, and neuronal size distribution. RESULTS: We found abnormalities in peripheral visual cortex in WMS-affected brains, but not in magnocellular subdivisions. There was a hemisphere by layer IV interaction and a layer IV left hemisphere and diagnosis interaction in cell-packing density. Williams syndrome-affected brains showed increased cell-packing density in left sublayer IVCbeta and an excess of small neurons in left layers IVA, IVCalpha, IVCbeta, V, and VI. CONCLUSIONS: Cell measurements differ in peripheral visual cortical fields of WMS, with significantly smaller, more closely packed cells in some layers on the left side. These cell-packing density and neuronal size differences may be related to visuospatial deficits in this population.

Adult↗