Parkinson's disease (PD) is associated with abnormal beta oscillations (13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30) in the basal ganglia and motor cortex (M1). Recent reports show that M1 beta-high gamma Hz) phase-amplitude coupling (PAC) is exaggerated in PD and is reduced following acute deep brain stimulation (DBS). Here we analyze invasive M1 electrocorticography recordings in PD patients on and off DBS, and in isolated cervical dystonia patients, and show that M1 beta oscillations are nonsinusoidal, having sharp and asymmetric features. These sharp oscillatory beta features underlie the previously reported PAC, providing an alternative to the standard interpretation of PAC as an interaction between two distinct frequency components. Specifically, the ratio between peak and trough sharpness is nearly perfectly correlated with beta-high gamma PAC (r = 0.96) and predicts PD-related motor deficit. Using a simulation of the local field potential, we demonstrate that sharp oscillatory waves can arise from synchronous synaptic activity. We propose that exaggerated beta-high gamma PAC may actually reflect such synchronous synaptic activity, manifesting as sharp beta oscillations that are "smoothed out" with DBS. These results support the "desynchronization" hypothesis of DBS wherein DBS counteracts pathological synchronization throughout the basal ganglia-thalamocortical loop. We argue that PAC can be influenced by more than one mechanism. In this case synaptic synchrony, rather than the often assumed spike-field coherence, may underlie exaggerated PAC. These often overlooked temporal features of the oscillatory waveform carry critical physiological information about neural processes and dynamics that may lead to better understanding of underlying neuropathology. IntroductionParkinson's disease (PD) is characterized by neuronal degeneration in multiple systems, including midbrain dopaminergic neurons. Though beta (13-30 Hz) oscillations are a normal feature of the basal ganglia-thalamocortical loop, PD is associated with excessive neuronal synchronization in the beta band (1, 2). Despite an established relationship between beta band neuronal synchronization and PD, the physiological mechanism causing motor dysfunction has been unclear. Excessive phase-amplitude coupling (PAC) between beta phase and high gamma amplitude (50-200 Hz) may offer an explanation (3)(4)(5). PAC between distant neural populations has been linked to enhanced neural information flow (6-8), long-term potentiation (9), and improved behavioral performance (10). However PAC strength is greater in M1 of PD patients compared to patients with isolated cervical dystonia or epilepsy (3), leading to the hypothesis that beyond its facilitative role, PAC may play a role in neural pathology (3,4,11).Analyses of PAC implicitly presuppose two separate, interacting physiological processes: a low-frequency component associated with an oscillation in the synaptic currents and a separate high-frequency component associated with local...
Pituitary apoplexy in a pre-existing pituitary tumor can result in serious and permanent neurologic deficits following cardiac surgical procedures. Several factors related to the altered physiology of cardiopulmonary bypass (CPB) contribute separately or in combination to the development of this syndrome. Over the last year we have encountered two such cases in whom emergency and prompt decompression of the adenoma resulted in an improvement of the initial clinical presentation but nevertheless persistence of residual and devastating ocular manifestations. In the literature six similar cases have been reported following cardiac surgical procedures, with similar outcomes. In this report we describe our experience and management of these two patients, and that published in the literature. We propose a possible role for a staged cardiac and neurosurgical procedure as a prophylactic measure in patients with known pituitary tumor. The role of cerebral monitoring is also discussed.
Commentary on Leone M et al., Lessons from 8 years' experience of hypothalamic stimulation in cluster headache n this issue, Leone et al. review the world experience with deep-brain stimulation (DBS) of the ipsilateral posterior hypothalamic region for medically intractable cluster headache (CH). The article is from the centre that pioneered this procedure and that has the greatest experience to date (16 patients). Results and physiological findings from 50 patients are described. Data from some of these patients were transmitted to the authors as personal communications. The procedure is fascinating in many respects. It is one of a number of new DBS applications that have been proposed based on findings from functional brain imaging. The target was selected as the region that has altered metabolic activity during a CH attack, as measured using H2 15 O-positron emission tomography. The time course for wash-in and wash-out of benefit has been formally studied in only one patient published thus far (1), but based on this and anecdotal observations, the time course for wash-in and wash-out of several weeks suggests long-term changes in synaptic efficacy may be taking place. The mechanism underlying its effectiveness, in those patients where it is effective, is not totally clear. The authors point out that in experimental animals, facial sensation may be conveyed to the hypothalamus by neurons of the trigeminohypothalamic tract, and that nociceptive inputs to the trigeminal nucleus caudalis can be modulated by differential regulation of orexin A and B receptors in the posterior hypothalamus. The authors mention several times that the procedure is now 'established' in the treatment of CH, but not all would agree with this. As shown in table 1, different centres performing this procedure have consistently shown that up to 50% of patients are non-responders. Formal blinded controlled studies have not been done. Our own experience now includes eight CH patients with at least 1 year's follow-up. Five of our eight patients are considered 'responders' based on a 50% reduction in either headache frequency or intensity, comparing headache diaries at last time point, compared with the preoperative baseline. Of the three non-responders, two in fact no longer use the device. For this invasive therapy to become accepted, a better predictor of outcome must be found, to avoid operating on patients who will receive no or minimal benefit. Predictors of outcome could potentially be found in detailed analysis of headache characteristics, responses to medication, or functional imaging features.
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