The first memory drum.

For most of the 20th century, the memory drum was the standard American apparatus for memory research. The first memory drum dates from 1887 in the work of G. E. Müller and Frederich Schumann, and an illustration of their device appeared 16 years later. This device apparently was invented to resolve the difficulties created by Ebbinghaus's method. The memory drum was a kymograph used to control the display of learning materials. Cattell used something similar for his dissertation with Wundt, though not for verbal material. From Müller's writings, images of this device and kymographs contemporary to Müller's innovation, characteristics, aspects, and difficulties of the development of this drum are presented in the context of its use to resolve the difficulties created by Ebbinghaus's method. An improved device was offered by instrument makers Diederichs in Göttingen and Zimmermann in Leipzig, both in 1894. Surprisingly, from 1903 Zimmermann offered only the original, unimproved device, mistakenly portraying it as appropriate for paired-associate learning procedures.

Distinct patterns of spatial frequency response by normal, recovered optic neuritis, and normal fellow eyes to a new linearly variable neutral density device.

Upon apparent recovery from optic neuropathy, structural damage to the optic nerve may remain while usual measures of visual function appear normal. To test for such damage, the logarithm of optical density to cause a pattern to disappear is read directly on the scale of our device. Patients in the first study observed the disappearance of a red Amsler grid; this Threshold Amsler Score, used jointly with acuity scores, separates normal eyes from eyes with optic neuropathies. Patients in the second study used the device to measure the disappearance of the highest contrast Vistech patterns to show that this device, used over a range of spatial frequencies, differentiates "subclinical" neuropathies (recovered optic neuritis eye; never symptomatic fellow eye to a diagnosed eye) from normal eyes. This device may measure the functional photopic brightness of the stimulus pattern; when the score from our device is higher, the range of photopic brightness for the stimulus is wider, and the retina is more sensitive to contrast.

Use of botulinum toxin in the treatment of one hundred patients with facial dyskinesias.

One hundred patients with involuntary eyelid and facial spasms resulting from essential blepharospasm, Meige syndrome, and hemifacial spasm continued to respond to repeated injections of botulinum toxin at expected time intervals during a 30-month period. This series of more than 372 injections done by one of us (JAM) supports the finding of earlier, smaller series that tolerance to the toxin does not develop. The drug had a greater duration of effect in patients with hemifacial spasm than in patients with blepharospasm; the duration of effect was 17.25 weeks in the former group and 12.6 weeks in the latter. Eighteen percent of patients required a higher than standard dose for a therapeutic response. Fourteen of 15 patients with lower facial spasms and one patient with torticollis had significant relief. Dry eye may be managed by titrating the lower lid dose.

Temporal orientation and education. A direct relationship in normal people.

Neurologists usually do not take socioeconomic status into account when evaluating temporal orientation. Our data indicate that this is a mistake: temporal orientation related directly to education, one measure os socioeconomic level, in New Jersey residents. The neurologist should suspect an abnormality in temporal orientation for patients with (1) some college training and (2) no education beyond high school, if they misstate the day of the month by more than one or three days, respectively.