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1.  Cognitive outcomes of patients undergoing therapeutic hypothermia after cardiac arrest 
Neurology  2013;81(1):40-45.
Objective:
We aimed to study the long-term cognitive abilities of patients surviving out-of-hospital cardiac arrest who were treated with therapeutic hypothermia (TH).
Methods:
We prospectively identified and examined consecutive survivors of out-of-hospital cardiac arrest who underwent TH at our institution from June 2006 to May 2011. The results of brain imaging, serum neuron-specific enolase (NSE) measurements, and EEGs were recorded. We assessed cognitive domains using the modified Telephone Interview for Cognitive Status. An education-adjusted score of ≥32 was considered normal.
Results:
Of 133 total patients, 77 (58%) were alive at a median follow-up of 20 months (interquartile range 14–24 months). We interviewed 56 patients (73% of those alive). Median age was 67 years (range 24–88 years). Fifty-one patients (91%) were living independently. Modified Telephone Interview for Cognitive Status scores ranged from 16 to 41. Thirty-three (60%) were considered cognitively normal and 22 (40%) were cognitively impaired. The time to assessment did not differ among the cognitive outcomes (p = 0.557). The median duration of coma was 2 days, possibly indicating that patients with severe anoxic injury were not included. Eighteen patients were not working at the time of their cardiac arrest (17 were retired and 1 was unemployed). Of the 38 patients who were working up to the time of the cardiac arrest, 30 (79%) returned to work. Cognitive outcome was not associated with age, time to return of spontaneous circulation, brain atrophy, or leukoaraiosis.
Conclusions:
The majority of surviving patients who underwent TH after cardiac arrest in this series had preserved cognitive function and were able to return to work.
doi:10.1212/WNL.0b013e318297ee7e
PMCID: PMC3770208  PMID: 23685933
2.  Impaired inhibition of prepotent motor actions in patients with Tourette syndrome 
Background
Evidence that tic behaviour in individuals with Tourette syndrome reflects difficulties inhibiting prepotent motor actions is mixed. Response conflict tasks produce sensitive measures of response interference from prepotent motor impulses and the proficiency of inhibiting these impulses as an act of cognitive control. We tested the hypothesis that individuals with Tourette syndrome show a deficit in inhibiting prepotent motor actions.
Methods
Healthy controls and older adolescents/adults with persistent Tourette syndrome without a history of obsessive–compulsive disorder or attention-deficit/hyperactivity disorder and presenting with stable mood functioning (i.e., no history of well-treated anxiety or depression) participated in this study. They performed a Simon task that induced conflict between prepotent actions and goal-directed actions. A novel theoretical framework distinguished group differences in acting impulsively (i.e., fast motor errors) from the proficiency of inhibiting interference by prepotent actions (i.e., slope of interference reduction).
Results
We included 27 controls and 28 individuals with Tourette syndrome in our study. Both groups showed similar susceptibility to making fast, impulsive motor errors (Tourette syndrome 26% v. control 23%; p = 0.10). The slope (m) reduction of the interference effect was significantly less pronounced among participants with Tourette syndrome than controls (Tourette syndrome: m = −0.07 v. control: m = −0.23; p = 0.022), consistent with deficient inhibitory control over prepotent actions in Tourette syndrome.
Limitations
This study does not address directly the role of psychiatric comorbidities and medication effects on inhibitory control over impulsive actions in individuals with Tourette syndrome.
Conclusion
The results offer empirical evidence for deficient inhibitory control over prepotent motor actions in individuals with persistent Tourette syndrome with minimal to absent psychiatric comorbidities. These findings also suggest that the frontal–basal ganglia circuits involved in suppressing unwanted motor actions may underlie deficient inhibitory control abilities in individuals with Tourette syndrome.
doi:10.1503/jpn.120138
PMCID: PMC3756119  PMID: 23820185
3.  Differential susceptibility to motor impulsivity among functional subtypes of Parkinson’s disease 
Background and objectives
Parkinson’s disease patients with predominant postural instability and gait difficulties (PIGD) may experience unique cognitive difficulties compared to patients with tremor predominant (TD) symptoms. PIGD patients are also at high risk for falling, and some of the worst fallers seem to react impulsively to their environment. We tested the hypothesis that PIGD patients show poorer control over motor impulses compared to TD patients.
Methods
34 PD participants were divided into predominant PIGD (n=17) or TD (n=17) functional subtypes based on their presenting symptoms in their optimally treated motor state. All participants performed a speeded reaction task that quantified motor impulsivity and the proficiency of inhibiting prepotent motor impulses.
