Treatment should not be initiated too soon in Parkinson's disease.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to Michael J Aminoff.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
OBJECTIVE: Acute anemia slows the responses to clinical tests of cognitive function. We tested the hypothesis that these slowed responses during acute severe isovolemic anemia in healthy unmedicated humans result from impaired central processing. METHODS: A blinded operator measured the latency of the P300 peak in nine healthy volunteers at each volunteer's baseline hemoglobin concentration (Hb), and again after isovolemic hemodilution to Hb 5 g/dL. At both Hb concentrations, the P300 latency was measured twice: with the blinded subject breathing air or 100% oxygen, administered in random order. RESULTS: Anemia increased P300 latency significantly from baseline values (P < 0.05). Breathing oxygen during induced anemia resulted in a P300 latency not different from that at baseline when breathing air (P = 0.5) or oxygen (P = 0.8). CONCLUSIONS: Impaired central processing is, at least in part, responsible for the slowed responses and deficits of cognitive function that occur during acute isovolemic anemia at Hb 5-6 g/dL. SIGNIFICANCE: The P300 latency appears to be a potential measure of inadequate central oxygenation. In healthy young adults with acute anemia, erythrocytes should be transfused to produce Hb>5-6 g/dL. As a temporizing measure, administration of oxygen can reverse the cognitive deficits and impaired central processing associated with acute anemia.
BACKGROUND AND PURPOSE: Many patients with Parkinson's disease (PD) experience sleep-related symptoms. Studies in other populations indicate that melatonin can increase sleep efficiency, decrease nighttime activity, and shorten sleep latency, but there has been little research on the use of melatonin in PD. The purpose of this study was to compare the effects of two doses of melatonin to placebo on sleep, daytime sleepiness, and level of function in patients with PD who complained of sleep disturbances. PATIENTS AND METHODS: A multi-site double-blind placebo-controlled cross-over trial was employed; 40 subjects completed the 10-week protocol. There was a 2-week screening period, 2-week treatment periods, and 1-week washouts between treatments. Nocturnal sleep was assessed by actigraphy and diaries, whereas daytime sleepiness and function were assessed by the Epworth Sleepiness Scale (ESS), Stanford Sleepiness Scale (SSS), and General Sleep Disturbance Scale (GSDS). RESULTS: Repeated measures analysis of variance revealed a significant improvement in total nighttime sleep time during the 50 mg melatonin treatment compared to placebo. There was significant improvement in subjective sleep disturbance, sleep quantity, and daytime sleepiness during the 5 mg melatonin treatment compared to placebo as assessed by the GSDS. CONCLUSIONS: Although we found a statistically significant improvement in actigraphically measured total sleep time on 50 mg melatonin compared to 5 mg or placebo, this small improvement (10 min) may not be clinically significant. However, the significant improvement found in subjective sleep disturbance suggests that these modest effects may be clinically relevant in this patient population.
Parkinson disease is the most common cause of parkinsonism, but other causes should always be excluded because they have a different prognosis, respond differently to medical treatment, and should not be managed by surgical means. However, diagnosis, even by experts, is challenging; one autopsy series showed an error rate of 24%. Distinction between various diagnostic possibilities depends on the history and examination findings. The use of certain medications, the rapid rate of disease progression, early onset of falling, the presence of certain dysautonomic symptoms, cognitive or behavioral changes, or a history of poor response to dopaminergic therapy may suggest an atypical form of parkinsonism. Postural hypotension, dementia, supranuclear ophthalmoparesis, or early postural instability should alert the examiner to consider an atypical cause of parkinsonism. Tests of autonomic function and brain imaging are often helpful in distinguishing these diseases.
