Inability of Cerebrospinal Fluid to Nourish the Spinal Cord

1955 ◽  
Vol 184 (1) ◽  
pp. 220-222 ◽  
Author(s):  
Peter H. Wolff ◽  
Robert D. Tschirgi

Cephalad perfusion with Tyrode's solution of the spinal subarachnoid space between a lumbar and cisternal tap in anesthetized cats had no effect on spinal reflexes, respiration or pupillary size for periods of 8 hours. Alteration of Ca++ or K+ concentration in the perfusate produced immediate changes in these indices, indicating the availability of the perfusate to neural elements. The onset and course of patellar areflexia, respiratory depression and pupillary dilatation resulting from i.v. insulin-induced hypoglycemia could not be influenced by including high concentrations of glucose, glutamate, succinate or a combination of these latter two in the subarachnoid perfusate. It is concluded that the cerebrospinal fluid cannot act as a sufficient medium for transport from the blood of nutrient substrates essential for maintaining function in the central nervous system.

Author(s):  
Peggy Mason

The central nervous system develops from a proliferating tube of cells and retains a tubular organization in the adult spinal cord and brain, including the forebrain. Failure of the neural tube to close at the front is lethal, whereas failure to close the tube at the back end produces spina bifida, a serious neural tube defect. Swellings in the neural tube develop into the hindbrain, midbrain, diencephalon, and telencephalon. The diencephalon sends an outpouching out of the cranium to form the retina, providing an accessible window onto the brain. The dorsal telencephalon forms the cerebral cortex, which in humans is enormously expanded by growth in every direction. Running through the embryonic neural tube is an internal lumen that becomes the cerebrospinal fluid–containing ventricular system. The effects of damage to the spinal cord and forebrain are compared with respect to impact on self and potential for improvement.


1958 ◽  
Vol 192 (3) ◽  
pp. 447-452 ◽  
Author(s):  
Sadayuki F. Takagi ◽  
Yutaka Oomura

The effect of nicotine on synaptic transmission in the frog and cat spinal cord was studied. Both a regular wick electrode and a microelectrode of the Ling-Gerard type were used. The reflex activity of the bullfrog spinal cord is facilitated by 0.01% nicotine solution, but is depressed and abolished by 0.1% solution. In the cat, intravenous administration of 150 mg/kg fails to block reflex activity, but topical application does block. The intracellular potential, of both frog and cat motoneurones, shows no change in the synaptic potential after application of the drug, but the spike appears after a shorter synaptic delay and one or more additional spikes appear. When the synaptic delay becomes sufficiently short, however, all spikes suddenly disappear, leaving the still unchanged synaptic potential. Occasionally the synaptic delay is again increased just before the spike potentials disappear. The excitability of a frog motoneurone was measured, by a recording microelectrode, before and after nicotine application. The drug first increased and then decreases excitability. Epinephrine can restore a reflex discharge depressed or abolished by nicotine. It is concluded that high concentrations of nicotine block synaptic transmission in the central nervous system, acting on the cell body but not on the synaptic potential.


2001 ◽  
Vol 69 (10) ◽  
pp. 6545-6548 ◽  
Author(s):  
Jun Fujii ◽  
Yoshimasa Kinoshita ◽  
Takashi Yutsudo ◽  
Hatsumi Taniguchi ◽  
Tom Obrig ◽  
...  

ABSTRACT The action of Shiga toxin (Stx) on the central nervous system was examined in rabbits. Intravenous Stx1 was 44 times more lethal than Stx2 and acted more rapidly than Stx2. However, Stx1 accumulated more slowly in the cerebrospinal fluid than did Stx2. Magnetic resonance imaging demonstrated a predominance of Stx1-dependent lesions in the spinal cord. Pretreatment of the animals with anti-Stx1 antiserum intravenously completely protected against both development of brain lesions and mortality.


1979 ◽  
Vol 51 (2) ◽  
pp. 251-253 ◽  
Author(s):  
Charles G. H. West

✓ A rare case of metastasis to the spinal subarachnoid space from a non-neuraxial primary tumor is presented. Dissemination was shown by computerized tomography to be via the cerebrospinal fluid from secondary deposits in the central nervous system and meninges. This route would seem to be the most common mode of spread to the spinal subarachnoid space.


2022 ◽  
Vol 19 (1) ◽  
Author(s):  
Yi Kung ◽  
Kuan-Yu Chen ◽  
Wei-Hao Liao ◽  
Yi-Hua Hsu ◽  
Chueh-Hung Wu ◽  
...  

Abstract Background The blood-cerebrospinal fluid (CSF) barrier (BCSFB) is critically important to the pathophysiology of the central nervous system (CNS). However, this barrier prevents the safe transmission of beneficial drugs from the blood to the CSF and thus the spinal cord and brain, limiting their effectiveness in treating a variety of CNS diseases. Methods This study demonstrates a method on SD rats for reversible and site-specific opening of the BCSFB via a noninvasive, low-energy focused shockwave (FSW) pulse (energy flux density 0.03 mJ/mm2) with SonoVue microbubbles (2 × 106 MBs/kg), posing a low risk of injury. Results By opening the BCSFB, the concentrations of certain CNS-impermeable indicators (70 kDa Evans blue and 500 kDa FITC-dextran) and drugs (penicillin G, doxorubicin, and bevacizumab) could be significantly elevated in the CSF around both the brain and the spinal cord. Moreover, glioblastoma model rats treated by doxorubicin with this FSW-induced BCSFB (FSW-BCSFB) opening technique also survived significantly longer than untreated controls. Conclusion This is the first study to demonstrate and validate a method for noninvasively and selectively opening the BCSFB to enhance drug delivery into CSF circulation. Potential applications may include treatments for neurodegenerative diseases, CNS infections, brain tumors, and leptomeningeal carcinomatosis.


