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The electroencephalogram, electromyogram, and electro-oculogram were recorded during wakefulness and sleep from two patients with palatal myoclonus. The myoclonus of branchial muscles was persistently present and irregularly varied around a fixed frequency. Its amplitude varied directly with the amplitude of background EMG activity both during wakefulness and in sleep. The complex abnormal ocular movements occurred at the same frequency as the branchial myoclonus. They disappeared during sleep to return during desynchronized sleep following a rapid eye movement. Voluntary extremity movements provoked in them a rhythmical myoclonus of identical frequency to the simultaneously recorded branchial myoclonus. These observations suggest that voluntary or involuntary muscle activity is necessary for the expression of palatal myoclonus and that the abnormal branchial muscle, ocular, and extremity movements are caused by a common pathophysiologic mechanism.

Vertigo can be caused by many lesions at many locations both in the peripheral organ and in the central nervous system. The lesions occurring in the central nervous system should be diagnosed and treated by a neurologist, but the otolaryngologist can be of great assistance through the study of the VIIIth cranial nerve function and its connections with the oculomotor system. As examples, four different brain stem syndromes are mentioned. (These were illustrated by movies at the meeting.)

In Reply .—The initial study (105 eyes) we performed with the Fieldmaster Model 101-PR automated perimeter 1 has now been validated in subsequent follow-up investigations of more than 1,000 eyes. 2-4 Evaluations performed by other investigators have also replicated our findings. 5.6 To date, our total clinical experience with automated suprathreshold static perimetry includes several automated devices 7 and extends to more than 4,000 eyes over a three-year period. We are therefore confident that these procedures can be highly effective for detecting visual field defects, provided the proper techniques are employed. It is unfortunate that Gerber and colleagues have experienced difficulties with automated suprathreshold static perimetry as performed by the Fieldmaster Model 101-PR. Most of the information we have received from practicing ophthalmologists has been very favorable. In the small number of instances in which problems have been reported, it has usually been possible to attribute the source of the

• Twenty-seven members of a family with dominantly inherited Charcot-Marie-Tooth disease (CMTD) were examined. Fifteen members had CMTD and 13 of these had varying amounts of myotonic pupillary abnormalities similar in some ways to Adie tonic pupil syndrome. Those with graver neurologic disease showed greater pupillary abnormalities. Ten of the 15 patients had pupillary constriction with methacholine chloride (Mecholyl) and some of these had extensive iris atrophy. Several affected patients received symptomatic relief from 0.025% pilocarpine. Seven other patients with CMTD who were not related to our initial family were checked for myotonic pupils; two had findings similar to our initial family. Pupillary abnormalities in certain patients with CMTD appear secondary to a parasympathetic denervation of the iris sphincter and ciliary muscle, as shown by a positive methacholine test, and probably represent part of the autonomic nervous system dysfunction associated with the polyneuropathy in CMTD.

• Fifteen patients with intentional or unintentional V1lesions one to five years after percutaneous radiofrequency trigeminal rhizotomy were examined. No corneal changes developed in the majority of patients. These findings raise the question as to the precipitating factor(s) for neuroparalytic keratitis. The suggested mechanism for preservation of corneal function appears to be intact axonal mechanism(s).

• A 58-year-old man with mycosis fungoides was treated with chemotherapeutic agents and radiation for the recurrent cutaneous form of this disease. Five years after the onset, he developed blurring of vision, neurologic signs, and then lapsed into coma. Chemotherapy and radiation treatment resulted in improvement of the ocular and systemic picture. Within three months, however, the patient's vision deteriorated and swelling of both optic discs, along with retinal and vitreous infiltrates, was noted. Local radiation of the eyes was followed by improvement of the ocular changes. Five months later the patient died. Results of a histologic examination of the eyes showed extensive involvement of the retina and vitreous by tumor cells. The CNS was remarkably free of tumor cells and it was assumed that the radiation and chemotherapy were responsible for this. ( Arch Ophthalmol 95:645-650, 1977)

Pseudotumor cerebri has been reported to cause serious unilateral or bilateral visual loss in up to 25% of patients and lesser degrees of visual impairment in up to 50% of patients.1-9The mechanism of visual field loss may be similar to that in glaucoma. In glaucoma, pressure inside the eye presumably damages the optic nerve, with loss of peripheral visual field. In pseudotumor cerebri, increased subarachnoid pressure is transmitted via the optic nerve sheath to the back of the optic nerve, resulting in papilledema, with eventual loss of peripheral visual field.1-9When medical therapy fails in glaucoma, a filtering procedure is often performed. When medical therapy fails in pseudotumor cerebri, another type of filtering procedure is often performed as a lumboperitoneal shunt. In 1971, Vander Ark et al10described the use of a lumboperitoneal shunt in the successful treatment of patients with pseudotumor cerebri who were experiencing

• Decompression of the perioptic meninges for intractable chronic papilledema was done in a patient with a right parietal temporal glioblastoma multiforme. The patient died 39 days postoperatively. Histologic study of the optic nerves indicated fistulas in the dura compatible with cerebrospinal fluid (CSF) egress and maintenance of a normal subarachnoid space around the nerve. Two additional patients with unilateral optic nerve decompression producing bilateral resolution of papilledema were studied. We contend that egress of CSF was the principle mode of action in these three cases. How long the dural fistula remains patent is unknown. Reports in the literature show considerable variation in the effects of optic nerve decompression. Anatomic variation of the intracanalicular subarachnoid space together with differences in underlying pathologic condition, surgical technique, and patient response may explain discrepancies among the results reported. ( Arch Ophthalmol 95:97-104, 1977)

At the American Academy of Ophthalmology meeting in 1978, we presented a set of goals for future development in automated perimetry. 1 The following are those goals with a few revisions: Precise detection and assessment of all forms of visual field loss in conjunction with a clinically acceptable false-positive rate. Accurate monitoring of progressive visual field loss. Standardization of stimulus conditions for various test procedures with easily interpreted data representation. Electronic monitoring of eye movements. Reduction in examination time. Administration of testing procedures by individuals with little or no perimetric training. A reliable machine at a reasonable purchase price. See also pp 339, 395 and 398. It has been about seven years since these goals were presented, and automated perimetry has undergone tremendous growth during that time. Has the automated perimetry industry successfully achieved these goals? In this editorial, we will briefly review the progress of automated perimetry for each

Previous reports have suggested that diphenylhydantoin may improve visual field loss resulting from ischemic disease of the optic nerves. Therefore, 15 patients with residual visual impairment after acute, presumably ischemic, optic neuropathy were treated alternately with diphenylhydantoin sodium and placebo in a double-blind study. Neither visual acuity nor visual fields improved during treatment. The importance of careful quantitative perimetry with preliminary repetitive testing until results are reproducible is stressed.