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Home arrow Psychology arrow Neuropsychiatric Symptoms of Cognitive Impairment and Dementia
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Renal Disorders

Patients with renal disorders are at an increased risk for developing cognitive impairment due to diverse conditions, including uremia and metabolic process associated with renal failure, high prevalence of cerebrovascular comorbid disorders, or even due to dialysis itself.

Uremic encephalopathy is an organic brain syndrome which occurs in patients with acute or chronic renal failure, usually, when renal function falls and remains in a very severe level. Severity and progression of the encephalopathy depend on the rate of decline in renal function, and, hence, symptoms are generally worse in patients with an acute deterioration. The clinical course is characterized by fluctuation of symptoms and may vary from mild (fatigue, apathy, inattention) to severe symptoms (seizures, coma). Intermediate manifestations may include neuropsychiatric symptoms (forgetfulness, emotional lability, sleep inversion, changes in abstract thinking and behavior, hallucinations and delusions, decreased level of consciousness), motor changes (discoordination, multifocal myoclonus, coarse postural tremor, paratonia, occasionally motor asymmetry and alternating during the course of the illness), and pathological reflexes (frontal lobe reflexes, pyramidal signs). Brain MRI may find reversible signal changes (low signal intensity on T1-weighted and high signal on T2-weighted images) in the basal ganglia and cerebral cortex, and the EEG is usually abnormal in the acute encephalopathic state. Prompt renal replacement therapy is critical to reverse encephalopathy symptoms caused by uremia [82].

Cognitive impairment and dementia are commonly seen in patients with chronic renal failure, particularly, in the advanced stages of the disease. Patients with chronic renal disease are at an increased risk for delirium due to several predisposing factors: susceptibility to derangements of water, electrolyte, and acid- base balance; changes in the metabolism of drugs with higher risk for adverse drug reaction; hospitalizations; co-occurrence of cerebrovascular disease and neuropathy; and polypharmacy. The prevalence of comorbid depression symptoms is also significant and should be sought and treated [83]. Moreover, many of the disorders that lead to the development of renal failure might be accompanied by neuropsychiatric manifestations that are independent of patient’s renal function, providing a potentially target treatment. In addition to these potentially reversible conditions, chronic renal failure itself represents an independent risk factor for progressive cognitive impairment and dementia, which are not fully explained by established vascular risk factors or cerebrovascular disease, highly prevalent in this population. Importantly, the risk for mental changes seems to be severity dependent, increasing over time with renal dysfunction progression, but it is not limited to those with end-stage renal failure or on dialysis treatment. Beside the severity of cerebrovascular disease, other mediators have been proposed for cognitive impairment in chronic renal failure (anemia, inflammation, oxidative stress, alterations in lipid, hyperhomocysteinemia, neurotoxicity of parathyroid hormone, and increased brain calcium content), but the exact pathogenesis remains unclear [84].

Cognitive impairment can also be associated with dialysis. An acute disturbance of cognition may be manifest when patients with severe uremia are rapidly dialyzed over a short period of time, representing a specific clinical entity called dialysis disequilibrium syndrome. Patients develop, during or soon after a dialysis session, headache, disorientation, confusion, fatigue, restless, other nonspecific symptoms such as nausea, cramps, tremor, blurred vision, and, in more severe and rare forms, seizures and coma. This syndrome is attributed to rapid shifts of fluid and solutes from the vascular compartment during dialysis, which induced cerebral edema. In nowadays, with modern dialysis regimens that encompass less intense dialysis sessions, this syndrome is now a relatively uncommon complication. In addition to acute cognitive impairment, dialysis has also been linked to progressive neuropsychiatric changes, so-called dialysis dementia syndrome. This rare disorder is characterized, initially, by a stuttering, hesitant speech immediately after dialysis, and some memory and personality change with apathy and depression. A subacute cognitive dysfunction ensues with dysarthria, aphasia, dysgraphia, apraxia, impaired memory, ataxia, myoclonus, seizures, and psychosis, evolving to frank dementia, akinetic mutism, and death, in 6-12 months in most untreated cases. Abnormalities in EEG may precede clinically overt symptoms. Epidemiological studies have recognized the aluminum content of dialysate fluid as the most likely cause for this serious syndrome, and, so, serum aluminum levels may help in establishing the diagnosis. Infusion of desferrioxamine, an aluminum-chelating agent, is the mainstay of management of dialysis dementia. Currently, the use of aluminum-free dialysate, due to modern techniques of water purification, seems to prevent the onset of the disease in patients who have just started dialysis [82]. Besides these two neurological complications associated with dialysis, moderate to severe cognitive impairment is common and undiagnosed in hemodialysis patients and is thought to be the result of multiple combined pathophysiological explanations [85]. Interestingly, studies have described improvements in cognition following renal transplantation, highlighting the potential reversibility, particularly, in memory problems observed during dialysis [86].

 
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