scholarly journals Neuro-Osteology

1998 ◽  
Vol 9 (2) ◽  
pp. 224-244 ◽  
Author(s):  
I. Kjær

Neuro-osteology stresses the biological connection during development between nerve and hard tissues. It is a perspective that has developed since associations were first described between pre-natal peripheral nerve tissue and initial osseous bone formation in the craniofacial skeleton (Kjær, 1990a). In this review, the normal connection between the central nervous system and the axial skeleton and between the peripheral nervous system and jaw formation are first discussed. The early central nervous system (the neural tube) and the axial skeleton from the lumbosacral region to the sella turcica forms a unit, since both types of tissue are developmentally dependent upon the notochord. In different neurological disorders, the axial skeleton, including the pituitary gland, is malformed in different ways along the original course of the notochord. Anterior to the pituitary gland/sella turcica region, the craniofacial skeleton develops from prechordal cartilage, invading mesoderm and neural crest cells. Also, abnormal development in the craniofacial region, such as tooth agenesis, is analyzed neuro-osteologically. Results from pre-natal investigations provide information on the post-natal diagnosis of children with congenital developmental disorders in the central nervous system. Examples of these are myelomeningocele and holoprosencephaly. Three steps are important in clinical neuro-osteology: (1) clinical definition of the region of an osseous or dental malformation, (2) embryological determination of the origin of that region and recollection of which neurological structure has developed from the same region, and (3) clinical diagnosis of this neurological structure. If neurological malformation is the first symptom, step 2 results in the determination of the osseous region involved, which in step 3 is analyzed clinically. The relevance of future neuro-osteological diagnostics is emphasized.

1963 ◽  
Vol 44 (3) ◽  
pp. 475-480 ◽  
Author(s):  
R. Grinberg

ABSTRACT Radiologically thyroidectomized female Swiss mice were injected intraperitoneally with 131I-labeled thyroxine (T4*), and were studied at time intervals of 30 minutes and 4, 28, 48 and 72 hours after injection, 10 mice for each time interval. The organs of the central nervous system and the pituitary glands were chromatographed, and likewise serum from the same animal. The chromatographic studies revealed a compound with the same mobility as 131I-labeled triiodothyronine in the organs of the CNS and in the pituitary gland, but this compound was not present in the serum. In most of the chromatographic studies, the peaks for I, T4 and T3 coincided with those for the standards. In several instances, however, such an exact coincidence was lacking. A tentative explanation for the presence of T3* in the pituitary gland following the injection of T4* is a deiodinating system in the pituitary gland or else the capacity of the pituitary gland to concentrate T3* formed in other organs. The presence of T3* is apparently a characteristic of most of the CNS (brain, midbrain, medulla and spinal cord); but in the case of the optic nerve, the compound is not present under the conditions of this study.


PEDIATRICS ◽  
1960 ◽  
Vol 25 (2) ◽  
pp. 309-315
Author(s):  
Harry H. White ◽  
Fred D. Fowler

Chronic lead encephalopathy must be considered in the differential diagnosis of pediatric patients who present with manifestations of schizophrenia, behavior disorders or degenerative diseases of the central nervous system. Determination of urinary coproporphyrin is a simple, fast screening procedure applicable to office practice. The prognosis for normal mental development following encephalopathy is poor. It is hoped that early recognition of the more subtle signs of central nervous system involvement will allow treatment to be instituted soon enough to prevent the crippling mental deterioration which is so often a sequela of lead poisoning.


1998 ◽  
Vol 13 (supplement) ◽  
pp. 120-121
Author(s):  
Masaharu NAKAJIMA ◽  
Tomoko OHTA ◽  
Nozomi KAWAKAMI ◽  
Susumu YAMATO ◽  
Kenji SHIMADA ◽  
...  

1937 ◽  
Vol 33 (9) ◽  
pp. 1142-1142
Author(s):  
B. Ivanov

In the picture of thyrotoxicosis, the foreground is the dysfunction of the thyroid gland; it should be borne in mind that the latter is under the influence of the central nervous system and hormonal centers (for example, the pituitary gland), changes in which affect the course and severity of the disease.


2021 ◽  
pp. 1057-1070
Author(s):  
Lily C. Wong-Kisiel

Abnormal development of the central nervous system is a common cause of developmental delay and epilepsy. An understanding of central nervous system malformation begins with an overview of normal embryology. Genetic advances in embryogenesis have unfolded a complex orchestration of gene expressions in place of the traditional developmental epochs (induction, neurulation, proliferation, migration, organization, synaptogenesis, and myelination). Causes of malformation of the central nervous system are multifactorial. Genetic causes, vitamin excess or deficiency, infections, or teratogens any time during pregnancy may disturb the preprogrammed mechanisms.


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