OCR Text |
Show }. Clin. Nturo-ophthalmol. 4: 197-208, 1984. Neuro-ophthalmology in the Recent European Literature Part II. The Motor System AVINOAM B. SAFRAN, M.D. In Part 11 in the series of articles reviewing neuro-ophthalmology in the recent European literature Uanuary to June 1983), the following topics will be discussed; eyelid motor disturbances and extrapyramidal disorders; the ocular motor system; and the autonomic nervous system. In order to faciUtate reprint requests, the name and address of the corresponding author of these papers are provided with the reference, when indicated, in the original paper. Eyelid Motor Disturbances and Extu.pyramidal Disorders In premature babies, fused eyelids carry such a bad prognosis when observed in neonatal period that many pediatricians do not even attempt resuscitation. Clinical significance of this si~ was reconsidered by Antoniou and McIntosh after they observed a 26-week gestation baby demonstrating tightly fused eyelids for 7 days without any respiratory problem. They reviewed 94 successive cases of recently born babies of less than 28-week gestation. Eight were noted to have fused eyelids. In six babies, gestation was 26 weeks or more. Out ot the eight babies, five died in the neonatal period and two within 14 months; one was still alive, though with major heart abnormalities. Possible involvement of facial nucleus in postparalytic hemifacial spasm was supported by MartineJlj et al.'s observations? Two new cases of widespread hemifacial spasm following injury of a peripheral branch of the facial nerve were reported. Mechanisms that make posterior fossa surgery successful in relieving hemifacial spasms were the subject of a lively debate by Janetta with Adams and Kaye in the correspondence section of the Journal of Nturolon, Neurosurgery and Psychiatry. Kaye and Adams) had recently reported that, in their experience, patients with hemifacial from tM Cliniqut d'ophth<lllmologie, HOpit<ll1 untooal Univmit. 1irt, ~<II, SwiturlMtd. September 1984 spasms inconsistently exhibit at operation vascular compression at the junction of the seventh nerve with the brain stem. janetta commented in a letter4 that Kaye and AdamsJ inability to consistently demonstrate vascular compression was presumably due to the fact that they had not properly looked for such a compression at oper~ ation. In an extensive reply. Adams and KayeS rejected janetta's assumption regarding their surgical procedure and presented eight reasons which had led them to disagree with janetta's concept of vascular compression at the root entry. They concluded that operation probably worked by persistent, bUI gentle trauma and fibrosis around the nerve. It was also indicated that, in a paper then in press, Adams et aI.' reported on the lack of significant vascular compression in most of 57 patients who underwent surgery for trigeminal neuralgia. In patients with manic-depressive illness and tardive dyskinesia, dyskinetic features can disappear during the manic phases. This phenomenon was also recenlly described by DePotter et al.' in a patient who, in addition, presented with parkinsonism-like symptoms. The authors noted that, in contrast with tardive dyskinesia phenomena, parkinsonism-like symptoms remained unchanged during the manic phases. Presence of a common dopamine receptor instability in the course of manic depression and tardive dyskinesia is probable. Physiopathological hypotheses were discussed taking account of the presence of parkinsonism-like symptoms and their dissociated evolution. Barnes et al.e studied purposeless movements in psychiatric patients treated with antipsychotic drugs and described in drug-induced. orofacial dyskinesia a characteristic pattern of movements that was different from that found in idiopathic orofacial dyskinesia. Sustained levodopa therapy in tardive dyskinesia failed to produce benefit in seven patients studied by Hardie et aI.' These fmdings contrasted with results of previously reported therapeutic trials, 10,11 but were in agreement with others. J2 197 Recent Literature: Part II Levodopa-induced involuntary movements were studied by Hardie et al. 13 and by Nielsen. 14 The former authors reported the occurrence of levodopa-induced peak dose chorea in a patient suffering from Meige's disease. The latter evaluated in 13 patients the effect of tiapride (Ndiethylaminoethyl- 2-methoxy-5-methylsulfanylbenzamide- hydrochloride) on levodopa-induced hyperkinesia and on-off phenomenon. No benefit was obtained by Nielsen with tiapride administration, in doses not accompanied by recurrence of Parkinsonian symptoms. Use of Nitoman@ (tetrabenazine) has been advocated in various hyperkinetic syndromes. Side effects during long-term treatment with Nitoman@ were for the first time assessed by Mikkelsen, 15 and the drug was found to be apparently safe. Extensive clinical reviews on tardive dyskinesia were provided by Woller and Tegelerl6 , and Briicher.17 In order to understand the effects of various pharmacology strategies employed in the management of Parkinson's and Huntington's diseases, tardive dyskinesia, and related disorders, Grovesl8 presented a remarkable review of the organization of the neostriatum in an apparently novel conceptual framework. Functional organization of the neostriatum was approached, as well as the way in which the cerebral cortex and brain stem play on the efferent systems of the neostriatum to effect neostriatal control of behavior. The function of the neostriatum in movement control is considered to involve preparation, execution, and guidance of voluntary movement in response to the analysis and volition of cortex. Striatal neurons were divided into two subsystems. One efferent subsystem contains the Spiny I neurons, which have been identified with the neuro transmitter gamma aminobutyric acid (GABA) and exert an inhibitory action on their target cells. The other efferent subsystem consists of excitatory efferents, the Spiny II cells, identified with substance P. In Parkinson's disease, an imbalance in excitability between the Spiny I and the Spiny II neurons would favor an excess of substance Pmediated excitatory neostriataI outflow. This leads, indirectly, to symptoms such as rigidity, resistance to passive movements, and a paucity of spontaneous behavior. In Huntington's disease, tardive dyskinesia, and related disorders characterized by involuntary movements, the influence of dopaminergic agonists and antagonists is known to be the inverse of their effects on Parkinsonian symptoms.The occurrence of involuntary movements may, therefore, result from increased excitability of the Spiny I neurons. In the management of Parkinsonian symptoms, it may be predicted that either an antagonist of substance P or an agonist of gamma aminobutyric acid might be effective. These substances, how- 198 ever, should be specific for the nondopaminergic targets of neostriatal efferents. The lack of su~h a specificity could be one of the many possIble reasons why exploratory attempts at symptom control have been disappointing. Conversely, an agonist of substance p/ ~r a.n antag~n!s.t?f ga~a aminobutyric acid, of SImIlar speClfICltles, Inlght produce symptom control in disorders characterized by involuntary movements. Recently, the hypothesis of viral etiology in Bell's palsy has received increasing attention, although conflicting reports on the matter have been published, and no virus has ever been isolated from affected patients. The assumption was, however, clearly supported by the findings of Aviel et al. 19 Based on the significant correlation which had been established between increased blood interferon levels, development of antiviral state in peripheral blood mononuclear cells, and presence