Reversible Cognitive Decline Research Articles

P.007 Web-based monitoring for cognitive decline following deep brain stimulation

Background: There is a pressing need to monitor the cognitive outcomes of patients undergoing deep brain stimulation (DBS) for movement disorders, despite the prevalence of pre-operative cognitive evaluations. Previous research has demonstrated the potential for DBS to induce reversible cognitive decline, highlighting the need for post-operative cognitive monitoring. Methods: To address this issue, the present study sought to improve upon the existing Autonomous Cognitive Examination through the development of a 5-minute web-based exam. This examination leverages the capacity of machine-learning algorithms to evaluate complex multimodal inputs, including cognitive and movement disorders, and is made available through a web-based platform for physicians to administer to their patients. Results: The outcome of this study was the development of a cognitive evaluation platform, which enables physicians to administer and view results of a brief cognitive examination with sensitivity to multiple domains of cognition, including movement disorders. The web-application based screening examination is easily accessible and can be used on any device. Conclusions: This web-based cognitive examination offers a crucial solution for monitoring longitudinal cognition in high-risk patient populations undergoing DBS for movement disorders. Its ability to assess complex multimodal inputs has broad applications beyond movement disorders and serves as a valuable tool for detecting cognitive decline.

Review of the Protective Effects of Statins on Cognition.

Elevated cholesterol is a major risk factor in the development of cardiovascular disease. Statins have proven to be effective in lowering low-density lipoprotein cholesterol as well as the incidence of cardiovascular events. As a result, statins are widely prescribed in the United States, with an estimated 35 million patients on statins. Many of these patients are older than age 65 and suffer from various comorbidities, including mild to severe cognitive impairment. Early studies looking at the effects of statins on cognition have shown that statin use may lead to mild reversible cognitive decline, although long-term studies have shown inconclusive findings. In recent years, studies have shown that the use of statins in certain groups of patients may lead to a reduction in the rate of cognitive decline. One hypothesis for this finding is that statin use can reduce the risk of cerebrovascular disease which may, in turn, reduce the risk of mild cognitive decline and dementia. With numerous patients currently prescribed statins and the likelihood that more patients will be prescribed the medication in the coming years, it is important to review the current literature to determine the association between statin use and cognitive decline, as well as determine how statins may be beneficial in preventing cognitive decline.

Valproate-induced reversible atrophy and cognitive decline: a case

Background: Valproate (VPA) has been previously described to cause reversible cerebral atrophy and cognitive decline, but few cases are reported and neuropsychological data is lacking. We report a case of VPA induced encephalopathy in an 11-year-old girl with temporal lobe epilepsy, presenting with impaired cognition and sedation combined with cerebral atrophy.
 Methods: Cognitive capacity was assessed using Wechsler Intelligence Scales for Children IV (WISC), non-standardised word lists and visual reproduction. Brain magnetic resonance imaging (MRI) was performed prior to, during and post VPA therapy.
 Results: Our patient demonstrated average full-scale intelligence quotient, verbal comprehension, perceptual reasoning and working memory. There was a marked discrepancy in processing speed, which ranked low average (score – 80; 9th percentile). Difficulties with mental abstraction and manipulation were noted. Brain MRI (3T) demonstrated mild generalised parenchymal atrophy. Cessation of VPA resulted in dramatic improvement in clinical symptoms (1 month after cessation) and normalisation of brain MRI (11 months after cessation). Progress neuropsychological testing 13 months after cessation showed marked improvements in processing speed. 
 Conclusion: This case provides an important reminder of this rare but importantly reversible syndrome with new information supporting the neuropsychological changes involved.

Cumulative Exposure to Frequent Intradialytic Hypotension Associates With New-Onset Dementia Among Elderly Hemodialysis Patients

Cumulative Exposure to Frequent Intradialytic Hypotension Associates With New-Onset Dementia Among Elderly Hemodialysis Patients

Valproate-associated reversible atrophy and cognitive decline: A case

Valproate-associated reversible atrophy and cognitive decline: A case

Acute dysphasia and reversible cognitive decline in a patient with probable cerebral amyloid angiopathy-related inflammation.

Cerebral amyloid angiopathy related inflammation (CAAri) is becoming increasingly recognised as a subset of cerebral amyloid angiopathy (CAA). CAAri generally presents with subacute cognitive decline, headaches, seizures, behavioral changes, and focal neurological deficits. We describe a patient who developed acute dysphasia and reversible cognitive decline due to probable CAAri. CT brain showed bilateral vasogenic edema in the cerebral hemispheres, predominantly involving the parietal and temporal lobes, left greater than right without enhancement. Magnetic resonance brain imaging showed extensive multifocal areas of subcortical white matter T2 hyperintensity in the frontal and temporal regions with associated mass effect, negligible enhancement, and multiple foci of microhemorrhage on susceptibility weighted imaging sequences consistent with a diagnosis of probable CAAri. She responded dramatically to a course of intravenous methylprednisolone followed by further immunosuppression with pulse intravenous cyclophosphamide. Her dysphasia resolved within 5 days of intravenous methylprednisolone therapy. Her MMSE improved from 11/30 at day 5 of admission to 28/30 at 6-month follow-up. The notable features of our case were the unusual CT findings, which were inconsistent with stroke and diagnostic utility of susceptibility-weighted magnetic resonance imaging in confirming the diagnosis which allowed for prompt institution of immunosuppression.

