IS THE CAUSE OF THE BRAIN PATHOLOGY OF MITOCHONDRIAL ENCEPHALOMYOPATHY, LACTIC ACIDOSIS, AND STROKE-LIKE EPISODES (MELAS) NON-ISCHEMIC?

1999 ◽  
Vol 58 (5) ◽  
pp. 561
Author(s):  
I. Nakano ◽  
M. Sawada ◽  
T. Somcya ◽  
K. Tamagawa ◽  
K. Saito ◽  
...  
2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yuji Suzuki ◽  
Matsuyuki Doi ◽  
Yoshiki Nakajima

Abstract Background Systemic anesthetic management of patients with mitochondrial disease requires careful preoperative preparation to administer adequate anesthesia and address potential disease-related complications. The appropriate general anesthetic agents to use in these patients remain controversial. Case presentation A 54-year-old woman (height, 145 cm; weight, 43 kg) diagnosed with mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes underwent elective cochlear implantation. Infusions of intravenous remimazolam and remifentanil guided by patient state index monitoring were used for anesthesia induction and maintenance. Neither lactic acidosis nor prolonged muscle relaxation occurred in the perioperative period. At the end of surgery, flumazenil was administered to antagonize sedation, which rapidly resulted in consciousness. Conclusions Remimazolam administration and reversal with flumazenil were successfully used for general anesthesia in a patient with mitochondrial disease.


2008 ◽  
pp. S101-S110
Author(s):  
A Chvátal ◽  
M Anděrová ◽  
H Neprašová ◽  
I Prajerová ◽  
J Benešová ◽  
...  

The pathological potential of glial cells was recognized already by Rudolf Virchow, Santiago Ramon y Cajal and Pio Del Rio-Ortega. Many functions and roles performed by astroglia in the healthy brain determine their involvement in brain diseases; as indeed any kind of brain insult does affect astrocytes, and their performance in pathological conditions, to a very large extent, determines the survival of the brain parenchyma, the degree of damage and neurological defect. Astrocytes being in general responsible for overall brain homeostasis are involved in virtually every form of brain pathology. Here we provide an overview of recent developments in identifying the role and mechanisms of the pathological potential of astroglia.


2005 ◽  
Vol 20 (2) ◽  
pp. 116-119 ◽  
Author(s):  
Hiroaki Kubota ◽  
Yuzo Tanabe ◽  
Jun-ichi Takanashi ◽  
Yoichi Kohno

1998 ◽  
Vol 56 (1) ◽  
pp. 93-97 ◽  
Author(s):  
LAZO JAVIER ◽  
ANTONIO CARLOS OLIVEIRA MENESES ◽  
ADEMIR ROCHA ◽  
MARCELO SIMÃO FERREIRA ◽  
JAIME OLAVO MARQUEZ ◽  
...  

Based on their own experience and on the literature, the authors compare the brain pathology due to HIV+ associated Trypanosoma cruzi reactived infection to that described for the natural history of the Chagas' disease (CD). The peculiar focal necrotizing chagasic meningoencephalitis (MECNF) which appears only in immunedeficient chagasics, especially when the deficiency is due HIV is a safe criterion for reactivation of CD. MECNF morphologic findings are unlike to those found either for some cases of acute phase CD or for chronic nervous form of CD.


2001 ◽  
Vol 280 (4) ◽  
pp. R1190-R1196 ◽  
Author(s):  
B. Bishop ◽  
G. Silva ◽  
J. Krasney ◽  
H. Nakano ◽  
A. Roberts ◽  
...  

When rats, acclimated to an ambient temperature (Ta) of 29°C, are exposed to 10% O2 for 63 h, the circadian rhythms of body temperature (Tb) and level of activity (La) are abolished, Tb falls to a hypothermic nadir followed by a climb to a hyperthermic peak, Laremains depressed (Bishop B, Silva G, Krasney J, Salloum A, Roberts A, Nakano H, Shucard D, Rifkin D, and Farkas G. Am J Physiol Regulatory Integrative Comp Physiol 279: R1378–R1389, 2000), and overt brain pathology is detected (Krasney JA, Farkas G, Shucard DW, Salloum AC, Silva G, Roberts A, Rifkin D, Bishop B, and Rubio A. Soc Neurosci Abstr 25: 581, 1999). To determine the role of Ta in these hypoxic-induced responses, Tb and La data were detected by telemetry every 15 min for 48 h on air, followed by 63 h on 10% O2 from rats acclimated to 25 or 21°C. Magnitudes and rates of decline in Tb after onset of hypoxia were inversely proportional to Ta, whereas magnitudes and rates of Tb climb after the hypothermic nadir were directly proportional to Ta. No hyperthermia, so prominent at 29°C, occurred at 25 or 21°C. The hypoxic depression of La was least at 21°C and persisted throughout the hypoxia. In contrast, Ta was a strong determinant of the magnitudes and time courses of the initial fall and subsequent rise in Tb. We propose that the absence of hyperthermia at 21 and 25°C as well as a persisting hypothermia may protect the brain from overt pathology.


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