Brain damage

The demonstration that injected or force-fed neonatal rodents given extremely high doses of MSG showed evidence of brain lesions, has led to much additional research to determine any possible link between neurotoxicity and human use of MSG (33). However, no evidence from animal tests indicates that MSG in the diet causes brain damage in humans (34). 

Numerous experiments on rodents, as well as dogs and monkeys, with dosage levels up to 43 g of MSG per kilogram of body weight have failed to show any link between dietary use of MSG and brain damage. In the case of dogs and monkeys, even experiments involving injection of MSG have not shown any effects on the brain. 

Further increase in rate and depth of respiration, further increase in pulse rate, performance failure, giddiness, poor judgment, lips blue, prolonged exposure possibly results in brain damage. 

The body temperature limits for health in terms of internal or core temperature are fairly limited. The limits are basically related to the function of nervous tissue. Body temperatures around 28 °C or less can result in cardiac fibrillation and arrest. Temperatures of 43 °C and greater can result in heat stroke, brain damage, and death. Often, too high a temperature causes irreversible shape changes to the protein molecules of nervous tissue. That is, cooling overheated tissue to normal temperatures may not restore its original function. 

The nervous system is vulnerable to attack from several directions. Neurons do not divide, and, therefore, death of a neuron always causes a permanent loss of a cell. The brain has a high demand for oxy gen. Lack of oxygen (hypoxia) rapidly causes brain damage. This manifests itself both on neurons and oligodendroglial cells. Anoxic brain damage may result from acute carbon monoxide, cyanide, and hydrogen sulfide poisonings. Carbon monoxide may also be formed in situ in the metabolism of dichloromethylene. 

Mikkelsen, S., Jorgensen, M., Browne, E., and Gyldensten, G. ( I 988). Mixed solvent exposure and organic brain damage A study of painters. Acta Neurol. Scand. 78, 1-143. 

Unconsciousness at once. Permanent brain damage or death may result unless rescued promptly and given artificial resuscitation. 

OA were aborted in 2003 due to the development of mild to moderate liver fibrosis in dogs treated for 9 months with high doses of pralnacasan. This was in spite of recent evidence demonstrating the effectiveness of pralnacasan treatment in the acute dextran sulfate sodium (DSS)-induced colitis model, which resembles Crohn s disease (CD) characteristics, and in transient ischemia induced brain damage. 

Findings obtained from experimental studies suggest that induction of iNOS mediates inflammatory or ischemic brain damage and that excessively activated nNOS under excitotoxic or ischemic conditions produces NO that is toxic to surrounding neurons. Selective inhibition of iNOS or nNOS may be neuroprotec-tive. This is also the case in glaucoma and diabetic... 

S100B Sensitive marker of hypoxic brain damage in infants and children undergoing open-heart surgery... 

Levels greater than 35 mcg/mL—hyperglycemia, hypotension, cardiac arrhythmias, tachycardia, seizures, brain damage... 

Chronic social use, characterized by daily social use for 5 or more years, which usually occurs among individuals with poor social skills and hm-ited education who are age 20—30 years and who may also have evidence of brain damage and minor legal problems... 

Chronic isolated use, characterized by a history of continuous solo use for 5 or more years among individuals age 20—29 years with poor social skills, limited education, and significant involvement in legal problems evidence of brain damage may be common in this group. 

Robinson TE, Berridge KC The neural basis of drug craving an incentive-sensitization theory of addiction. Brain Res Brain Res Rev 18 247—291, 1993 Rosenberg J Brain damage and epilepsy in a sailor on a ship with chemicals. Tidsskr Nor Laegeforen 102 576-577, 1982... 

Acute clinical signs of neurotoxicity, manifested by hyperexcitability, dyspnea, decreased respiration, tremors, and convulsions, were identified in the available literature as effects caused by high doses of endosulfan. Exposure to high levels of endosulfan in humans may possibly be associated with permanent brain damage as manifested by cognitive and emotional deterioration, memory impairment, and... 