OBJECTIVE: We prospectively investigated the role of magnetoencephalography (MEG) in localizing the seizure focus and in predicting outcome to surgical resections for intractable temporal lobe epilepsy (TLE). METHODS: We performed simultaneous interictal EEG and MEG recording (two 37-channel system) in 26 TLE patients followed by MEG source localization. We correlated early modeling dipoles with intracranial EEG, temporal surgical resection and surgical outcome. RESULTS: There were 12 patients who had anterior temporal horizontal or tangential dipoles to the anterior infero-lateral temporal tip cortex. Two patients underwent selective amygdalo-hippocampectomy (SAH) and nine patients had antero-medial temporal lobectomy (AMTL). All patients had successful outcome except for one patient who initially failed SAH, but became seizure-free after AMTL. There were 11 patients who demonstrated anterior temporal vertical or tangential oblique dipoles. Five patients had AMTL and three had SAH; all became seizure free. Five of above 23 patients had invasive EEG and demonstrated mesial seizure onset. Three TLE patients had lateral vertical dipoles that were concordant with intracranial EEG and these became seizure free after temporal neocortical resections. CONCLUSIONS: MEG source analysis produces distinct source patterns that provide useful localizing information, predict surgical outcome, and may aid in planning limited surgical resection in TLE.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
BACKGROUND: The relationship between the event-related cerebral potential (ERP) and perceptual awareness by the subject is poorly understood. The authors manipulated the process of stimulus recognition to examine the effect of changes in a subject's awareness on different components of the ERP and on behavioral (motor) responses. METHODS: Ten subjects listened to a series of 400 tone pips, one of which (frequent tone) was slightly louder than the other (rare tone; 14% of trials). Stimuli were presented in blocks of 10 tones and, following each block, subjects were asked how many rare tones they had detected and if they were aware of any errors that they had made during that block. Cerebral and motor responses were recorded by surface electrodes. RESULTS: When subjects were aware of having responded erroneously to either the rare or frequent tone, their response times were shorter than for correct responses to that tone. When subjects were unaware of such errors, however, the response times were delayed compared to correct responses and to error responses of which the subject was aware. When the subject made an error by responding to the rare tone as if it were frequent and was aware of the error, the N2 and P3 latencies were delayed. By contrast, when subjects were unaware of such errors, no N2 or P3 components were present. Similar findings were noted when subjects responded to a frequent tone as if it were rare. CONCLUSIONS: These results suggest that the N2 and P3 components of the ERP reflect the awareness of the subject that an unexpected event has occurred, regardless of whether it is an unexpected stimulus or an unexpectedly erroneous response to that stimulus. The recording of ERP may provide a means of measuring perceptual awareness in other contexts.
PURPOSE: We evaluated visual patterns and source localization of ictal magnetoencephalography (MEG) in patients with intractable temporal lobe epilepsy (TLE) and extratemporal epilepsy (ETE). METHODS: We performed spike and seizure recording simultaneously with EEG and MEG on two patients with TLE and five patients with ETE. Scalp EEG was recorded from 21 channels (10-20 international system), whereas MEG was recorded from two 37-channel sensors. We compared ictal EEG and MEG onset, frequency, and evolution and performed MEG dipole source localization of interictal spikes and early ictal discharges and co-registered dipoles to brain magnetic resonance imaging (MRI). We correlated dipole characteristics with intracranial EEG, surgical resection, and outcome. RESULTS: Ictal MEG lateralized seizure onset in both TLE patients and demonstrated ictal onset, frequency, and evolution in accordance with EEG. Ictal MEG source analysis revealed tangential vertical dipoles in the anterolateral angle in one patient, and anterior dipoles with anteroposterior orientation in the other. Intracranial EEG revealed regional entorhinal seizure onset in the first patient. Both patients became seizure free after temporal lobectomy. In ETE, ictal MEG demonstrated visual patterns similar to ictal EEG and had concordant localization with interictal MEG in all five patients. Two patients underwent surgery. Ictal MEG localization was concordant with intracranial EEG in both cases. One patient had successful outcome after surgery. The second patient did not improve after limited resection and multiple subpial transections. CONCLUSIONS: Ictal MEG can demonstrate ictal onset frequency and evolution and provide useful localizing information before epilepsy surgery.
