Hemorrhagic Encephalopathy Research Articles

Central Nervous System Hemorrhages Induced by Heparin in Rats with Allergic Encephalomyelitis

SummaryMany cases of acute necrotizing hemorrhagic encephalopathy have massive hemorrhages. The experimental model for this disease, hyperacute allergic encephalomyelitis, has only microscopic hemorrhages. Treatment of affected rats with heparin converted microscopic to massive hemorrhages, thus completing the analogy between human and experimental diseases. There was no evidence that hemorrhage can precede inflammation. Nor were hemorrhages observed in the ordinary form of allergic encephalomyelitis, in which permeability changes were less profound.

ALLERGIC ENCEPHALOMYELITIS: A HYPERACUTE FORM.

The hyperacute form of allergic encephalomyelitis is characterized by its short incubation period, 100 percent incidence, overwhelming severity, and high mortality and by the massive quantities of polymorphonuclear neutrophils, fibrin, and edema fluid which infiltrate the central nervous system. The hyperacute form has been produced with the aid of aqueous pertussis vaccine as an adjuvant. This is the first reproducible laboratory model for human acute necrotizing hemorrhagic encephalopathy.

Mass accidental salt poisoning in infancy. A study of a hospital disaster.

In the first known incidence of a mass salt poisoning of infants, the case fatality rate was 6 of 14 exposed. Five died before the situation was recognized. All five whose brains were examined at autopsy showed hemorrhagic encephalopathy consistent with previous reports of salt poisoning in humans and animals. Eleven of 14 of these infants manifested neurological symptoms. Peritoneal dialysis was attempted in four patients, three of whom survived despite severe illness in two of them. The technique proved feasible under ordinary hospital conditions and may be instrumental in the recovery of patients. Some suggestions for improvement have come from the experience.

The treatment of sleeping sickness (mainly due to Trypanosoma rhodesiense) with melarsoprol : I. Reactions observed during treatment

1. 1) Though the physical and mental state of patients with sleeping sickness due to T. rhodesiense and T. gambiense is usually markedly improved during melarsoprol therapy, unwanted drug-effects are common. 2. 2) In a total of 110 patients treated with melarsoprol, central nervous system reactions, mainly reactive encephalopathy, occurred in 14 cases (12.7 per cent.). 3. 3) Five deaths (4.5 per cent.) occurred during treatment. One was due to haemorrhagic encephalopathy, probably caused by relative overdosage, and three were primarily due to trypanosomal meningo-encephalitis. In the remaining patient, not examined at autopsy, death was attributed speculatively to a severe reactive encephalopathy. 4. 4) Angioneurotic or skin reactions occurred in five cases (4.5 per cent.). 5. 5) Agranulocytosis occurred once. 6. 6) Erythema nodosum leprosum reaction (preferably called erythema induratum leprosum) occurred once in a patient with both leprosy and trypanosomiasis treated with melarsoprol. 7. 7) Other reactions (5.5 per cent.) included arthralgia and renal and hepatic effects. The pyrexial reaction, occurring especially in parasitaemic cases, on initial treatment is similar to the Jarisch-Herxheimer effect in syphilis. 8. 8) Though aetiological diagnosis of a melarsoprol toxic reaction is readily made, the importance of endeavouring to make a pathogenetic diagnosis is emphasized.

Varicella complicated by acute hemorrhagic encephalopathy.

Acute encephalopathy occasionally complicates the clinical course of varicella. It is characterized by depression in the level of consciousness, seizures, and frequently by ataxia. This complication, although usually mild and without residuum, occasionally assumes serious or even fatal proportions. In 1955 Lander1published a clinicopathological study of an adult with acute hemorr h a g i c leukoencephalitis complicating varicella, a condition not previously recorded. The patient described in the present report survived her illness, and, for this reason, no final conclusions can be reached. Report of Case Case1.—This 19-month-old white girl, born Sept. 6, 1958, was admitted to the hospital on April 10, 1960, after having had a major seizure. Six days before admission to the hospital she developed a chickenpox rash but was only moderately ill. Three days prior to admission, she was seen by a pediatrician because of some bruises on her trunk and extremities, and

Hemorrhagic Encephalopathy in Chicken Embryos Infected with Influenza Virus

Summary Prior allantoic infection with homologous or heterologous influenza viruses, or Newcastle disease virus, protected chicken embryos against the hemorrhagic and lethal effects of neurotropic (NWS) influenza virus inoculated intravenously. The titers of NWS virus in brains of protected embryos were appreciably lower than those in fully susceptible controls, suggesting that the protective effect of prior allantoic infection was related to inhibition of NWS virus multiplication. The refractory state to intravenous challenge with NWS virus did not depend on the amount of interfering virus inoculated intra-allantoically but did require that active allantoic infection be established 8 to 16 hr prior to intravenous challenge. Intra-allantoic inoculation of myxovirus inactivated by heat or u.v. irradiation, or neutralized by immune serum, did not enhance resistance to NWS virus challenge. The small quantity of infectious virus disseminated from the allantoic site of infection to the tissues of the embryo seems insufficient to account for interference with NWS virus multiplication. However, multiple intravenous or intra-allantoic injections of infected allantoic fluid, freed of infectious influenza virus by centrifugation and heating, protected embryos against hemorrhagic encephalopathy. These studies are consistent with the hypothesis that the protective effect of prior allantoic infection is related to in vivo production of an interferon that gains access to the embryonic circulation from the infected allantois.

