Four persons developed marked parkinsonism after using an illicit drug intravenously. Analysis of the substance injected by two of these patients revealed primarily 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP) with trace amounts of 1-methyl-4-phenyl-4-propionoxy-piperidine (MPPP). On the basis of the striking parkinsonian features observed in our patients, and additional pathological data from one previously reported case, it is proposed that this chemical selectively damages cells in the substantia nigra.

https://science.sciencemag.org/content/sci/219/4587/979.full.pdf

Chronic Parkinsonism in humans due to a product of meperidine-analog synthesis

ropathic pain (7–10), and this and other putative mechanisms will be discussed The clinical features, diagnosis, and management of the focal and multifocal neuropathies will be described A major portion of this review will discuss the clinical features, assessment, and management of the patient with the most common form of DN, diabetic distal sensory polyneuropathy (DPN) The late sequelae of DPN and their prevention will also be described Finally, practical guidelines for the screening of DPN in clinical practice will be provided For further details on this topic, please refer to recent reviews (11– 18)

https://care.diabetesjournals.org/content/diacare/27/6/1458.full.pdf

Diabetic Somatic Neuropathies

As in last year's review, only a few selected topics of particular interest are discussed here. A limited number of papers have been reviewed; thus many significant contribu¬ tions in other areas of research on the cornea and sclera have been omitted. The list of references includes only those which are mentioned in the text. However, a complete bibliography for the period Oct 1, 1962, through Sept 30, 1963, containing close to 800 references, may be obtained on micro¬ film upon request.

https://jamanetwork.com/journals/OPHTH/articlepdf/627472/archopht_71_2_021.pdf

Cornea and Sclera

The causes of paralysis of the third, fourth and sixth cranial nerves.

The definition of apraxia specifies that the disturbance of performed skilled movements cannot be explained by the more elemental motor disorders typical of patients with movement disorders. Generally this does not present a significant diagnostic problem when dealing with 'higher-level' praxic disturbances (e.g. ideational apraxia), but it can be a major confound in establishing the presence of limb-kinetic apraxia. Most motor disturbances characteristic of extrapyramidal disorders, particularly bradykinesia and dystonia, will compromise the ability to establish the presence of loss of dexterity and deftness that constitutes this subtype. The term 'apraxia' has also been applied to other motor disturbances, such as 'gait apraxia' and 'apraxia of eyelid opening', that perhaps are misnomers, demonstrating the lack of a coherent nomenclature in this field. Apraxia is a hallmark of corticobasal degeneration (CBD) and historically this has received the most attention among the movement disorders. Corticobasal degeneration is characterized by various forms of apraxia affecting limb function, particularly ideomotor apraxia and limb-kinetic apraxia, although buccofacial and oculomotor apraxia can be present as well. The syndrome of parkinsonism and prominent apraxia, designated the 'corticobasal syndrome' (CBS), may be caused by a variety of other central nervous system pathologies including progressive supranuclear palsy (PSP), Alzheimer's disease, dementia with Lewy bodies and frontotemporal dementias. Distinct from the CBS, PSP and Parkinson's disease can demonstrate varying degrees of apraxia on selected tests, especially in those patients with more severe cognitive dysfunction. Diseases that cause the combination of apraxia and a primary movement disorder most often involve a variety of cerebral cortical sites as well as basal ganglia structures. Clinical-pathological correlates and functional imaging studies are compromised by both this diffuse involvement and the confusion experienced in the clinical evaluation of apraxia in the face of the additional elemental movement disorders. Finally, although apraxia results in clear disability in patients with the CBS, it is not clear how milder ideomotor apraxia found on specific testing contributes to patients' overall day-to-day motor disability.