of viral infection, Aviel et al. assessed interferon levels in 32 consecutive patients with Bell's palsy, and searched for antiviral state in 15 of them. They observed that 66% of patients had abnormally high interferon levels, and 72% had increased interferon values and/or were in acute viral state. Nevertheless, no correlation could be established between interferon levels, presence of acute viral state, and degree of paralysis or recovery from neurological impairment. However, new morphological and electrophysiological data recall precisely the now somewhat overshadowed anatomical theories of the development of acute idiopathic facial ralsy. These were reviewed by Fisch and Felix/2 and should be taken into account in the complex pathogenesis of Bell's palsy. A family with recurrent idiopathic facial palsy was described and previously ~ublished cases were reviewed by Rousseau et al. I This common condition was found to occur in about 1.4%0 of the general population, and inheritance was found to be generally autosomal-dominant. Recurrence rate was usually about 6%. If another member of the family exhibited a recurrent form of the disease, the recurrence probability was increased to 38%. Residual impairment was not greater in familial than in isolated form of the disease. It was recently demonstrated by Abramsky et al. 22 that familial recurrent peripheral Bell's facial palsy is frequently associated with immunological disorders. Ptosis in the differential diagnosis of neurological disorders has been reviewed by Hartman et al23 and by Gastaut et al.24 Loss of ability of unilateral volitional blinking and palpebral motor impersistence were reviewed by Larmande et al/25 who also described an additional case presenting with these signs as a result of a right parietal tumor. The exceptional importance of ocular move- Journal of Clinical Neuro-ophthalmology ments in patients with athethoid syndrome was stressed by Foley26 in a review of his personal experience with 165 cases. Affected patients make up about a quarter of the cerebral palsied population. Responsible lesions are mainly located in the basal ganglia, and most often result from either intra natal asphyxia or neonatal jaundice. One of the remarkable features of the condition is the relative preservation of ocular movements, while every other kind of movement is completely disorganized. As emphasized by Foley, many of these often intelligent patients depend on eye movements as their only means of communication in their early and middle childhood; during this period of their life, they may indeed be incapable of speaking. Eye-code is sometimes limited to yes-no responses. However, even such simple messages can be difficult to decipher by the uninitiated interlocutor. In fact, it has been shown that ocular motor system is not completely uninvolved in these patients. 27 Foley26 carefully evaluated 106 patients and noted impairment of upward gaze in 18%, abnormalities of eye tracking in 20%, and alteration in optokinetic nystagmus in 29%. Nevertheless, these patients showed apparently well-preserved vestibulo- ocular reflex, that enabled globes to remain stable despite the head being tossed in all directions. D-penicillamine therapy has been associated with neuromuscular disorders. 28 It has been suggested that oral zinc therapy is a suitable alternative for the management of Wilson's disease, because of zinc and copper competition in gastrointestinal tract absorption. Hoogeraad and Van den Hamer29 recently reported on their extended experience with oral zinc therapy in Wilson's disease. Clinical and biochemical results were good in all four patients studied over a follow-up period of 3 years. No toxic side effects were seen. The unusual association of corneal signs of both type II tyrosinosis and Wilson's disease were reported by Thiel and Weidle30 in a 23-year-old man. The Ocular Motor System Supranuclear and Nuclear Disorders When an object of interest appears in the periphery of the visual field, saccades are the best suited ocular movements for bringing the object to the central fixation point. Latency between time of visual perception of the peripheral target and actual beginning of the saccade has been termed saccadic reaction time. Saccadic reaction time varies significantly according to circumstances. It is usually about 200 msec. However, as reported by Lachenmayr,31 saccadic reaction time to peripheral suprathreshold stimuli may be increased by a factor of about 1.5 when attention September 1984 Safran of the subject is occupied by a visual load. This phenomenon has of course clear implications in occupational and traffic medicine. Human saccadic reaction time is also prolonged with aging. 32 Furthermore, as also recently indicated by Vitte et a1.,33 and Schmidt-Burgk et a1./4 it is increased in numerous disorders of the central nervous system, and correlates well with impairment of pursuit movements. Conversely, saccadic reaction time can be markedly reduced when the previous fixation point disappears before the new target appears.15. 36 The existence of a special type of saccades showing reaction time as short as 70 msec was demonstrated by Fischer and Boch36 in trained monkeys. These saccades were termed Hexpresssaccades. HThey occurred only when the previous fixation point was withdrawn 140 msec or more before the appearance of the new peripheral target. It is conceivable that the extinction of the fixation point starts a process leading to the decision to initiate the saccade. The eyes do not move until the new target becomes visible. At that point, the time of execution of the eye movement and the coordinates of the goal-target are known, and there is a minimal delay before the retinal signal reaches the eye muscles. The time period of about 140 msec may represent the delay required for making the decision to initiate the saccade. The brain stem generator may be relatively unaffected by age, unlike the higher centers involved in programming the saccades. This was suggested by the findings of a detailed study of the effect of age on saccade characteristics, conducted by Abel et a1. 32 The assumption was based on: 1) a lack of major decrease in overall saccadic velocity with age; 2) an increase in saccadic latency with age; and 3) a reduction in saccade accuracy of elderly subjects' as compared with younger subjects' performances. Subclinical eye movement disorders were studied by Reulen et al37 in 84 patients with multiple sclerosis and in 21 with optic neuritis. Saccadic latency, maximum saccadic velocity, accuracy of saccadic eye movements, and tracking eye movements were evaluated, and presence of nystagmus was assessed on recordings. Subclinical eye movement disorders were found in 80% of the definite, in 74% of the probable and in 60% of the possible multiple sclerosis patients. In addition, five of the 21 patients with optic neuritis showed ocular motor involvement. Reulen et a1. noted that saccadic latency and pursuit abnormalities were not correlated with prolonged visual evoked potential latencies, and concluded that these ocular motor disturbances probably do not, for the most part, result from lesions located within primary visual pathways. Conversely, occurrence of prolonged saccadic latency correlated 199 Recent Literature: Part II well with pursuit impairment, as also recently indicated by Vitte et al.33 Furthermore, Reulen et at. showed a significant association of internuclear ophthalmoplegia with prolonged saccadic latency. The authors concluded that, in patients with internuclear ophthalmoplegia, lesions often extended to structures other than medial longitudinal fasciculus. Patients recovering from downgaze paralysis sometimes complain of stumbling and