Peritoneal Dialysis for Salt Poisoning

SALT poisoning in infancy constitutes a medical emergency because increased levels of sodium in serum are damaging to the central nervous system and may produce severe hemorrhagic encephalopathy.1 2 3 After diagnosis several methods may be considered for alleviating the disturbance by removal of excess sodium chloride. The one most commonly employed is the intravenous administration of glucose in water, a method that depends upon renal excretion to rid the body of excess ions. However, there is evidence that renal function may be impaired in hypernatremic states,4 so that sodium excretion is slower than one might otherwise anticipate. Thus, the devastating effects . . .

Central hemorrhagic encephalopathy of early infancy.

Central hemorrhagic encephalopathy of early infancy.

Hemorrhagic encephalopathy induced by hypernatremia. II. Experimental observations on hyperosmolarity in cats.

Hypernatremia as a cause of acute neurological disorder is being recognized with increasing frequency.1-11Common clinical and metabolic features in infants with fatal outcome were described in the previous paper.12At autopsy, extensive venous occlusion and subarachnoid, subdural, and intracerebral bleeding were prominent findings. Mechanisms for production of these vascular changes and their relative importance in the clinical picture were not clear. It was not known, for example, to what degree hemorrhagic encephalopathy was an integral manifestation of the underlying metabolic disturbance, or whether these vascular lesions merely represented nonspecific, secondary results of transiently disturbed intracranial-pressure relationships. Hyperosmolarity, of order of magnitude similar to that encountered in patients (375-400 mOsm/L.), produces comparable clinical alterations in experimental animals.13,14Within 30 minutes after intraperitoneal injection of hypertonic solutions, cats develop marked tremor, ataxia, muscle twitching, stupor, and occasional convulsions. One cat in three dies within a few hours. In

Hemorrhagic encephalopathy induced by hypernatremia. I. Clinical, laboratory, and pathological observations.

Hyperosmolarity is characterized by an increase in the solute concentration of body fluids brought about by loss of water, inadequate water intake, or administration of large amounts of hypertonic solutions. When the osmolar concentration of the extracellular fluid is increased, transfer of water from cells to extracellular fluid exceeds that in the opposite direction. Net water movement is thus out of the cells, with resultant dilution of extracellular fluid and concentration of the fluid within cells themselves. If the solute which increases the extracellular fluid osmolarity is one which is in the main excluded from intracellular fluid, such as sodium and chloride ions, this disturbance in water distribution cannot be mitigated by movement of solute into cells. Hence, the ultimate effect of hypernatremia is dehydration of cells. This physicochemical disorder is most frequently encountered in infants and children with severe diarrhea and vomiting, but it also occurs in adults. Schmidt,

Thrombotic thrombocytopenic purpura: a review of the literature with report of a case.

Excerpt Thrombotic thrombocytopenic purpura has become recognized as a clinical entity only in recent years. This uniformly fatal disease, which may affect either sex at any age, is characterized b...

Agonal nature of the cerebral ring hemorrhages.

CEREBRAL ring hemorrhages are seen in a variety of diseases, such as fat embolism, laceration of the brain, acute Plasmodium falciparum malaria, postvaccinial and parainfectious encephalitides, pernicious anemia, aplastic anemia and leukemia, and intoxications (barbiturates, neoarsphenamine, arsphenamine), as reviewed by Kirschbaum,1Dietrich,2Weimann,3Lindau,4Durck,5Wolff,6Winblad,7Sjovall,8and others. These hemorrhages may occur in such large numbers throughout the white matter that the hemorrhagic tendency is considered one of the important features of the disease process. This justifies the use of the term brain purpura (Schmidt9), acute hemorrhagic leucoencephalitis (Alexander and Putnam,10Hurst,11Henson and Russell12), and acute necrotizing hemorrhagic encephalopathy (Adams, Cammermeyer, and Denny-Brown13). The effusions of blood are thought to take place in diseases in which the nerves to the vessels have been paralyzed and stasis has thereby been furthered, with diapedesis hemorrhages, as

Haemorrhagic Encephalopathy after Arsenical Therapy

Haemorrhagic Encephalopathy after Arsenical Therapy

ARSPHENAMINE ENCEPHALOPATHY

The clinical and pathologic observations in cases of hemorrhagic encephalopathy due to arsphenamine usually present a fairly characteristic picture. A few hours or days after an intravenous injection of an arsphenamine preparation acute cerebral symptoms develop, especially headache, nausea, vomiting and fever, and the patient rapidly becomes comatose. Meningitic signs are usually absent except in cases in which subarachnoid bleeding has occurred. The cerebrospinal fluid is usually normal except for having increased pressure. Autopsy generally reveals marked dilatation and engorgement of the meningeal and cerebral vessels, varying degrees of vascular necrosis and perivascular hemorrhages, typically of the ring type. Meningeal hemorrhages may be present. A mild perivascular inflammatory infiltration is sometimes noted. Perivascular softening and demyelinization as the outstanding lesion has been described. 1 The case herein reported is unusual in that it presented a frank meningitic as well as encephalopathic syndrome and because of the unusually intense leukocytic inflammatory