Results
The groups showed similar reaction times, but compared to TD patients, PIGD patients made significantly more impulsive motor errors. Notably, when the initial impulsive erroneous response was avoided, PIGD and TD groups were similar in their ability to suppress the incorrect motor impulse from further interfering with the selection of a correct action.
Conclusions
PD patients with PIGD predominant symptoms show greater susceptibility to acting on prepotent motor impulses compared to TD patients. This finding may have direct implications for fall risk and also points to dissociable neurocognitive pathologies in TD and PIGD subtypes. Clinically, the use of specific cognitive instruments to assess the expression and inhibition of motor impulses may help identify PD patients who have difficulty ‘thinking before they leap’ and are at high risk of falling.
doi:10.1136/jnnp-2012-303056
PMCID: PMC3704227  PMID: 22917670
4.  Trends and Issues in Characterizing Early Cognitive Changes in Parkinson's Disease 
In this review, we first discuss trends and issues in measuring cognitive changes in PD, including recent efforts to define the diagnostic classification of “PD Mild Cognitive Impairment” (PD-MCI). After reviewing some limitations associated with this diagnosis, we discuss how measures derived from the neurocognitive sciences offer better precision in detecting early cognitive changes in PD. To support this idea, we highlight 2 influential lines of current investigation that are unveiling novel insights about specific cognitive processes that are vulnerable early in PD and of critical importance to clinicians involved in treating PD: action control and reward learning and decision making. We conclude by highlighting some extant issues and unresolved questions for future investigations.
doi:10.1007/s11910-012-0312-5
PMCID: PMC3692293  PMID: 22949166
Parkinson disease; Mild cognitive impairment; Action control; Reward
5.  The Risky Business of Dopamine Agonists in Parkinson Disease and Impulse Control Disorders 
Behavioral neuroscience  2011;125(4):492-500.
Risk-taking behavior is characterized by pursuit of reward in spite of potential negative consequences. Dopamine neurotransmission along the mesocorticolimbic pathway is a potential modulator of risk behavior. In patients with Parkinson's Disease (PD), impulse control disorder (ICD) can result from dopaminergic medication use, particularly Dopamine Agonists (DAA). Behaviors associated with ICD include hypersexuality as well as compulsive gambling, shopping, and eating, and are potentially linked to alterations to risk processing. Using the Balloon Analogue Risk task, we assessed the role of agonist therapy on risk-taking behavior in PD patients with (n=22) and without (n=19) active ICD symptoms. Patients performed the task both ‘on’ and ‘off’ DAA. DAA increased risk-taking in PD patients with active ICD symptoms, but did not affect risk behavior of PD controls. DAA dose was also important in explaining risk behavior. Both groups similarly reduced their risk-taking in high compared to low risk conditions and following the occurrence of a negative consequence, suggesting that ICD patients do not necessarily differ in their ability to process and adjust to some aspects of negative consequences. Our findings suggest dopaminergic augmentation of risk-taking behavior as a potential contributing mechanism for the emergence of ICD in PD patients.
doi:10.1037/a0023795
PMCID: PMC3144294  PMID: 21604834
Impulse Control Disorders; Dopamine Agonists; Parkinson Disease; Risk behavior
6.  Sleep disturbances in Parkinson’s disease patients and management options 
Nature and Science of Sleep  2011;3:125-133.
Sleep disturbances are among the most common nonmotor complaints of patients with Parkinson’s disease (PD), and can have a great impact on quality of life. These disturbances manifest in a variety of ways; for instance, insomnia, sleep fragmentation, and excessive daytime sleepiness. Sleep-related movement disorders such as restless legs syndrome and periodic leg movements may share a common pathophysiology, and occurrence of rapid eye movement behavior disorder may predate the onset of PD or other synucleinopathies by several years. Medications for PD can have a significant impact on sleep, representing a great challenge to the treating physician. Awareness of the complex relationship between PD and sleep disorders, as well as the varied way in which sleep disturbances appear, is imperative for successful long-term management.