difficulties in looking at the floor, while full downward ocular excursions are demonstrated during clinical examination by finger tracking. However, when these patients are asked to perform refixation saccades, downward rapid eye movements show gross alteration. In an interesting study of two patients with downgaze paralysis followin@ brain stem infarction, Weder and Meienberg3 stressed it is not unusual that smooth and rapid eye movements recover at different speeds. Furthermore, they showed that isolated impairment of downgaze saccades can be markedly disabling. They described a patient who was incapable of making downward refixation saccades and developed a strategy for bringing her eyes relatively rapidly into her lower field of gaze. The strategy consisted of closing her eyes, bending her head forward, and reopening her eyes. This was interpreted as taking advantage of the relatively fast reflex downward ocular movement which reverses Bell's phenomenon when eyes are opened. Listeriosis encephalitis usually causes multiple small abcesses, that are predominantly located in the medullopontine area. In 1978, Safran et at.39 were the first to report internuclear ophthalmoplegia with listeriosis rhomboencephalitis. They noted the frequent occurrence of this ocular motor disorder in the description of previously reported cases, although it had not been diagnosed properly. Petit et al.40 recently described a case of large listerian abcess located in the pontine area. The ocular findings of the patient were upgaze and right abducens palsy, right internuclear ophthalmoplegia and, later, right trigeminal and facial involvement. It is conceivable that the large abcess resulted from coalescence of microabcesses. Therapeutic management of the condition was discussed. Internuclear opthalmoplegia following arc aortography was observed by Goodman and Crawford41 in a 49-year-old woman, who had been involved in a traffic accident 6 days before. Traumatic aneurysm formation of the proximal right vertebral artery was demonstrated by angiography. The authors suggested that the occurrence of ocular motor disorder was induced either by an embolism originating from the vertebral artery aneurysm or by a direct complication of aortography. 200 Tracking a moving target generally implies combined eye and head movements. In ~rder to prevent the eyes from remaining stable ~ space because of the vestibulo-ocular reflex, this reflex must be suppressed. This phenomenon has been termed cancellation or suppression of vestibuloocular reflex. The relationship between performances of pursuit and vestibulo-ocular reflex suppression was analysed by Chambers and Gresty42 in 10 normal and 20 diseased subjects presenting a wide spectrum of neurological disorders. In individual subjects, performances of pursuit and visual suppression were generally comparable, for either normal or impaired condition. Exceptions were three subjects with normal pursuit and disturbed visual suppression, and two patients showing the inverse pattern. Results suggested that pursuit and visual suppression have similar dynamics and share a common pathway up to the level of the cerebellum. The key area appeared to be the flocculus. The authors postulated that, beyond that, there may be an anatomical and functional dissociation of these subsystems. Few simple clinical tests have been devised for bedside evaluation of visual suppression of vestibulo- ocular reflex. In 1978, Benson and Barnes43 suggested assessing visual suppression by determining possible changes in visual acuity while the Eatient was asked to shake the head. In 1978, Zee 4 proposed the use of an ophthalmoscope in looking for relative movement of the optic disc while the patient is re~uested to shake head from side to side. Wist et al 5 recently developed a test based on the detection of oscillopsia. A disc 1 em in diameter is attached to a wall at the level of the eyes, and the patient is placed in front of the disc 1 m from the wall. The patient is then asked to fixate monocularly on the disc while oscillating the head laterally. Rotatory head movements should be of ± 20° amplitude, and frequency of oscillation I cycle/second. A metronome will help keeping the right oscillation frequency. If oscillopsia occurs, amplitude of the apparent lateral motion of the disc is measured on the wall. Wist et at. found that with these head movements, stabilization of the retinal image was complete in normals. If oscillopsia is reported with 1 cycle/ second head oscillation, pathology is indicated. Both patients and normal subjects reported oscillopsia with head movements of 2 cycles/second. A new type of ocular oscillation was described by Doslak et at.46: multiple double saccadic pulses. The 37-year-old man presenting with this ocular phenomenon was considered to suffer from multiple sclerosis. He also showed saccadic overshoot dysmetria, flutter dysmetria, macrosaccadic oscillations and square-wave jerks, reflecting cerebellar and possibly coexisting brain stem Journal of Clinical Neuro-ophthalmology dysfunction. Like flutter and flutter dysmetria, double saccadic pulses were interpreted as pause cell instabilities in the pulse generator itself. Ocular bobbing in a patient with central pontine myelinolysis was observed by Zegers de Beyl et a1.47 Diagnosis was confirmed by necropsy findings. Acquired pendular nystagmus was studied by Ell et a1.48 in a personal series of 18 cases and in 34 previously reported cases. Most of the affected patients had multiple sclerosis, while 30% had suffered a brain stem vascular disease. Ell et a1. emphasized visual impairment and reading difficulties resulting from these conditions. They suggested that acquired pendular nystagmus reflected membrane instability in structures of ocular motor nuclei. Abnormally frequent saccadic intrusions ("square-wave jerks") were demonstrated by Jones et a1.49 to occur in Alzheimer-type dementia. They appeared during fixation and slow smooth pursuit tasks in all four patients studied. Verbal instructions to fixate on the target were followed by an increased saccadic intrusion amplitude in three of the four patients. These eye movement abnormalities were interpreted as resulting from alteration in the ocular motor system. Changes in neurotransmitter concentration and morphological abnormalities have been observed in midbrain and pons of patients with Alzheimer disease, and support the authors' assumption. Schizophrenics often show alteration in ocular motor control. Schmid-Burgk et a1. 34 indicated that eye movement disorders include prolonged saccadic reaction time, saccadic undershoot, and impaired pursuit movements. In contrast with the consistent dysmetria that is observed in certain patients with brain stem or cerebellar lesions, dysmetric saccades of schizophrenics occurred irregularly, interspersed between normal refixation movements. Schmidt-Burgk et a1., therefore, suggested that dysmetric saccades did not result from brain stem or cerebellar lesions. In manicdepressive and alcoholic patients, dysmetria was found less often. Occurrence of other ocular motor changes, however, was comparable with that in schizophrenics. Three new cases of periodic alternating n6stagmus were reported by Norre and Puls.5 The authors emphasized the difficulty of properly assessing the vestibular function in these patients, and proposed an appropriate schema for vestibular stimulation and evaluation of responses. Differential diagnosis and mechanisms of druginduced disorders of the ocular motor system were reviewed by Esser and Brandt.51 Frequent involvement of the vestibulocerebellar system was emphasized. The first extensive report of a large family with September 1984 Safran inherited Moebius syndrome