Neuronal damage variability

Histopathological findings in fatal cases of lead encephalopathy in children include cerebral edema, altered capillaries, and perivascular glial proliferation. Neuronal damage is variable and may be caused by anoxia (EPA 1986a). 

Two different methods have been used to determine the structure-activity relations of the neurotoxic action of the excitatory amino acids. With the first, the amino acids are administered by peripheral injection, which produces neuronal damage in areas of the brain to which the excitotoxins gain access. The second approach involves direct intracranial injection with analysis of the affected area to determine the scope and specificity of the lesion. While the latter method allows for more precise definition of toxic potencies and avoids variables such as metabolism and penetration of the blood-brain barrier, the systemic administration of these compounds was exploited first and continues to be used. 

Effects In Humans. Neither postmortem nor functional cerebrospinal fluid (CSF) studies in humans provide firm evidence for similar, long-term damages or alterations to monoaminergic neurons in chronic stimulant abusers. In part, the lack of demonstrable neurochemical changes may well be due to the obvious preclusion of well-controlled prospective experimentation in humans, as well as to variability in critical variables (e.g., individual sensitivity or pattern of abuse) encountered in clinical research. Possible relationship of the various complications of stimulant abuse including hyperpyrexia, seizure, anoxia, and metabolic exhaustion to neuronal chromatolysis, terminal destruction, and monoamine and enzymatic depletion have not been systematically explored in human autopsy eases. It should be also noted that, under nonperturbed conditions, overt behavioral deficits are rare in... 

Platinum-based chemotherapeutics induced hair cell death in rodents, albeit in variable patterns. In guinea pig, mice, and rat, cisplatin caused hearing loss that correlated to the loss of hair cells [36]. In the chinchilla, cisplatin predominantly affected outer hair cells and neurons [57], In contrast, carboplatin damaged IHCs, vestibular hair cells and auditory nerves only in chinchillas, and showed little ototoxic potency in other rodents and humans [41, 57, 58]. 

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