PubMed Health⌕ Search

Biomedical subjects

A L Wolff

Publications and source records attributed to A L Wolff.

4 recordsLinked to original sources
PubMed2000

Functional neuroanatomy of smooth pursuit and predictive saccades.

We used PET to study differences in cerebral blood flow (CBF) in smooth pursuit, predictive saccades and fixation. Eye movements were monitored in the scanner. Compared with fixation, pursuit and predictive saccades activated a network of highly similar areas, including frontal eye fields, supplementary eye fields, V5 and medial cuneus. Our findings are consistent with non-human primate studies that suggest that pursuit and saccades are controlled by similar and adjacent neural areas. Pursuit was associated with greater activation of caudate than saccades, suggesting a role for basal ganglia in pursuit that is consistent with studies of neurological populations. Saccades were associated with greater activation of cerebellum and frontal eye fields. A frontal-cerebellar loop may be important in coordinating the preparation and timing of saccades in predictive tracking.

Adult↗
PubMed1999

Neural correlates of eye tracking deficits in first-degree relatives of schizophrenic patients: a positron emission tomography study.

BACKGROUND: Schizophrenia is thought to arise from the interaction of genetically mediated and environmentally triggered abnormalities in brain function. Reduced frontal activation, reported in schizophrenic patients, may be one expression of genetic risk. The present study investigated whether frontal activation in relatives of schizophrenic patients would be related to eye tracking deficits (ETD), which are considered a behavioral marker of risk for schizophrenia. METHODS: Subjects were first-degree relatives of schizophrenic patients (n = 17) and controls (n = 11). Relatives were divided into those with normal and abnormal pursuit based on qualitative ratings. Subjects were scanned using positron emission tomography and the H(2)15O bolus subtraction technique while performing smooth pursuit and fixation. Brain areas more active in pursuit than fixation were identified in the 3 groups. Correlations were used to investigate the relationship between activation of pursuit regions and pursuit gain in the relatives. RESULTS: Controls significantly activated frontal eye fields (FEFs) and posterior areas, including the motion processing area, V5, and cuneus. The 2 groups of relatives activated the same posterior regions as controls, but differed from each other in activation of FEFs. Relatives with normal tracking activated right dorsal FEFs while relatives with ETD did not. Individual subtractions revealed that 90% of controls and 100% of the relatives with normal tracking activated FEFs during pursuit compared with 42% of relatives with ETD (P = .009). Pursuit gain was significantly and selectively associated with percent activation of right dorsal FEFs (r = 0.74). CONCLUSIONS: Subtle frontal dysfunction seems to be a pathophysiological substrate of ETD in relatives of schizophrenic patients, and may be one aspect of genetically mediated differences in brain function relevant to schizophrenia.

Eye Movements↗
PubMed1999

Motor deficits and schizophrenia: the evidence from neuroleptic-naïve patients and populations at risk.

Patients with schizophrenia and high-risk populations have elevated rates of eye movement abnormalities. However, it is not known whether these abnormalities are specific to eye movements or whether they are also found in more traditional domains of motor control. Most studies examining the motor function of patients with schizophrenia have involved patients treated with medication; abnormalities in motor function could be a result of treatment rather than the disease itself. If motor abnormalities are related to schizophrenia, they should also be found in neuroleptic-naïve patients and possibly in high-risk populations in whom eye movement abnormalities are also observed. We reviewed relevant empirical papers published in the last 35 years. Results suggest that approximately one-fifth of neuroleptic-naïve patients with schizophrenia have increased rates of parkinsonism and neurological soft signs. In high-risk populations, replicated findings include delayed motor development in preschizophrenia subjects, and poor motor skills in the offspring of patients with schizophrenia. In first-degree relatives, increased rates of neurological soft signs were reported. These findings suggest that motor abnormalities are not limited to eye movements and may constitute markers of vulnerability. The literature has several weaknesses that should be addressed in future studies.

Adult↗