doi:10.2147/NSS.S18897
PMCID: PMC3630958  PMID: 23616723
sleep disorders; insomnia; restless legs syndrome; Parkinson disease; fatigue; REM behavior disorder
7.  Modeling Accuracy and Variability of Motor Timing in Treated and Untreated Parkinson’s Disease and Healthy Controls 
Parkinson’s disease (PD) is characterized by difficulty with the timing of movements. Data collected using the synchronization–continuation paradigm, an established motor timing paradigm, have produced varying results but with most studies finding impairment. Some of this inconsistency comes from variation in the medication state tested, in the inter-stimulus intervals (ISI) selected, and in changeable focus on either the synchronization (tapping in time with a tone) or continuation (maintaining the rhythm in the absence of the tone) phase. We sought to re-visit the paradigm by testing across four groups of participants: healthy controls, medication naïve de novo PD patients, and treated PD patients both “on” and “off” dopaminergic medication. Four finger tapping intervals (ISI) were used: 250, 500, 1000, and 2000 ms. Categorical predictors (group, ISI, and phase) were used to predict accuracy and variability using a linear mixed model. Accuracy was defined as the relative error of a tap, and variability as the deviation of the participant’s tap from group predicted relative error. Our primary finding is that the treated PD group (PD patients “on” and “off” dopaminergic therapy) showed a significantly different pattern of accuracy compared to the de novo group and the healthy controls at the 250-ms interval. At this interval, the treated PD patients performed “ahead” of the beat whilst the other groups performed “behind” the beat. We speculate that this “hastening” relates to the clinical phenomenon of motor festination. Across all groups, variability was smallest for both phases at the 500-ms interval, suggesting an innate preference for finger tapping within this range. Tapping variability for the two phases became increasingly divergent at the longer intervals, with worse performance in the continuation phase. The data suggest that patients with PD can be best discriminated from healthy controls on measures of motor timing accuracy, rather than variability.
doi:10.3389/fnint.2011.00081
PMCID: PMC3245650  PMID: 22207839
motor timing; Parkinson’s disease; temporal processing; synchronization; continuation; dopamine; linear mixed model
8.  Posterior Reversible Encephalopathy Syndrome: Associated Clinical and Radiologic Findings 
Mayo Clinic Proceedings  2010;85(5):427-432.
OBJECTIVE: To identify and define clinical associations and radiologic findings of posterior reversible encephalopathy syndrome (PRES).
PATIENTS AND METHODS: Patients prospectively diagnosed as having PRES from October 1, 2005, through April 30, 2009, were pooled with retrospectively identified patients admitted from August 1, 1999, through September 30, 2005. We performed a detailed review of clinical information, including demographics, presenting symptoms, medical history, and risk factors. All patients underwent computed tomography of the brain or magnetic resonance imaging. Findings on magnetic resonance imaging were analyzed independently by 2 neuroradiologists.
RESULTS: We identified 120 cases of PRES in 113 patients (mean age, 48 years). Mean peak systolic blood pressure was 199 mm Hg (minimum-maximum, 160-268 mm Hg), and mean peak diastolic blood pressure was 109 mm Hg (minimum-maximum, 60-144 mm Hg). Etiologies of PRES included hypertension (n=69 [61%]), cytotoxic medications (n=21 [19%]), sepsis (n=8 [7%]), preeclampsia or eclampsia (n=7 [6%]), and multiple organ dysfunction (n=1 [1%]). Autoimmune disease was present in 51 patients (45%). Clinical presentations included seizures (n=84 [74%]), encephalopathy (n=32 [28%]), headache (n=29 [26%]), and visual disturbances (n=23 [20%]). In the 115 cases (109 patients) for which magnetic resonance imaging findings were available, the parieto-occipital regions were the most commonly involved (n=108 [94%]), followed by the frontal lobe (n=88 [77%]), temporal lobe (n=74 [64%]), and cerebellum (n=61 [53%]). Cerebellar involvement was significantly more frequent in patients with a history of autoimmunity (P=.008), and patients with sepsis were more likely to have cortical involvement (P<.001).
CONCLUSION: A substantial proportion of patients with PRES have underlying autoimmune conditions that may support endothelial dysfunction as a pathophysiologic mechanism. On brain imaging, the location and severity of vasogenic edema were mostly similar for the different clinical subgroups.
This study involved 120 cases of posterior reversible encephalopathy syndrome in 113 patients; a substantial proportion of these patients have underlying autoimmune conditions that may support endothelial dysfunction as a pathophysiologic mechanism. On brain imaging, the location and severity of vasogenic edema were mostly similar for the different clinical subgroups.
doi:10.4065/mcp.2009.0590
PMCID: PMC2861971  PMID: 20435835

Results 1-8 (8)