The Blood-Cerebrospinal Fluid Barrier in Tuberculous Meningitis and Allied Conditions

Smith, Harriet J; Taylor, L.M.; Hunter, G.

doi:10.1136/jnnp.18.4.237

Cited by 21 publications

(4 citation statements)

References 13 publications

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“…When small numbers of virulent cryptococci were injected intravenously into normal mice, tissue populations rose markedly in all organs studies during s Unpublished studies by the author have demonstrated that the blood-cerebrospinal fluid bromide ratio fails from the normal 2.5 to 3.0:1 to 1:1 in cryptococeal meningitis in man. These findings are similar to those found in tuberculous meningitis (33) and indicate a marked alteration in the blood-cerebrospinal fluid barrier.…”

Section: Discussionsupporting

confidence: 88%

Specific and Non-Specific Immunity in Experimental Cryptococcosis in Mice

Louria

1960

The Journal of Experimental Medicine

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Host defense mechanisms often appear to be inadequate following cryptococcal invasion (1-4). Significant antibody response has not been demonstrated with any regularity in man or experimental animals during torula infection. Furthermore, cellular response in cryptococcosis is frequently sparse. The apparent inadequacy of host antibody and cellular defenses during torula infection has been related to the presence of a large capsule, surrounding the cryptococcus cell, which consists primarily of several polysaccharides (5).Benham (6) was able to produce antibodies to cryptococci in rabbits only after the capsule had been removed with hydrochloric acid. Evans and Kessel (7,8) and Neill, CastiUo, Smith, and Kapros (9), however, demonstrated precipitating and agglutinating antibodies in the rabbit following immunization with large numbers of heat-or formalin-killed cryptococci. These antibodies were dearly shown to be directed against the capsular material. The rabbit does not ordinarily develop progressive cryptococcosis so that no inference could be drawn as to the protective effect of such immunization in this animal.In recent studies, Gadebusch (10) reported that he could delay death in mice following cryptococcal challenge by the administration of immune rabbit serum. These as yet unconfirmed studies suggested that immune rabbit serum not only contained antibody directed against the cryptococcal capsule, but also was able to modify the course of a lethal cryptococeal infection. However, the challenge organisms were suspended in mucin, and the antisera and challenge were both given intraperitoneaUy within 2 hours of each other. It is quite possible that the apparent protection was related to dumping of fungi by the agglutinating antisera, thus in actuality reducing the size of the inoculum. Furthermore, mucin itself can at first reduce and later increase resistance non-specifically to many infections (11). Thus temporary dumping of fungus cells by antisera might retard the acute infection long enough to allow nonspecific resistance to develop.Gadebusch (12) also reported that death was delayed in mice infected with a lethal

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Section: Discussionsupporting

confidence: 88%

Specific and Non-Specific Immunity in Experimental Cryptococcosis in Mice

Louria

1960

The Journal of Experimental Medicine

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“…Both returned to normal as the meningitis re gressed. No changes in bromide transfer were noted in other types of lympho cytic meningitis (96). Similar qualitative observations have been made for penicillin (98), and oxytetracycline (99).…”

Section: Clinical Implications Of Blood-brain Barrier Studiessupporting

confidence: 67%

Mechanisms of Drug Absorption and Excretion Passage of Drugs in and out of the Central Nervous System

Rall¹,

Zubrod²

1962

Annu. Rev. Pharmacol.

144

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“…Initially, patients with tuberculous meningitis were treated with PPD intrathecally with the aim of creating a sterile meningitis and thereby increase, because of the resultant breakdown of BBB, the delivery of the systemic antituberculous drugs within the CNS. The Oxford workers noticed an apparent success with this treatment (intrathecal PPD) in MS patients who also suffered from tuberculous meninigitis (Smith et al ., 1955). This formed the basis of a controlled trial of intrathecal tuberculin (PPD) in MS (Kelly and Jellinek, 1961).…”

Section: Discussionmentioning

confidence: 99%

Acute cervical hyperextension–hyperflexion injury may precipitate and/or exacerbate symptomatic multiple sclerosis

Chaudhuri

Behan

2001

Euro J of Neurology

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We report here 39 cases in which definite multiple sclerosis (MS) was precipitated or exacerbated by specific hyperextension-hyperflexion cervical cord trauma. The worsening or onset of the symptomatic disease bore a striking temporal relationship to the focal injury. Our data suggests that central nervous system (CNS)-specific acute physical trauma such as cervical cord hyperextension-hyperflexion injury may aggravate latent clinical symptoms in MS. The deterioration of MS bore no direct relationship with the severity of neck injury. Possible pathogenic mechanisms of focal CNS-specific trauma aggravating the course of asymptomatic or benign MS are discussed. This may have implications in improving our understanding of the factors that may modify the clinical course of MS.

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The Blood-Cerebrospinal Fluid Barrier in Tuberculous Meningitis and Allied Conditions

Cited by 21 publications

References 13 publications

Specific and Non-Specific Immunity in Experimental Cryptococcosis in Mice

Specific and Non-Specific Immunity in Experimental Cryptococcosis in Mice

Mechanisms of Drug Absorption and Excretion Passage of Drugs in and out of the Central Nervous System

Acute cervical hyperextension–hyperflexion injury may precipitate and/or exacerbate symptomatic multiple sclerosis

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