Periventricular leukomalacia in adults. Clinicopathological study of four cases.

The pathological findings in four patients with courses characterized by acute coma and respiratory insufficiency occurring in obscure circumstances are presented. Carbon monoxide intoxication was excluded. After an early partial recovery from coma, the patients remained in a persistent vegetative state, with a tetrapyramidal syndrome. Pathologic changes consisted of infarction and demyelination of periventricular white matter, with associated necrotic foci in the basal ganglia in some cases. We propose that the prolonged hypoxia and ischemia produce a "no reflow" phenomenon causing brain edema (more pronounced in the white matter); this resulted in infarctions of white matter in the periventricular arterial end and border zones.

[1]  J. Dereuck,et al.  Periventricular leukoencephalopathy and meningo-cortical arterio-venous malformation. , 1974 .

[2]  R. Myers,et al.  Experimental carbon monoxide encephalopathy in the primate I. Physiologic and metabolic aspects. , 1974, Archives of neurology.

[3]  R. Myers,et al.  Experimental carbon monoxide encephalopathy in the primate. II. Clinical aspects, neuropathology, and physiologic correlation. , 1974, Archives of neurology.

[4]  I. Feigin,et al.  DEGENERATION OF WHITE MATTER IN HYPOXIA, ACIDOSIS AND EDEMA , 1973, Journal of neuropathology and experimental neurology.

[5]  H. Schaumburg,et al.  Periventricular atherosclerotic leukoencephalopathy , 1972, Neurology.

[6]  J. Dereuck.  The cortico-subcortical arterial angio-architecture in the human brain. , 1972 .

[7]  E. Richardson,et al.  Pathogenesis and evolution of periventricular leukomalacia in infancy. , 1972, Archives of neurology.

[8]  F. Plum,et al.  Persistent vegetative state after brain damage. A syndrome in search of a name. , 1972, Lancet.

[9]  M. Kowada,et al.  Cerebral ischemia. II. The no-reflow phenomenon. , 1968, The American journal of pathology.

[10]  M. Kowada,et al.  Cerebral ischemia. III. Vascular changes. , 1968, The American journal of pathology.

[11]  M. Tommasi,et al.  [Leukoencephalopathy with large bilateral symmetrical cavitation. Post-traumatic decortication syndrome]. , 1968, La Presse medicale.

[12]  F. Romanul,et al.  CHANGES IN BRAIN AND PIAL VESSELS IN ARTERIAL BORDER ZONES; A STUDY OF 13 CASES. , 1964, Archives of neurology.

[13]  F. Plum,et al.  Delayed neurological deterioration after anoxia. , 1962, Archives of internal medicine.

[14]  S. Strich,et al.  DIFFUSE DEGENERATION OF THE CEREBRAL WHITE MATTER IN SEVERE DEMENTIA FOLLOWING HEAD INJURY , 1956, Journal of neurology, neurosurgery, and psychiatry.

[15]  N. Malamud,et al.  CRANIAL TRAUMA AND EXTRAPYRAMIDAL INVOLVEMENT: CEREBRAL CHANGES SIMULATING THOSE OF ANOXIA A CLINICOPATHOLOGIC REPORT OF THREE CASES , 1947, Journal of neuropathology and experimental neurology.

[16]  M. Ginsberg,et al.  Hypoxic-ischemic leukoencephalopathy in man. , 1976, Archives of neurology.

[17]  J. Reuck,et al.  The anatomy of the late radiation encephalopathy. , 1975 .

[18]  J. Reuck,et al.  The Human Periventricular Arterial Blood Supply and the Anatomy of Cerebral Infarctions , 1971 .

[19]  J. Reuck.  Arterial vascularisation and angioarchtitecture of the nucleus caudatus in human brain. , 1971 .

[20]  J. D. Reuck.  La limite du territoire profond de l’artère Sylvienne chez l’homme , 1969 .

[21]  J. Brucher.  Neuropathological problems posed by carbon monoxide poisoning and anoxia. , 1967, Progress in brain research.

[22]  M. Fardeau,et al.  The central nervous system and carbon monoxide poisoning. II. Anatomical study of brain lesions following intoxication with carbon monixide (22 cases). , 1967, Progress in brain research.

[23]  H. M. Eecken.  The anastomoses between the leptomeningeal arteries of the brain : their morphological, pathological, and clinical significance , 1959 .