and limb abnormalities was provided by Wishnick et a1.52 Twenty affected members were examined. Transmission was autosomal dominant with variable expressivity and incomplete penetrance. Soft tissue syndactyly was a common familial trait. Associated findings included double elevator palsy, hypoplastic pectoralis muscles, pectus excavatum, and club feet. Surgical management of facial weakness in Moebius syndrome was discussed by Stricker et a1.53 Intranuclear Disorders A new hereditary neuromuscular disorder including ophthalmoplegia and intestinal pseudoobstruction was identified by Ionasescu et a1.54 Four affected patients were studied. Inheritance pattern was presumably autosomal recessive. Ptosis and diplopia began in childhood. In the second decade, patients progressively developed intestinal pseudo-obstruction and complained of nausea, vomiting, postprandial discomfort, and diarrhea. Digestive impairment resulted in marked weight loss and death occurred before the age of 30. Segmental weakness of the pupillary sphincters was also observed, and interpreted as probably resulting from myopathic alteration. Histological studies disclosed primary myopathic lesions of smooth and striate muscles. In addition, changes in peripheral nerves and 10mbar posterior columns were found. Clinical and histopathological features of the condition were compared with those of other neuromuscular disorders affecting ocular motility. An apparently unique autosomal recessive disorder including an external ophthalmoplegia and spastic paraplegia was described by Staal et a1.55 in five adult siblings. Optic nerve atrophy was present in three of the five, dementia in two, extrapyramidal signs and cerebellar ataxia in one. Complete neuro-ophthalmological evaluation was performed on four patients. All four showed retraction of the upper lids and preservation of doll's head phenomenon, but impairment of voluntary ocular motor movements. In one patient, adduction was reportedly limited in one eye. Optokinetic response was described as normal in two of the patients, and altered in two others. Electroretinogram was recorded in two patients and showed no abnormality. Necropsy was performed in one case. Loss of ganglion cells was noted in macular and temporal retina, and axons were absent in the corresponding path of the optic nerve. Ocular motor nuclei were unremarkable. Demyelination of spinocerebellar and olivocerebellar pathways was observed, as well as loss of Purkinje cells, of cells in Clarke's column and in the inferior olives. Dentate nucleus was gliotic. 201 Recent Literature: Part II Sequence of demyelination-remyelination in Guillain-Barre disease was studied by Wexler,56 with serial measurements of nerve conduction. Demyelination was observed to follow a centripetal course, appearing first in the most distal segments of nerve and progressing to the spinal root level as the patient weakened. This pattern of demyelination may explain the characteristically late rise in cerebrospinal fluid proteins in patients with Guillain-Barre disease. Motor and sensory fibers appeared equally affected, although motor weakness was clinically more obvious. The first nerve segments to be demyelinated were the last to be remyelinated. Association of superior oblique myokymia with systemic neurological diseases was rerorted in two patients by Neetens and Martin.5 One patient presented with lead intoxication, the other suffered from adrenoleucodystrophy. The authors suggested that patients with superior oblique myokymia should be fully examined in order to determine whether the ocular motor disturbance may be associated with diffuse subclinical involvement of the central nervous sys-tem. , Oculomotor palsy with cyclic sfsasms was reported by Bateman and Saunders 8 in an elderly woman who demonstrated an enhancing mass in the left supraclinoid region on computerized tomography scanning examination. The lesion was thought to be either an aneurysm or a meningioma. Angiography could not be performed. The oculomotor disorders were characterized by limitation of upward and downward movements of the left eye, and marked lid lag on looking down. Spastic phases occurred every 3-7 minutes and lasted 45-90 seconds. They consisted of overelevation of the slight depression and adduction of the globe. No pupillary changes were noted. The authors felt that this case report provided evidence that oculomotor palsy with cyclic spasm may result from a peripheral lesion. Although alternating involvement of ocular motility is not unusual with diabetes, it has rarelx been reported in young patients. Davous et al. 9 described a 22-year-old patient showing regressive painless third nerve palsy with pupillary involvement, who 6 months later, developed controlateral painful complete ophthalmoplegia. General examination including serological tests for syphilis and anti-DNA antibody titer, cerebral computerized tomography scanning, and carotid and vertebral arteriograms showed normal results, with the exception of a high fasting blood sugar level. Paralysis was, therefore, felt to be diabetic in origin. The pattern of ocular motor involvement in this patient supports the views of Annabi et al.60 about third nerve vascularization. According to Annabi et aI., arterial branches to the third nerve give off no collaterals in the 202 posterior region of the circle of Willis, .whereas vascularization of the third nerve in the mtracavernous region is associated with that of the fifth, fourth sixth and occasionally second and sev- I I 59 enth cranial nerves. The patient of Davous et al. was thought to demonstrate involvement of the proximal segment of the third nerve on one side, and intracavernous ischemia on the other side. Neetens61 stressed the fact that ocular muscle palsy following minor head trauma could be the presenting sign of basal intracranial tumor. Mechanisms of ocular motor nerve impairment in head trauma were reviewed. More than 80 million people were affected in 1971 and 1981 by two epidemics of acute hemorrhagic conjunctivitis. This disease was caused by a newly identified virus called Enterovirus 70. A number of the subjects eventually developed a polio-like paralytic disorder with high resultant disability. Neurological involvement was recentll; studied by Wadia et al. 62 and by Katiyar et al. 3 While in 1971 epidemic paralysis remained confined to the lower limbs, in 1981, limb and/or cranial nerve impairment occurred. In the latter epidemic, cranial nerve palsies were seen in approximately half of the patients with neurological impairment. Involvement of the seventh and fifth (motor) nerves was most common, whereas optic and ocular motor nerve impairment was unusual. Poor recovery was noted in patients with ocular nerve involvement and in those with severe cranial nerve palsies. Differential diagnosis included Guillain-Barre syndrome and poliomyelitis, but also common isolated palsies such as Bell's palsy, because focal motor impairment following Enterovirus 70 has also been reported without prior conjunctivitis. Even during interepidemic periods, the possibility of an Enterovirus 70 etiology should be borne in mind when one is evaluating acquired peripheral motor palsy. The authors suggested, as a top priority, the development of a vaccine for immunization. In 1981, the epidemic mainly affected the Indian subcontinent, Central America, and Zaire. Cases were also reported in Key West, Florida. Ocular motor disturbances in various craniofacial dysostosis conditions were analyzed in a paper by Morax et al.,64 based on a study of 64 cases. ·V" syndrome with double ·up-shoot" and limitation of movement in the fields of superior oblique muscles was the most commonly encountered abnormality. Mechanisms