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Biomedical subjects

B R Brooks

Publications and source records attributed to B R Brooks.

At least 127 records · Page 7Linked to original sources
PubMed1980

Cerebrospinal-fluid lymphocyte populations and immune complexes in active multiple sclerosis.

A specific subpopulation of mononuclear cells bearing a surface receptor for the Fc portion of IgG was considerably reduced in the cerebrospinal fluid (CSF) of multiple sclerosis (MS) patients during exacerbation, but returned toward normal levels as the patient entered remission. Low concentrations of immune complexes were found in the CSF in nearly 50% of MS patients during exacerbations but immune complexes were not found in patients with stable MS.

Acute Disease↗
PubMed1980

A diagnostic index of active demyelination: myelin basic protein in cerebrospinal fluid.

We have developed a radioimmunoassay to measure a specific neurological component, the basic protein of myelin, and have used this test for assessing this component in spinal fluid. The levels of basic protein in spinal fluid correlate closely with the clinical activity of multiple sclerosis; therefore the test can be used for objective evaluation of disease activity in patients with that disorder. Moreover, it is a useful adjunct in the diagnosis of multiple sclerosis and evaluation of potential therapy. In addition, the test is helpful in diagnosing other diseases in which acute breakdown of myelin occurs, especially leukoencephalopathy resulting from irradiation and chemotherapy for treatment of leukemia in children.

Demyelinating Diseases↗
PubMed1980

Norepinephrine and gamma-aminobutyric acid in amyotrophic lateral sclerosis.

Patients with amyotrophic lateral sclerosis have increased levels of the neutrotransmitter norepinephrine in blood and cerebrospinal fluid and depressed levels of the inhibitory neurotransmitter gamma-aminobutyric acid in cerebrospinal fluid. These neurochemical alterations are most marked in patients bedridden with advanced disease, appear interrelated, and lead to cardiovascular alterations in patients with amyotrophic lateral sclerosis.

Adult↗
PubMed1979

CSF viral antibodies. Evaluation in amyotrophic lateral sclerosis and late-onset postpoliomyelitis progressive muscular atrophy.

Serum and CSF from 48 patients with amyotrophic lateral sclerosis and six patients with late-onset postpoliomyelitis progressive muscular atrophy were investigated for the presence of antibody to poliovirus types 1, 2, and 3, coxsackie viruses B3 and B4, influenza A, measles, rubella, mumps, herpes simplex types 1 and 2, cytomegalovirus, varicella-zoster, and Toxoplasma gondii. These results were compared with those from 53 control patients with neuromuscular disease matched for age, sex, race, and poliovirus vaccine exposure. There was no difference either in distribution of serum or CSF antibody titers or the geometric-mean antibody titers. There was no evidence suggesting the presence of locally produced specific viral antibody within the CNS to any of the agents studied. In particular, there was no serological evidence to suggest an association between persistent infection with any poliovirus type and amyotrophic lateral sclerosis or late-onset postpoliomyelitis progressive muscular atrophy.

Adult↗
PubMed1978

Decreased spinal cord cGMP in murine (wobbler) spontaneous lower motor neuron degeneration.

Of the secondary messengers, cyclic quanosine monophosphate, but not cyclic adenosine monophosphate, was reduced by 80% in the cervical spinal cord and by 56% in the cerebellum of clinically affected homozygote "wobbler" mice compared to sex- and age-matched litter-mate clinically unaffected control mice. A neurotransmitter, gamma aminobutyric acid, and high-energy intermediates, adenosine triphosphate and phosphocreatine, were not significantly different in affected or unaffected mice.

Animals↗
PubMed1977

Blood-to-cerebrospinal fluid barrier for cyclic adenosine monophosphate in man.

A definite blood to lumbar CSF barrier for cyclic adenosine monophosphate (cAMP) exists in man under physiologic conditions. Lumbar CSF cAMP level remained unchanged, while the CSF glucose level rose significantly after a glucagon hydrochloride infusion that caused a 40-fold increase in the plasma cAMP level.

Blood-Brain Barrier↗
PubMed1977

Cerebrospinal fluid norepinephrine alterations during electrical stimulation of cerebellar, cerebral surfaces in epileptic patients.

Lumbar cerebrospinal fluid norepinephrine concentrations were determined by radioenzymatic assay in five epileptic patients receiving double-blind cerebellar stimulation and in three epileptic patients with subdural cerebral surface electrodes. Mean CSF norepinephrine levels were significantly elevated by chronic cerebellar stimulation and significantly depressed after intermittent cerebral cortical stimulation. Lumbar CSF cyclic adenosine monophosphate levels determined by radioimmunoassay were not significantly altered by either cerebellar or cerebral surface stimulation. Our study suggests that (1) electrical stimulation of the anterodorsal cerebellum in man evokes alterations in noradrenergic metabolism. Cerebellar stimulation-induced elevations in norepinephrine may inhibit cerebellar, cerebral, and spinal neuronal activity. In addition, (2) noradrenergic responses to brain surface stimulation may exhibit regional specificity, and (3) noradrenergic alterations evoked by cerebral surface stimulation may not mimic those induced in isolated brain preparations.

Adolescent↗