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Enhanced vascular permeability in acute disseminated vasculomyelinopathy.

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Enhanced Vascular
Permeability in
Acute Disseminated
Richard A. Rudick, MD,’ and Thomas A. Eskin, M D t
In his stimulating article “Disseminated vasculomyelinopathy: an immune complex disease” [5], D r Reik reemphasized the perivascular distribution of inflammatory demyelination [4] and legitimately raised the issue of serum
factors involved in pathogenesis.
Enhanced brain vascular permeability is the first pathological event in experimental allergic encephalomyelitis (EAE) [3], the widely accepted animal model for
human acute disseminated encephalomyelitis. Vascular
permeability changes in EAE precede mononuclear
cell infiltration and demyelination. T h e mechanism of
enhanced vascular permeability (vascular injury) in EAE
has not been defined, but since it precedes mononuclear
cell infiltration, serum factors may be involved. Circulating
immune complexes, as suggested by Dr Reik, are only one
of numerous possible causes.
Because many neurological conditions are associated
with enhanced vascular permeability but not with concomitant inflammatory dernyelination, other factors (probably humoral) must be involved. Serum factors such as immunoglobulins with myelinotoxic activity [ 11 or lymphocytes sensitized to myelin antigens [2] may participate in
the actual demyelination. These factors might act only in
the presence of enhanced vascular permeability, however.
Elucidation of humoral factors responsible for enhanced
brain vascular permeability in EAE (such as immune complexes) might be important in understanding the pathogenesis of acute disseminated encephalomyelitis.
‘Department of Neurology and Center for Brain Research
+Department of Pathology, Neuropathology Division
University of Rochester School of Medicine
601 Elmwood Ave
Rochester, N Y 14642
Louis Reik, Jr, M D
I share with Drs Rudick and Eskin the beliefs that vascular
injury occurs first in vasculomyelinopathy, that serum factors (immune complexes) initiate vascular injury, and that
other factors (sensitized lymphocytes) may subsequently
participate in demyelination.
I agree that enhanced vascular permeability alone is insufficient to cause inflammatory demyelination. Circulating
immune complexes d o more than alter vascular permeability, however. Complexes are trapped in vessel walls, activate complement, and attract inflammatory cells that
release proteolytic enzymes, causing tissue injury. If components of complement represent the other humoral factors
that they suggest are involved in inflammatory demyelination, our views coincide.
Understanding demyelination is not necessarily the key
to understanding human vasculomyelinopathy, though.
Often the initial vascular lesions are more common in gray
than in white matter [I, 21, and the frequency of subsequent dernyelination may be overestimated [2, 33. Demyelination may not be an obligatory part of the illness.
Finally, even though vascular changes occur in EAE and
precede demyelination, EAE may not be the correct model
for vasculomyelinopathy. Its antecedents are unlike those
of any human illness save the neurological complications
that follow inoculation against rabies with the nerve tissue
antirabies vaccine.
Department of Neurology
University of Connecticut Health Center
Farmington, C T 06032
Carpenter S, Lampert PW: Post-infectious perivenous encephalitis and acute hemorrhagic leukoencephalitis. In
Minckler J (ed): Pathology of the Nervous System. New York,
McGraw-Hill, 1972, vol 3, pp 2260-2269
Hart MN, Earle KM: Haemorrhagic and perivenous encephalitis: a clinical-pathoiogical review of 38 cases. J Neurol
Neurosurg Psychiatry 38:585-591, 1975
Poser CM: Diseases of the myelin sheath. In Baker AB, Baker
LH (eds): Clinical Neurology. Hagerstown, MD, Harper &
Row, 1978, vol 2, pp 80-104
1. Bornstein MB, Appel SH: The application of tissue culture to
the study of experimental “allergic”encephalomyelitis. I. Patterns of demyelination. J Neuropathol Exp Neurol 20:141157, 1961
2. Dau PC, Peterson RDA: Transformation of rodent lymphoid
cells by an encephalitogen of human origin. Int Arch Allergy
35:353-368, 1969
3. Oldstone MBA, Dixon FJ: Immunohistochemical study of allergic encephalomyelitis. Am J Pathol 52:25 1-263, 1968
4. Poser CM: Disseminated vasculomyelinopathy: a review of the
clinical and pathological reactions of the nervous system in
hyperergic diseases. Acta Neurol Scand 45:7-44, 1969
5. Reik L Jr: Disseminated vasculomyelinopathy: an immune
complex disease. Ann Neurol 7:291-296, 1980
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disseminated, vascular, vasculomyelinopathy, enhance, acute, permeability
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