involved in the pathogenesis of the ocular motor disorders were discussed. They included orbital torsion resulting in pseudoectopia maculae syndrome and extorsion of the four recti muscles, as well as plagiocephalia- induced sagittalization of inferior oblique muscles. Muscle agenesis was rarely observed. Prognosis of ocular myasthenia in childhood was addressed in a paper by Schmidt.65 Seven Journal of Clinical Neuro-ophthalmology children with "juvenile" type myasthenia and two with "familial" type myasthenia were described. Schmidt found a good long-term prognosis in the studied cases. Previous reports were also reviewed extensively. Various factors have been shown to precipitate myasthenic crisis. A case of myasthenic crisis following an infusion of low-sodium biodinated contrast medium (iothalamic acid, Conray 60%®) has been reported by Canal and Franceschi.66 Iothalamic acid is a common contrast medium that was used in this patient for enhancing computerized tomography of the mediastinum. The reaction was not attributed to cholinergic crisis because the patient had taken no anticholinesterase agent in the 3 previous days. Valesini et al. 67 had the rare opportunity to relate the appearance of anti-acetylcholine receptor antibodies to the onset of muscle weakness in a patient with myasthenia gravis. This patient also suffered from systemic lUpus erythematosus. Sera were available from 18 months before the occurrence of weakness. Anti-acetylcholine receptor antibodies were absent until about the time that weakness appeared, increased over the subsequent 4-6 months and then remained constant. During this period, antinuclear antibody titer declined, and anti-ds-DNA antibodies were negative. A new highly potent and probably safe drug has been used successfully in three patients with Eaton-Lambert syndrome. Lundh et al. 68 reported on the therapeutical trial of 3, 4-diaminopyridine in two patients with cryptogenic Eaton-Lambert syndrome, and one exhibiting this syndrome in conjunction with cancer of the gallbladder. Intravenous infusions of 6-9 mg four times a day with 0.5 mg atropine, or oral administration of 24 mg four times a day caused marked improvement which persisted over a follow-up period of 5 months in one patient and 4 months in another. The third patient died after a short time, following pulmonary embolism. With simultaneous administration of atropine, no side effects were noted in the first patient, while the second complained of temporary perioral paresthesias and transitory pain in her arm after intravenous injection. 3-4 diaminopyridine has experimentally been demonstrated to be less convulsant and more potent in improving neuromuscular transmission than 4aminopyridine which has been clinically tested previously. In the second patient studied, a prior treatment attempt with 4-aminopyridine had caused a seizure. Creatine-kinase has been considered to be the most useful laboratory test in the investigation of muscle disorders. Recently, however, Heath et al. 69 demonstrated that determination of plasma carbonic anhydrase III is probably more sensitive than creatine-kinase. Plasma levels of both en- September 1984 Safran zymes were assessed in 44 patients with a variety of neuromuscular disorders, and it was found that marked elevation in creatine-kinase levels was associated with similar increase in carbonic anhydrase III levels. However, in nine patients, only the carbonic anhydrase III was elevated, whereas two patients showed rise in creatinekinase levels only. Nuclear filamentous inclusions were found by Coquet et al. 70 in striate muscles of six patients with oculopharyngeal dystrophy. They had also been reported in five recent studies on oculopharyngeal dystrophy. Coquet et al. felt that they may be characteristic of the disease as they have apparently never been seen in other disorders. Association of progressive external ophthalmoplegia and Hashimoto's thyroiditis was reported by Leger et al. 71 in a 43-year-old woman. Mitochondrial abnormalities were demonstrated in muscle tissue. The Autonomic Nervous System The boundary between simple anisocoria and pupillary inequality in Homer's syndrome was further delineated by the studies of van der Wiel and van Gjin.72. 73 These authors evaluated two clinical criteria commonly used in diagnosis of anisocoria due to sympathetic impairment: 1) dilatation lag, i.e., relative delay of the affected pupil to dilate in darkness as compared to the fellow pupil; and 2) failure to dilate with hydroxyamphetamine eyedrops, that induce release of presynaptic norepinephrine in the iris. Van der Wiel and Van Gjin72 first confirmed the clinical value of dilatation lag for differentiating unilateral oculosympathetic impairment from simple anisocoria, but noted that dilatation lag is diagnostic for Homer's syndrome only when it exceeds 0.4 mm after 5 seconds in darkness, without a further lag in the next S seconds. Smaller dilatation lags were observed both in controls and in patients with oculosympathetic defects. These findin~s are in agreement with those of Safran et aI., 4 who independently conducted a study on the same matter. Three of the 12 patients with clinically presumed oculosympathetic denervation who were studied by van der Wiel and van Gjin failed to meet these criteria. In this study, lag was evaluated by taking photographs, without using associated psychosensory stimuli to enhance pupil dilatation and dilatation lag. Only four of the 10 patients with presumably postganglionic sympathetic lesions demonstrated significantly abnormal response with hydroxyamphetamine eyedrops, while a normal response was elicited in allIS patients with preganglionic lesions, in the second study by van der Wiel and van Gjin. 73 Of interest is the fact that in 203 Recent Literature: Part II four patients with postganglionic lesions who unexpectedly showed normal results, oculosympathetic dysfunction disappeared within 2 years. Finally, it should be noted that only 12% of normal control pupils demonstrated peak dilatation between 40 and 50 minutes, whereas all other pupils reached or continued a plateau of maximal dilatation between 50 and 60 minutes. The authors, therefore, suggested measuring hydroxyamphetamine- induced anisocoria between 50 and 60 minutes after eyedrop administration. Central corneal thickness was found to be increased with Homer's syndrome in a study conducted by Nielsen75 in 14 patients with unilateral ocular sympathetic impairment. Duration of innervational disorder ranged from 6 months to 36 years. No significant change was found in intraocular pressure or corneal sensitivity as evaluated by means of the Cochet-Bonnet esthesiometer. No perilimbal hyperemia was noted. Adrenergic substances have been shown to be sEecific agonists of rece~tors in the epithelium76 and the endothelium of the cornea, enhancing the production of cyclic AMP. These data support the author's assumption that the observed increase in corneal thickness may result from an increase in the water content of the cornea. In diabetic autonomic neuropathy, pupils are often small and show altered response to darkness. Shirley A. Smith and S. E. Smith78 examined 34 insulin-treated diabetics to determine whether these pupillary changes were due to autonomic dysfunction or to primary myopathy. Sixteen of the 34 patients studied failed to dilate normally to darkness. Small pupils exhibited supersensitivity reactions to topical 2% phenylephrine, whereas response to topical 0.5% hydroxyamphetamine was within the normal range when compared with pupillary reaction of age-matched healthy subjects. The authors suggested that impairment of pupil dilatation in response to darkness resulted from decrease in sympathetic outflow. The