The main concern regarding tetraalkyl lead has been about human health hazards, a concern that has resulted in the progressive replacement of leaded petrol by unleaded petrol in most countries (Environmental Health Criteria 85). There has been particular concern about possible brain damage to children in polluted urban areas. Little work has been done on the effects of organolead compounds on wildlife or ecosystems, so the following account will be brief. 

All defects in urea synthesis result in ammonia intoxication. Intoxication is more severe when the metabolic block occurs at reactions 1 or 2 since some covalent linking of ammonia to carbon has already occurred if citrulline can be synthesized. Clinical symptoms common to all urea cycle disorders include vomiting, avoidance of high-protein foods, intermittent ataxia, irritability, lethargy, and mental retardation. The clinical features and treatment of all five disorders discussed below are similar. Significant improvement and minimization of brain damage accompany a low-protein diet ingested as frequent small meals to avoid sudden increases in blood ammonia levels. 

As the name implies, the odor of urine in maple syrup urine disease (brancbed-chain ketonuria) suggests maple symp or burnt sugar. The biochemical defect involves the a-keto acid decarboxylase complex (reaction 2, Figure 30-19). Plasma and urinary levels of leucine, isoleucine, valine, a-keto acids, and a-hydroxy acids (reduced a-keto acids) are elevated. The mechanism of toxicity is unknown. Early diagnosis, especially prior to 1 week of age, employs enzymatic analysis. Prompt replacement of dietary protein by an amino acid mixture that lacks leucine, isoleucine, and valine averts brain damage and early mortality. 

In many respects the classic findings of neuropsychology have formed the bedrock of much of what we know about how we see, hear, speak, move and even feel. Nonetheless, neuropsychology has not always influenced theories about how the intact brain carries out tasks. This is partly because nature is a poor surgeon accidental brain damage is usually spatially diffuse, interrupts several functions, is irreversible and the time of its occurrence cannot be predicted. Another problem with the lesion method in general, even when specific areas can be removed from animals, is that... 

The stimulation method could not address the role of the elaboration areas and the study of brain damaged patients or lesion studies of animals is hampered by the lack of temporal resolution. What is needed for another wave of reverse engineering, then, is the ability to stimulate the brain while it is doing something, or to be able to reversibly disrupt its functioning to give the lesion method a temporal dimension. The story of how we are able to achieve both of these takes us back to Faraday.. . . ... 

Chapman GA, Moores K, Harrison D, Campbell CA, Stewart BR, Strijbos PJ (2000) Fractalkine cleavage from neuronal membranes represents an acute event in the inflammatory response to excitotoxic brain damage. J Neurosci 20 RC87... 

Ereret T, Valable S, Chazalviel L, Saulnier R, Mackenzie ET, Petit E, Bemaudin M, Boulouard M, Schumann-Bard P. Delayed administration of deferoxamine reduces brain damage and promotes functional recovery after transient focal cerebral iscbemia in tbe rat. Eur J Neurosci 2006 23 1757-1765. 

Sironi L, Cimino M, Guerrini U, Calvio AM, Lodetti B, Asdente M, Balduini W, Paoletti R, Tremoli E. Treatment with statins after induction of focal ischemia in rats reduces the extent of brain damage. Arterioscler Thromb Vase Biol 2003 23 322-327. 

Krieger DW, De Georgia MA, Abou-Chebl A, Andrefsky JC, Sila CA, Katzan IL, Mayberg MR, Furlan AJ. Coohng for acute ischemic brain damage (cool aid) an open pilot study of induced hypothermia in acute ischemic stroke. Stroke 2001 32 1847-1854. 

De GeorgiaMA, Krieger DW, Abou-Chebl A, Devlin TG, Jauss M, Davis SM, Koroshetz WJ, Rordorf G, Warach S. Cooling for acute ischemic brain damage (cool aid) a feasibility trial of endovascular cooling. Neurology 2004 63 312-317. 

PulsineUi WA, Waldman S, Rawhnson D, Plum F. Moderate hyperglycemia augments ischemic brain damage a neuropathologic study in the rat. Neurology 1982 32(11) 1239-1246. 

---