Reversible parkinsonism and cognitive decline due to a possible interaction of valproic acid and quetiapine

Combination therapy with valproic acid plus quetiapine is recommended as one of the first-line approaches to treatment of manic or mixed episodes in patients with bipolar disorder. A 66-year-old patient with this psychiatric disease developed parkinsonism and cognitive decline during concomitant treatment with both drugs. The rapid onset of symptoms soon after use of the combination suggested an interaction/using the Karch-Lasagna criteria, the interaction was judged to be definite. Their evidence on a pharmacokinetic drug interaction between the two drugs is conflicting but possible underlying mechanisms proposed include CYP3A4 inhibition. As concomitant use of valproate and quetiapine is now quite frequent in bipolar disorder, this potential interaction should be closely monitored, especially in the elderly.

Cognitieve stoornissen en parkinsonisme bij gebruik van valproïnezuur

Two patients presented with progressive cognitive impairment and parkinsonism related symptoms while being treated with sodium valproate. Both patients suffered from progressive cognitive decline and mobility disorders with an insidious onset over a period of months to years. After discontinuation of sodium valproate both debilitating symptoms resolved nearly completely. There is a growing prevalence and incidence of epilepsy above the age of 60 and a great number of these patients are on sodium valproate treatment. All clinicians treating elderly patients should be aware of the fact that this treatment can cause reversible cognitive decline and parkinsonism probably due to impairment of mitochondrial complex I function. Discontinuation of sodium valproate is strongly recommended in all patients with development of cognitive impairment or parkinsonism or both during sodium valproate treatment.

Reversible progressive cognitive decline due to herpes simplex type 2 encephalitis with normal MR imaging

Reversible progressive cognitive decline due to herpes simplex type 2 encephalitis with normal MR imaging

Reversible cognitive decline after DBS STN in PD and displacement of electrodes

Cognitive decline may follow deep brain stimulation (DBS) of the subthalamic nucleus (STN).1,2 Changes in cognition between stimulation on and off have also been described.3 We describe a patient with severe decline after STN DBS and postoperative electrode displacement. The patient is a 43-year-old woman diagnosed with Parkinson disease (PD) 8 years prior to DBS STN for severe response fluctuations and dyskinesias. Neuropsychological evaluation was normal (table). She used levodopa/carbidopa slow release 400/100 mg daily. View this table: Table Stimulation characteristics, motor scores, and neuropsychological test results at the evaluation times Surgery was performed using MRI, four-tract microrecordings, and macrostimulation for target localization (12 mm lateral, 2 mm posterior, and 4 mm inferior to the midcommissural point [MCP]). The left electrode (model 3389; Medtronic) was implanted in the central trajectory, with the deepest contact 7 mm below MCP. There was considerable CSF leakage from the burr holes. On the right side, no typical STN activity could be recorded. Because test stimulation along the medial trajectory induced a large reduction in rigidity and bradykinesia, the …

The Frequency of Reversible Parkinsonism and Cognitive Decline Associated with Valproate Treatment: A Study of 364 Patients with Different Types of Epilepsy

We report the frequency of parkinsonism and cognitive decline (P/CD) in patients treated with valproate (VPA) after 1 year of treatment and at least 1 year of follow-up. Three hundred sixty-four patients with various epileptic syndromes and seizure types were treated with VPA mono- or polytherapy for more than 1 year. We found five cases of P/CD (1.37%; 95% CI, 0.18-2.56%). Among 140 patients with different adverse effects (AEs) of VPA, P/CD were among the rarest in frequency but significant in terms of drug discontinuation (five of 17). Early identification of this type of AE and discontinuation of the drug led to complete recovery in affected patients.

Reversible cortical atrophy and cognitive decline induced by valproic acid

An 18-year-old male suffered from familial progressive myoclonic epilepsy from the age of 7 years. In addition to seizures, there was a marked decline in school performance. At the age of 14 years, sodium valproate was started as add-on therapy; 2 weeks later he was hospitalized in a stuporous state. The serum level of valproate was within the therapeutic range. Cognitive evaluation disclosed moderate mental retardation. No metabolic abnormalities were detected. Valproate was discontinued and during the 4 following months, a slow but significant improvement was documented in cognitive functions. Repeated assessment was within the range of mild mental retardation. Initially, magnetic resonance imaging (MRI) showed mild cortical atrophy. A subsequent MRI study performed 2 years later was normal.

Reversible cognitive decline during high-dose α-interferon treatment

The cognitive effects of high-dose human leukocyte α-interferon (IFN-α) treatment were evaluated among 15 patients with the newly diagnosed spinal form of amyotrophic lateral sclerosis (ALS). To confirm the earlier findings showing reversible effects on cognitive performance and to exclude confounding effects, a randomized blinded placebo controlled study was conducted. Twelve patients with continuous intravenous IFN-α-infusion treatment over five days and 3 placebo control patients were neuropsychologically evaluated. The neuropschological examination included tests of intelligence, memory, complex mental processing, visuoconstructional skills, writing, and calculation. A clear difference in the performance profiles of the placebo and the IFN-α-treated patient groups was detected: The IFN-α group showed significant deterioration during treatment in the digit span backwards task, logical verbal memory task, calculation ability, and writing time, while improvement was seen after treatment. Concomitant fever did not explain the findings. In the placebo group an improvement indicating a learning effect in the three consecutive measurements was found. The reversible cognitive deterioration indicates a clear CNS effect during the IFN-α treatment.