BACKGROUND: Previous studies have found subtle slowing of responses in tests of addition and digit-symbol substitution during acute severe isovolemic anemia to a hemoglobin concentration of 5 g/dl in healthy unmedicated humans. In this study, the authors tested the hypothesis that such changes relate to the slowing of afferent neural traffic. METHODS: The median nerve was stimulated at the wrist in seven healthy unmedicated volunteers before and after induction of acute isovolemic anemia to a nadir hemoglobin concentration of 5.1 +/- 0.3 g/dl (mean +/- SD). Times for neural impulses to travel from the stimulus site to the brachial plexus, cervical spinal cord, and cerebral cortex were measured using somatosensory evoked potentials. Tests were repeated during acute anemia with the subject breathing oxygen. As a control for time and intrasubject variation, the testing was repeated on a separate day when anemia was not produced at times equivalent to those on the experimental day. RESULTS: Induced acute severe isovolemic anemia decreased nerve conduction latencies from the wrist to the contralateral cerebral cortex (i.e., to the N20 peak) by 2.3 +/- 1.6% compared with values at a mean hemoglobin concentration of 12.7 g/dl (P < 0.01). These decreased latencies were due solely to an increased peripheral conduction velocity, from the wrist to the brachial plexus (P < 0.05), and were not altered when subjects breathed oxygen (P > 0.05). Conduction velocity from the brachial plexus or cervical spinal cord to the cerebral cortex did not change with acute anemia (P > 0.05). Latencies did not differ on the control day among the times of testing (all P > 0.05), nor did they differ at baseline between the control and experimental days (all P > 0.05). CONCLUSION: Somatosensory evoked potential latencies were not increased by acute severe isovolemic anemia, making it unlikely that the afferent portion of the neural system is responsible for slowing of cognitive responses previously observed during acute anemia. Because severe isovolemic anemia did not increase somatosensory evoked potential latencies, etiologies other than anemia should be sought if latencies are increased during intraoperative monitoring.
Magnetic resonance imaging (MRI) and (1)H magnetic resonance spectroscopy (MRS) of the substantia nigra, basal ganglia, and cerebral cortex were performed on 10 patients with Parkinson's disease (PD) and 13 age-matched, healthy control subjects. Compared to controls, PD patients had approximately 24% lower creatine in the region of the substantia nigra and smaller volumes of the putamen (11%), globus pallidus (16%), and prefrontal cortex (6%; all P < 0.05). No other significant between-group differences were found in nine regions examined. Thus, quantitative MRI may show regional neurodegenerative changes outside the substantia nigra in PD but PD-linked extranigral metabolic abnormalities, if they exist, may be difficult to detect with current (1)H MRS methods. In additional, exploratory tests, volumes of the caudate (r = -0.56), putamen (r = -0.66), and globus pallidus (r = -0.60; all P < 0.05) were negatively correlated with the volume of the substantia nigra pars compacta in controls. In PD these correlations did not hold. Instead, pallidal volume in PD was positively correlated with compacta volume (r = 0.64; P < 0.05). This relationship suggests that basal ganglia volumes may be influenced by dopaminergic innervation from the substantia nigra in normal and PD subjects.
Explore the source record for details and available documents.
The electrophysiological evaluation of root or spinal cord disease is complementary to neuroimaging studies, providing information about functional rather than anatomical integrity and information that is important for diagnostic and prognostic purposes. The electrophysiological findings help to localize a lesion but are not pathognomonic of specific diseases. The findings may also provide insight into underlying physiological mechanisms that have been disrupted. A number of different electrophysiological techniques are now in widespread use. Each of these techniques provides different information and thus has distinct utility and limitations. The optimal evaluation of patients with root or spinal cord disease requires an understanding of how these techniques complement each other and depends on the individual clinical problem for which electrophysiological assessment is requested.