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Wernicke-Korsakoff Syndrome

Whereas the clinical symptoms of somnolence, ataxia, and ophthalmoplegia can be attributed to the Wernicke syndrome, the Korsakoff psychosis is characterized mainly by amnesia, disorientation, and suggestibility with confabulation. Neither of the two syndromes is a distinct entity since the transitions between them are fluid both clinically and pathologically. Both types of changes must be attributed to alcohol intoxication in combination with a thiamine deficiency (Butterworth 1989; Laforenza et al. 1990), as well as activation of microglia and astroglia (Todd and Butterworth 1999). An acute course must be distinguished from a more chronic course.

The acute course is characterized by disorientation, confusion, and autonomic deficits and has a poor prognosis. Both macroscopically and microscopically new, sometimes non-reactive capillary hemorrhages can be demonstrated; they are located mainly in the mammillary bodies, but also in the paraventricular nuclei, especially the supraoptic nu

Fig. 18.4a-d. Wernicke-Korsakoff Syndrome. Microscopically the mammillary bodies are characterized by hemorrhages of different age, a spongy desintegration (a), an intense vascularization and astrogliosis (b, c), as well as fibrinoid degeneration of arterioles and capillaries with morphologically intact neurons (d) (a, c van Gieson stain; b Prussian blue reaction; c trichrome stain; magnification a X100, b X500, c x50, d X1000)

Fig. 18.4a-d. Wernicke-Korsakoff Syndrome. Microscopically the mammillary bodies are characterized by hemorrhages of different age, a spongy desintegration (a), an intense vascularization and astrogliosis (b, c), as well as fibrinoid degeneration of arterioles and capillaries with morphologically intact neurons (d) (a, c van Gieson stain; b Prussian blue reaction; c trichrome stain; magnification a X100, b X500, c x50, d X1000)

cleus and quadrigeminal plate (Colmant 1965). The acute course is rare.

The chronic course exhibits both of the aforementioned clinical pictures (Wernicke's syndrome, Korsakoff psychosis). Morphologically the following changes are encountered.

The gross appearance is dominated by atrophic, brownish mammillary bodies (Fig. 18.3) and periventricular hemorrhages (Fig. 18.4a) of varying age at the level of the third and fourth ventricles and the aqueduct. Histology reveals astrogliosis and capillary proliferation (Fig. 18.4c) plus siderophages (Fig. 18.4a) and spongy disintegration of the neuro-pil and demyelination as well. The vascular changes include angiectasis, looping, and swelling of endo-thelium as well as fibrinoid degeneration (Fig. 18.4d) selectively affecting arterioles and capillaries (Oke-da et al. 1995). The neuronal elements remain largely intact and only occasionally exhibit swelling with chromatolysis. A large proportion of cases also have neuronal changes in the thalamic nucleus (53-100%, Harper and Butterworth 1997, especially in the mediodorsal and anterior principal nuclei), including perineuronal vacuoles and degenerating neurons, some with eosinophilic cell change and cytoplasmic vacuolization (Olney 1990; Meldrum and Garthwaite

1991). All of these morphological phenomena have been reproduced experimentally by reductions in thiamine intake. In chronic alcoholics, they are explained by impaired intestinal absorption caused by alcoholic gastroenteritis.

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