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T Hedley-Whyte

Publications and source records attributed to T Hedley-Whyte.

6 recordsLinked to original sources
PubMed1999

[The role of radiotherapy in the treatment of malignant meningiomas].

PURPOSE: Most malignant meningiomas will recur following surgical resection only. The role of irradiation and radiation dose levels is poorly defined. This study reviews a single institution experience using both, conventional and high doses > or = 60 Gy/CGE radiation regimen. PATIENTS AND METHODS: Between 1974 and 1995 16 patients with histologically proven malignant meningioma underwent radiation therapy (RT). Age at diagnosis ranged between 6 and 79 years (median: 49 years). Three patients reported previous irradiation to the head at least 14 years prior to diagnosis. Ten patients were treated for primary, and 6 patients for recurrent disease. Six patients underwent gross total and 10 patients subtotal resection (Table 1). RT was delivered using conventional, megavoltage photons or combined 160 MeV proton and photon irradiation. Except 1 patient, who died during RT, the radiation doses ranged between 40 and 70 Gy/CGE (= Cobalt Gray Equivalent) (median: 58 Gy/CGE, Table 2). RESULTS: With median observation time of 59 months (range: 10 to 155 months), actuarial local control rates at 5 and 8 years were 52% and 17%, respectively. Target doses > or = Gy/CGE resulted in significantly improved tumor control (100%) compared to < 60 Gy/CGE (17%) (p = 0.0006, Table 3 and Figure 1). Improved local control translated also in increased overall survival: 87% (> or = 60 Gy/CGE) versus 15% (< 60 Gy/CGE) at 5 years (p = 0.025, Figure 2). At time of analysis, 6/16 patients (38%) were alive. Two patients developed symptomatic brain damage at doses of 59.3 and 72 Gy/CGE. CONCLUSION: Conformal, radiation therapy with target doses > or = 60 Gy/CGE, in this study by use of combined proton and photon irradiation, can significantly improve chances of long-term local control and survival for patients diagnosed with these challenging tumors.

Adolescent↗
PubMed1989

Neuropathological distinction between Parkinson's dementia and Parkinson's plus Alzheimer's disease.

The distinctive clinical features of dementia in Parkinson's disease (PDD) and Parkinson's plus Alzheimer's disease (PD + AD) suggest different patterns of cerebral atrophy in these conditions. To determine the pathoanatomical substrates of dementia in PDD and PD + AD, morphometric analysis of 5 standardized coronal slices was used to identify volumetric changes in cerebral tissue. In PDD (n = 4) there were 9 to 23% reductions in cross-sectional area of cerebral cortex, a 38% loss of tissue in the globus pallidus + putamen, and an 18% reduction in area of the amygdala, whereas in PD + AD (n = 6) there was severe global atrophy of the cerebral cortex (27-29% reductions), moderate atrophy of white matter (10-19% reductions), and 40% reductions in areas of globus pallidus + putamen and the amygdala relative to neuropathologically intact controls (n = 14). Immunostaining with anti-glial fibrillary acidic protein disclosed significant gliosis of all four major subdivisions of neocortex in PD + AD and gray matter of the caudate, putamen, globus pallidus, and thalamus in both PDD and PD + AD relative to controls. The findings suggest that dementia in PDD is mainly subcortical in origin and due to neuronal degeneration in basal ganglia, the amygdala, and thalamus. In PD + AD the same pattern and degree of subcortical degeneration is evident, but there are clearly superimposed lesions involving cortical neurons and long projection fibers coursing through cerebral white matter that most likely account for the distinctive manifestations of dementia in this condition compared with PDD.

Aged↗
PubMed1983

Childhood brain tumor update.

In this review of recent studies of the cerebellar tumors of childhood we have discussed the limitations of traditional approaches to the classification of childhood brain tumors for the purposes of estimating prognosis. While these traditional approaches have provided considerable information about cells of origin, they have left behind the ancient tradition of pathology of considering the tumor in all its aspects, not just its histologic features. As an alternative we have introduced an approach that does not depend ona priori assumptions but rather allows prognosis to be estimated directly from histologic features or from clusters of histologic, clinical, and surgical features-- namely the use clustering strategies as applied to the cerebellar tumors. We have also discussed the preliminary work of the Childhood Brain Tumor Consortium, which has collected a large amount of data to serve as a source of prognostic information in the design of studies of alternative therapies. The preliminary data indicate that there is a disquietingly wide array of overlapping histologic features in three common childhood brain tumors-- medulloblastomas, pilocytic astrocytomas, and ependymomas. Clinicians who seek to reduce the number of deaths among children with brain tumors need specific prognostic information to decide among alternative therapies and to design studies of therapies for biologically homogeneous tumors, rather than studies of therapies of tumor "names" that encompass extraordinarily wide ranges of histologic features. Clinicians must also be extremely wary of "historical" controls; they cannot allow themselves to fall into the trap of believing that a new therapy is better because their patients "would have been expected" to have succumbed sooner. For each proposed therapy new studies must be designed, each with its control population, no matter how difficult this is. Historical controls assume that 1) the tumors were classified properly, 2) the sites of the tumors in different groups of patients were comparable, and 3) tumors with the same name (each encompassing an extremely wide range of histologic features) are comparable in every histologic respect to the study population, and 4) the outlook for patients with tumors with this name has not changed over the half century since the name came into common usage (i.e., that the morbidity associated with these tumors has not changed). For these reasons the use of historical controls must be condemned and all studies of therapies based on such controls discarded. Studies of therapies must compare populations of patients homogeneous as to site, histologic features, and such clinical features as age.

Astrocytoma↗