Eight chronic alcoholics received repeated computed tomography scans. Four, who maintained abstinence and functionally improved, showed partially reversible cerebral atrophy. Two nonabstinent patients and two abstinent patients who had completed functional improvement before the first scan showed no change in atrophy.

We present a fully differential 128-channel integrated neural interface. It consists of an array of 8 X 16 low-power low-noise signal-recording and generation circuits for electrical neural activity monitoring and stimulation, respectively. The recording channel has two stages of signal amplification and conditioning with and a fully differential 8-b column-parallel successive approximation (SAR) analog-to-digital converter (ADC). The total measured power consumption of each recording channel, including the SAR ADC, is 15.5 ¿W. The measured input-referred noise is 6.08 ¿ Vrms over a 5-kHz bandwidth, resulting in a noise efficiency factor of 5.6. The stimulation channel performs monophasic or biphasic voltage-mode stimulation, with a maximum stimulation current of 5 mA and a quiescent power dissipation of 51.5 ¿W. The design is implemented in 0.35-¿m complementary metal-oxide semiconductor technology with the channel pitch of 200 ¿m for a total die size of 3.4 mm × 2.5 mm and a total power consumption of 9.33 mW. The neural interface was validated in in vitro recording of a low-Mg²⁺/high-K⁺ epileptic seizure model in an intact hippocampus of a mouse.

Seventy-three soldiers who had traumatic amputations were examined from 1 to 6 months after limb loss. All experienced phantom limb sensations and 67 percent experienced phantom limb pains, usually transient. Stump pain occurred in 43 percent and was associated with phantom pain in 54 percent of these. Of the 23 percent of the entire group who had evident stump pathology, 33 percent had phantom pains only, 20 percent had stump pains only, 40 percent had both, and 7 percent were pain-free. All stump ends exhibited an area of hyperpathia with hypoesthesia. Phantom pain probably results from peripheral or spinal cord mechanisms, or both, rather than from more rostra1 mechanisms.