Deletion of the Kv2.1 delayed rectifier potassium channel leads to neuronal and behavioral hyperexcitability.

The Kv2.1 delayed rectifier potassium channel exhibits high-level expression in both principal and inhibitory neurons throughout the central nervous system, including prominent expression in hippocampal neurons. Studies of in vitro preparations suggest that Kv2.1 is a key yet conditional regulator of intrinsic neuronal excitability, mediated by changes in Kv2.1 expression, localization and function via activity-dependent regulation of Kv2.1 phosphorylation. Here we identify neurological and behavioral deficits in mutant (Kv2.1(-/-) ) mice lacking this channel. Kv2.1(-/-) mice have grossly normal characteristics. No impairment in vision or motor coordination was apparent, although Kv2.1(-/-) mice exhibit reduced body weight. The anatomic structure and expression of related Kv channels in the brains of Kv2.1(-/-) mice appear unchanged. Delayed rectifier potassium current is diminished in hippocampal neurons cultured from Kv2.1(-/-) animals. Field recordings from hippocampal slices of Kv2.1(-/-) mice reveal hyperexcitability in response to the convulsant bicuculline, and epileptiform activity in response to stimulation. In Kv2.1(-/-) mice, long-term potentiation at the Schaffer collateral - CA1 synapse is decreased. Kv2.1(-/-) mice are strikingly hyperactive, and exhibit defects in spatial learning, failing to improve performance in a Morris Water Maze task. Kv2.1(-/-) mice are hypersensitive to the effects of the convulsants flurothyl and pilocarpine, consistent with a role for Kv2.1 as a conditional suppressor of neuronal activity. Although not prone to spontaneous seizures, Kv2.1(-/-) mice exhibit accelerated seizure progression. Together, these findings suggest homeostatic suppression of elevated neuronal activity by Kv2.1 plays a central role in regulating neuronal network function.

Radial nerve palsy caused by open humeral shaft fractures.

Although radial nerve palsy associated with a closed humeral shaft fracture may be managed by observation, it is our experience that an open humeral shaft fracture with radial nerve palsy requires exploration of the nerve. In a series of 14 patients with radial nerve palsy caused by an open humeral shaft fracture, 9 (64%) of the 14 patients had a radial nerve that was either lacerated or interposed between the fracture fragments. There was an equal incidence of radial nerve lacerations or entrapments in types I, II, and III open humeral shaft fractures. Epineural radial nerve repair, done primarily or secondarily, provided a satisfactory return of radial nerve function. Rigid fixation of the associated fracture is the recommended treatment.

Four-bone ligament reconstruction for treatment of chronic complete scapholunate separation.

This study reviews the results of a four-bone ligamentous weave reconstruction for treatment of chronic complete scapholunate separation. This reconstruction between the radius, lunate, capitate, and scaphoid employs a dorsal and palmar approach weaving a long strip of the extensor carpi radialis brevis through the four bones reducing and stabilizing the scaphoid and lunate with a wire loop. Thirty-six consecutive cases of operated chronic complete scapholunate separation were evaluated in a 2- to 10-year follow-up. Average length of follow-up was 4.8 years. Average age was 34 years. Average postoperative range of motion was 52 degrees extension and 37 degrees flexion. Grip strength averaged 73% of the noninvolved side. All preoperative scapholunate gaps seen on radiographs were greater than 4 mm, at surgery greater than 1.0 cm, and the postoperative gaps radiographically averaged 3.3 mm. Eighty-six percent of patients returned to preinjury activities including heavy labor. The most significant finding was no x-ray evidence of advancing arthritic changes.