ascorbic-acid and Paralysis

Several data suggest that excitotoxicity due to excessive glutamatergic neurotransmission may be an important factor in the mechanisms of motor neuron (MN) death occurring in amyotrophic lateral sclerosis (ALS). We have previously shown that the overactivation of the Ca(2+)-permeable α-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) glutamate receptor type, through the continuous infusion of AMPA in the lumbar spinal cord of adult rats during several days, results in progressive rear limb paralysis and bilateral MN degeneration. Because it has been shown that energy failure and oxidative stress are involved in MN degeneration, in both ALS and experimental models of spinal MN degeneration, including excitotoxicity, in this work we tested the protective effect of the energy substrates pyruvate and β-hydroxybutyrate (βHB) and the antioxidants glutathione ethyl ester (GEE) and ascorbate in this chronic AMPA-induced neurodegeneration.. AMPA infusion induced remarkable progressive motor deficits, assessed by two motor tasks, that by day seven reach bilateral rear limb paralysis. These effects correlate with the death of >80% of lumbar spinal MNs in the infused and the neighbor spinal cord segments, as well as with notable astrogliosis in the ventral horns, detected by glial fibrillary acidic protein immunohistochemistry. Co-infusion with pyruvate or βHB notably prevented the motor deficits and paralysis, decreased MN loss to <25% and completely prevented the induction of astrogliosis. In contrast, the antioxidants tested were ineffective regarding all parameters analyzed.. Chronic progressive excitotoxicity due to AMPA receptors overactivation results in MN death and astrogliosis, with consequent motor deficits and paralysis. Because of the notable protection against these effects exerted by pyruvate and βHB, which are well established mitochondrial energy substrates, we conclude that deficits in mitochondrial energy metabolism are an important factor in the mechanisms of this slowly developed excitotoxic MN death, while the lack of protective effect of the antioxidants indicates that oxidative stress seems to be less significant factor. Because excitotoxicity may be involved in MN degeneration in ALS, these findings suggest possible preventive or therapeutic strategies for the disease.

Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Antioxidants; Ascorbic Acid; Cell Death; Disease Models, Animal; Extremities; Gliosis; Glutathione; Hydroxybutyrates; Male; Mitochondria; Motor Activity; Motor Neurons; Nerve Degeneration; Neuroprotection; Oxidative Stress; Paralysis; Pyruvic Acid; Rats; Rats, Wistar; Receptors, AMPA; Spinal Cord; Treatment Outcome

On the basis of in vitro studies, the antioxidant nutrients vitamins E and C are postulated to interact in vivo.. We developed a guinea pig model to evaluate the combined deficiency of vitamins E and C in vivo.. Weanling guinea pigs were fed a control diet or a vitamin E-deficient diet for 14 d, after which one-half of each group had vitamin C removed from their diet, thus creating 4 diet groups. Some animals were observed for clinical signs. Others were killed for evaluation.. Of 21 guinea pigs that were observed after being fed the diet deficient in both vitamins, 8 died 9 +/- 2 d (x +/- SD) after starting the diet. Eight additional guinea pigs developed a characteristic syndrome at 11 +/- 3 d. First, they became paralyzed in the hind limbs. Within a few hours, the paralysis progressed to include all 4 limbs and caused difficulty in breathing, which would have caused death had the animals not been euthanized. Histopathologic evaluation did not identify a lesion in the muscles or nervous system that could account for the paralysis. Biochemical measurements confirmed the deficiencies and indicated that the double deficiency caused lipid peroxidation in the central nervous system.. A distinct clinical syndrome of combined vitamin E and vitamin C deficiency occurs in guinea pigs. This syndrome indicates that these antioxidant vitamins are related in vivo. We speculate that acute oxidative injury in the central nervous system underlies the clinical syndrome.

Topics: alpha-Tocopherol; Animals; Ascorbic Acid; Ascorbic Acid Deficiency; Brain; Disease Models, Animal; Guinea Pigs; Male; Osmolar Concentration; Paralysis; Sciatic Nerve; Spinal Cord; Vitamin E Deficiency

A four-year-old male child was reported with sudden inability to stand walk of 10 days duration. Acute paralytic poliomyelitis was diagnosed in the presence of fever, respiratory infection, muscle tenderness, and weakness in lower extremity in an unimmunized child. Reevaluation after a week showed swelling, thickening, and tenderness of left femur. Plain x-ray of the left thigh was advised to exclude underlying osteomyelitis of the femur. X-ray showed features of scurvy. The child responded well to parenteral vitamin C therapy and resumed normal walking with in two weeks. Scurvy can present as pseudoparalysis of acute onset without any other signs even in older children. It emphasized the need for an index of suspicion of scurvy in a case of suspected paralysis. Dramatic response to vitamin C therapy can be used to confirm the diagnosis in the absence of laboratory support. Health education can be accelerated to prevent a disease like scurvy.

Topics: Ascorbic Acid; Child, Preschool; Diagnosis, Differential; Humans; Knee; Male; Paralysis; Poliomyelitis; Radiography; Scurvy

The authors observed a lesion of the peripheral nerves in 13 of 401 children with supracondylar humerus fractures (3.2%). Most frequently, the radial nerve was injured. All patients with neural lesions healed spontaneously, a surgical revision of the nerve was not necessary. The authors' opinion is that neural lesions accompanying supracondylar fractures can be treated conservatively. Exceptions are clear indications for surgical revision, as persisting ischaemia of the forearm or extensive open fractures. When treating conservatively, it is necessary to make a thorough clinical and EMG investigation to set exactly the diagnosis of the neural lesion immediately after removing the plaster cast (mostly 3 weeks after the injury). This investigation is to be repeated regularly, as the reinervation dynamics of the affected region is to be followed up. At the same time it is advantageous to perform electrostimulation until reinervation potentials appear, vitaminotherapy and intensive active exercise with the involved extremity. If no signs of reinvertion in the affected area appear within 6 months, a surgical revision of the nerve is to be considered.

Topics: Ascorbic Acid; Brachial Plexus; Electric Stimulation; Electromyography; Female; Humans; Humeral Fractures; Male; Median Nerve; Nerve Regeneration; Paralysis; Radial Nerve; Ulnar Nerve; Vitamin B Complex; Vitamin E

Topics: Ascorbic Acid; Ascorbic Acid Deficiency; Child; Extremities; Fractures, Spontaneous; Humans; Paralysis; Radiography; Spinal Dysraphism

Topics: Anemia; Animals; Ascorbic Acid; Chickens; Diet; Folic Acid; Paralysis; Paresis; Riboflavin; Vitamin A; Vitamin B Complex; Vitamins