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  • Author or Editor: William J. McBride x
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Naresh P. Patel, Neill M. Wright, William W. Choi, Duncan Q. McBride and J. Patrick Johnson

Object. Forestier Disease (FD) is a progressive skeletal disorder affecting predominantly older men. It is also known as diffuse idiopathic skeletal hyperostosis (DISH) and is characterized by massive anterior longitudinal ligament calcification that forms a bridge on the anterior border of the thoracic and subaxial cervical spine. To the authors' knowledge, retroodontoid masses associated with FD have not been described.

Methods. Five patients with FD and multilevel subaxial cervical fusion were treated for retroodontoid masses and cervicomedullary junction (CMJ) compression. There were four men and one woman (mean age 73 years, range 54–86 years). All patients suffered progressive neurological symptoms resulting from anterior compression of the CMJ.

Four patients underwent combined transoral resection of the ligamentous mass followed by an occipitocervical fusion procedure. One patient with circumferential CMJ compression underwent a posterior decompression and occipitocervical fusion. Histopathological examination of the mass showed hypertrophic degenerative fibrocartilage. Early postoperative neurological improvement was noted in all patients. The follow-up period ranged from 4 to 19 months. At the end of the follow-up period, four patients experienced neurological improvement. One patient died 3 weeks postsurgery of pulmonary complications.

Conclusions. The osseous elements of the occipitoatlantoaxial complex are not directly affected by FD. The ligamentous structures of the odontoid process, however, are exposed to significantly altered biomechanics resulting from fusion of the subaxial cervical spine associated with FD. Stress-induced compensatory ligamentous hypertrophic changes at the craniovertebral junction cause CMJ compression and subsequent neurological deterioration. This previously undescribed entity should be considered in patients with FD or DISH who present with progressive quadriparesis. Transoral decompression and posterior fusion are often needed in patients with large masses and severe progressive neurological deficits. Selected patients with smaller masses and milder neurological symptoms may be treated with posterior fusion alone.

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Jessica A. Wilden, Kurt Y. Qing, Sheketha R. Hauser, William J. McBride, Pedro P. Irazoqui and Zachary A. Rodd


There is increasing interest in deep brain stimulation (DBS) for the treatment of addiction. Initial testing must be conducted in animals, and the alcohol-preferring (P) rat meets the criteria for an animal model of alcoholism. This study is composed of 2 experiments designed to examine the effects of 1) pharmacological inactivation and 2) DBS of the nucleus accumbens shell (AcbSh) on the consumption of alcohol by P rats.


In the first experiment, the effects of reversible inactivation of the AcbSh were investigated by administering intracranial injections of γ–aminobutyric acid (GABA) agonists. Bilateral microinjections of drug were administered to the AcbSh in P rats (8–10 rats/group), after which the animals were placed in operant chambers containing 2 levers—one used to administer water and the other to administer 15% EtOH—to examine the acquisition and maintenance of oral EtOH self-administration. In the second experiment, a DBS electrode was placed in each P rat's left AcbSh. The animals then received 100 or 200 μA (3–4 rats/group) of DBS to examine the effect on daily consumption of oral EtOH in a free-access paradigm.


In the first experiment, pharmacological silencing of the AcbSh with GABA agonists did not decrease the acquisition of EtOH drinking behavior but did reduce EtOH consumption by 55% in chronically drinking rats. Similarly, in the second experiment, 200 μA of DBS consistently reduced EtOH intake by 47% in chronically drinking rats. The amount of EtOH consumption returned to baseline levels following termination of therapy in both experiments.


Pharmacological silencing and DBS of the AcbSh reduced EtOH intake after chronic EtOH use had been established in rodents. The AcbSh is a neuroanatomical substrate for the reinforcing effects of alcohol and may be a target for surgical intervention in cases of alcoholism.