"Organ reserve" refers to the ability of an organ to successfully return to its original physiological state following repeated episodes of stress. Clinical evidence shows that organ reserve correlates with the ability of older adults to cope with an added workload or stress, suggesting a role in the process of aging. Although organ reserve is well documented clinically, it is not clearly defined at the molecular level. Interestingly, several metabolic pathways exhibit excess metabolic capacities (e.g., bioenergetics pathway, antioxidants system, plasticity). These pathways comprise molecular components that have an excess of quantity and/or activity than that required for basic physiological demand in vivo (e.g., mitochondrial complex IV or glycolytic enzymes). We propose that the excess in mtDNA copy number and tandem DNA repeats of telomeres are additional examples of intrinsically embedded structural components that could comprise excess capacity. These excess capacities may grant intermediary metabolism the ability to instantly cope with, or manage, added workload or stress. Therefore, excess metabolic capacities could be viewed as an innate mechanism of adaptability that substantiates organ reserve and contributes to the cellular defense systems. If metabolic excess capacities or organ reserves are impaired or exhausted, the ability of the cell to cope with stress is reduced. Under these circumstances cell senescence, transformation, or death occurs. In this review, we discuss excess metabolic and structural capacities as integrated metabolic pathways in relation to organ reserve and cellular aging.

Five additional cases of ataxic-hemiparesis are reported. In 3 cases, computed tomography showed an area of decreased attenuation in the posterior limb of the internal capsule, and in 1 case, 2 areas of attenuation in the corona radiata. A review of previously reported cases suggest that brainstem ataxic-hemiparesis may be separated from supratentorial forms of ataxic-hemiparesis by the presence of nystagmus, dysarthria, cranial neuropathy, and the absence of sensory abnormality.

Nearly half of all cases of acute encephalitis did not have an identifiable cause. Autoimmune (antibody-mediated) etiology has gained more recognition over the recent years. It is important to consider the diagnosis by the clinical findings of acute limbic encephalopathy, new onset schizophrenia, or new onset medically refractory seizures. Identification of the antibodies is important in defining the underlying causes including underlying malignancies. Antibodies against intracellular proteins are more likely to be paraneoplastic and T-cell mediated. Antibodies against cell surface or synaptic antigens are mostly B-cell mediated and they are more responsive to immunotherapy. In addition to high index of clinical suspicion, MRI, serum and CSF antibody testing are most helpful in making the final diagnosis.

Wernicke's encephalopathy (WE) is a neuropsychiatric condition caused by thiamine deficiency often associated with alcoholism. Other less common causes include prolonged gastroenterology problems or dietary insufficiencies associated with hyperemesis gravidarum, bariatric surgery, and eating disorders. Prolonged WE without proper treatment can lead to the chronic and irreversible condition, Wernicke-Korsakoff syndrome. Despite being known for its classic triad of clinical symptoms (nystagmus/ophthalmoplegia, gait ataxia, and confusion), WE patients more commonly present with nonspecific symptoms of altered mental status. Obscure clinical presentations often led to delays in the appropriate of patients with WE. We are presenting a case of WE that is unusual because the underlying cause is schizophrenia and the lack of alcohol use. For a punctual diagnosis, a high index of suspicion is essential to prevent further exacerbation of neuronal death seen in WE. IV thiamine should be administered to any patient with acute encephalopathy or altered mental status, given its low cost and lack of side effects.