assertion is supported by the significant correlation that was noted in the studied diabetic patients between small pupil diameter, cardiac vagal dysfunction, and somatic sensory loss. It has been hypothesized that in diabetic autonomic neuropathy, alteration of light pupil reflex results from the reduced pupil size usually found in these patients, that would mechanically impair further contraction. The findings by Shirley A. Smith and S. E. Smith79 did not support this assumption. By comparing the light reflex in diabetic patients with that in healthy subjects (mostly elderly) who also have small pupils, these authors demonstrated that decrease of diabetic pupillary reflexes exceeds that to be expected from the small pupil alone. Smith and Smith suggested that reduction of light reflex in dia- 204 betics could result from a loss of parasympathetic function, and possibly from an associated primary myopathic process. . When illumination of the eye is suddenly mcreased to a new steady level, pupil first constricts, then slowly redilates. This phenomeno~n has been named pupillary escape. Sun and Stark demonstrated with five healthy subjects that pupillary escape depends on initial pupil size. Escape was observed with large pupilS, but not with smaller ones. The effect of operating level of the pupil size on escape phenomenon remained unexplained. Retinal operating level apparently does not play an essential role in pupillary escape, because dependence on initial pupil size was demonstrated either by changing background illumination or by varying accommodation level. Brain stem connections to the Edinger-Westphal nucleus were investigated by Breen et al.81 in the cat, by means of retrograde tracers. The authors were able to show a direct pathway from the olivary pretectaI nucleus to the mesencephalic pupilloconstrictor area. This may indicate that neurons of the olivary pretectal nucleus, which receives an input from the retina, may play a major role in the light reflex. Breen et al. also demonstrated an input from the nucleus of the posterior commissure, that was more extensive than has previously been thought. These results provided further evidence that there may be an ascending inhibitory input to the pupilloconstrictor outflow. Electrical activity attributed to the efferent arc of the light pupillary reflex was recorded in man by Bracher et al.82 by means of surface corneal electrodes similar to those used for electroretinogram recording. If the pupil was large before stimulation, a corneopositive potential synchronous with pupillary constriction was observed. In contrast, with an initially narrow pupil, a corneonegative deflection dominated, which was also synchronous with phasic pupillary constriction. Parasympathicolytic or parasympathicomimetic drugs abolished both of the above-mentioned potentials. In ophthalmology departments, glaucoma specialists will perhaps join neuro-ophthalmologists in their interest in bromocriptine, since it was demonstrated recently by Mekki et al.,83 that oral bromocriptine significantly lowers intraocular pressure in man. Reduction in intraocular presst, lfe was not associated with alteration of pupil diameter. Furthermore, no changes in heart rate, blood pressure, or systolic time intervals were found in the six healthy volunteers studied.* • Note. For prescribing above-mentioned treatments, please refer to the original articles. Journal of Clinical Neuro-ophthalmology References 1. Antoniou, AG. and McIntosh, N.: Do fused eyelids indicate inevitable neonatal death? Lancet 1: 878879, 1983. Reprints: A G. Antoniou, Neonatal Unit, St. George's Hospital, London SW 17 ORE, England. 2. Martinelli, P., Gabellini, AS., and Lugaresi, E.: Facial nucleus involvement in post-paralytic facial spasm. (Letter.) J. Neurol. Neurosurg. Psychiatry 46: 586-587, 1983. 3. Kaye, AH., and Adams, CB.T.: Hemifacial spasm: A long term follow-up of patients treated by posterior fossa surgery and facial nerve wrapping. J. Neurol. Neurosurg. Psychiatry 44: 1100-1103, 1981. 4. Janetta, P.: Hemifacial spasm: Treatment by posterior fossa surgery. (Letter.) J. Neurol. Neurosurg. Psychiatry 46: 465, 1983. 5. Adams, CB.T., and Kaye, AH.: Hemifacial spasm: Treatment by posterior fossa surgery (Reply letter.) J. Neurol. Neurosurg. Psychiatry 46: 465-466, 1983. 6. Adams, CB.T., Kaye, AH., and Teddy, P.J.: The treatment of trigeminal neuralgia by posterior fossa microsurgery. J. Neurol. Neurosurg. Psychiatry (In press.) 7. Potter, RW.de, Linkowski, P., and Mendlewicz, J.: State-dependent tardive dyskinesia in manic-depressive illness. J. Neurol. Neurosurg. Psychiatry 46: 666-668, 1983. Reprints: Prof. J. Mendlewicz, Dept. of Psychiatry, Hopital Erasme, 808 Route de Lennik, B-1070 Bruxelles, Belgium. 8. Barnes, T.RE., Rossor, M., and Trauer, T.: A comparison of purposeless movements in psychiatric patients treated with antipsychotic drugs, and normal individuals. J. Neurol. Neurosurg. Psychiatry 46: 540-546, 1983. Reprints: Dr. T.RE. Barnes, Psychiatric Research Unit, Old Addenbrooke's Hospital, Trumpington St., Cambridge CB 2 2QE, England. 9. Hardie, RJ., Lees, AJ. and Stem, G.M.: Sustained levodopa therapy in tardive dyskinesia. (Letter.) J. Neurol. Neurosurg. Psychiatry 46: 685, 1983. 10. Alpert, M., Friedhoff, AJ., and Diamond, F.: Use of dopamine receptor agonists to reduce dopamine receptor number in tardive dyskinesia. In Experimental Therapeutics ofMovement Disorders, S. Fahn, D.B. CaIne, and I. Shoulson, Eds. Raven Press, New York, 1983, pp. 253-258. 11. Shoulson, I.: Carbidopa/levodopa therapy of coexistent drug-induced Parkinsonism and tardive dyskinesia. In Experimenal Therapeutics of Movement Disorders, S. Fahn, D.B. CaIne, and I. Shoulson, Eds. Raven Press, New York, 1983, pp. 259266. 12. Casey, D.E., Gerlach, J., and Bjf/lmdal, N.: Levodopa and receptor sensitivity modification in tardive dyskinesia. Psychopharmacology 78: 89-92, 1982. 13. Hardie, RJ., Lees, AJ., and Stem, G.M.: Levodopa induced chorea in Meige syndrome. (Letter.) J. Neurol. Neurosurg. Psychiatry 46: 286, 1983. 14. Nielsen, 8.M.: Tiapride in levodopa-induced involuntary movements. Acta Neurol. Scand. 67: 372375, 1983. Reprints: B. Mejer Nielsen, Department of Neurology, University of Copenhagen, Hvi- September 1984 Safran dovre Hospital, Hvidovre, Denmark. 15. Mikkelsen, B.O.: Tolerance of tetrabenazine during long-term treatment; Acta Neurol. Scand. 68: 57-60, 1983. Reprints: Birgit Ohrt Mikkelsen, M.5c., Department of Clinical Research, Roche Ltd., Industriholmen 59, DK-2650 Hvidovre, Denmark. 16. Woller, W., and Tegeler, J.: Spate Extrapyramidale Hyperkinesen Klinik-Pravalenz-Pathophysiologie. Fortschr, Neurol. Psychiatr. 51: 131-157, 1983. Reprints: Dr. W. Woller, Psychiatry Klinik der Univ. Dusseldorf, Bergisch Landstrasse 2, D-4000 Dusseldorf 12, Germany. 17. Briicher, K.: Die Spatdyskinesien-eine Uebersicht uber KIinik, Pathogenese, Prophylaxe und Therapie eines spaten neuroleptischen Seiteneffekts. Fortschr. Neurol. Psychiatr. 51: 183-199,1983. Reprints: K. Briicher, Psychiatrische KIinik und Poliklinik der Universitat Marburg, Marburg, Federal Republic of Germany. 18. Groves, P.M.: A theory of the functional organization of the neostriatum and the neostriatal control of voluntary movement. Brain Res. Rev. 5: 109112, 1983. Reprints: Philip M. Groves, University of California, San Diego School of Medicine, Department of Psychiatry (M-003), La Jolla, California 92093. 19. Aviel, A, Hahn, T., Levin, S. et al; Interferon antiviral system in Bell's palsy. Acta Otolaryngol. 95: 69-73, 1983. Reprints: A Aviel, Department of Otolaryngology, Kaplan Hospital, Rehovot 76100, Israel. 20. Fisch, U., and Felix H.: On the pathogenesis of Bell's palsy. Acta Otolaryngol. 