Radiosurgical Pallidotomy for Parkinson's Disease.

Deep brain stimulation (DBS) has been widely accepted as a tool for treating many symptoms of Parkinson's disease (PD); pallidotomy has been nearly abandoned. Concerns about both the safety and efficacy of pallidotomy are based on small series, isolated case reports, and techniques that would now be considered obsolete. The senior author recently reviewed long-term follow-up of a series of patients who had gamma knife pallidotomy (GKP) for advanced PD. GKP leads to durable, clinically significant benefit. Bilateral GKP adds incremental improvement. The complication rate was 4% when calculated on a per lesion basis. GKP is not quite as effective as DBS for tremor and bradykinesia; the results of GKP and DBS are equivalent for dyskinesia. GKP should be considered in patients who are not candidates for DBS. GKP is not as invasive as radiofrequency pallidotomy and avoids the problems and expenses associated with DBS. Patients on anticoagulants, with cognitive deficits or with other contraindications to DBS can be offered GKP to alleviate many of the motor symptoms of PD.

Hippocampal neuron damage in human epilepsy: Meyer's hypothesis revisited.

Whether hippocampal neuron loss and/or hippocampal sclerosis is the 'cause' or 'consequence' of seizures has been a fundamental question in human epilepsy studies for over a century. To address this question, this study examined hippocampal specimens from temporal lobe epilepsy patients (TLE; n = 572) and those with extra-temporal seizures and pathologies (n = 73) for qualitative signs of hippocampal sclerosis and quantitative neuron loss using cell counting techniques. Patients were additionally classified based on pathological substrate, and history of an initial precipitating injury (IPI). Results showed that: (1) Hippocampal sclerosis was strongly linked with an IPI in both TLE and extra-temporal seizure patients. (2) In TLE cases, IPIs showed an early age preference and often involved seizures, but IPIs were not age dependent and older IPI cases showed sclerosis that was indistinguishable from younger IPI patients. (3) In TLE patients, longer seizure durations were associated with decreased neuronal densities in all hippocampal subfields. The decrease was independent of the neuron loss linked with IPIs, it occurred in all pathological groups, it occurred over 30 years or more, and was not a consequence of aging. (4) Intractable seizures in the young human hippocampus were not associated with neuronal damage, but were linked with decreased postnatal granule cell development and aberrant axon sprouting. These results support the concept that hippocampal sclerosis is likely an acquired pathology, and most of the neuronal loss occurs with the IPI. In addition, there is progressive hippocampal damage from intractable TLE regardless of pathology. Hence, hippocampal neuron loss can be the 'consequence' of repeated limbic seizures over 30 years or more, but is unlikely to 'cause' hippocampal sclerosis unless there is also an IPI.