Endocrinology ◽  
2010 ◽  
Vol 151 (10) ◽  
pp. 4908-4915 ◽  
Author(s):  
Ana P. Fernández ◽  
Julia Serrano ◽  
Ricardo Martínez-Murillo ◽  
Alfredo Martínez

Adrenomedullin (AM) is a regulatory peptide, coded by the adm gene, which is involved in numerous physiological processes, including pain sensitivity. Previous studies have shown that intrathecal injection of AM induced hyperalgesia in the rat. Here, we explore pain sensitivity in a mouse conditional knockout for adm in neurons of the central nervous system, including the spinal cord and dorsal root ganglia. Double immunofluorescence in wild-type (WT) animals shows that AM immunoreactivity is found in calcitonin gene-related peptide-positive neurons of the dorsal root ganglia but not in neurons that bind isolectin B4. Mice lacking adm had modified expression of canonical sensorial neuropeptides, having significantly more calcitonin gene-related peptide and less substance P and enkephalin than their WT littermates. Furthermore, the spinal cord of adm knockout mice expressed higher levels of the AM receptor components, suggesting a compensation attempt to deal with the lack of afferent AM signaling. Behavioral nociceptive tests also found differences between genotypes. In the tail-flick test, which measures mostly spinal reflexes, the adm-null animals had a longer latency than their WT counterparts. On the other hand, in the hotplate test, which requires encephalic processing, mice lacking adm had shorter latencies than normal littermates. These results suggest that AM acts as a nociceptive modulator in spinal reflexes, whereas it may have an analgesic function at higher cognitive levels. This study confirms the important role of AM in pain sensitivity processing but unveils a more complex scenario than previously surmised.


2019 ◽  
Author(s):  
Iva Vassileva Vesselinova

Myelomeningocele is the most common and severe congenital malformation of the central nervous system, associated with substantial neurological morbidity, devastating lifelong medical disability and increased mortality. This review focuses on the perioperative anesthesia considerations of postnatal correction of myelomeningocele. This contains 3 tables, and 34 references. Key words: myelomeningocele, Arnold Chiari malformation, tethered spinal cord syndrome, hydrocephalus, cerebrospinal fluid, ventriculo-peritoneal shunt, latex hypersensitivity, morbidity, mortality.


Author(s):  
Mark Harrison

This chapter describes the anatomy of the central nervous system as it applies to Emergency Medicine, and in particular the Primary FRCEM examination. The chapter outlines the key details of the structure, anatomy, and arteries of the cerebral hemispheres, blood supply and venous drainage, brainstem, cerebrospinal fluid, cerebellum, spinal cord, and core blood supply. This chapter is laid out exactly following the RCEM syllabus, to allow easy reference and consolidation of learning.


1992 ◽  
Vol 82 (1) ◽  
pp. 93-97 ◽  
Author(s):  
D. G. Weir ◽  
A. M. Molloy ◽  
J. N. Keating ◽  
P. B. Young ◽  
S. Kennedy ◽  
...  

1. Pigs were maintained in air or in an atmosphere of nitrous oxide which dramatically changes the S-adenosyl-l-methionine to S-adenosyl-l-homocysteine ratio in neural tissues. Samples of cerebrospinal fluid, cortex, cerebellum and spinal cord were then extracted and analysed for S-adenosyl-l-methionine and S-adenosyl-l-homocysteine. Regression analyses were carried out on values obtained in cerebrospinal fluid and in neural tissues. 2. Highly significant correlations were obtained between levels of S-adenosyl-l-homocysteine (r2 = 0.42-0.69; P < 0.001) and S-adenosyl-l-methionine/S-adenosyl-l-homocysteine ratios (r2 = 0.56-0.65; P < 0.001) in cerebrospinal fluid and levels and ratios in cortex, cerebellum and spinal cord. The levels of S-adenosyl-l-methionine did not show a significant correlation. 3. We conclude that the ratio of these metabolites in the cerebrospinal fluid may reflect the ratio in the central nervous system and we suggest that this may also be true in human tissues. This finding will permit the determination of the probable methylation ratio in the central nervous system in human conditions, such as vitamin B12 deficiency and acquired immune deficiency syndrome, where a similar myelopathy occurs to that seen in the nitrous oxide-treated pig. All three myelopathies may arise from an inhibition of methyltransferases involved in the synthesis of myelin that would occur when the methylation ratio is reduced.


1983 ◽  
Vol 20 (5) ◽  
pp. 553-562 ◽  
Author(s):  
J. Beech

The cytology of cerebrospinal fluid samples from horses is described. The samples were obtained from 24 normal horses. 35 horses with axonal degeneration and/or spinal cord compression. 29 horses with encephalomyelitis, 14 horses with other lesions of the nervous system, and eight horses with signs of neurologic dysfunction of undetermined origin. (Three of the latter were suspected botulinum intoxications.) Fluid was aspirated from the atlanto-occipital space following general anesthesia or immediately after a lethal dose of barbiturate. In two horses, fluid also was aspirated from the lumbosacral space. Small mononuclear cells were predominant in normal horses, and in most horses with axonal degeneration and encephalomyelitis. Several horses with encephalomyelitis also had neutrophils, eosinophils, and some mitotic figures. Although the cytologic findings were abnormal in many of the horses with disease of the central nervous system, in most horses the cytologic findings were normal.


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