ascorbic-acid and Ataxia

The aim of this article is to correct a very general error in scientific articles, in textbooks and in the Internet that has become an accepted fact. In this literature, the term "vitamin E″ is used for several similar molecules (both tocopherols and tocotrienols) that have never been shown to have vitamin property, i.e. a protective effect against the human deficiency disease. In fact, the name "vitamin E″ should only be used to define molecules that prevent the human deficiency disease "Ataxia with Vitamin E Deficiency" (AVED). Only one such molecule is known, α-tocopherol. This error may confuse consumers as well as medical doctors, who prescribe vitamin E without realizing that the current use of the name includes molecules of unknown, if not unwanted functions.

Topics: alpha-Tocopherol; Antioxidants; Ascorbic Acid; Ataxia; Calcitriol; Dietary Supplements; Humans; Rickets; Scurvy; Stereoisomerism; Terminology as Topic; Tocotrienols; Vitamin E; Vitamin E Deficiency

Oxidative stress is considered to be involved in the pathogenesis of primary blast-related traumatic brain injury (bTBI). We evaluated the effects of ascorbic acid 2-glucoside (AA2G), a well-known antioxidant, to control oxidative stress in rat brain exposed to laser-induced shock waves (LISWs). The design consisted of a controlled animal study using male 10-week-old Sprague-Dawley rats. The study was conducted at the University research laboratory. Low-impulse (54 Pa•s) LISWs were transcranially applied to rat brain. Rats were randomized to control group (anesthesia and head shaving, n = 10), LISW group (anesthesia, head shaving and LISW application, n = 10) or LISW + post AA2G group (AA2G administration after LISW application, n = 10) in the first study. In another study, rats were randomized to control group (n = 10), LISW group (n = 10) or LISW + pre and post AA2G group (AA2G administration before and after LISW application, n = 10). The measured outcomes were as follows: (i) motor function assessed by accelerating rotarod test; (ii) levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG), an oxidative stress marker; (iii) ascorbic acid in each group of rats. Ascorbic acid levels were significantly decreased and 8-OHdG levels were significantly increased in the cerebellum of the LISW group. Motor coordination disorder was also observed in the group. Prophylactic AA2G administration significantly increased the ascorbic acid levels, reduced oxidative stress and mitigated the motor dysfunction. In contrast, the effects of therapeutic AA2G administration alone were limited. The results suggest that the prophylactic administration of ascorbic acid can reduce shock wave-related oxidative stress and prevented motor dysfunction in rats.

Topics: Animals; Ascorbic Acid; Ataxia; Brain; Brain Injuries, Traumatic; Cerebellum; Male; Oxidative Stress; Rats; Rats, Sprague-Dawley

Male Swiss-Webster mice were administered ethanol immediately before a motor coordination test. Controls and animals treated with 1, 2 or 3 g/kg, IP, of ethanol remained on a suspended meter stick for 240 +/- 0, 232 +/- 8, 93 +/- 2 and 75 +/- 5 sec, respectively. Blood ethanol levels at the end of the test period (4 min) or when the animal fell from the meter stick were 1.02 +/- 0.03, 2.13 +/- 0.09 and 2.24 +/- 0.07 mg/ml for the 1, 2 and 3 g/kg dose of ethanol, respectively. Thirty min prior to ethanol (2 g/kg, IP) animals received L-ascorbic acid in doses of 500 or 1000 mg/kg, IP. Both doses of L-ascorbic acid significantly enhanced the duration of time that the animals spent on the meter stick. When animals were given 1 g/kg, IP, of ethanol their rate of walking (cm/min) on the meter stick was significantly increased over controls. Administration of L-ascorbic acid (1000 mg/kg, IP) 30 min prior to ethanol (1 g/kg) did not change the rate of locomotion. In experiments on ethanol-induced hypnosis (sleep-time), animals received L-ascorbic acid (250, 500, 1000 or 1500 mg/kg, IP) or saline 30 min prior to ethanol (4 g/kg, IP). L-ascorbic acid increased the time of onset of hypnosis significantly at doses of 1000 and 1500 mg/kg. With these doses of L-ascorbic acid sleep duration and blood ethanol content were not altered. L-ascorbic acid, however, increased ethanol-induced hypnosis at a dose of 500 mg/kg.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Ascorbic Acid; Ataxia; Central Nervous System Depressants; Drug Interactions; Ethanol; Hypnotics and Sedatives; Male; Mice; Psychomotor Performance

Six cases of PCP intoxication in young children age 5 years and younger seen at UCLA Medical Center recently and 10 other cases from the literature are described and their clinical findings summarized. PCP intoxication should be suspected in young children and infants presenting with rapid onset of lethargy or coma, strange behavior, staring spells, ataxia, and nystagmus. Other findings less frequent but still suspect are opisthotonos, hypertension, tachypnea or hyperpnea, miosis, hyperreflexia, hypertonia, and rigidity. Once suspected, the diagnosis is most easily made by finding PCP in the urine. Proper diagnosis of PCP intoxication is important to ensure that rapid, appropriate treatment is given, costly diagnostic workups are avoided, and family evaluations are instituted. One case strongly suggests that intoxication in infants may result from accidental inhalation when near individuals who are smoking PCP.

Topics: Ascorbic Acid; Ataxia; Diagnosis, Differential; Environmental Exposure; Female; Fluid Therapy; Humans; Infant; Infant, Newborn; Infant, Newborn, Diseases; Male; Nystagmus, Pathologic; Phencyclidine; Sleep Stages; Spasm