chiniofon and Cardiovascular-Diseases

Due to an unexpected increase in serious cardiovascular events in MS patients treated with Linomide, a synthetic immunomodulator, two phase-III multinational relapsing remitting (RR) and secondary progressive (SP) MS trials had to be discontinued. MRI results of 413 patients who participated for at least 3 months were analysed. Patients received placebo, 2.5 or 5 mg Linomide. Scans were performed at pre-enrolment, month 3 and termination. The number and volume of enhancing lesions (ELV), and the number of active scans were evaluated. At month 3, the decrease in the number of enhancing lesions in the placebo group was 11%, compared with 15% in the 2.5 mg group (P=0.027) and 23% in the 5 mg group (P=0.057). Using the percentage of active scans as outcome parameter, the odds ratio for improvement between placebo and 2.5 mg group was 1.62 (P=0.14); between placebo and 5 mg Linomide group 3.58 (P=0.003). At termination, a rebound effect was noted in the 2.5 mg group (P=0.01). Analysis of the ELV showed no significant difference between placebo and treatment groups. Although Linomide has unacceptable side effects, it seems to have a modest effect on MS disease activity, as measured by MRI. Multiple Sclerosis (2000) 6, 99 - 104

Topics: Adjuvants, Immunologic; Adolescent; Adult; Cardiovascular Diseases; Humans; Hydroxyquinolines; Magnetic Resonance Imaging; Middle Aged; Multiple Sclerosis, Chronic Progressive; Multiple Sclerosis, Relapsing-Remitting; Treatment Outcome

Topics: Bismuth; Cardiovascular Diseases; Diazepam; Drug Therapy; Endocrine System Diseases; Gastrointestinal Diseases; Glafenine; Hepatitis; Humans; Hydroxyquinolines; Hypersensitivity; Infections; Kidney Diseases; Metabolic Diseases; Neoplasms; Nervous System Diseases; Practolol; Respiratory Tract Diseases; Rheumatic Diseases

Acute vestibular paralysis may not be considered as a nosologic entity but as a syndrome. Symptomatology (vertigo, spontaneous and provoked vestibular nystagmus, absence of cochlear signs) shows an uniform picture. The results of the caloric test as well as the nystagmic responses induced by galvanic stimulation and the development of central vestibular compensation however indicate that the site of the lesion is not only confined to the labyrinth but may also occur at the level of the peripheral neuron or even the vestibular nuclei. Etiology and pathology are still vague. Our own clinical observations as well as the scarce data in literature about morphological and experimental studies suggest in a way that vascular and infectious disorders are of importance as primary releasing factors. Hypothetically, vestibular loss of function may either be caused by a disturbance of labyrinthine microcirculation, initiated in a great majority of cases by infection, or by a direct lesion of the peripheral neuron as well as the vestibular nuclei. Retrolabyrinthine lesions may be due to menigoencephalitis, caused by a neurotropic virus or other infectious agents such as Toxoplasma gondii. Acute vestibular paralysis should be strictly distinguished from vestibular neuronitis. While vestibular paralysis is a syndrome, vestibular neuronitis must be considered as a nosologic entity, including a lesion of the peripheral neuron as well as evidence of an infectious event.

Topics: Adolescent; Adult; Aged; Amphetamines; Audiometry; Bacterial Infections; Cardiovascular Diseases; Child; Child, Preschool; Female; Humans; Hydroxyquinolines; Labyrinth Diseases; Male; Metabolic Diseases; Middle Aged; Nystagmus, Pathologic; Phenytoin; Toxoplasmosis; Vertigo; Vestibular Function Tests; Vestibule, Labyrinth; Virus Diseases