A laboratory for the study of the activity of the central nervous sytem in the higher animals.

2006 ◽  
pp. 144-146
Author(s):  
Ivan Petrovitch Pavlov
Author(s):  
Elisabeth J. Rushing

SummaryIdentification of the underlying genetic and epigenetic alterations in an increasing number of tumors of the nervous system is contributing to a more clinically relevant classification. In the following article, the 7 cIMPACT-NOW publications, which adumbrate the upcoming 5th edition of the WHO Classification of Tumours of the Central Nervous Sytem are summarized.


2000 ◽  
Vol 102 (2) ◽  
pp. 189-198 ◽  
Author(s):  
Joel F Kaye ◽  
Nicole Kerlero de Rosbo ◽  
Itzhack Mendel ◽  
Shlomo Flechter ◽  
Michael Hoffman ◽  
...  

1983 ◽  
Vol 6 (3) ◽  
pp. 331
Author(s):  
J. Triepel ◽  
W.G. Forssmann

2019 ◽  
Vol 46 (2) ◽  
pp. 61-65
Author(s):  
Mohammad Hossain ◽  
Nazmin Ahmed ◽  
Narendra Shalike ◽  
Md Rokibul Islam ◽  
Soumen Samadder ◽  
...  

Choroid plexus tumors are rare intracranial tumors which account for 0.4-0.6% of all brain tumors. Choroid plexus tumors represent a spectrum of neoplasms derived from papillary epithelium of normal choroid plexus, including well-differentiated papilloma (WHO grade I), intermediate form as atypical Choroid Plexus Papilloma (WHO grade II) and highly aggressive choroid plexus carcinomas (WHO grade III). Though rare, it is responsible for the communicating hydrocephalus in children due to overproduction of cerebrospinal fluid. Due to advances in molecular biology and better understanding of the tumorigenesis of choroid plexus papilloma, now it is established that several genetic syndromes and central nervous sytem abnormalities are associated with this tumor. Here, we reported a case of a 10 months old child who presented with sudden deterioration of consciousness level and after thorough evaluation, diagnosed as a case of Choroid Plexus Papilloma with Dandy Walker Variant. Till date, this is the first reported case of the association/ co-existence of such two conditions which needs further evaluation. Bangladesh Med J. 2017 May; 46 (2): 61-65


1984 ◽  
Vol 60 (5) ◽  
pp. 1089-1094 ◽  
Author(s):  
Hiroshi Hasegawa ◽  
Shoji Bitoh ◽  
Hideo Otsuki ◽  
Masaaki Fujiwara ◽  
Tomio Yamamoto ◽  
...  

✓ A case is reported of malignant schwannomatosis (malignant transformation of von Recklinghausen's disease) with catecholamine production in a patient with multiple intracranial aneurysms. The patient had a history of episodic hypertension and elevated levels of catecholamines in the serum and 24-hour urinary excretion. Postmortem examination revealed diffuse central nervous sytem (CNS) dissemination of the tumor from the thoracolumbar spinal malignant schwannoma. A high concentration of catecholamines was demonstrated in the tumor tissue, and histochemical and electron microscopy studies suggested the presence of catecholamines in the cytoplasm of some of the tumor cells. This patient's clinical and radiological features, including severe headache, vomiting, stiff neck, ptosis of the eye ipsilateral to the internal carotid-posterior communicating artery aneurysms, and local arterial narrowing, mimicked those of subarachnoid hemorrhage from a ruptured aneurysm. However, the clinical picture was caused by diffuse CNS dissemination of the tumor, another primary malignant schwannoma of the oculomotor nerve, and intimal fibrous thickening of the arterial wall.


2008 ◽  
Vol 32 (1) ◽  
pp. 79-86 ◽  
Author(s):  
Nathalie Mallol-Mesnard ◽  
Florence Menegaux ◽  
Brigitte Lacour ◽  
Olivier Hartmann ◽  
Didier Frappaz ◽  
...  

1980 ◽  
Vol 58 (6) ◽  
pp. 633-637
Author(s):  
John C. Costella ◽  
Bruce B. Virgo

Carbohydrate metabolism and central nervous sytem (CNS) intoxication were investigated as causes of dieldrin-induced congenital inviability. The 24-h LD50 was calculated using 5-day-old normal mice (CD-1 strain), fasted for 24 h, and gavaged with dieldrin. The LD50, 27 mg/kg, was 5% of the cumulative dose received by the dieldrin-treated, pregnant females. Acutely poisoned pups convulsed and tremored, inviable pups do not. Inviable pups were caesarian delivered on day 18 from dieldrin-treated females (p.o., 2 mg/kg per day, from day 6 to day 18), and aspects of carbohydrate metabolism were measured 0, 19, and 24 h postdelivery. Inviable and control pups weighed the same at all times but the liver weight of inviable pups was reduced by 0, 8, and 21%, at 0, 19, and 24 h, respectively (control: 61, 48, and 41 mg/g body weight). The inviable pups were hypoglycemic at delivery (0.69 vs. 0.95 mg/mL plasma in the controls), at 19 h (0.53 vs. control values of 0.94 mg/mL), and were aglycemic at 24 h (normal pups: 0.32 mg/mL). Liver glycogen, normal in inviable pups at birth (control: 71 mg/g liver), was reduced by 38% at 19 h (control: 19 mg/g) and by 77% at 24 h (control: 4.5 mg/g). Cardiac glycogen was reduced in treated pups only at 24 h (5.5 mg/g vs. control levels of 11.0 mg/g). Muscle glycogen was also reduced only at 24 h (2.2 mg/g vs. control levels of 5.4 mg/g). Prenatal dieldrin did not affect blood lactate, pyruvate, or urea, nor did it alter hepatic lactate dehydrogenase (LDH) or fructose diphosphatase (FDPase) activities. It is concluded that the inviability is not caused by CNS stimulation; it is associated with congenital hypoglycemia, enhanced glycogenolysis, and apparently normal gluconeogenesis.


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