Cortical deficits in multiple sclerosis on the basis of subcortical lesions.

Patients suffering from multiple sclerosis have a high frequency of cognitive deficits usually attributable to demyelination and axonal loss in the subcortical white matter. Neurologic abnormalities referable to cortical function are uncommon but have been described. The present study describes three patients with clinically definite MS with deficits in cognitive function referable to cortical location. Two of the patients underwent positron emission tomography and showed profound cortical hypometabolism adjacent to subcortical white matter lesions seen on MRI. This paper points out that neurologic deficits referable to cortical sites may be caused by subcortical white matter lesions and that cognitive dysfunction in patients with MS may progress rapidly in the absence of motoria deficits or other evidence of clinical deterioration. Multiple Sclerosis (2000) 6 50 - 55

Diazepam improves recording of lumbar and neck somatosensory evoked potentials.

To determine whether the decrease in muscle artifact provided by diazepam is of sufficient clinical value to justify its use, somatosensory evoked potentials recorded in examinations of 73 consecutive patients were compared with those recorded from 33 subsequent patients who were given 10 mg of diazepam orally just before the examination. With diazepam pretreatment there was clear improvement in the quality of lumbar and neck recordings--increased reproducibility and definition and ease of measurement--and also greater tolerance of the procedure and a slight shortening of time required for the test.

Elevation of serum creatine kinase B-subunit levels by radiographic contrast agents in patients with neurologic disorders.

The effect of radiographic contrast agents on the central nervous system was evaluated by measurement of serum creatine kinase B-subunit (CKB) levels with use of radioimmunoassay in 58 patients who underwent computed tomographic (CT) scanning and 46 patients who underwent cerebral angiography for evaluation of cerebrovascular diseases, brain tumors, and other neurologic disorders. In 11 patients (10.6%), the CKB increased to abnormally high levels within 4 hours after the radiographic procedures, and the median value after 30 minutes was significantly higher than the corresponding precontrast value (P less than 0.01). Eight of the 11 patients had recent ischemic cerebrovascular diseases, and 7 of the 11 had undergone CT scanning. On the basis of the information available in the literature, elevation of the serum CKB levels may be interpreted as reflecting breakdown of the blood-brain barrier and neural damage. Intravascularly administered radiographic media are generally safe, but the results of the current investigation suggested the potential for detrimental effects, particularly in patients with recent cerebrovascular diseases.

Serum creatine kinase B concentrations in acute cerebrovascular diseases.

Serum creatine kinase B (CKB) concentrations were measured every 12 hours for five days in 38 patients during acute cerebrovascular diseases and in nine controls. Mean CKB concentration was 6.2 +/- 0.8 ng/mL. The fluctuation of the CKB concentration following ischemic stroke was as notable as the elevation immediately after the ischemic event. The two abnormalities were observed in 13 of 17 patients with acute cerebral infarction, and the extent of abnormalities roughly correlated with the volume of tissue damage. The profiles were normal for patients with transient vascular events. Patients with subarachnoid hemorrhage demonstrated wide fluctuation along with high CKB concentration. Although transient elevation of the CKB concentration in some patients with subarachnoid hemorrhage was observed after angiography or clinical worsening, the fluctuation in patients with ischemic stroke was not associated with worsening of neurologic conditions or recurrence of ischemic events.

Creatine kinase BB isoenzyme in CSF in neurologic diseases. Measurement by radioimmunoassay.

The concentration of creatine kinase BB isoenzyme (CK BB) was measured by radioimmunoassay in CSF from 306 patients with various neurologic disorders. Levels above 2.0 ng/mL were not found in patients without neurologic disease. Whereas mean CSF CK BB level was less than 2.0 ng/mL in groups of patients with systemic malignant neoplasms, latent syphilis, peripheral neuropathy, disk disease, polyradiculopathy, myelopathy, multiple sclerosis, neurodegenerative disease, encephalopathy, and hydrocephalus, it was elevated in groups of patients with convulsive disorder, CNS neoplasm, cerebrovascular disease, vasculitis, and meningoencephalitis.