Spinal ganglia and peripheral nerves from a patient with Tay-Sachs disease

1985 ◽  
Vol 66 (3) ◽  
pp. 239-244 ◽  
Author(s):  
T. Abe ◽  
K. Ogawa ◽  
H. Fuziwara ◽  
K. Urayama ◽  
K. Nagashima
2001 ◽  
Vol 91 (7) ◽  
pp. 361-364 ◽  
Author(s):  
Joonhyun Yoon ◽  
Christopher Crabtree ◽  
Georgeanne Botek

Painful legs and moving toes syndrome is characterized by spontaneous causalgic pain in the lower extremities associated with peculiar involuntary movements of the lower extremities, especially the toes and feet. The pain is diffuse, intractable, aching, and deep. The movements consist of persistent writhing movements in the digits that cannot be limited voluntarily. The syndrome has been observed after a variety of abnormalities affecting the posterior nerve roots, the spinal ganglia, and the peripheral nerves. This article reviews commonly reported findings and current concepts in the etiology and management of this condition. (J Am Podiatr Med Assoc 91(7): 361-364, 2001)


1955 ◽  
Vol 102 (2) ◽  
pp. 213-236 ◽  
Author(s):  
Byron H. Waksman ◽  
Raymond D. Adams

In experimental allergic encephalomyelitis (EAE), produced by injecting rabbits with whole rabbit spinal cord together with tubercle bacilli and mineral oil, lesions comparable to those seen in the central nervous system are found in the nerve roots, spinal ganglia, and peripheral nerves. When special fractions of bovine white matter are used as antigen in rabbits, the same distribution of lesions is seen but peripheral nerve involvement is relatively less frequent. When rabbit sciatic nerve or spinal ganglia are used as antigen in rabbits, lesions occur only in the roots, ganglia, and peripheral nerves. Lesions are not produced in the central nervous system, nor is there a meningitis. This disease picture has been called experimental allergic neuritis (EAN). The antigenicity of rabbit nerve is not impaired by autoclaving. Sciatic nerve of other mammalian species produces the same disease in rabbits as does rabbit nerve. Optic nerve, used as antigen, produces the typical picture of EAE, not EAN. The optic nerves are not affected in EAN, whereas they commonly contain lesions in EAE. There are differences of symptomatology, referable to the difference in distribution of lesions, between EAE and EAN. The spinal fluid of EAE shows an increase both in the number of cells and in the total protein content. In EAN, the same changes in protein are observed, but usually the cell count remains normal. The cell count appears to be related to the involvement of cerebral and spinal meninges, which is an almost invariable accompaniment of EAE. The skin tests and serologic studies made with homologous and heterologous antigens were essentially non-contributory, apparently as a consequence of the diversity of antigens present in the inoculated materials. The similarity between EAN and certain of the human polyneuritides is indicated and discussed.


2003 ◽  
Vol 40 (1) ◽  
pp. 63-70 ◽  
Author(s):  
R. J. Panciera ◽  
K. E. Washburn ◽  
R. N. Streeter ◽  
J. G. Kirkpatrick

Nine Gelbvieh calves originating in four herds and clinically presenting with rear limb ataxia/ paresis had histopathologically confirmed peripheral neuropathy and a proliferative glomerulopathy. Degenerative lesions were severe in peripheral nerves, dorsal and ventral spinal nerve roots, and less marked in dorsal fasciculi of the spinal cord. Cell bodies of spinal ganglia were minimally diseased; ventral horn neurons occasionally had central chromatolysis and nuclear displacement. Glomerular lesions ranged from mild mesangial hypercellularity to glomerulosclerosis. Pedigree analysis of affected animals from one herd indicated a strong familial relationship and probable hereditary basis for the syndrome.


1971 ◽  
Vol 17 (2) ◽  
pp. 103-113 ◽  
Author(s):  
S. Le Vay ◽  
C. Meier ◽  
P. Glees

Author(s):  
D. M. DePace

The majority of blood vessels in the superior cervical ganglion possess a continuous endothelium with tight junctions. These same features have been associated with the blood brain barrier of the central nervous system and peripheral nerves. These vessels may perform a barrier function between the capillary circulation and the superior cervical ganglion. The permeability of the blood vessels in the superior cervical ganglion of the rat was tested by intravenous injection of horseradish peroxidase (HRP). Three experimental groups of four animals each were given intravenous HRP (Sigma Type II) in a dosage of.08 to.15 mg/gm body weight in.5 ml of.85% saline. The animals were sacrificed at five, ten or 15 minutes following administration of the tracer. Superior cervical ganglia were quickly removed and fixed by immersion in 2.5% glutaraldehyde in Sorenson's.1M phosphate buffer, pH 7.4. Three control animals received,5ml of saline without HRP. These were sacrificed on the same time schedule. Tissues from experimental and control animals were reacted for peroxidase activity and then processed for routine transmission electron microscopy.


Author(s):  
T. G. Merrill ◽  
B. J. Payne ◽  
A. J. Tousimis

Rats given SK&F 14336-D (9-[3-Dimethylamino propyl]-2-chloroacridane), a tranquilizing drug, developed an increased number of vacuolated lymphocytes as observed by light microscopy. Vacuoles in peripheral blood of rats and humans apparently are rare and are not usually reported in differential counts. Transforming agents such as phytohemagglutinin and pokeweed mitogen induce similar vacuoles in in vitro cultures of lymphocytes. These vacuoles have also been reported in some of the lipid-storage diseases of humans such as amaurotic familial idiocy, familial neurovisceral lipidosis, lipomucopolysaccharidosis and sphingomyelinosis. Electron microscopic studies of Tay-Sachs' disease and of chloroquine treated swine have demonstrated large numbers of “membranous cytoplasmic granules” in the cytoplasm of neurons, in addition to lymphocytes. The present study was undertaken with the purpose of characterizing the membranous inclusions and developing an experimental animal model which may be used for the study of lipid storage diseases.


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