95: 532-538, 1983. Reprints: U. Fisch, M.D., ORL-Klinik, University Hospital, CH-8091 Zurich, Switzerland. 21. Rousseau, J.J., Godfroi, M.E., and Husquinet, H.: Paralysie faciale idiopathique familiale recurrente. Acta Neurol. Belg. 83: 23-28, 1983. Reprints: J.J. Rousseau, Centre Hospitalier de Sainte-Ode, B6970 Baconfoy, Belgium. 22. Abramsky, 0., Livhits, T., and Brautbar, c.: Familial recurrent peripheral Bell facial palsy with immunologic observations. Neurology 32: A183, 1982. 23. Hartmann, A, Berendes, K., and Berlit, P.: Die Ptosis in der differentialdiagnose Neurologischer Erkrankungen. Klin. Monatsbl. Augenheilk 182: 113-120, 1983. Reprints: Prof. Dr. A Hartmann, Neurologische Univ.-Klinik, Siegmund-FreudStrasse, D-5300 Bonn 1, Federal Republic of Germany. 24. Gastaut, J.L., Pellissier, J.F., Pouget, J., et al.: Le ptosis en pathologie neuro-musculaire. Rev. Otoneuroophthalmol. 55: 85-98, 1983. Reprints: J.L. Gastaut, Clinique Rhumatologique et des Maladies Neuro-musculaires, Groupe Hospitalier de la Timone, F-13385 Marseille Cedex 4, France. 25. Larmande, P., Larmande, A, and Rolland, J.: Perte de l'occlusion volontaire unilaterale des paupieres et impersistance motrice palpebrale par lesion parietale tumorale. Rev. Otoneuroophthalmol. 55: 7783, 1983. Reprints: P. Larmande, Service d'Ophthalmologie, CH.U. Bretonneau, F-37033 Tours Cedex, France. 26. Foley, J.: The athetoid syndrome. A review of a personal series. J. Neurol. Neurosurg. Psychiatry 46: 205 Recent Literature: Part II 283-298, 1983. Reprints: Dr. John Foley, The Cheyne Centre for Spastic Children, 61 Cheyne Walk, London SW3, United Kingdom. 27. Hoyt, C.S., Billson, F.A., and Alpins, N.: The supranuclear disturbances of gaze in kernicterus. Ann. Ophthalmol. 10: 1487-1492, 1978. 28. Carrano, J.: Myasthenia gravis and D-penicillamine. J. Rheumatol. (Suppl) 7: 169-174, 1981. 29. Hoogenraad, T.U., and Van den Hamer, C.J.A: Three years of continuous oral zinc therapy in 4 patients with Wilson's disease. Acta Neurol. Scand. 67: 356-364, 1983. Reprints: T.U. Hoogenraad, M.D., Department of Neurology, State University Hospital, P.O. Box 16250, 3500 CG Utrecht, The Netherlands. 30. Thiel, H.J., and Weidle, E.: Tyrosinosis and Hepatolentikulaare Degeneration (M. Wilson). Klin. Monatsbl. Augenheilk 182: 232-234, 1983. 31. Lachenmayr, B.: Inhibition des Sakkadischen Systems Durch eine Visuelle Belastung. Fortschr. Ophthalmol. 79: 542-544, 1983. Reprints: B. Lachenmayr, Institut fur Medizinische Optic der Univ. Munchen, Barbarastrasse 16, 0-8000 Munchen 40, Federal Republic of Germany. 32. Abel, L.A, Troost, B.T., and Dell'Osso, L.F.: The effects of age on normal saccadic characteristics and their variability. Vision Res. 23: 33-37, 1983. Reprints: Larry A Abel, Ocular Motor Neurophysiology Laboratory, Veterans Administration Medical Center, Case Western Reserve University, Cleveland, Ohio 44106. 33. Vitte, E., Ulmer, E., Chaumette, A et al.: Mesure des latences des saccades oculaires voluntaires et de correction. Son interet en oto-neurologie. Ann. Otolaryngol. 100: 85-97. 1983. Reprints: Prof. P. Dialoux, Clinique ORL, Hopital Lariboisiere, 2 rue F.7501O Ambroise-Pare, Paris, France. 34. Schmid-Burgk, W., Becker, W. Diekmann, V., et al.: Disturbed smooth pursuit and saccadic eye movements in schizophrenia. Arch. Psychiatr. Nervenkr. 232: 381-389, 1983. Reprints: H.H. Kornhuber, Abteilung fur Neurologie, Universitat Ulm, Steinhovelstrasse, D-7900 Ulm, Federal Republic of Germany. 35. Saslow. M.G.: Effects of components of displacement- step stimuli upon latency of saccadic eye movements. J. Ophthalmol. Soc. Am. 57: 1024-1029, 1967. 36. Fischer, B., and Boch, R: Saccadic eye movements after extremely short reaction times in the monkey. Brain Res. 260: 21-26, 1983.Reprints: B. Fischer, Dept. of Neurophysiology, University of Freiburg, Freiburg i/B., Federal Republic of Germany. 37. Reulen, J.P.H., Sanders, E.AC.M., and Hogenhuis, L.AH.: Eye movement disorders in multiple sclerosis and optic neuritis. Brain 106: 121-140, 1983. Reprints: J.P.H. Reulen, Department of Medical PhysicS, Vrije Universiteit, 1081 BT Amsterdam, The Netherlands. 38. Weder, B., and Meienberg, 0.: Downgaze paralysis due to brain stem infarction. Clinical course in two cases. Neuro-ophthalmology 3: 29-35, 1983. Reprints: Dr. O. Meienberg, Neurologische Universitatsklinik, Inselspital, CH-3010 Bern, Switzerland. 39. Safran, AB., Berney, J., and Rilliet, B.: L'ophthal- 206 moplegie internucleaire dans les enceph~li~e~ infectieuses: Observation d'un cas de listenose. Schweiz. Arch. Neurol. Neurochir. Psychiatr. 123: 179-185,1978. 40. Petit, H., Destee, A, Leys, D., et al.: Volumineux abces listerien du tronc cerebral. Effet favorable de l'antibiotherapie. Rev. Neurol. 139: 149-154, 1983. Reprints: H. Petit, Service de Neurologie, Hopital Regional, F-59037 Lille, France. 41. Goodman, G.K., and Crawford, K.H.: Internuclear ophthalmoplegia following arch aortography. Occurrence in asssociation with an occult vertebral artery aneurysm. Neuroradiology 25: 171-172, 1983. Reprints: Dr. GX Goodman, Kentucky Lions Eye Research Institute, University of Louisville School of Medicine, 301 East Muhammed Ali Boulevard, Louisville, Kentucky 40202. 42. Chambers, B.R., and Gresty, M.A: The relationship between disordered pursuit and vestibuloocular reflex suppression. J. Neurol. Neurosurg. Psychiatry 46: 61-66,1983. Reprints: Dr. M. A Gresty, National Hospital, Queen Square, London WC1N 3BG, England. 43. Benson, AJ., and Barnes, G.R: Vision during angular oscillation: The dynamic interaction of visual and vestibular mechanisms. Aviat. Space Environ. Med. 49: 340-345, 1978. 44. Zee, D.5.: Ophthalmoscopy in examination of patients with vestibular disorders. Ann. Neurol. 3: 373-374,1978. 45. Wist, E.R., Brandt, Th., and Krafczyk, S.: Oscillopsia and retinal slip. Evidence supporting a clinical test. Brain. 106: 153-168, 1983. Reprints: Eugene R. Wist, Psychological Institute, University of DUsseldorf, Federal Republic of Germany. 46. Doslak, M.}., Dell'Osso, L.F., and Daroff, RB.: Multiple double saccadic pulses occurring with other saccadic intrustions and oscillations.Neuroophthalmology 3: 109-116, 1983. Reprints: L.F. Dell'Osso, Ph.D., Ocular Motor Neurophysiology Lab. (127A), Veterans Administration Medical Center, Cleveland, Ohio 44106. 47. Zeger de Beyl, D., Flament-Durand, L Borenstein, S., et al.: Ocular bobbing and myoclonus in central pontine myelinolysis. J. Neurol. Neurosurg. Psychiatry 46: 564-565, 1983. Reprints: Dr. D. Zeber de beyl, Dept. of Neurology, 808 route de Lennik, B1070 Brussels, Belgium. 48. Ell, J.J., Gresty, M.A., and Findley, L.J.: Acquired pendular nystagmus. (abstract.) J. Neurol. Neurosurg. Psychiatry 46: 189-191, 1983. 49. Jones, A, Friedland, RP., Koss, B., et al.: Saccadic intrusions in Alzheimer-type dementia. J. Neurol. 229: 189-194, 1983. Reprints: R.P. Friedland, Department of Neurology, University of California, Davis, California 95616. 50. Norre, M.E., and Puis, T.: Nystagmus alternant. Rev. Otoneuro-ophthalmol. 55: 149-155, 1983. Reprints: M.E. Norre, Department d'Otoneurologie et d'Equilibriometrie Clinique Otorhinolaryngologique, Akademisch Ziekenhuis St Rafael, Kath. Universiteit Leuven, Leuven, Belgium. 51. Esser, J., and Brandt, Th.: Pharmakologische verusachte Augenbewegunsstorungen-Differentialdiagnose und Wirkungsmechanismen. Fortschr. Journal of Clinical Neuro-ophthalmology Neurol. Psychiatr. 51: 41-56, 1983. Reprints: Dr. Joachim Esser, Neurologische Klinik mit klinischer Neurophysiologie, Alfred-Krupp-Krankenhaus, D4300 Essen, Federal Republic of Germany. 52. Wishnick, M.M., Nelson, L.B., Huppert, L., et al.: Mobius syndrome and limb abnormalities with dominant inheritance. Ophthal. Paediatr. Genet. 