Apraxia in movement disorders

Sparing of the pupil with paralysis of the third cranial nerve has been reported to be characteristic of diabetic ophthalmoplegia. 1,2 This has been borne out by a number of case reports. 3-5 In a large series of oculomotor paralyses, Rucker 6 found that 18 of 21 diabetics showed sparing of the pupil. The one histopathologic study of diabetic third nerve paralysis (Dreyfus, Hakim, and Adams 7 ) suggested that the normal pupillary reactions were due to sparing of the circumferential portion of the third nerve. It is the purpose of this paper to report the pupillary findings in our cases of diabetic ophthalmoplegia and to make a spot check of pupillary reactivity in third nerve paralysis unassociated with diabetes. An attempt has also been made to define the characteristics of diabetic third nerve paralysis as seen in our cases. The diagnosis of diabetes mellitus was made either by overt disease

https://jamanetwork.com/HttpHandlers/ArticlePdfHandler.ashx?journal=ophth&articleId=626350&pdfFileName=archopht_64_4_018.pdf

Diabetic Ophthalmoplegia with Special Reference to the Pupil

Apraxia of lid opening is a nonparalytic motor abnormality characterized by the patient's difficulty in initiating the act of lid elevation. It differs from paralytic ptosis by being present only momentarily at the start of lid opening, and it differs from ordinary forms of blepharospasm by occurring without unusual contraction of the orbicularis oculi. Although apraxia of lid closure has long been documented in the literature (Lewandowsky, 1907),1apraxia of lid opening has scarcely been mentioned. Schilder (1927)2described it, however, in two patients who had difficulty with both opening and closing their eyes. One of these patients had Huntington's chorea and both patients developed a trick of opening their eyes by a thrust of their heads backward. Riese (1930)3described apraxia of lid opening in a patient with a bullet injury to his frontotemporal region. We have not found other reports of this abnormality but suspect

https://jamanetwork.com/journals/OPHTH/articlepdf/627870/archopht_73_2_003.pdf

Apraxia of lid opening

Sclerocornea has been described most frequently in conjunction with the entity cornea plana, 1-7 but it may also occur as an isolated congenital anomaly. 8 The scleralization may affect only a limited area in the peripheral cornea or may involve the entire cornea. In addition to cornea plana, other ocular defects, as well as extraocular anomalies, 9 have been noted to accompany sclerocornea. Seven cases of sclerocornea which we have seen will be described in this paper. These demonstrate different degrees of scleralization and various associated anomalies, some of which have not been previously reported. Report of Cases Case 1. —A 4-month-old white female was noted to have had cloudy corneas since birth. The infant had been the product of a full-term pregnancy, during which period there had been no maternal illnesses, and the delivery had been uncomplicated. Birth weight was 6 pounds and 7 ounces. The parents, to the

Sclerocornea and associated congenital anomalies.

Ocular motor dysmetria 1 and skew deviation 2,3 are characteristic manifestations of disease in the posterior cranial fossa. However, no attempt has been made previously to assess the localizing value of dysmetria as to sidedness and recent observations on skew deviation 4 have suggested findings at variance with those previously reported. 5-7 Clarification of these uncertainties is clearly indicated. To determine whether or not these signs had lateralizing value, 51 cases were selected in which surgical exploration or clinical signs indicated convincingly whether the lesion was unilateral or bilateral. The dysmetria and skew deviation were not necessarily present in the same patient and 10 of the patients have been previously included in a report on internuclear ophthalmoplegia. 4 Dysmetria was manifest by an overshoot of the eyes when fixation was alternately directed from an eccentrically placed object on either side to a midline point. In instances in which the dysmetria

Lateralizing value of ocular motor dysmetria and skew deviation.

In most instances of optic neuropathy associated with multiple sclerosis it is difficult to ascribe the onset of visual symptoms to a particular precipitating factor. However, some patients with multiple sclerosis have an optic neuropathy that is initially provoked or temporarily aggravated by physical exertion (Uhthoff's symptom 1 ). It is the purpose of this paper to report four cases of multiple sclerosis with optic neuropathy in which episodes of visual impairment occurred during periods of exercise. Report of Cases Case 1. —A 25-year-old female was admitted to the Massachusetts General Hospital for evaluation of recurrent episodes of visual impairment that had started four years previously. Initially she had experienced numbness of her right lower extremity which lasted for four weeks. Shortly thereafter the vision in her left eye became limited to identification of large objects but returned to normal in about a month. Immediately after the birth of her child,

Jack E. Goldstein

Papers

Diabetic Ophthalmoplegia with Special Reference to the Pupil

Apraxia of lid opening

Sclerocornea and associated congenital anomalies.

Lateralizing value of ocular motor dysmetria and skew deviation.

Exercise and the optic neuropathy of multiple sclerosis.