Summary:Background: Nonconvulsive status epilepticus (NCSE) is a usually underdiagnosed and potentially treatable cause of altered awareness in the elderly. To assess etiologies, associations with other medical problems, and prognosis of NCSE in a population aged >75 years we performed a nested casecontrol study.Methods: We retrospectively evaluated the clinical manifestations and EEG findings in 19 consecutive elderly patients (mean age 83.3 years) presenting with NCSE and compared them with 34 elderly patients (mean age 83.3 years) with altered mental status but without EEG evidence of NCSE. The variables compared included brain lesions on CT or MRI, number of concomitant chronic active diseases, previous neurological disorders, acute medical problems, the use and withdrawal of medications, and outcome. Statistical analysis was performed using chi-square test, t-test, Fisher's exact two-tailed test, and Wilcoxon rank sum test.Results: The etiology of NCSE was epilepsy in 2, acute medical disorders in 14, and a cryptogenic cause in 4. The NCSE group had a more frequent history of epilepsy, 35% versus 8.8% (p = 0.028); tramadol use, 31% versus 0% (p = 0.00151); longer hospitalization, 25 days versus 7 days (p = 0.0004); and unfavorable outcome, 50% versus 5.8% (p = 0.00031). No significant differences were found in the other variables. Unfavorable outcome was associated with a higher number of comorbidities (>2) and to a severely altered mental status.Conclusions: NCSE is a serious cause of altered mental status in the elderly. Although its direct role in brain damage is controversial, elderly patients with NCSE have higher morbidity and worst prognosis than those with altered mental status without NCSE.

Objective: To describe the clinical features, etiology, findings from neuroimaging, and treatment results in a series of 29 patients with Holmes tremor (HT).Methods: A retrospective study was performed based on review of medical records and videos of patients with HT diagnosis.Results: A total of 16 women and 13 men were included. The mean age at the moment of CNS insult was 33.9 6 20.1 years (range 8-76 years). The most common causes were vascular (48.3%), ischemic, or hemorrhagic. Traumatic brain injury only represented 17.24%; other causes represented 34.5%. The median latency from lesion to tremor onset was 2 months (range 7 days-228 months). The most common symptoms/signs associated with HT were hemiparesis (62%), ataxia (51.7%), hypoesthesia (27.58%), dystonia (24.1%), cranial nerve involvement (24.1%), and dysarthria (24.1%). Other symptoms/signs were vertical gaze disorders (6.8%), bradykinesia/rigidity (6.8%), myoclonus (3.4%), and seizures (3.4%). Most of the patients had lesions involving more than one area. MRI showed lesions in thalamus or midbrain or cerebellum in 82.7% of the patients. Levodopa treatment was effective in 13 out of 24 treated patients (54.16%) and in 3 patients unilateral thalamotomy provided excellent results. Conclusions:The most common causes of HT in our series were vascular lesions. The most common lesion topography was mesencephalic, thalamic, or both. Treatment with levodopa and thalamic stereotactic lesional surgery seems to be effective.

Over the last few years, cases of movement disorders induced by flunarizine and cinnarizine have been increasingly reported. We describe a series of 101 patients, whose ages ranged from 37 to 84 years (mean 69.1), developing abnormal movements frequently associated with depression, secondary to treatment with either or both drugs. Symptoms closely resembled those induced by neuroleptic drugs and remitted on drug discontinuance in all but five cases after 5-22 months' follow-up. Whether or not such undesirable side effects are attributable to calcium antagonism and/or dopamine receptor blockade, long-term treatment with flunarizine or cinnarizine should be discouraged, particularly in the elderly.

We studied nitrogen radical nitric oxide (.NO) release and reactive oxygen species (ROS) production by isolated neutrophils after phorbol myristate acetate (PMA) stimulation in 12 newly diagnosed and nine treated Parkinson's disease (PD) patients and 10 age-matched healthy controls. Neutrophils of both groups of PD patients had an elevated PMA-activated release of .NO [61 and 57%, respectively, higher than that of controls (p < 0.05)]. In contrast, H2O2 release was only significantly increased by 56% in chronically treated patients. In agreement, the maximum rate of luminol-dependent chemiluminescence, which partly represents O2- H2O2- .NO interactions, was increased only in the treated group. When other blood markers of oxidative stress were compared, only erythrocyte catalase activity was decreased in both PD patient series by 33 and 39%, respectively (p < 0.05), whereas plasma antioxidant capacity and erythrocyte superoxide dismutase activity levels were decreased only in treated PD patients. This study suggests that neutrophils express a primary alteration of .NO release in PD patients, whereas H2O2 and oxidative-stress parameters are more probably related to the evolution of PD or to effects of treatment with L-dopa.