2: 77-81,1983. Reprints: Marcia M. Wishnick, Ph.D., M.D., Department of Pediatrics, Division of Human Genetics, New York University Medical Center, 550 First Avenue, New York, New York 10016. 53. Stricker, M., Meley, M., and Chassagne, J.P.: Le syndrome de Moebius, Possibilites chirurgicales. Rev. Otoneuro-ophthalmol. 55: 157-161, 1983. Reprints: M. Meley, Service de Chirurgie maxillofaciale, C.H.R de Nancy, 29, avo du Ml. de Lattrede- Tassigny, F-54037 Nancy Cedex, France. 54. Ionasescu, V., Thompson, S.H., Ionasescu, R, et al.: Inherited ophthalmoplegia with intestinal pseudo-obstruction. J. Neurol. Sci. 59: 215-228, 1983. Reprints; V. Ionasescu, M.D., Department of Pediatrics, University Hospitals, Iowa City, Iowa 52242. 55. Staal, A, Stefanko, S.l., Jennekens, F.G.I., Penning De Vries-Bos, L.H., and Van Gijn, J.: Autosomal recessive spino olivo-cerebellar degeneration without ataxia. J. Neurol. Neurosurg. Psychiatry 46: 648-652, 1983. Reprints: A Staal, University Hospital Rotterdam (Dijkzigt), 40 Dr. Molewaterplein, 3015 GD Rotterdam, The Netherlands. 56. Wexler, I.: Sequence of demyelination-remyelination in Guillain-Barre disease. J. Neurol. Neurosurg. Psychiatry 46: 168-174, 1983. Reprints: Dr. Ira Wexler, 11085 LittlePatuxent Parkway, Columbia, Maryland,21044. 57. Neetens, A, and Martin, J,J.: Superior oblique myokymia in a case of adrenoleucodystrophy and in a case of lead intoxication. Neuro-ophthalmology 3: 103-108, 1983. Reprints: Prof. A Neetens, Institute of Ophthalmology, University of Antwerp, Antwerp, Belgium. 58. Bateman, D.E., and Saunders, M.: Cyclic oculomotor palsy: Description of a case and hypothesis of the mechanism. J. Neurol. Neurasurg. Psychiatry 46: 451-453, 1983. Reprints: Dr. D.E. Bateman, Regional Neurological Centre, Newcastle General Hospital, Westgate Road, Newcastle upon Tyne NE4 6BE, Great Britain. 59. Davous, P., Demierre, B., and Massiou, H.: Recurrent alternating ophthalmoplegia with iridoplegia in a young diabetic. fur. Neural. 22: 157-160, 1983. Reprints; Patrie Davous, M.D., Hopital SainteAnne, 1, rue Cabanis, F-75014 Paris, France. 60. Annabi, A, Lasjaunias, P., and Lapresle, J.: Paralysies de la IIIe paire au cours du diabete et vascularisation du moteuroculaire commun. J. Neurol. Sci. 41: 359-367, 1979. 61. Neetens, A: Extraocular muscle palsy from minor head trauma. Initial sign of intracranial tumor. Neuro-ophthalmology 3: 43-48, 1983. Reprints: Prof. A Neetens, Department of Ophthalmology, University of Antwerp, U.I.A, Antwerp, Belgium. 62. Wadia, N.H., Wadia, P.N., Katrak, S.M., et al.: A study of the neurological disorder associated with acute haemorrhagic conjunctivitis due to entero- September 1984 Safran virus 70. J. Neurol. Neurosurg. Psychiatry 46: 599610, 1983. Reprints: Prof. N.H. Wadia, Ben Nevis, B. Desai Road, Bombay 400 036, India. 63. Katiyar, B.C., Misra, S., Singh, RB., et al.: Adult polio-like syndrome following enterovirus 70 conjunctivitis (natural history of the disease). Acta Neurol. Scand. 67: 263-274, 1983. Reprints: B.C. Katiyar, M.D., A-2, New Medical Enclave, Division of Med. Neurology, Institute of Med. Sciences, Banaras Hindu University, Varanasi-221 005, India. 64. Morax, S., Pascal, D., and Barraco, P.: Signfication du syndrome V avec double 'up shoot.' Insuffisance des deux grands obliques au cours des malformations cranio-faciales. J. Fram;. Ophthalmol. 6: 295-310, 1983. Reprints: S. Morax, Fondation Rothschild, 24, rue Manin, F-75019 Paris, France. 65. Schmidt, D.: Prognosis of ocular myasthenia in childhood. Neuro-ophthalmology 3: 117- 124,1983. Reprints: Dieter Schmidt, Universitatsaugenklinik, Killianstrasse 5 D-7800 Freiburg, Federal Republic of Germany. 66. Canal, N., and Franceschi, M.: Myasthenic crisis precipitated by iothalamic acid. (Letter.) Lancet 1: 1288,1983. 67. Valesini, G., Pastore, R, De Berardinis, P.G., et al.: Appearance of anti-acetylcholine receptor antibodies coincident with onset of myasthenic weakness in patient with systemic lupus erythematosus. (Letter.) Lancet 1: 831,1983. 68. Lundh, H., Nilsson, 0., and Rosen, I.: Novel drug of choice in Eaton-Lambert syndrome. (Letter.) J. Neural. Neurosurg. Psychiatry 46: 684-685,1983. 69. Heath, R, Schwartz, M.S., Brown, I.RF., et al.: Carbonic anhydrase III in neuromuscular disorders. J. Neurol. Sci. 59: 383-388, 1983. Reprints: Robert Heath, Department of Child Health and Chemical Pathology, St. George's Hospital Medical School, London SW17 ORE, England. 70. Coquet, M., Vallat, J.M., Vital, c., et al.: Nuclear inclusions in oculopharyngeal dystrophy. An ultrastructural study of six cases. J. Neurol. Sci. 60: 151156, 1983. Reprints: Dr. M. Coquet, Centre de Microscopie Electronique, Universite de Bordeaux II, 146, rue Leo Saignat, F-33076 Bordeaux Dedex, France. 71. Leger, J.M., Fardeau, M., and Doumith, R: Ophthalmoplegie externe progressive et thyroidite de Hashimoto. Rev. Neurol. 139: 305-306, 1983. Reprints: J. M. Leger, Service de Neurologie, Hopital de la Salpetriere, 47, Bd de I'Hopital, F-75651 Paris Cedex 13, France. 72. Van Der Wiel, H.L., and Van Gijn, J.: Homer's syndrome-Criteria for oculosympathetic denervation. J. Neural. Sci. 56: 293-298, 1982. 73. Van Der Wiel, H.L., and Van Gijn, J.: Localization of Homer's syndrome. Use and limitations of the hydroxyamphetamine test. J. Neurol. Sci. 59: 229235, 1983. Reprints: H.L. van der Wiel, Department of Neurology, University Hospital Rotterdam (Dijkzigt), Rotterdam, The Netherlands. 74. Safran, AB., Petrovic, D., Roth, A, and Assimacopoulos, A: Les limites de l'anisocorie physiologique. Bull. Mem. Soc. Fr. Ophtalmol. (In press.) 207 Recent Literature: Part II 75. Nielsen, P.J.: The central corneal thickness in patients with Horner's syndrome. Acta Ophthalmol. 61: 467-473, 19~3. Reprints: Per Julius Nielsen, ~jenafdeling J, Arhus Kommune Hospital, 8000 Arhus, Denmark. 76. Zadunaisky, J.A, Lande, M.A., Chalfie, M., and Neufeld, AM.: Ion pump in the cornea and their stimulation by epinephrine and cyclic AMP. Exp. Eye Res. 15: 577-584, 1973. 77. Walkenbach, R.J., and Le Grand, R.D.: Inhibition of adenyl cyclase activity in the corneal epithelium by antinflammatory steroids. Exp. Eye Res. 34: 161168, 1982. 78. Smith, S.A., and Smith, S.E.: Evidence for a neuropathic aetiology in the small pupil of diabetes mellitus. Br. J. Ophthalmol. 67: 89-93, 1983. Reprints: Dr. S.A Smith, Department of Pharmacology, St Thomas's Hospital Medical School, London SE1 7EH, England. 79. Smith, SA, and Smith, S.E.: Reduced pupillary light reflexes in diabetic autonomic neuropathy. Diabetologia 24: 330-332, 1983. Reprints: see above. 208 80. Sun, F., and Stark, L.: Pupillary escape intensified by large pupillary size. Vision Res. 23: 611-615, 1983. Reprints: Lawrence Stark, Department of Physiological Optics and Engineering Sciences, Univ. of California, Berkeley, California 94720. 81. Breen, L.A, Burde, R.M., and Loewy, AD.: Brain stem connections to the Edinger-Westphal nucleus of the cat: A retrograde tracer study. Brain Res. 261: 303-306, 1983. Reprints: Ronald M. Burde, Department of Ophthalmology-Box 8096, 660 Street, Euclid Avenue, St Louis, Missouri 63110. 82. Bracher, D., Biitikofer, R., Garrett, F., and Ludin, H.P.: Changes in corneal DC-potentials associated with changes in pupillary diameter. Graefe's Arch. Chir. Exp. Ophthalmol. 220: 122-129, 1983. Reprints: D. Bracher, M.D., Weltpoststrasse 16, CH3015 Berne, Switzerland. 83. Mekki, Q.A, Hassan, S.M., and Turner, P.: Bromocriptine lowers intraocular pressure without affecting blood pressure. Lancet 1: 1250-1251, 1983. Reprints: P. Turner, Department of Clinical Pharmacology. St Bartholomew's Hospital Medical College, London EClA 7BE, England. Journal of Clinical Neuro-ophthalmology |